Surgery

First Edition 2021

Dr Thomas Watchman
MbChB (hons) BSc (Psychology) MSc (Medical Education) MRCGP
MRCP (UK) DCH DRCOG FHEA
General Practitioner (GP)
Manchester, United Kingdom

Copyright Zero to Finals 2021. All rights reserved.

No part of this book can be reproduced or transmitted in any way

without prior permission from Dr Thomas Watchman at Zero to Finals.
Email: tom@zerotofinals.com.
 Acknowledgements
I am incredibly grateful to the following people for their help with
proofreading, fact-checking and making suggestions to improve this book:
Adam Louani - Final-Year Medical Student
Amy Cooke - Final-Year Medical Student
Beth Jones - Fourth-Year Medical Student
Bryony Patrick - Anaesthetics Specialty Registrar
Carolyn Cairns - Final-Year Medical Student
Charles McVickers - Foundation Year 1 Doctor
Christie Mellor - Foundation Year 2 Doctor
David Perry - Anaesthetics Specialty Registrar
Elin Wynne - Final-Year Medical Student
Isabelle Sumner - Final-Year Medical Student
Joel Lambert - Surgical Specialty Registrar
Melina Kellermann - Final-Year Medical Student
Merili Pugh - Doctor and Loving Wife
Rachel Grant - Anaesthetics Core Trainee Year 2
Rhiannon Jo Berkeley - Student Physician Associate
Rory Scott-Wilson - Final-Year Medical Student
Stephanie McDonald - Third-Year Medical Student
Thomas Dale MacLaine - Final-Year Medical Student
 Disclaimer
It is essential to use Zero to Finals for its intended purpose: as a
resource to help students and health professionals prepare for exams. It
is not intended and should not be used as a resource, guideline or
reference for clinical practice or decision making. It is certainly not
designed for patients looking for medical information or advice. There are
plenty of excellent resources for the above, not least your senior
colleagues, guidelines, research papers or personal doctor. By using the
Zero to Finals resources, you agree that Zero to Finals and those involved
in creating the resources are not responsible for any actions you take or
do not take based on the information provided.

The skills needed to practice medicine, surgery, and other healthcare

roles are broad and complex. There is a limit to what you can learn from
one resource. You need to develop clinical judgment, experience and
context-specific decision-making skills that cannot be learned in one
place. It is crucial to develop your ability to find the best resources and
data to guide your clinical practice. Attend clinical placements, listen to
your tutors and supervisors and ask for help. Use a variety of up to date
guidelines, protocols, research and other resources when preparing for
exams and treating patients. Nothing is entirely reliable and accurate.

I employ extensive effort to ensure the information is accurate and up

to date. However, it is not perfect, and research, guidelines and best
practice are constantly changing. There will be errors despite my best
efforts. I would be very grateful if you point them out when you find them.
Do not accept anything as fact without questioning it.

The Zero to Finals books are supplemented by the resources at

zerotofinals.com. There is a webpage on each topic with illustrations,
diagrams, podcasts and videos that tackle the problem from every angle.

To get in touch or report an error, please email me at

tom@zerotofinals.com.
 For Joan and Peter
Two very important and special people in my life
 Contents
General Surgery
Urology
Vascular Surgery
Cardiothoracic Surgery
Breast Surgery
Ear, Nose and Throat
Orthopaedics
Anaesthetics
 General Surgery
Basics of Surgery
Pre-Operative Care
Consent and Capacity
Post-Operative Care
Intravenous Fluids
Acute Abdomen
Appendicitis
Bowel Obstruction
Ileus
Volvulus
Hernias
Haemorrhoids
Diverticular Disease
Mesenteric Ischaemia
Bowel Cancer
Stomas
Gallstones
Acute Cholecystitis
Acute Cholangitis
Cholangiocarcinoma
Pancreatic Cancer
Pancreatitis
Liver Transplant
 Basics of Surgery
There are a number of basic definitions and concepts that are worth
learning before starting a surgical rotation or learning about surgical
topics.

Prefixes

Prefixes generally refer to an area of the body:

• Laparo- refers to the abdomen (e.g., laparotomy - open surgery on
the abdomen)
• Thoraco- refers to the chest (e.g., thoracotomy - open surgery on
the chest)
• Colo- refers to the colon (e.g., colectomy - removal of the colon)
• Cysto- refers to the bladder (e.g., cystoscopy - putting a
endoscopic camera into the bladder)
• Gastro- refers to the stomach (e.g., gastroscopy - putting a
endoscopic camera into the stomach)
• Mammo- refers to the breast (e.g., mammogram - imaging of the
breast)
• Masto- refers to the breast (e.g., mastectomy - removal of the
breast)
• Myo- refers to muscle tissue (e.g., myotomy - where the muscle
tissue is cut open)
• Nephro- refers to the kidneys (e.g., nephrectomy - removal of a
kidney)
• Pneumo- refers to the lungs (e.g., pneumonectomy - removal of a
lung)
• Orchid- refers to the testes (e.g., orchidectomy - removal of a
testicle)
• Rhino- refers to nose (e.g., rhinoplasty - changing the shape of the
nose)
• Lobo- refers to a lobe of an organ (e.g., lobectomy - removal of a
lobe of the lung)

Suffixes
 Suffixes generally refer to what is happening with a particular area of
the body:
• -otomy refers to surgically cutting open (e.g., laparotomy - open
surgery on the abdomen)
• -oscopy refers to viewing with a scope and keyhole surgery (e.g.,
colonoscopy, laparoscopy and thoracoscopy)
• -ectomy refers to removal (e.g., tonsillectomy - removal of the
tonsils)
• -plasty refers to changing the shape (e.g., rhinoplasty - changing
the shape of the nose)
• -pexy refers to fixing something in place (e.g., orchidopexy -
surgery to fix a testicle in the correct place)
• -centesis refers to puncturing with a needle (e.g., thoracocentesis -
removing air or fluid from the pleural space)
• -ostomy refers to creating a new opening (e.g., colostomy -
opening the colon onto the surface of the abdomen)
• -itis refers to inflammation (e.g., prostatitis - inflammation of the
prostate)
• -algia refers to pain (e.g., mastalgia - breast pain)
• -gram refers to recording or imaging (e.g., electrocardiogram or
echocardiogram)

More Definitions

There are some further key definitions that are worth becoming
familiar with:
• Adhesions: scar-like tissue inside the body that bind surfaces
together
• Fistula: an abnormal connection between two epithelial surfaces
• Tenesmus: the sensation of needing to open the bowels without
being able to produce stools (often with pain)

TOM TIP: I have randomly been asked to define certain terms by

surgeons whilst on ward rounds and in clinics. Having key
definitions ready to recite can make you look clever. I particularly
recommend learning the definition of a fistula as “an abnormal
connection between two epithelial surfaces”, as I have been asked
this on several occasions.
Specific Operations

Operations with unique names to be familiar with include:

• Hemicolectomy - removing a portion of the large intestine (colon)
• Hartmann’s procedure (proctosigmoidectomy) - removal of the
rectosigmoid colon with closure of the anorectal stump and
formation of a colostomy
• Anterior resection - removal of the rectum
• Whipple procedure (pancreaticoduodenectomy) - removal of the
head of the pancreas, duodenum, gallbladder and bile duct

Incisions and Scars

Upper abdominal surgery:

• Kocher incision - open cholecystectomy
• Chevron / rooftop incision - liver transplant, Whipple procedure,
pancreatic surgery or upper GI surgery
• Mercedes Benz incision - liver transplant

Abdominal organ surgery:

• Midline incision - for a general laparotomy, allows good access to
abdominal organs
• Paramedian incision - laparotomy (midline usually used instead)
• Hockey-stick incision - renal transplant

Appendix surgery:
• Battle incision (paramedian) - open appendicectomy
• Gridiron incision / McBurney incision (oblique) - open
appendicectomy
• Lanz incision (transverse) - open appendicectomy
• Rutherford Morrison incision (extended version of gridiron) -
open appendicectomy and colectomy

Caesarean section:
• Pfannenstiel incision - curved incision two fingers width above
the pubic symphysis
• Joel-Cohen incision - straight incision that is slightly higher (this is
the recommended incision)
 Laparoscopic surgery involves several 5-10mm incisions to allow the
cameras and instruments to be inserted into the abdomen via port sites.
A site just above or below the umbilicus is usually used as a port site.

Diathermy

Diathermy uses a high-frequency electrical current to cut through

tissues or to cauterise small blood vessels to stop bleeding. It causes
targeted localised burning of tissues. It is useful for making targeted
incisions with minimal bleeding.

Monopolar diathermy can be used in small or large operations. A

diathermy probe is used by the surgeon and produces an electrical
current. A grounding plate or grounding pad is placed under the leg or
buttock. A circuit is formed in the patient's body, where the electricity goes
in through the diathermy instrument and out through the grounding plate.
At the site where the electrical energy is applied, it causes localised
burning and tissue damage. As the electrical current spreads through the
body to the grounding plate, which has a large surface area, it becomes
less intense and does not cause damage to other tissues.

Bipolar diathermy involves an instrument with two electrodes. A

current passes between the electrodes affecting the tissues in this area.
This is often used in microsurgery, for example, operations on the hand. It
is also helpful to prevent the electrical current from passing through the
rest of the body, for example in patients with a pacemaker.

Sutures

There are all sorts of sutures available, which suit different purposes
and are used on different tissues. The two main categories of suture are
absorbable and non-absorbable.

Absorbable sutures are slowly absorbed and disappear over time.

Examples include Vicryl and Monocryl. They are used for tissues that
will heal well and remain sealed after the suture has been absorbed, such
as within the abdominal cavity and closing the tissues beneath the
epidermis.

Non-absorbable sutures remain in place for a long time and provide

support to the tissues. Examples include silk, nylon and polypropylene.
Examples of how they might be used include:
• Closing the skin by interrupted or mattress suture technique (see
below), removed later once the skin has healed
• Fixing drains in place, removed later with the drain
• Connective tissues that heal slowly, such as repairing tendons

The surface layer or skin (the epidermis) can be closed with various
techniques:
• Staples are a rapid way of closing the skin and need removing
later
• Interrupted sutures involve a series of individual knots
• Mattress sutures involve a series of individual sutures that each
go from one side of the wound, under and out the other side, then
back under again to the original side
• Continuous sutures involve a single suture that goes in and out
along the wound in a spiral shape
• Subcuticular sutures involve using a single absorbable suture
side to side just below the skin to pull the skin edges together
 Drains

Drains are tubes left inside body cavities to allow air and fluid to drain
away, usually into a bottle beside the bed. This prevents air, blood, pus or
other fluids from collecting within a space. They are often secured and left
in place after an operation. They are removed when they stop draining (or
are draining very little) and it is assumed whatever has been drained will
no longer build up if the drain is removed.

Chest drains provide a method of removing air and fluid from the
pleural space. The external end of the drain is placed underwater,
creating a seal to prevent air from flowing back through the drain into the
chest. Air can exit the chest cavity and bubble through the water, but the
water prevents air from re-entering the drain and chest. It works like a
one-way valve. During normal respiration the water in the drain will rise
and fall due to changes in pressure in the chest (described as
“swinging”).
 WHO Surgical Safety Checklist

The WHO Surgical Safety Checklist (2009) is carried out for each
operation. The aim is to reduce the risk of human error. The checklist is
completed at 3 stages:
• Before the induction of anaesthesia
• Before the first skin incision
• Before the patient leaves theatre

It involves multiple members of the team (e.g., theatre nurse,

anaesthetic nurse, operating department practitioner, anaesthetist and
surgeon) checking essential factors, such as:
• Introductions of all team members
• Patient identity
• Allergies
• Operation
• Risk of bleeding
• Anticipated critical events
• Counting the number of swabs and needles to ensure nothing is left
inside the patient
 Pre-Operative Care
Before going to theatre for an operation, there are a number of things
that need to be addressed:
• Pre-operative assessment (pre-op)
• Consent
• Bloods (including group and save / crossmatch)
• Fasting
• Medication changes
• Venous thromboembolism assessment

Pre-Operative Assessment

Patients need to be assessed to determine if they are fit to undergo

the specific operation. This involves exploring their co-morbidities, risk
from anaesthesia, their frailty status and their cardiorespiratory fitness.

They require a full history of:

• Past medical problems
• Previous surgery
• Previous adverse responses to anaesthesia
• Medications
• Allergies
• Smoking
• Alcohol use

Pregnancy needs to be considered in women of childbearing age.

Consider asking about a family history of sickle cell disease. A general
examination is performed to look for cardiovascular and respiratory
disease.

Patients who may be malnourished (e.g., BMI under 18.5 or

significant unintentional weight loss) may need input from a dietician and
additional nutritional support before surgery and during admission.

ASA Grade
 The American Society of Anesthesiologists (ASA) grading system
classifies the physical status of the patient for anaesthesia. Patients are
given a grade to describe their current fitness prior to undergoing
anaesthesia/surgery:
• ASA I - normal healthy patient
• ASA II - mild systemic disease
• ASA III - severe systemic disease
• ASA IV - severe systemic disease that constantly threatens life
• ASA V - “moribund” and expected to die without the operation
• ASA VI - declared brain-dead and undergoing an organ donation
operation
• E - this is used for emergency operations

Pre-Operative Investigations

NICE guidelines (2016) are available outlining recommendations for

routine preoperative tests for elective surgery, based on individual patient
factors and the size of the operation. There will also be local guidelines. If
in doubt, get advice from an anaesthetist.

Investigations may be required prior to surgery depending on the co-

morbidities:
• ECG if there is known or possible cardiovascular disease or over 65
years
• Echocardiogram if there are heart murmurs, cardiac symptoms or
heart failure
• Lung function tests may be required if there is known or possible
respiratory disease
• Arterial blood gas testing may be required if there is known or
possible respiratory disease
• HbA1C (within the last 3 months) for people with known diabetes
• U&Es for patients at risk of developing an acute kidney injury or
electrolyte abnormalities (e.g., taking diuretics)
• FBC may be required if there is possible anaemia, cardiovascular
or kidney disease
• Clotting testing may be required if there is known or possible liver
disease
 Group and save refers to sending off a sample of the patient’s blood
to establish their blood group. The sample is saved in case they require
blood to be matched to them for a blood transfusion. A group and save is
done routinely where there is a lower probability that they will require
blood products. No blood is assigned to the patient at this stage. A group
and save sample will only be valid for a certain period (e.g., 7 days)
depending on the local trust policy, after which a repeat sample is
required.

Crossmatching involves the process of actually taking a unit or more

of blood off the shelf and assigning it to the patient in case they need it
quickly. This is done where there is a higher probability that they will
require blood products, so that the blood is ready to go if required.

MRSA screening is routinely performed on all patients being admitted

to hospital. This is usually arranged automatically by the nursing staff, so
you don’t need to think about this.

Fasting Before Surgery

Patients undergo ‘fasting’ before surgery to ensure they have an

empty stomach for the duration of their operation. The aim is to reduce
the risk of reflux of food around the time of surgery (particularly during
intubation and extubation), which subsequently can result in the patient
aspirating their stomach contents into their lungs.

Fasting for an operation typically involves:

• 6 hours of no food or feeds before the operation
• 2 hours of no clear fluids (fully “nil by mouth”)

TOM TIP: When you assess an acutely unwell surgical patient,

always consider whether there is any possibility they require
emergency surgery. Acutely unwell surgical patients that potentially
require emergency surgery are made nil by mouth and given
maintenance IV fluids. Allowing them to eat and drink could have
significant consequences if they need emergency surgery, and the
anaesthetist and senior surgeon won’t be happy. This decision will
often be reversed on the post-take ward round if the consultant or
senior surgeon decides they are unlikely to need to go to theatre.
 Specific Medications

Anticoagulants need to be stopped before major surgery. The INR

can be monitored in patients on warfarin to ensure it returns to normal
before the operation. Warfarin can be rapidly reversed with vitamin K in
acute scenarios. Treatment dose low molecular weight heparin or an
unfractionated heparin infusion may be used to bridge the gap
between stopping warfarin and surgery in higher-risk patients (e.g.,
mechanical heart valves or recent VTE), and stopped shortly before
surgery depending on the risk of bleeding and thrombosis. DOACs (e.g.,
apixaban, rivaroxaban or dabigatran) are stopped 24-72 hours before
surgery depending on the half-life, procedure and kidney function.

Oestrogen-containing contraception (e.g., the combined

contraceptive pill) or hormone replacement therapy (e.g., in
perimenopausal women) need to be stopped 4 weeks before surgery to
reduce the risk of venous thromboembolism (NICE guidelines 2010).

Long-term corticosteroids, equivalent to more than 5mg of oral

prednisolone, require additional management around the time of surgery.
Surgery adds additional stress to the body, which normally increases
steroid production. In patients on long-term steroids, there is adrenal
suppression that prevents them from creating the extra steroids required
to deal with this stress. Management involves:
• Additional IV hydrocortisone at induction and for the immediate
postoperative period (e.g., first 24 hours)
• Doubling of their normal dose once they are eating and drinking
for 24 - 72 hours depending on the operation

Diabetes

The stress of surgery increases blood sugar levels. However, fasting

may lead to hypoglycaemia. In general, the risk of hypoglycaemia is
greater than hyperglycaemia.

Certain oral anti-diabetic medications may need to be adjusted or

omitted around surgery:
 • Sulfonylureas (e.g., gliclazide) can cause hypoglycaemia and
are omitted until the patient is eating and drinking
• Metformin is associated with lactic acidosis, particularly in
patients with renal impairment
• SGLT2 inhibitors (e.g., dapagliflozin) can cause diabetic
ketoacidosis in dehydrated or acutely unwell patients

In patients on insulin going for surgery (follow the local policy):

• Continue a lower dose (BNF recommends 80%) of their long-acting
insulin
• Stop short-acting insulin whilst fasting or not eating, until eating and
drinking again
• Start a variable rate insulin infusion alongside a glucose, sodium
chloride and potassium infusion (“sliding-scale”) to carefully control
their insulin, glucose and potassium balance

VTE Prophylaxis

Every patient admitted to hospital should be assessed for their risk

of venous thromboembolism (VTE). Surgery, particularly where the
patient is likely to be immobilised (e.g., orthopaedic surgery), significantly
increases the risk of venous thromboembolism. There are local and
national policies on reducing the risk that involve:
• Low molecular weight heparin (LMWH) such as enoxaparin
• DOACs (e.g., apixaban or rivaroxaban) may be used as an
alternative to LMWH
• Intermittent pneumatic compression (inflating cuffs around the
legs)
• Anti-embolic compression stockings
 Consent and Capacity
Patients should make informed decisions about their treatment. This
means they need to be given information in a way that allows them to
adequately understand the purpose, benefits and risks of treatment to
make a decision.

Patients are allowed to make unwise decisions provided they fully

understand the decision and have capacity. Making an unwise decision
does not mean they lack capacity.

It is worth noting that you do not have to provide treatment requested

by a patient if you do not think it is appropriate (e.g., requesting
inappropriate opioid medications or unwarranted surgery). They have the
right to a second opinion.

TOM TIP: Your ability to help patients make informed decisions is

tested with every OSCE explanation station. The key to scoring the
highest marks is to tailor your explanation to the individual patient’s
current understanding, ideas, concerns and expectations. This
means spending most of the time listening and asking questions,
rather than telling the patient information. Check what the patient
currently knows and then fill in the gaps using small chunks of
information. Offer the patient options with an explanation of each
option (even if the choice seems obvious), rather than telling them
what to do. This includes offering the option to do nothing, even if
this results in poor outcomes. OSCE explanation stations are often
set up with a particular patient agenda, such as wanting to avoid a
certain treatment, and if you don’t ask, you won’t identify this and
may do poorly on that station.

Capacity

The legal framework around capacity and making decisions for

patients that lack capacity is the Mental Capacity Act (2005).
 All adults are assumed to have capacity. Where there is a doubt about
a patient’s capacity, it is assessed based on each individual decision. For
example, a patient with cognitive impairment may be able to make a
decision to consent to someone taking their blood, but not to consent to
major surgery with potentially-life threatening risks.

A person’s capacity to make a decision may fluctuate, meaning on a

“good day” they can make a decision. The decision should be delayed if
safe to do so and they are likely to be able to make it for themselves at a
later time.

There are four criteria a patient needs to meet to demonstrate

capacity to make a decision:
• Understand the decision
• Retain the information long enough to make the decision
• Weigh up the pros and cons
• Communicate their decision

TOM TIP: It is worth committing these four criteria for capacity to

memory. I have lost count of the number of times I have been asked
for or needed to apply these criteria. They also frequently feature in
exam questions, both in written exams and OSCEs.

Treatment decisions for patients that lack capacity are taken in their
best interest, taking into account their individual wishes and values.
Significant decisions can be made at a best interest meeting, with a
multidisciplinary group that includes professions (e.g., doctors, nurses
and social workers), the patient’s next of kin and other relevant people,
such as close friends or family members.

Lasting power of attorney (LPA) is when a person legally nominates

a person of their choice to make decisions on their behalf if they lack
mental capacity. LPA only comes into effect if the patient lacks the
capacity to decide for themselves. It does not give the person with LPA
control over a decision if they can still make that decision for themselves.

Deprivation of liberty safeguards (DoLS) involves an application

made by a hospital or care home for patients who lack capacity to allow
them to provide care and treatment. Whilst in hospital, or a care home,
the patient is under control and is not able to leave. This means they are
“deprived of their liberty” and require a legal framework to protect them.

Gaining Consent

Gaining consent involves the full process of providing information to

allow the patient to make an informed decision. How formal this process
is varies depending on the intervention. For example, to examine a
patient’s hands, informed consent is simply implied by them allowing you
to inspect their hands. Starting a patient on a medication generally only
requires an explanation and verbal consent. Gaining consent for surgery
is a much more rigorous process and requires a signed consent form.

The person that gains consent for a surgical procedure should be

involved with that procedure and have a sufficient understanding of it,
including the intended benefits, risks and the possible complications.
These should be explained to the patient in a way they can understand,
so that they can make an informed decision. The alternative options
should also be discussed.

A copy of the consent form is given to the patient and another is filed
in the notes. Patients can withdraw their consent at any time prior to the
procedure, provided they retain capacity to change their mind.

Consent Forms

There are four different consent forms that can be used in different
scenarios that you may come across in the NHS:
• Content Form 1: Patient consenting to a procedure
• Consent Form 2: Parental consent on behalf of a child
• Consent Form 3: Where the patient won’t have their
consciousness impaired (e.g., a breast biopsy)
• Consent Form 4: Where the patient lacks capacity
 Post-Operative Care
Immediately after the operation, the patient will go to the recovery
room to be monitored closely whilst they regain consciousness. Once
they are conscious and stable, they can return to the ward. Patients may
be transferred to HDU or ICU depending on their condition and the
monitoring requirements post-operatively.

Enhanced Recovery

Enhanced recovery aims to get patients back to their pre-operative

condition as quickly as possible, by encouraging independence, early
mobility and appropriate diet. There are increased nutritional
requirements after the physiological stress of surgery, so sufficient
calories are very important. The aim is to discharge as soon as possible.
This leads to better outcomes for the patient.

The principles of enhanced recovery are:

• Good preparation for surgery (e.g., healthy diet and exercise)
• Minimally invasive surgery (keyhole or local anaesthetic where
possible)
• Adequate analgesia
• Good nutritional support around surgery
• Early return to oral diet and fluid intake
• Early mobilisation
• Avoiding drains and NG tubes where possible, as well as early
catheter removal
• Early discharge

Analgesia

Adequate analgesia in the post-operative period is important to

encourage the patient to:
• Mobilise
• Ventilate their lungs fully (reducing the risk of chest infections and
atelectasis)
 • Have an adequate oral intake

Analgesia is usually started in theatre by the anaesthetist, with regular

paracetamol, NSAIDs and opiates if required (e.g., regular modified-
release oxycodone with immediate-release oxycodone as required for
breakthrough pain). The surgeon may put local anaesthetic into the
wound to help with the initial pain after the procedure. Analgesia should
be reduced and stopped as symptoms improve. There is more detail on
analgesia in the anaesthetics section.

Non-steroidal anti-inflammatory drugs (NSAIDs) such as

ibuprofen, naproxen and diclofenac may be inappropriate or
contraindicated in patients with:

• Asthma
• Renal impairment
• Heart disease
• Stomach ulcers

Patient Controlled Analgesia

Patient-controlled analgesia (PCA) involves an intravenous infusion

of a strong opiate (e.g., morphine, oxycodone or fentanyl) attached to a
patient-controlled pump. This involves the patient pressing a button as
pain starts to develop, for example during a contraction in labour, to
administer a bolus of this short-acting opiate medication. The button will
stop responding for a set time after administering a bolus to prevent over-
use. Only the patient should press the button (not a nurse or doctor).

Patient-controlled analgesia requires careful monitoring. There needs

to be input from an anaesthetist, and facilities in place if adverse events
occur. This includes access to naloxone for respiratory depression,
antiemetics for nausea, and atropine for bradycardia. The anaesthetist
may prescribe background opiates (e.g., patches) in addition to a PCA.
Other “as required” opiates should be avoided whilst a PCA is in use. The
machine is locked to prevent tampering.

Post-Operative Nausea and Vomiting

 Nausea and vomiting are common in the 24 hours after an operation
and is called post-operative nausea and vomiting (PONV). There are
many causes, including the surgical procedure, anaesthetic, pain and
opiates.

Risk factors for post-operative nausea and vomiting are:

• Female
• History of motion sickness or previous PONV
• Non-smoker
• Use of postoperative opiates
• Younger age
• Use of volatile anaesthetics

Antiemetics are often given at the end of the procedure by the

anaesthetist to prevent post-operative nausea and vomiting. Common
options for prophylaxis given at the end of the operation are:
• Ondansetron (5HT3 receptor antagonist) - avoided in patients at
risk of prolonged QT interval
• Dexamethasone (corticosteroid) - caution in diabetic or
immunocompromised patients
• Cyclizine (histamine (H1) receptor antagonist) – caution with heart
failure and elderly patients

Examples of “rescue” antiemetics used in the post-operative period if

nausea or vomiting occur are:
• Ondansetron (5HT3 receptor antagonist) - avoid in patients at risk
of prolonged QT interval
• Prochlorperazine (dopamine (D2) receptor antagonist) - avoid in
patients with Parkinson’s disease
• Cyclizine (histamine (H1) receptor antagonist) - caution with heart
failure and elderly patients

Some local guidelines also refer to the P6 acupuncture point on the

inner wrist. There is evidence that pressure to this area can reduce
nausea.

Tubes
 Post-operative patients may have a catheter, drains or nasogastric
tube, and these will be monitored and removed when appropriate:
• Drains are usually removed once they are draining minimal or no
blood or fluid
• Nasogastric tubes are removed when they are no longer required
for intake or drainage of gas or fluid
• Catheters are removed when the patient can mobilise to the toilet

Removal of a catheter is called a trial without catheter (TWOC). It is

called this as there is a risk the patient will find it difficult to pass urine
normally and go into urinary retention, and the catheter may need to be
reinserted for a period before removal can be tried again. This is quite
common, more so in male patients.

Nutritional Support

Good nutrition is important for healthy wound healing and overall

recovery from surgery. A dietician may be involved.

Where possible, patients should get their nutrition via their

gastrointestinal tract. Having nutrition via the gastrointestinal tract is
called enteral feeding. This could be by:
• Mouth
• NG tube
• Percutaneous endoscopic gastrostomy (PEG) - a tube from the
surface of the abdomen to the stomach

Total parenteral nutrition (TPN) involves meeting the full ongoing

nutritional requirements of the patient using an intravenous infusion of a
solution of carbohydrates, fats, proteins, vitamins and minerals. This is
used where it is not possible to use the gastrointestinal tract for nutrition.
It is prescribed under the guidance of a dietician. TPN is very irritant to
veins and can cause thrombophlebitis, so is normally given through a
central line rather than a peripheral cannula.

Post-Operative Complications

Patients are monitored for a long list of complications that can occur in
the post-operative period:
 • Anaemia
• Atelectasis is where a portion of the lung collapses due to under-
ventilation
• Infections (e.g., chest, urinary tract or wound site)
• Wound dehiscence is where there is separation of the surgical
wound, particularly after abdominal surgery
• Ileus is where peristalsis in the bowel is reduced (typically after
abdominal surgery)
• Haemorrhage with bleeding into a drain, inside the body creating a
haematoma or from the wound
• Deep vein thrombosis and pulmonary embolism
• Shock due to hypovolaemia (blood loss), sepsis or heart failure
• Arrhythmias (e.g., atrial fibrillation)
• Acute coronary syndrome (myocardial infarction) and
cerebrovascular accident (stroke)
• Acute kidney injury
• Urinary retention requiring catheterisation
• Delirium refers to fluctuating confusion and is more common in
elderly and frail patients

Anaemia

A post-op full blood count (FBC) is used to measure the

haemoglobin (Hb).

Treatment of anaemia is based on individual factors and preferences,

alongside local guidelines. As a rough guide (local policies will vary):
• Hb under 100 g/l – start oral iron (e.g., ferrous sulphate 200mg three
times daily for three months)
• Hb under 70-80 g/l – blood transfusion in addition to oral iron

Patients with symptoms of anaemia or underlying cardiovascular or

respiratory disease may need a transfusion with higher haemoglobin
levels.

It is worth noting that Jehovah’s Witnesses may refuse blood

transfusions. They often have a written advanced directive to state that
even in an emergency scenario where they lose capacity, blood
transfusions are prohibited. Provided they have capacity and are making
an informed decision, they have the right to autonomy. Measures are
taken before surgery to optimise any anaemia, and careful steps are
taken during surgery to minimise blood loss.
 Intravenous Fluids
Prescribing IV fluids is a common task within surgery, as well as
practically all inpatient medical jobs. The information here is designed to
help you understand the concepts for your exams. When prescribing
fluids, follow national and local guidelines and consult seniors if you are in
doubt. You should not use this as a guide to prescribing.

Fluid Compartments

Fluid within the body is distributed across different “spaces”. Water,

electrolytes, glucose, and proteins constantly move between the fluid
spaces to find balance and carry out functions. There are two categories
of fluid spaces in the body:
• Intracellular space (inside the cells) - 2/3 of the total body fluids
• Extracellular space (outside the cells) - 1/3 of the total body fluids

The extracellular space is subdivided into three spaces:

• Intravascular space (inside blood vessels) - 20% of the
extracellular fluid
• Interstitial space - the functional tissue space between and
around cells - 80% of the extracellular fluid
• The “third space” - the “third" extracellular space

The “third space” refers to areas of the body that do not normally
contain fluid and where fluid collection is not functional or desirable. This
includes areas such as the:
• Peritoneal cavity (forming ascites)
• Pleural cavity (forming pleural effusions)
• Pericardial cavity (forming a pericardial effusion)
• Joints (forming joint effusions)

The third space also refers to the non-functional and excessive

collection of fluid in the interstitial space, resulting in oedema.
 Third-spacing refers to fluid shifting into the non-functional third
space. Often this refers to the development of oedema, as excessive
fluid moves into the interstitial space. It also refers to the development of
ascites, effusions or other non-functional fluid collections within the body.
When fluid moves into a non-functional space, this may come at the
expense of the intravascular space, resulting in hypotension and
reduced perfusion of the body tissues.

Fluid Balance

Monitoring fluid balance is common in hospitals and involves

recording all the fluid intake and all the fluid output on a fluid balance
chart. It is particularly helpful in acutely unwell patients (e.g., sepsis),
surgical patients and those with fluid balance issues, such as diarrhoea
and vomiting, heart failure or kidney disease.

Some patients require a specific fluid restriction (e.g., heart failure,

renal failure or hyponatraemia), meaning the total fluid intake is capped
(e.g., 1.5 litres per day). Extra caution needs to be taken in these patients
to calculate their input accurately. Seek advice from seniors when in
doubt.

Sources of fluid intake include:

• Oral fluids
• Nasogastric or PEG feeds
• Intravenous fluids (including IV medications)
• Total parenteral nutrition

Sources of fluid output include:

• Urine output
• Bowel or stoma output (particularly diarrhoea)
• Vomit or stomach aspiration
• Drain output
• Bleeding
• Sweating

Insensible fluid loss is a term that refers to fluid output that is difficult
to measure, such as through respiration (breathed out), in stools, through
burns and from sweat. This varies a lot and can only be estimated. It may
account for a large volume (over 800mls per day) in patients with
significant diarrhoea, high stoma output or sweating with a high fever.

TOM TIP: The fluid balance chart helps assess whether the input
matches the output to guide the prescription of IV fluids. When
prescribing fluids, always look at the fluid balance chart from that
day and the previous day to see whether they have a positive or
negative fluid balance. If they have a negative fluid balance, they
may require additional IV fluids, and if they have a positive fluid
balance, they may require less IV fluid. Sometimes a bit of
scepticism needs to be applied, as the chart might not be
completely accurate. The patient may be visiting the toilet or
sneaking large drinks without informing the nurse, or there may be
omissions from the chart, particularly when the ward is very busy.

Assessing Fluid Status

Having an abnormally low amount of extracellular fluid can be

referred to as hypovolaemia or volume depletion. A negative fluid
balance is when more fluid is leaving the body than coming in, leading to
hypovolaemia.

Having an abnormally high amount of extracellular fluid in the body

can be referred to as hypervolaemia or fluid overload. A positive fluid
balance is when more fluid is entering the body than being removed and
will lead to hypervolaemia.

Signs of hypovolaemia (inadequate fluid) are:

• Hypotension (systolic < 100 mmHg)
• Tachycardia (heart rate > 90)
• Capillary refill time > 2 seconds
• Cold peripheries
• Raised respiratory rate
• Dry mucous membranes
• Reduced skin turgor
• Reduced urine output
• Sunken eyes
• Reduced body weight from baseline
 • Feeling thirsty

Signs of fluid overload are:

• Peripheral oedema (check the ankles and sacral area)
• Pulmonary oedema (shortness of breath, reduced oxygen
saturation, raised respiratory rate and bibasal crackles)
• Raised JVP
• Increased body weight from baseline (regular weights are an
important way of monitoring fluid balance)

Patients with third-spacing may have a low level of fluid in the

intravascular space, but excessive fluid in other areas (such as the
interstitial space or peritoneal cavity). This can give signs of
hypovolaemia (e.g., hypotension, tachycardia and prolonged capillary
refill time) and signs of fluid overload (e.g., oedema and ascites).

Indications for IV Fluids

The main indications for IV fluids are:

• Resuscitation (e.g., sepsis or hypotension)
• Replacement (e.g., vomiting and diarrhoea)
• Maintenance (e.g., nil by mouth due to bowel obstruction)

Generally, IV fluids should be avoided if the patient can adequately

meet their fluid requirements with oral fluids.

Types of IV Fluid

There are two main groups of IV fluids:

• Crystalloids
• Colloids

Crystalloids are essentially water with added salts and glucose. The
contents of crystalloid solutions will redistribute throughout the different
fluid compartments of the body. Common examples are:
• 0.9% sodium chloride (“normal saline”)
• 5% dextrose
• 0.18% sodium chloride in 4% glucose
• Hartmann’s solution
 • Plasma-Lyte 148

A 1 litre bag of normal 0.9% saline solution contains:

• 1 litre of water
• 154 mmol sodium (note that this is a lot of sodium, and lots of saline
can result in hypernatraemia)
• 154 mmol chloride

A 1 litre bag of 5% dextrose contains:

• 1 litre of water
• No electrolytes (note that lots of 5% dextrose can result in
hyponatraemia and oedema)
• 50 g of glucose

A 1 litre bag of 0.18% sodium chloride in 4% dextrose contains:

• 1 litre of water
• 31 mmol sodium
• 31 mmol chloride
• 40 g of glucose

A 1 litre bag of Hartmann’s solution contains:

• 1 litre of water
• 131 mmol sodium
• 111 mmol chloride
• 5 mmol potassium
• 2 mmol calcium
• 29 mmol lactate (helps to buffer the solution - reducing the risk of
acidosis)

A 1 litre bag of Plasma-Lyte 148 contains:

• 1 litre of water
• 140 mmol sodium
• 98 mmol chloride
• 5 mmol potassium
• 1.5 mmol magnesium
• 27 mmol acetate (helps to buffer the solution - reducing the risk of
acidosis)
 • 23 mmol gluconate (helps to buffer the solution - reducing the risk
of acidosis)

TOM TIP: Normal 0.9% saline has a concentration of sodium of

154 mmols/L. The normal blood concentration of sodium is 135-145
mmols/L. When you use normal saline, you are adding a lot of
sodium into the system, significantly increasing the risk of
hypernatraemia. Normal saline also carries a risk of causing
metabolic acidosis due to adding so much chloride
(hyperchloraemic acidosis). For these reasons, Hartmann’s or
Plasma-Lyte are often better options.

Colloids contain larger molecules that stay in the intravascular

space longer. Theoretically, this helps to retain fluid in the intravascular
space. However, the research suggests there is no benefit to using them
in resuscitation scenarios.

One example of a colloid is human albumin solution, which may be

used in patients with decompensated liver disease. Albumin is an
important component of plasma and increases the plasma volume. It
increases the oncotic pressure of the plasma, drawing in and retaining
fluid. In decompensated liver disease, the patient’s liver is not producing
adequate albumin, leading to reduced oncotic pressure in the
intravascular space, resulting in reduced circulating blood volume.
Human albumin solution may be used to help correct this, although the
effects are only temporary.

TOM TIP: During most medical and surgical jobs, you will
practically only prescribe crystalloid fluids. I don’t remember ever
prescribing a colloid solution as a junior doctor working in
hospitals, other than albumin in patients with ascitic drains, on the
instructions of the gastroenterology team.

Tonicity

Tonicity refers to the osmotic pressure gradient between two fluids

across a membrane. This determines whether water molecules will move
across the membrane by osmosis, from the area of lower concentration
of solutes to the area of higher concentration of solutes. The normal
serum osmolality is 275 - 295 mOsmol/Kg.

Isotonic solutions (e.g., 0.9% saline, Hartmann’s and Plasma-Lyte)

match the concentration of solutes (osmolality) in the plasma.

Hypotonic solutions (e.g., 5% dextrose and 0.18% sodium chloride)

have a lower concentration of solutes than the plasma.

Hypertonic solutions (e.g., 3% saline) have a higher concentration of

solutes than the plasma.

Water will flow from an area of lower concentration of solutes to an

area of higher concentration of solutes by osmosis. Theoretically, if
you dilute the blood with a hypotonic solution, water will flow out of the
blood into the interstitial space. This is why hypotonic solutions (e.g., 5%
dextrose) are not used for fluid resuscitation. Hypotonic solutions also
carry a risk of hyponatraemia (low sodium) by diluting the sodium
content of the blood.

Resuscitation IV Fluids

Where your assessment suggests the patient is hypovolaemic and

needs fluid resuscitation, you can prescribe boluses of IV fluid to rapidly
improve their fluid status. Seek senior input where you are unsure, or
there is shock (circulatory failure).

An isotonic fluid should be used for fluid resuscitation. This usually

means a choice of either:
• 0.9% saline
• Hartmann’s solution
• Plasma-Lyte 148

An ABCDE assessment of the patient is used to determine their fluid

status. Signs such as hypotension, tachycardia and prolonged capillary
refill time indicate the need for fluid resuscitation (see above for a full list).

Establish the underlying cause of the hypovolaemia (e.g., sepsis).

 The NICE guidelines suggest:
• An initial 500 ml fluid bolus over 15 minutes (“stat”), followed by
reassessment with an ABCDE approach
• Repeat boluses of 250 - 500 mls of fluid if required, each time
followed by a reassessment
• Seek expert help if the patient is not responding, particularly after 2
litres of fluid

TOM TIP: You can’t give a rapid infusion of a fluid that has a high
potassium content. Under normal circumstances, the rate of
potassium infusion should not exceed 10 mmol/hour, as there is a
risk of inducing an arrhythmia or cardiac arrest. Higher rates are
only used in specific scenarios under expert supervision with
cardiac monitoring and through a central line (rather than a
peripheral cannula).

Replacement IV Fluids

IV fluids can be used to replace fluids in a patient with a negative

fluid balance, where the fluid losses are greater than the fluid intake.
This involves calculating or estimating the losses and prescribing
additional fluids to account for these losses.

Maintenance IV Fluids

Maintenance IV fluids are used for the shortest time possible where
the patient is unable to take fluid , for example, while nil by mouth
waiting for surgery or in bowel obstruction. As soon as they are able to
meet their nutritional needs orally, the IV fluids should be stopped.

The NICE guidelines give approximate requirements of maintenance

IV fluids:
• 25-30 ml / kg / day of water
• 1 mmol / kg / day of sodium, potassium and chloride
• 50-100 g / day of glucose (this is to prevent ketosis, not to meet their
nutritional needs)

The weights are based on the ideal body weight rather than their
actual body mass index. This avoids excessive prescriptions for obese
patients.

For example, if you had a 70kg man, they would require:

• Approximately 2 litres of water
• Approximately 70 mmol sodium, chloride and potassium
• 50-100 g glucose

You can select a bag of IV fluid with additional potassium added to

meet the potassium requirements of the patient. Fluids may come with an
additional 20 mmol or 40 mmol of potassium in a 1 litre bag. Potassium
should not be added to fluids. The mixtures should come ready-made
from the manufacturer.

The NICE guidelines suggest starting with 25-30 ml/kg/day of 0.18%

sodium chloride in 4% glucose with 27 mmol/l of added potassium. This is
available as a ready-made solution. They point out that more than 2.5
litres of this fluid increases the risk of hyponatraemia, as it is hypotonic.

1 Litre
0.18%
sodium
Maintenance 70kg
chloride in 2
Requirements Requirements / Man /
4% glucose Litres
Day Day
with 27
mmol/l
potassium
2
2
Water 25 - 30 ml / kg litres 1 litre
litres
(approx)
70 62
Sodium 1 mmol / kg 31 mmol
mmol mmol
70 62
Chloride 1 mmol / kg 31 mmol
mmol mmol
70 54
Potassium 1 mmol / kg 27 mmol
mmol mmol
50 - 80
Glucose 50 - 100 g 40 g
100 g g
 Daily monitoring (at least) is required to ensure the correct fluids are
prescribed. This includes assessment of their fluid status, fluid balance
chart and U&E blood tests. A maximum of 24 hours of fluids are
prescribed at one time.

Too much fluid can lead to dilution of important components of the

blood:
• Sodium (with hypotonic solutions)
• Potassium (if potassium is not included)
• Other electrolytes, e.g., calcium or magnesium
• Haemoglobin and haematocrit (red blood cells in the blood)
causing anaemia
• Clotting factors, platelets and fibrinogen causing coagulopathy
(clotting problems)

To avoid fluid overload and problems with abnormal fluid or electrolyte

distribution, take additional caution and seek senior guidance with:
• Elderly or frail patients
• Significant oedema
• Sodium imbalance (hyponatraemia or hypernatraemia)
• Heart failure
• Renal impairment
• Liver impairment

TOM TIP: Surgeons and anaesthetists often prescribe

Hartmann’s solution or Plasma-Lyte 148 as maintenance fluids, as
they are balanced, isotonic solutions. They are less likely to cause
hyponatraemia than hypotonic solutions (e.g., 5% dextrose or 0.18%
sodium chloride), which is important in surgical patients. They are
also less likely to cause hypernatraemia than normal saline.

Practicalities of Prescribing

A fluid prescribing chart will typically require you to fill in the following
sections:
 When prescribing the rate, the typical options are:
• Stat - indicates it should be given as quickly as it will run through
the cannula
• Over X hours - indicating the number of hours you want it to be
infused across
• X ml / hour - e.g., 125 ml / hour will give 1 litre over 8 hours (volume
of fluid / number of hours)

TOM TIP: When prescribing maintenance fluids during a normal

working day, try to ensure enough bags of fluid are prescribed to
last through to the next working day (unless you want the fluids to
stop). If the bag of fluid runs out at 2 AM and no further bags are
prescribed, the on-call junior doctor will get a bleep to attend the
ward and prescribe more fluids. Not only does this interrupt
whatever that doctor is doing at the time, but they have to work out
what to prescribe for a patient that they don’t know. This might
involve waking the patient up, disturbing important rest. If the fluids
are being stopped out of hours, remember to give clear instructions
to the nurses and in the notes.
 Acute Abdomen
An acute abdomen refers to a recent, rapid onset of urgent abdominal
or pelvic pathology, usually presenting with abdominal pain. This is a
common presentation and has a wide variety of causes.

Differential Diagnoses of Acute Abdominal Pain

It may be helpful to think of the causes as being related to pathology in

the organs located in the area of the pain. Keep in mind that the pain may
not always be localised in the typical area, so be open-minded for other
possible differentials. This list is not exhaustive, and there will always be
more differentials to consider.
Generalised abdominal pain:
• Peritonitis
• Ruptured abdominal aortic aneurysm
• Intestinal obstruction
• Ischaemic colitis

Right upper quadrant pain:

• Biliary colic
• Acute cholecystitis
 • Acute cholangitis

Epigastric pain:
• Acute gastritis
• Peptic ulcer disease
• Pancreatitis
• Ruptured abdominal aortic aneurysm

Periumbilical (central) abdominal pain:

• Ruptured abdominal aortic aneurysm
• Intestinal obstruction
• Ischaemic colitis
• Early stages of appendicitis

Right iliac fossa pain:

• Acute appendicitis
• Ectopic pregnancy
• Ruptured ovarian cyst
• Ovarian torsion
• Meckel’s diverticulitis

Left iliac fossa pain:

• Diverticulitis
• Ectopic pregnancy
• Ruptured ovarian cyst
• Ovarian torsion

Suprapubic pain:
• Lower urinary tract infection
• Acute urinary retention
• Pelvic inflammatory disease
• Prostatitis

Loin to groin pain:

• Renal colic (kidney stones)
• Ruptured abdominal aortic aneurysm
• Pyelonephritis

Testicular pain:
 • Testicular torsion
• Epididymo-orchitis

Peritonitis

Peritonitis refers to inflammation of the peritoneum, the lining of the

abdomen. The signs of peritonitis are:
• Guarding - involuntary tensing of the abdominal wall muscles
when palpated to protect the painful area below
• Rigidity - involuntary persistent tightness / tensing of the
abdominal wall muscles
• Rebound tenderness - rapidly releasing pressure on the abdomen
creates worse pain than the pressure itself
• Coughing test - asking the patient to cough to see if it results in
pain in the abdomen
• Percussion tenderness - pain and tenderness when percussing
the abdomen

Localised peritonitis is caused by underlying organ inflammation, for

example, appendicitis or cholecystitis.

Generalised peritonitis may be caused by perforation of an

abdominal organ (e.g., perforated duodenal ulcer or ruptured appendix)
releasing the contents into the peritoneal cavity and causing generalised
inflammation of the peritoneum.

Spontaneous bacterial peritonitis is associated with spontaneous

infection of ascites in patients with liver disease. This is treated with
broad-spectrum antibiotics and carries a poor prognosis.

Initial Assessment

Initial assessment of an acutely unwell patient is with an ABCDE

approach, assessing and treating:
• A – Airway: Ensure the patient’s airway is patent and secure.
• B – Breathing: Assess the breathing, respiratory rate and oxygen
saturations. Listen to the lungs. Provide oxygen if required.
• C – Circulation: Assess the blood pressure, heart rate, heart
sounds and perfusion (e.g., capillary refill time). Gain IV access
 (wide-bore cannulae are better), take bloods and provide an IV
bolus of fluid if required.
• D – Disability: Assess the consciousness level using AVPU or
GCS scoring systems. Check the blood glucose level.
• E – Exposure: Finish the full assessment, including examination of
the abdomen.

TOM TIP: When asked “how would you manage this acute
presentation?” in an exam or teaching session, the obvious and
easy answer to start with is “I would start with an ABCDE
approach”. This is a good answer because it shows you are
considering the immediate assessment and stabilisation of the
unwell patient ahead of jumping to more definitive management that
would come after the initial assessment (such as “I would perform
an immediate right hemicolectomy”). However, don’t use this
answer for non-acute presentations.

Investigations

The following investigations are useful for obtaining a diagnosis and

preparing the patient for theatre.

Full blood count (FBC) gives an indication of bleeding (drop in Hb)

and infection / inflammation (raised WBC).

Urea and electrolytes (U&Es) give an indication of electrolyte

imbalance and kidney function (useful prior to CT scans, as they require a
contrast injection that can damage the kidneys).

Liver function tests (LFTs) give an indication of the state of the

biliary and hepatic system.

C-reactive protein (CRP) gives an indication of inflammation and

infection.

Amylase gives an indication of inflammation of the pancreas in acute

pancreatitis.
 International normalised ratio (INR) gives an indication of the
synthetic function of the liver and the patient's clotting function (which is
useful prior to procedures).

Serum calcium is required to score acute pancreatitis and for other

reasons (e.g., clotting and cardiac function).

Serum human chorionic gonadotropin (hCG) or a urine

pregnancy test is essential in females of child bearing age.

Arterial blood gas (ABG) analysis will show the lactate (an
indication of tissue ischaemia) and pO2 (used for scoring in acute
pancreatitis).

Serum lactate gives an indication of tissue ischaemia. It is a product

of anaerobic respiration and can also be raised in dehydration or
hypoxia. Lactate is also available on an ABG result as mentioned above.

Group and save is essential prior to theatre in case the patient

requires a blood transfusion.

Blood cultures are used if infection is suspected.

Abdominal x-ray can provide evidence of bowel obstruction by

showing dilated bowel loops.

Erect chest x-ray can demonstrate air under the diaphragm when
there is an intra-abdominal perforation.

Abdominal ultrasound can be useful in checking for gallstones,

biliary duct dilatation and gynaecological pathology.

CT scans are often required to identify the cause of an acute

abdomen and determine correct management.

Management

Initial management involves:

• ABCDE assessment
 • Alert seniors of unwell patients: escalating to the registrar,
consultant and critical care as required
• Nil by mouth if surgery may be required or they have features of
bowel obstruction
• NG tube in cases of bowel obstruction
• IV fluids if required for resuscitation or maintenance
• IV antibiotics if infection is suspected
• Analgesia as required for pain management
• Arranging investigations as required (e.g., bloods, group and
save and scans)
• Venous thromboembolism risk assessment and prescription if
indicated
• Prescribing regular medication on the drug chart if they are
being admitted (some may need to be withheld)

Patients being admitted to an acute surgical unit will usually be seen

by a junior doctor, then reviewed by the surgical registrar if required. A
consultant will then review that patient on the post-take ward round,
creating a management plan that is then carried out by the junior doctors.
This may involve further investigations, preparations for surgery or
discharge depending on the presentation.

Further management steps if the patient requires surgery:

• Taking consent for surgery (by someone suitably qualified)
• Review by an anaesthetist
• Adding to the theatre list
• Crossmatch units of blood if required
 Appendicitis
Appendicitis is inflammation of the appendix. The peak incidence of
appendicitis is in patients aged 10 to 20 years. It can occur at any age but
is less common in young children and adults over 50 years.

Basic Anatomy

The appendix is a small, thin tube arising from the caecum. It is

located at the point where the three taeniae coli meet (the taeniae coli
are longitudinal muscles that run the length of the large intestine). There
is a single opening to the appendix that connects it to the bowel, and it
leads to a dead end.
 Basic Pathophysiology

Pathogens can get trapped due to obstruction at the point where the
appendix meets the bowel. Trapping of pathogens leads to infection and
inflammation. The inflammation may proceed to gangrene and rupture.
When the appendix ruptures, faecal contents and infective material
are released into the peritoneal cavity. This leads to peritonitis, which is
inflammation of the peritoneal lining.

Signs and Symptoms

 The key presenting feature of appendicitis is abdominal pain. This
typically starts as central abdominal pain that moves down to the right
iliac fossa (RIF) within the first 24 hours, eventually becoming localised
in the RIF.

On palpation of the abdomen, there is tenderness at McBurney’s

point. McBurney’s point refers to a specific area one third of the distance
from the anterior superior iliac spine (ASIS) to the umbilicus.

Other classic features are:

• Loss of appetite (anorexia)
• Nausea and vomiting
• Low-grade fever
• Rovsing’s sign (palpation of the left iliac fossa causes pain in the
RIF)
• Guarding on abdominal palpation
• Rebound tenderness in the RIF (increased pain when
suddenly releasing the pressure of deep palpation)
 • Percussion tenderness (pain and tenderness when percussing
the abdomen)

Rebound tenderness and percussion tenderness suggest

peritonitis, potentially indicating a ruptured appendix.

Diagnosis

The Alvarado score can be used to calculate the probability of

appendicitis.

Diagnosis is based on the clinical presentation and raised

inflammatory markers.

Performing a CT scan can be useful in confirming the diagnosis,

particularly where another diagnosis is more likely. An ultrasound scan
is often used in female patients to exclude ovarian and gynaecological
pathology. Ultrasound can also be useful in children, where a CT scan is
less appropriate due to the dose of radiation.

Appendicitis is mostly a clinical diagnosis (meaning it is based on

signs and symptoms rather than diagnostic tests). Where the diagnosis is
unclear, a period of observation may be used, with repeated
examinations over time to see whether the symptoms resolve or worsen.

When a patient has a clinical presentation suggestive of

appendicitis, but investigations are negative, the next step is to perform a
diagnostic laparoscopy to visualise the appendix directly. The surgeon
can perform an appendicectomy during the same procedure, if indicated.

Key Differential Diagnoses of Appendicitis

Ectopic Pregnancy
Consider ectopic pregnancy in females of childbearing age. This is a
gynaecological emergency with a relatively high mortality if mismanaged.
A serum or urine human chorionic gonadotropin (hCG) to exclude
pregnancy is essential.

Ovarian Cysts
 Ovarian cysts can cause pelvic and iliac fossa pain, particularly with
rupture or torsion.

Meckel’s Diverticulum
Meckel’s diverticulum is a malformation of the distal ileum that occurs
in around 2% of the population. It is usually asymptomatic and does not
require any treatment. However, it can bleed, become inflamed, rupture or
cause a volvulus or intussusception.

Mesenteric Adenitis
Mesenteric adenitis describes inflamed abdominal lymph nodes. It
presents with abdominal pain, usually in younger children, and is often
associated with tonsillitis or an upper respiratory tract infection. No
specific treatment is required.

TOM TIP: When seeing females of child-bearing age assume they

are pregnant until proven otherwise with a pregnancy test. This is
especially important in patients with abdominal pain (where ectopic
pregnancy is a key differential), or where you are requesting x-rays
or CT scans. Serum HCG is typically part of the normal abdominal
pain blood panel in A&E.

Appendix Mass

An appendix mass occurs when the omentum surrounds and sticks

to the inflamed appendix, forming a mass in the right iliac fossa. This is
typically managed conservatively with supportive treatment and
antibiotics, followed by appendicectomy once the acute condition has
resolved.

Management

Patients with suspected appendicitis need emergency admission to

hospital under the surgical team. Older children (e.g., above 10 years) will
often be managed by adult general surgical teams (with support from
paediatrics).

Removal of the inflamed appendix (appendicectomy) is the definitive

management for appendicitis. Laparoscopic surgery is associated with
fewer risks and faster recovery compared to open surgery (laparotomy).

Complications of Appendicectomy

• Bleeding, infection, pain and scars

• Damage to bowel, bladder or other organs
• Removal of a normal appendix
• Anaesthetic risks
• Venous thromboembolism (deep vein thrombosis or pulmonary
embolism)
 Bowel Obstruction
A bowel obstruction refers to when the passage of food, fluids and gas
through the intestines becomes blocked. Small bowel obstruction is more
common than large bowel obstruction. Obstruction results in a build up of
gas and faecal matter proximal to the obstruction (before the obstruction).
This causes back-pressure, resulting in vomiting and dilatation of the
intestines proximal to the obstruction. Bowel obstruction is a surgical
emergency.

The gastrointestinal tract secretes fluid that is later absorbed in the

colon. When there is an obstruction, and fluid cannot reach the colon, it
cannot be reabsorbed. As a result, there is fluid loss from the
intravascular space into the gastrointestinal tract. This leads to
hypovolaemia and shock. This abnormal loss of fluid is referred to
as third-spacing. The higher up the intestine the obstruction, the greater
the fluid losses as there is less bowel over which the fluid can be
reabsorbed.

Causes

The “big three” causes account for around 90% of cases of bowel
obstruction:
• Adhesions (small bowel)
• Hernias (small bowel)
• Tumours (large bowel)

Other causes include:

• Volvulus (large bowel)
• Diverticular disease
• Strictures (e.g., secondary to Crohn’s disease)
• Intussusception (in young children aged 6 months to 2 years)

TOM TIP: Learn to recite the “big three” causes of obstruction

without any hesitation. These are the three causes of bowel
obstruction you should produce if asked on a ward round or in an
OSCE examination. When patients present with symptoms of bowel
obstruction, don’t just think about obstruction, but also consider
what the cause of the obstruction would be. Ask about hernias,
change in bowel habit, weight loss and PR bleeding (bowel cancer)
and about previous abdominal surgery that may have resulted in
adhesions.

Adhesions

Adhesions are pieces of scar tissue that bind the abdominal contents
together. They can cause kinking or squeezing of the bowel, leading to
obstruction. Adhesions typically cause obstruction in the small bowel,
rather than the large bowel.

The main causes of intestinal adhesions are:

• Abdominal or pelvic surgery (particularly open surgery)
• Peritonitis
• Abdominal or pelvic infections (e.g., pelvic inflammatory disease)
• Endometriosis

Less commonly, they can be congenital or secondary to radiotherapy

treatment.

Closed-Loop Obstruction

Closed-loop obstruction describes a situation where there are two

points of obstruction along the bowel; meaning that there is a middle
section sandwiched between two points of obstruction. This might happen
with:
• Adhesions that compress two areas of bowel
• Hernias that isolate a section of bowel blocking either end
• Volvulus where the twist isolates a section of intestine
• A single point of obstruction in the large bowel, with an ileocaecal
valve that is competent

A competent ileocaecal valve does not allow any movement back

into the ileum from the caecum. When there is a large bowel obstruction
and a competent ileocaecal valve, a section of bowel becomes isolated
and the contents cannot flow in either direction.
 The contents of a “closed-loop” section of bowel do not have an open
end where they can drain and decompress. Therefore, the closed-loop
section will inevitably continue to expand, leading to ischaemia and
perforation. Closed-loop obstruction requires emergency surgery.

Presentation

The key features of bowel obstruction are:

• Vomiting (particularly green bilious vomiting)
• Abdominal distention
• Diffuse abdominal pain
• Absolute constipation and lack of flatulence
• “Tinkling” bowel sounds may be heard in early bowel obstruction

Abdominal X-ray
 The key x-ray finding in bowel obstruction is distended loops of
bowel.

The upper limits of the normal diameter of bowel are:

• 3 cm small bowel
• 6 cm colon
• 9 cm caecum

Valvulae conniventes are present in the small bowel and

are mucosal folds that form lines extending the full width of the bowel.
These are seen on an abdominal x-ray as lines across the entire width of
the bowel.

Haustra are like pouches formed by the muscles in the walls of the
large bowel. They form lines that do not extend the full width of the
bowel. These are seen on an abdominal x-ray as lines that extend only
part of the way across the bowel.

Initial Management

As with any unwell patient, start with an ABCDE approach. Patients

with bowel obstruction may be haemodynamically unstable and require
urgent intervention if they have developed:
• Hypovolaemic shock due to fluid stuck in the bowel rather than
the intravascular space (third-spacing)
• Bowel ischaemia
• Bowel perforation
• Sepsis

A full set of bloods are required, as with any acute abdomen. Key
things to look out for with bowel obstruction are:
• Electrolyte imbalances (U&Es)
• Metabolic alkalosis due to vomiting stomach acid (venous blood
gas)
• Bowel ischaemia (raised lactate - either on a venous blood gas
or laboratory sample)

The initial management of bowel obstruction is casually described as

“drip and suck”:
 • Nil by mouth (don’t put food or fluids in if there is a blockage)
• IV fluids to hydrate the patient and correct electrolyte imbalances
• NG tube with free drainage to allow stomach contents to freely
drain and reduce the risk of vomiting and aspiration

Abdominal x-ray may be the initial imaging investigation. However,

depending on the signs and symptoms, this may be skipped, and the
patient sent straight for a CT scan.

Erect chest x-ray can demonstrate air under the diaphragm when
there is an intra-abdominal perforation.

A contrast abdominal CT scan is usually required to confirm the

diagnosis of bowel obstruction and establish the site and cause of the
obstruction. It can also be used to diagnose an intra-abdominal
perforation, if present.

TOM TIP: Patients need a cannula and a U&E blood test before a
contrast CT scan. The cannula is required to give the contrast, and
the U&Es are necessary to ensure the patient has adequate renal
function, given the risk of contest-induced nephropathy.

Surgical Intervention

Conservative management may be used in the first instance in

stable patients with obstruction secondary to adhesions or volvulus.
Where this fails, surgery is required.

The definitive management of bowel obstruction is with surgery (either

laparoscopy or laparotomy) to correct the underlying cause:
• Exploratory surgery in patients with an unclear underlying cause
• Adhesiolysis to treat adhesions
• Hernia repair
• Emergency resection of an obstructing tumour

Stents may be inserted into the bowel (during a colonoscopy) in

patients with obstruction due to a tumour. Stents hold the tumour out of
the way, creating space for the bowel contents to move through.
 Ileus
Ileus is a condition affecting the small bowel, where the normal
peristalsis that pushes the contents along the length of the intestines,
temporarily stops. It may be referred to as paralytic ileus or adynamic
ileus.

Pseudo-obstruction is a term used to describe a functional

obstruction of the large bowel, where patients present with intestinal
obstruction, but no mechanical cause is found. This is less common than
ileus, which affects the small bowel.

Causes

There is a long list of things that can make the bowel unhappy, leading
to ileus. Common causes are:
• Injury to the bowel
• Handling of the bowel during surgery
• Inflammation or infection in, or nearby, the bowel (e.g., peritonitis,
appendicitis, pancreatitis or pneumonia)
• Electrolyte imbalance (e.g., hypokalaemia or hyponatraemia)

The most common time you will see ileus is following abdominal
surgery. This usually resolves with supportive care within a few days.

Signs and Symptoms

The signs and symptoms are akin to bowel obstruction, with:

• Vomiting (particularly green bilious vomiting)
• Abdominal distention
• Diffuse abdominal pain
• Absolute constipation and lack of flatulence
• Absent bowel sounds (as opposed to the “tinkling” bowel sounds of
mechanical obstruction)

Management
 The ileus will usually resolve with treatment of the underlying cause.
Management involves supportive care.

Supportive care involves:

• Nil by mouth or limited sips of water
• NG tube if vomiting
• IV fluids to prevent dehydration and correct the electrolyte
imbalances
• Mobilisation to helps stimulate peristalsis
• Total parenteral nutrition (TPN) may be required whilst waiting for
the bowel to regain function
 Volvulus
Volvulus is a condition where the bowel twists around itself and the
mesentery that it is attached to. The mesentery is the membranous
peritoneal tissue that creates a connection between the bowel and the
posterior abdominal wall. The bowel gets its blood supply from the
mesentery (through the mesenteric arteries).

Twisting in the bowel leads to a closed-loop bowel obstruction,

where a section of bowel is isolated by obstruction on either side.

The blood vessels that supply the bowel can be involved, cutting off
the blood supply to the bowel, which leads to bowel ischaemia. Ischaemia
leads to death of the bowel tissue (necrosis), and bowel perforation.

Types of Volvulus

There are two main types of volvulus depending on the area affected:
• Sigmoid volvulus
• Caecal volvulus

Sigmoid volvulus is more common and tends to affect older patients.

The twist affects the sigmoid colon. A key cause is chronic constipation
and lengthening of the mesentery attached to the sigmoid colon. The
sigmoid colon becomes overloaded with faeces, causing it to sink
downwards, resulting in a twist. It is also associated with a high fibre diet
and the excessive use of laxatives.

Caecal volvulus is less common and tends to affect younger patients.

The twist occurs in the caecum.
Risk Factors

• Neuropsychiatric disorders (e.g., Parkinson’s)

• Nursing home residents
• Chronic constipation
• High fibre diet
• Pregnancy
• Adhesions
 Presentation

The signs and symptoms are akin to bowel obstruction, with:

• Vomiting (particularly green bilious vomiting)
• Abdominal distention
• Diffuse abdominal pain
• Absolute constipation and lack of flatulence

Diagnosis

Abdominal x-ray can show the “coffee bean” sign in sigmoid

volvulus, where the dilated and twisted sigmoid colon looks like a giant
coffee bean.

A contrast CT scan is the investigation of choice to confirm the

diagnosis and identify other pathology.

TOM TIP: Remember the “coffee bean” sign for your MCQ exams.
It is worth looking up photographs so that you can recognise it and
immediately know the diagnosis (sigmoid volvulus) if it comes up.

Management

The initial management is the same as with bowel obstruction (nil by

mouth, NG tube and IV fluids).

Conservative management with endoscopic decompression can

be attempted in patients with sigmoid volvulus (without peritonitis). A
flexible sigmoidoscope is inserted carefully, with the patient in the left
lateral position, resulting in a correction of the volvulus. A flatus tube /
rectal tube is left in place temporarily to help decompress the bowel, and
is later removed. There is a risk of recurrence (around 60%).

Surgical management involves:

• Laparotomy (open abdominal surgery)
• Hartmann’s procedure for sigmoid volvulus (removal of the
rectosigmoid colon and formation of a colostomy)
• Ileocaecal resection or right hemicolectomy for caecal volvulus
 Hernias
Hernias occur when there is a weak point in a cavity wall, usually
affecting the muscle or fascia. This weakness allows a body organ (e.g.,
bowel) that would normally be contained within that cavity to pass through
the cavity wall.

Presentation
 There are many types of hernias that present differently depending on
where they are and what organs are involved.

The typical features of an abdominal wall hernia are:

• A soft lump protruding from the abdominal wall
• The lump may be reducible (it can be pushed back into the normal
place)
• The lump may protrude on coughing (raising intra-abdominal
pressure) or standing (pulled out by gravity)
• An aching, pulling or dragging sensation

Complications

There are three key complications of hernias:

• Incarceration
• Obstruction
• Strangulation

Incarceration is where the hernia cannot be reduced back into the

proper position (it is irreducible). The bowel is trapped in the herniated
position. Incarceration can lead to obstruction and strangulation of the
hernia.

Obstruction is where a hernia causes a blockage in the passage of

faeces, fluids and gas through the bowel. Obstruction presents with
vomiting, generalised abdominal pain and absolute constipation (not
passing faeces or flatus).

Strangulation is where a hernia is non-reducible (it is trapped with

the bowel protruding) and the base of the hernia becomes so tight that it
cuts off the blood supply, causing ischaemia. This will present with
significant pain and tenderness at the hernia site. Strangulation is a
surgical emergency. The bowel will die quickly (within hours) if not
corrected with surgery. There will also be a mechanical obstruction when
this occurs.

TOM TIP: Hernias that have a wide neck, meaning that the size of
the opening that allows abdominal contents through is large, are at
lower risk of complications. The contents can easily pass out of this
opening but can also easily be put back, which puts them at a lower
risk of incarceration, obstruction and strangulation. When
assessing a hernia, always comment on the size of the neck/defect
(narrow or wide), as this will help formulate a risk assessment and
management plan for the hernia (such as how urgently they need to
be operated on).

Richter’s Hernia

A Richter’s hernia is a very specific situation that can occur in any

abdominal hernia. This is where only part of the bowel wall and lumen
herniate through the defect, with the other side of that section of the
bowel remaining within the peritoneal cavity. They can become
strangulated, where the blood supply to that portion of the bowel wall is
constricted and cut off. Strangulated Richter’s hernias will progress very
rapidly to ischaemia and necrosis and should be operated on
immediately.

Maydl’s Hernia

Maydl’s hernia refers to a specific situation where two different loops

of bowel are contained within the hernia.
 General Management Options

There are general management options that apply to abdominal wall

hernias. These are:
• Conservative management
• Tension-free repair (surgery)
• Tension repair (surgery)

Conservative management involves leaving the hernia alone. This is

most appropriate when the hernia has a wide neck (low risk of
complications) and in patients that are not good candidates for surgery
due to co-morbidities.

Tension-free repair involves placing a mesh over the defect in the

abdominal wall. The mesh is sutured to the muscles and tissues on either
side of the defect, covering it and preventing herniation of the cavity
contents. Over time, tissues grow into the mesh and provide extra
support. This has a lower recurrence rate compared with tension repair,
but there may be complications associated with the mesh (e.g., chronic
pain).

Tension repair involves a surgical operation to suture the muscles

and tissue on either side of the defect back together. Tension repairs are
rarely performed and have been largely replaced by tension-free repairs.
The hernia is held closed (to heal there) by sutures applying tension. This
can cause pain and there is a relatively high recurrence rate of the hernia.
 Inguinal Hernias

Inguinal hernias present with a soft lump in the inguinal region (in the
groin). There are two types:
• Indirect inguinal hernia
• Direct inguinal hernia

There are a number of differential diagnoses for a lump in the inguinal

region:
• Femoral hernia
• Lymph node
• Saphena varix (dilation of saphenous vein at junction with femoral
vein in groin)
• Femoral aneurysm
• Abscess
• Undescended / ectopic testes
• Kidney transplant

Indirect Inguinal Hernias

An indirect inguinal hernia is where the bowel herniates through the

inguinal canal.

The inguinal canal is a tube that runs between the deep inguinal ring
(where it connects to the peritoneal cavity), and the superficial inguinal
ring (where it connects to the scrotum).

In males, the inguinal canal is what allows the spermatic cord and
its contents to travel from inside the peritoneal cavity, through the
abdominal wall and into the scrotum.

In females, the round ligament is attached to the uterus and passes

through the deep inguinal ring, inguinal canal and then attaches to the
labia majora.

During fetal development, the processus vaginalis is a pouch of

peritoneum that extends from the abdominal cavity through the inguinal
canal. This allows the testes to descend from the abdominal cavity,
through the inguinal canal and into the scrotum. Normally, after the testes
descend through the inguinal canal, the deep inguinal ring closes and
the processus vaginalis is obliterated. However, in some patients, the
inguinal ring remains patent, and the processus vaginalis remains
intact. This leaves a tract or tunnel from the abdominal contents, through
the inguinal canal and into the scrotum. The bowel can herniate along this
tract, creating an indirect inguinal hernia.
 There is a specific clinical finding of indirect inguinal hernias that
helps differentiate them from direct inguinal hernias. When an indirect
hernia is reduced and pressure is applied (with two fingertips) to the deep
inguinal ring (at the mid-way point from the ASIS to the pubic tubercle),
the hernia will remain reduced.

Direct Inguinal Hernias

Direct inguinal hernias occur due to weakness in the abdominal wall at

Hesselbach’s triangle. The hernia protrudes directly through the
abdominal wall, through Hesselbach’s triangle (not along a canal or
tract like an indirect inguinal hernia). Pressure over the deep inguinal ring
will not stop the herniation.

Hesselbach’s triangle boundaries (RIP mnemonic):

• R - Rectus abdominis muscle - medial border
• I - Inferior epigastric vessels - superior / lateral border
• P - Poupart’s ligament (inguinal ligament) - inferior border

Femoral Hernias

Femoral hernias involve herniation of the abdominal contents through

the femoral canal. This occurs below the inguinal ligament, at the top of
the thigh.

The opening between the peritoneal cavity and the femoral canal is
the femoral ring. The femoral ring leaves only a narrow opening for
femoral hernias, putting femoral hernias at high risk of:

• Incarceration
• Obstruction
• Strangulation

Boundaries of the femoral canal (FLIP mnemonic):

• F - Femoral vein laterally
• L - Lacunar ligament medially
• I - Inguinal ligament anteriorly
• P - Pectineal ligament posteriorly

Don’t get the femoral canal confused with the femoral triangle. The
femoral triangle is a larger area at the top of the thigh that contains the
femoral canal. You can remember the boundaries with the SAIL
mnemonic:
• S - Sartorius - lateral border
• A - Adductor longus - medial border
• IL - Inguinal Ligament - superior border

Use the NAVY-C mnemonic to remember the contents of the

femoral triangle from lateral to medial across the top of the thigh:
• N - Femoral Nerve
 • A - Femoral Artery
• V - Femoral Vein
• Y - Y-fronts
• C - Femoral Canal (containing lymphatic vessels and nodes)

Incisional Hernias

Incisional hernias occur at the site of an incision from previous

surgery. They are due to weakness where the muscles and tissues were
closed after a surgical incision. The bigger the incision, the higher the risk
of a hernia forming. Medical co-morbidities put patients at higher risk due
to poor healing.

Incisional hernias can be difficult to repair, with a high rate of

recurrence. They are often left alone if they are large, with a wide neck
and low risk of complications, particularly in patients with multiple co-
morbidities.

Umbilical Hernias

Umbilical hernias occur around the umbilicus due to a defect in the

muscle around the umbilicus. Umbilical hernias are common in neonates
and can resolve spontaneously. They can also occur in older adults.

Epigastric Hernias

An epigastric hernia is simply a hernia in the epigastric area (upper

abdomen).

Spigelian Hernias

A Spigelian hernia occurs between the lateral border of the rectus

abdominis muscle and the linea semilunaris. This is the site of the
spigelian fascia, which is an aponeurosis between the muscles of the
abdominal wall. Usually, this occurs in the lower abdomen and may
present with non-specific abdominal wall pain. There may not be a
noticeable lump.
 An ultrasound scan can establish the diagnosis.

Spigelian hernias generally have a narrower base, increasing the risk

of incarceration, obstruction and strangulation.

Diastasis Recti

Diastasis recti may also be called rectus diastasis and recti

divarication. It refers to a widening of the linea alba, the connective
tissue that separates the rectus abdominis muscle, forming a larger gap
between the rectus muscles. It is not technically a hernia. This gap
becomes most prominent when the patient lies on their back and lifts their
head. There is a protruding bulge along the middle of the abdomen.

The linea alba is the aponeurosis of the two sides of the rectus
abdominis muscle. The gap is created because the linea alba is
stretched and broad.
 Diastasis recti can be congenital (in newborns) or due to weakness in
the connective tissue, for example following pregnancy or in obese
patients.

No treatment is required in most cases, but surgical repair is possible.

Obturator Hernias

Obturator hernias are where the abdominal or pelvic contents herniate

through the obturator foramen at the bottom of the pelvis. They occur
due to a defect in the pelvic floor and are more common in women,
particularly in older age, after multiple pregnancies and vaginal deliveries.
They are often asymptomatic but may present with irritation to the
obturator nerve, causing pain in the groin or medial thigh.

Howship–Romberg sign refers to pain extending from the inner thigh

to the knee when the hip is internally rotated, and is due to compression
of the obturator nerve.

It can also present with complications of:

• Incarceration
 • Obstruction
• Strangulation

CT or MRI of the pelvis can establish the diagnosis. It may be found

incidentally during pelvic surgery.

Hiatus Hernias

An hiatus hernia refers to the herniation of the stomach up through the

diaphragm. The diaphragm opening should be at the level of the lower
oesophageal sphincter and should be fixed in place. A narrow opening
helps to maintain the sphincter and stop acid and stomach contents
refluxing into the oesophagus. When the opening of the diaphragm is
wider, the stomach can enter through the diaphragm and the contents of
the stomach can reflux into the oesophagus.

There are four types of hiatus hernia:

• Type 1: Sliding
• Type 2: Rolling
• Type 3: Combination of sliding and rolling
• Type 4: Large opening with additional abdominal organs entering
the thorax

Sliding hiatus hernia is where the stomach slides up through the

diaphragm, with the gastro-oesophageal junction passing up into the
thorax. Rolling hiatus hernia is where a separate portion of the stomach
(i.e., the fundus), folds around and enters through the diaphragm opening,
alongside the oesophagus.
 Type 4 hiatus hernia refers to a large hernia that allows other intra-
abdominal organs to pass through the diaphragm opening (e.g., bowel,
pancreas or omentum).

Key risk factors are increasing age, obesity and pregnancy.

Hiatus hernias present with dyspepsia (indigestion), with symptoms of:

• Heartburn
• Acid reflux
• Reflux of food
• Burping
• Bloating
• Halitosis (bad breath)

Hiatus hernias can be intermittent, meaning they may not be seen on

investigations. Hiatus hernias may be seen on:
• Chest x-rays
• CT scans
• Endoscopy
• Barium swallow tests

Treatment is either:
• Conservative (with medical treatment of gastro-oesophageal
reflux)
 • Surgical repair if there is a high risk of complications or symptoms
are resistant to medical treatment

Surgery involves laparoscopic fundoplication. This involves tying

the fundus of the stomach around the lower oesophagus to narrow the
lower oesophageal sphincter.
 Haemorrhoids
Haemorrhoids are enlarged anal vascular cushions. It is not clear
why they become enlarged and swollen, but they are often associated
with constipation and straining. They are also more common with
pregnancy, obesity, increased age and increased intra-abdominal
pressure (e.g., weightlifting or chronic coughing).

They often occur in pregnancy, most likely due to constipation,

pressure from the baby in the pelvis and the effects of hormones that
relax the connective tissues.

Anal Cushions

The anal cushions are specialised submucosal tissue that contain

connections between the arteries and veins, making them very vascular.
They are supported by smooth muscle and connective tissue. They help
to control anal continence, along with the internal and external sphincters.
The blood supply is from the rectal arteries.
 The location of pathology at the anus is described as a clock face. 12
o’clock is towards the genitals and 6 o’clock is towards the back. The anal
cushions are usually located at 3, 7 and 11 o’clock.

Classification

The classification of haemorrhoids depends on their size and whether

they prolapse from the anus:
• 1st degree: no prolapse
 • 2nd degree: prolapse when straining and return on relaxing
• 3rd degree: prolapse when straining, do not return on relaxing, but
can be pushed back
• 4th degree: prolapsed permanently

Symptoms

Haemorrhoids may be asymptomatic. They are often associated with

constipation and straining.

A common presentation is with painless, bright red bleeding,

typically on the toilet tissue or seen after opening the bowels. The blood is
not mixed with the stool (this should make you think of an alternative
diagnosis).

Other symptoms include:

• Sore / itchy anus
• Feeling a lump around or inside the anus

Examination

• External (prolapsed) haemorrhoids are visible on inspection as

swellings covered in mucosa
• Internal haemorrhoids may be felt on a PR exam (although this is
generally difficult or not possible)
• They may appear (prolapse) if the patient is asked to “bear down”
during inspection

Proctoscopy is required for proper visualisation and inspection. This

involves inserting a hollow tube (proctoscope) into the anal cavity to
visualise the mucosa.

Management

Consider the differential diagnoses in patients presenting with

symptoms such as rectal bleeding:
• Anal fissures
• Diverticulosis
• Inflammatory bowel disease
 • Colorectal cancer

Consider testing for anaemia if there is prolonged bleeding or clinical

signs of anaemia.

Topical treatments can be given for symptomatic relief and to help

reduce swelling, for example:
• Anusol (contains chemicals to shrink the haemorrhoids -
“astringents”)
• Anusol HC (also contains hydrocortisone - only used short term)
• Germoloids cream (contains lidocaine - a local anaesthetic)
• Proctosedyl ointment (contains cinchocaine and hydrocortisone -
short term only)

Prevention and treatment of constipation involves:

• Increasing the amount of fibre in the diet
• Maintaining a good fluid intake
• Using laxatives where required
• Consciously avoiding straining when opening their bowels

There are a number of non-surgical treatments for haemorrhoids:

• Rubber band ligation (fitting a tight rubber band around the base
of the haemorrhoid to cut off the blood supply)
• Injection sclerotherapy (injection of phenol oil into the
haemorrhoid to cause sclerosis and atrophy)
• Infra-red coagulation (infra-red light is applied to damage the
blood supply)
• Bipolar diathermy (electrical current applied directly to the
haemorrhoid to destroy it)

Surgical Options

Haemorrhoidal artery ligation involves using a proctoscope to

identify the blood vessel that supplies the haemorrhoids and suturing it to
cut off the blood supply.

Haemorrhoidectomy involves excising the haemorrhoid. Removing

the anal cushions may result in faecal incontinence.
 Stapled haemorrhoidectomy involves using a special device that
excises a ring of haemorrhoid tissue at the same time as adding a circle
of staples in the anal canal. The staples remain in place long-term.

Thrombosed Haemorrhoids

Thrombosed haemorrhoids are caused by strangulation at the base

of the haemorrhoid, resulting in thrombosis (a clot) in the haemorrhoid.
This can be very painful.

Thrombosed haemorrhoids appear as purplish, very tender, swollen

lumps around the anus. A PR examination is unlikely to be possible due
to the pain.

The thrombosis will resolve with time, although it can take several
weeks.

The NICE clinical knowledge summaries (2016) suggests considering

admission if the patient present within 72 hours with extremely painful
thrombosed haemorrhoids. They may benefit from surgical management.
 Diverticular Disease
A diverticulum (plural diverticula) is a pouch or pocket in the bowel
wall, usually ranging in size from 0.5 – 1cm.

Diverticulosis refers to the presence of diverticula, without

inflammation or infection. Diverticulosis may be referred to as
diverticular disease when patients experience symptoms.

Diverticulitis refers to inflammation and infection of diverticula.

Pathophysiology

The wall of the large intestine contains a layer of muscle called the
circular muscle. The points where this muscle layer is penetrated by
blood vessels are areas of weakness. Increased pressure inside the
lumen over time can cause a gap to form in these areas of the circular
muscle. These gaps allow the mucosa to herniate through the muscle
layer and pouches to form (diverticula).

Diverticula do not form in the rectum, because it has an outer

longitudinal muscle layer that completely surrounds the diameter of the
rectum, adding extra support. In the rest of the colon, there are three
longitudinal muscles that run along the colon, forming strips or ribbons
called teniae coli. The teniae coli do not surround the entire diameter of
the colon, and the areas that are not covered by teniae coli are
vulnerable to the development of diverticula.

Diverticulosis

Diverticulosis is sometimes described in layman’s terms as “wear and

tear of the bowel”. The most commonly affected section of the bowel is
the sigmoid colon. However, it can affect the entire large intestine in some
patients. Small bowel diverticula are also possible but much less
common.
 Diverticulosis is very common with increased age. Additional risk
factors are:
• Low fibre diet
• Obesity
• Use of NSAIDs

The use of NSAIDs increases the risk of diverticular haemorrhage.

Diverticulosis is often diagnosed incidentally on colonoscopy or CT

scans. Treatment is not necessary where the patient is asymptomatic.
However, advice regarding a high fibre diet and weight loss is
appropriate.

Diverticulosis may cause lower left abdominal pain, constipation or

rectal bleeding.

Management is with increased fibre in the diet and bulk-forming

laxatives (e.g., ispaghula husk). Stimulant laxatives (e.g., Senna)
should be avoided. Surgery to remove the affected area may be required
where there are significant symptoms.

Acute Diverticulitis

Diverticulitis refers to inflammation in the diverticula. Acute

diverticulitis presents with:
• Pain and tenderness in the left iliac fossa / lower left abdomen
• Fever
• Diarrhoea
• Nausea and vomiting
• Rectal bleeding
• Palpable abdominal mass (if an abscess has formed)
• Raised inflammatory markers (e.g., CRP) and white blood cells

The NICE clinical knowledge summaries (updated January 2021)

suggest management of uncomplicated diverticulitis in primary care with:
• Oral co-amoxiclav (at least 5 days)
• Analgesia (avoiding NSAIDs and opiates, if possible)
• Only taking clear liquids (avoiding solid food) until symptoms
improve (usually 2-3 days)
• Follow-up within 2 days to review symptoms

Patients with severe pain or complications require admission to

hospital. Hospital treatment involves management as with any patient
with an acute abdomen or sepsis, including:
• Nil by mouth or clear fluids only
• IV antibiotics
• IV fluids
• Analgesia
• Urgent investigations (e.g., CT scan)
• Urgent surgery may be required for complications

Complications of acute diverticulitis are:

• Perforation
• Peritonitis
• Peridiverticular abscess
• Large haemorrhage requiring blood transfusions
• Fistula (e.g., between the colon and the bladder or vagina)
• Ileus / obstruction
 Mesenteric Ischaemia
Mesenteric ischaemia is caused by a lack of blood flow through the
mesenteric vessels supplying the intestines, resulting in intestinal
ischaemia.

Blood Supply

There are three main branches of the abdominal aorta that supply the
abdominal organs:
• Coeliac artery
• Superior mesenteric artery
• Inferior mesenteric artery

The foregut includes the stomach, part of the duodenum, biliary

system, liver, pancreas and spleen. This is supplied by the coeliac
artery.

The midgut is from the distal part of the duodenum to the first half
of the transverse colon. This is supplied by the superior mesenteric
artery.

The hindgut is from the second half of the transverse colon to the
rectum. This is supplied by the inferior mesenteric artery.

Chronic Mesenteric Ischaemia

Chronic mesenteric ischaemia (also known as intestinal angina) is

the result of narrowing of the mesenteric blood vessels by
atherosclerosis. This results in intermittent abdominal pain, when the
blood supply cannot keep up with the demand. It is similar to the
pathophysiology of angina, where the blood supply is reduced by
coronary artery disease, resulting in intermittent symptoms.

The typical presentation is with a “classic triad” of:

• Central colicky abdominal pain after eating (starting around 30
minutes after eating and lasting 1-2 hours)
 • Weight loss (due to food avoidance, as this causes pain)
• Abdominal bruit may be heard on auscultation

Risk factors for chronic mesenteric ischaemia are the same as any
other cardiovascular disease:

• Increased age
• Family history
• Smoking
• Diabetes
• Hypertension
• Raised cholesterol

Diagnosis is by CT angiography.

Management involves:
• Reducing modifiable risk factors (e.g., stop smoking)
• Secondary prevention (e.g., statins and antiplatelet medications)
• Revascularisation to improve the blood flow to the intestines

Revascularisation may be performed by:

• Endovascular procedures first-line (i.e., percutaneous
mesenteric artery stenting)
• Open surgery (i.e endarterectomy, re-implantation or bypass
grafting)

Acute Mesenteric Ischaemia

Acute mesenteric ischaemia is typically caused by a rapid blockage in

blood flow through the superior mesenteric artery. This is usually caused
by a thrombus (blood clot) stuck in the artery, blocking blood flow. The
blood clot may be a thrombus that has developed inside the artery or an
embolus from another site that has got stuck in the artery.

A key risk factor is atrial fibrillation, where a thrombus forms in the

right atria, then mobilises (thromboembolism) down the aorta to the
superior mesenteric artery, where it becomes stuck and cuts off the blood
supply.
 Acute mesenteric ischaemia presents with acute, non-specific
abdominal pain. The pain is disproportionate to the examination findings.
Patients can go on to develop shock, peritonitis and sepsis.

Over time, the ischaemia to the bowel will result in necrosis of the
bowel tissue and perforation.
A contrast CT is the diagnostic test of choice for acute mesenteric
ischaemia, allowing the radiologist to assess both the bowel and the
blood supply. Patients will have metabolic acidosis and raised lactate
level due to ischaemia.

Patients require surgery to achieve two objectives:

• Remove necrotic bowel
• Remove or bypass the thrombus in the blood vessel (open surgery
or endovascular procedures may be used)

There is a very high mortality (over 50%) with acute mesenteric

ischaemia.
 Bowel Cancer
Bowel cancer is the fourth most prevalent cancer in the UK, behind
breast, prostate and lung cancer. Bowel cancer usually refers to cancer of
the colon or rectum. Small bowel and anal cancers are less common.

Risk Factors

There are a number of factors that increase the risk of colorectal

cancer:
• Family history of bowel cancer
• Familial adenomatous polyposis (FAP)
• Hereditary nonpolyposis colorectal cancer (HNPCC), also
known as Lynch syndrome
• Inflammatory bowel disease (Crohn’s or ulcerative colitis)
• Increased age
• Diet (high in red and processed meat and low in fibre)
• Obesity and sedentary lifestyle
• Smoking
• Alcohol

Familial adenomatous polyposis (FAP) is an autosomal dominant

condition involving malfunctioning of the tumour suppressor genes
called adenomatous polyposis coli (APC). It results in many polyps
(adenomas) developing along the large intestine. These polyps have
the potential to become cancerous (usually before the age of 40). Patients
have their entire large intestine removed prophylactically to prevent the
development of bowel cancer. This procedure is called a
panproctocolectomy.

Hereditary nonpolyposis colorectal cancer (HNPCC) is also known

as Lynch syndrome. It is an autosomal dominant condition that results
from mutations in DNA mismatch repair (MMR) genes. Patients are at a
higher risk of a number of cancers, but particularly colorectal cancer.
Unlikely FAP, it does not cause multiple adenomas.
 Presentation

The red flags that should make you consider bowel cancer are:
• Change in bowel habit (usually to more loose and frequent stools)
• Unexplained weight loss
• Rectal bleeding
• Unexplained abdominal pain
• Iron deficiency anaemia (microcytic anaemia with low ferritin)
• Abdominal or rectal mass on examination

The NICE guidelines for suspected cancer recognition and referral

(updated January 2021) give various criteria for a “two week wait” urgent
cancer referral, depending on the patient’s age and combination of
symptoms. For example:
• Over 40 years with abdominal pain and unexplained weight loss
• Over 50 years with unexplained rectal bleeding
• Over 60 years with a change in bowel habit or iron deficiency
anaemia

Patients may present acutely with obstruction if the tumour blocks

the passage through the bowel. This presents as a surgical emergency
with vomiting, abdominal pain and absolute constipation.

TOM TIP: Iron deficiency anaemia on its own without any other
explanation (i.e., heavy menstruation) is an indication for a “two
week wait” cancer referral for colonoscopy and gastroscopy (“top
and tail”) for GI malignancy. This is because GI malignancies such
as bowel cancer can cause microscopic bleeding (not visible in
bowel movements) that eventually lead to iron deficiency anaemia.

Faecal Immunochemical Test (FIT) and Bower Cancer

Screening

Faecal immunochemical tests (FIT) look very specifically for the

amount of human haemoglobin in the stool. FIT replaced the older
faecal occult blood (FOB) test, which detected blood in the stool but
could give false positives by detecting blood in food (e.g., from red
meats).
 FIT tests can be used as a test in general practice to help assess for
bowel cancer in specific patients who do not meet the criteria for a two
week wait referral, for example:
• Over 50 with unexplained weight loss and no other symptoms
• Under 60 with a change in bowel habit

FIT tests are used for the bowel cancer screening program in
England. In England, people aged 60 - 74 years are sent a home FIT test
to do every 2 years. If the results come back positive they are sent for a
colonoscopy.

People with risk factors such as FAP, HNPCC or inflammatory bowel

disease are offered a colonoscopy at regular intervals to screen for bowel
cancer.

Investigations

Colonoscopy is the gold standard investigation. It involves an

endoscopy to visualise the entire large bowel. Any suspicious lesions can
be biopsied to get a histological diagnosis, or tattooed in preparation for
surgery.

Sigmoidoscopy involves an endoscopy of the rectum and sigmoid

colon only. This may be used in cases where the only feature is rectal
bleeding. There is the obvious risk of missing cancers in other parts of the
colon.

CT colonography is a CT scan with bowel prep and contrast to

visualise the colon in more detail. This may be considered in patients that
are less fit for a colonoscopy. It is less detailed than a colonoscopy and
does not allow for a biopsy.

Staging CT scan involves a full CT thorax, abdomen and pelvis (CT

TAP). This is used to look for metastasis and other cancers. It may be
used after a diagnosis of colorectal cancer, or as part of the initial workup
in patients with vague symptoms (e.g., weight loss) in addition to
colonoscopy as an initial investigation to exclude other cancers.
 Carcinoembryonic antigen (CEA) is a tumour marker blood test for
bowel cancer. This is not helpful in screening, but it may be used for
predicting relapse in patients previously treated for bowel cancer.

Dukes’ Classification

Dukes’ classification is the system previously used for bowel cancer. It

has now been replaced in clinical practice by the TNM classification, but
you may come across it in older textbooks or question banks. A brief
summary is:
• Dukes A – confined to mucosa and part of the muscle of the bowel
wall
• Dukes B – extending through the muscle of the bowel wall
• Dukes C – lymph node involvement
• Dukes D – metastatic disease

TNM Classification

T for Tumour:
• TX – unable to assess size
• T1 – submucosa involvement
• T2 – involvement of muscularis propria (muscle layer)
 • T3 – involvement of the subserosa and serosa (outer layer), but not
through the serosa
• T4 – spread through the serosa (4a) and reaching other tissues or
organs (4b)

N for Nodes:
• NX – unable to assess nodes
• N0 – no nodal spread
• N1 – spread to 1-3 nodes
• N2 – spread to more than 3 nodes

M for Metastasis:
• M0 – no metastasis
• M1 – metastasis

Management

After a patient has a diagnosis, they are discussed at a

multidisciplinary team (MDT) meeting. The colorectal MDT involves
surgeons, oncologists, radiologists, histopathologists, specialist nurses
and other health professionals to agree on the most appropriate
management options.

The choice of management depends on many factors:

• Clinical condition
• General health
• Stage
• Histology
• Patient wishes

Options for managing bowel cancer (in any combination) are:

• Surgical resection
• Chemotherapy
• Radiotherapy
• Palliative care

Surgical Resection
 The ideal scenario with bowel cancer is to surgically remove the entire
tumour. Removal of the section of bowel affected by the tumour can be
potentially curative. Surgery can also be used palliatively, to reduce the
size of the tumour and improve symptoms.

Laparoscopic surgery (where possible) generally gives better

recovery and fewer complications compared with open surgery. Robotic
surgery is increasingly being used, which is essentially a more advanced
laparoscopic technique.

Surgery involves:
• Identifying the tumour (it may have been tattooed during an
endoscopy)
• Removing the section of bowel containing the tumour
• Creating an end-to-end anastomosis (sewing the remaining ends of
bowel back together)
• Alternatively creating a stoma (bringing the open section of bowel
onto the skin)

Operations

Right hemicolectomy involves removal of the caecum, ascending

and proximal transverse colon.

Left hemicolectomy involves removal of the distal transverse and

descending colon.

High anterior resection involves removing the sigmoid colon (may

be called a sigmoid colectomy).

Low anterior resection involves removing the sigmoid colon and

upper rectum but sparing the lower rectum and anus.

Abdomino-perineal resection (APR) involves removing the rectum

and anus (plus or minus the sigmoid colon) and suturing over the anus. It
leaves the patient with a permanent colostomy.

Hartmann’s procedure is usually an emergency procedure that

involves the removal of the rectosigmoid colon and creation of an
colostomy. The rectal stump is sutured closed. The colostomy may be
permanent or reversed at a later date. Common indications are acute
obstruction by a tumour, or significant diverticular disease.

Complications

There is a long list of potential complications of surgery for bowel

cancer:
• Bleeding, infection and pain
• Damage to nerves, blood vessels, bladder, ureter or bowel
• Post-operative ileus
• Anaesthetic risks
• Laparoscopic surgery converted during the operation to open
surgery (laparotomy)
• Leakage or failure of the anastomosis
• Requirement for a stoma
• Failure to remove the tumour
• Change in bowel habit
• Venous thromboembolism (DVT and PE)
• Incisional hernias
 • Intra-abdominal adhesions

Low Anterior Resection Syndrome

Low anterior resection syndrome may occur after resection of a

portion of bowel from the rectum, with anastomosis between the colon
and rectum. It can result in a number of symptoms, including:
• Urgency and frequency of bowel movements
• Faecal incontinence
• Difficulty controlling flatulence

Follow-Up

Patients will be followed up for a period of time (e.g., 3 years) following

curative surgery. This includes:
• Serum carcinoembryonic antigen (CEA)
• CT thorax, abdomen and pelvis
 Stomas
Stomas are artificial openings of a hollow organ (for example the
bowel). The bowel or urinary system is artificially opened onto the surface
of the abdomen, allowing faeces or urine to drain, bypassing the distal
portions of the bowel or urinary tract. A specially adapted bag (stoma
bag) is fitted around the stoma to collect the waste products and is
emptied as required.

A colostomy is where the large intestine (colon) is brought onto the

skin. Colostomies drain more solid stools, as much of the water is
reabsorbed in the remaining large intestine. They can be flatter to the
skin (compared with ileostomies which have a spout), as the solid
contents are less irritating to the surrounding skin. They are typically
located in the left iliac fossa (LIF).

An ileostomy is where the end portion of the small bowel (ileum) is

brought onto the skin. Ileostomies drain more liquid stools, as the fluid
content is normally reabsorbed later, in the large intestine. They have a
spout, which allows them to drain directly into a tightly fitting stoma bag
without the contents coming into contact with the surrounding skin. They
are typically located in the right iliac fossa (RIF).

A gastrostomy involves creating an artificial connection between the

stomach and the abdominal wall. This can be used for providing feeds
directly into the stomach in patients that cannot meet their nutritional
needs by mouth. Percutaneous endoscopic gastrostomy (PEG) refers
to when the gastrostomy is fitted by an endoscopy procedure.

A urostomy involves creating an opening from the urinary system

onto the skin. They have a spout and are typically located in the right
iliac fossa (RIF).

All patients with stomas should have training on how to manage the
stoma and have regular follow-up with a specialist stoma nurse.
 End Colostomy / End Ileostomy

An end colostomy is created after the removal of a section of the

bowel, where the end part of the proximal portion of the bowel is brought
onto the skin. Faeces are able to drain out of the end colostomy into a
stoma bag. The other open end of the remaining bowel (the distal part) is
sutured and left in the abdomen. It may be reversed at a later date, where
the two ends are sutured together creating an anastomosis.

End colostomies are permanent after an abdomino-perineal

resection (APR) because the entire rectum and anus have been
removed. These are usually located in the lower left abdomen.

End ileostomies are permanent after a panproctocolectomy (total

colectomy with removal of the large bowel, rectum and anus), for
example in the treatment of inflammatory bowel disease or familial
adenomatous polyposis (FAP). An alternative to this is to create an
ileo-anal anastomosis (J-pouch). This is where the ileum is folded back
on itself and fashioned into a larger pouch that functions a bit like a
rectum. This “J-pouch” is then attached to the anus and collects stools
prior to the person passing a motion.

Loop Colostomy / Loop Ileostomy

A loop colostomy is a temporary colostomy used to allow the distal

portion of the bowel and the anastomosis to heal after surgery, before
being reversed around 6-8 weeks later. The bowel is partially opened and
folded so that there are two openings on the skin side-by-side, attached in
the middle.

“Loop” is used because a loop of bowel has been taken through the
abdominal wall, the looped middle section removed, and the two ends
(proximal and distal) are left open. The proximal end (the productive side)
is turned inside out to form a spout to protect the surrounding skin. This
distal end is flatter. This allows you to distinguish between the proximal
and distal portions of the bowel.
 Urostomy

A urostomy is used to drain urine from the kidney, bypassing the

ureters, bladder and urethra. This may be used after a cystectomy
(removal of the bladder).

Forming a urostomy involves creating an ileal conduit. A section of

the ileum (15 - 20cm) is removed and an end-to-end anastomosis is
created so that the bowel is continuous. The ends of the ureters are
connected to the separated section of the ileum. The end of the section is
brought out onto the skin as a stoma and drains urine directly from the
ureters into a urostomy bag.
 Urostomy bags need to fit tightly around the urostomy to avoid urine
coming in contact with the skin. Urine in contact with the skin will cause
irritation and skin damage.

Complications

Stomas have a number of possible complications:

• Psycho-social impact
• Local skin irritation
• Parastomal hernias
• Loss of bowel length leading to high output, dehydration and
malnutrition
• Constipation (colostomies)
• Stenosis
• Obstruction
• Retraction (sinking into the skin)
• Prolapse (telescoping of bowel through hernia site)
• Bleeding
• Granulomas causing raised red lumps around the stoma
 Gallstones
Gallstones are small stones that form within the gallbladder. The
stones form from concentrated bile in the bile duct. Most stones are made
of cholesterol.

Gallstones may be completely asymptomatic. They can also cause

pain and lead to complications, such as acute cholecystitis, acute
cholangitis and pancreatitis.

Gallstones blocking the drainage of the pancreas (via the pancreatic

duct) result in pancreatitis.

Basic Anatomy

The right hepatic duct and left hepatic duct leave the liver and join
together to become the common hepatic duct. The cystic duct from the
gallbladder joins the common hepatic duct halfway along. The
pancreatic duct from the pancreas joins with the common hepatic duct
further along. When the common bile duct and the pancreatic duct join
they become the ampulla of Vater, which then opens into the duodenum.
The sphincter of Oddi is a ring of muscle surrounding the ampulla of
Vater that controls the flow of bile and pancreatic secretions into the
duodenum.
 Key Definitions

There are some key definitions that it is helpful to be familiar with

relating to the gallbladder and gallstones:
• Cholestasis: blockage to the flow of bile
• Cholelithiasis: gallstone(s) are present
• Choledocholithiasis: gallstone(s) in the bile duct
• Biliary colic: intermittent right upper quadrant pain caused by
gallstones obstructing drainage of the gallbladder
• Cholecystitis: inflammation of the gallbladder
• Cholangitis: inflammation of the bile ducts
• Gallbladder empyema: pus in the gallbladder
• Cholecystectomy: surgical removal of the gallbladder
• Cholecystostomy: inserting a drain into the gallbladder

Risk Factors

The risk factors for gallstones can be remembered with the four F’s
mnemonic:

• F - Fat
• F - Fair
 • F - Female
• F - Forty

Presentation

Patients with gallstones may be completely asymptomatic.

The typical symptom of gallstones is biliary colic. Biliary colic is

caused by stones temporarily obstructing drainage of the gallbladder.
They may get lodged at the neck of the gallbladder or in the cystic duct,
then when they falls back into the gallbladder the symptoms resolve. This
causes symptoms of:
• Severe, colicky epigastric or right upper quadrant pain
• Often triggered by meals (particularly high fat meals)
• Lasting 30 minutes to 8 hours
• May be associated with nausea and vomiting

Alternatively, patients may present with a complication of gallstones,

such as:
• Acute cholecystitis
• Acute cholangitis
• Obstructive jaundice (if the stone blocks the ducts)
• Pancreatitis

TOM TIP: Fat entering the digestive system causes

cholecystokinin (CCK) secretion from the duodenum. CCK triggers
contraction of the gallbladder, which leads to biliary colic. Patients
with gallstones and biliary colic are advised to avoid fatty foods to
prevent CCK release and gallbladder contraction. Exam questions
may test this mechanism, so it is worth remembering.

Liver Function Tests

Bilirubin

Bilirubin normally drains from the liver, through the bile ducts and into
the intestines. Raised bilirubin (jaundice) with pale stools and dark
urine represents an obstruction to flow within the biliary system.
Obstruction may be due to:
 • A gallstone in the bile duct
• An external mass pressing on the bile ducts (e.g.,
cholangiocarcinoma or tumour of the head of the pancreas)

Alkaline Phosphatase

Alkaline phosphatase (ALP) is a non-specific marker. It is an enzyme

originating in the liver, biliary system and bone, and abnormal results can
indicate liver, biliary or bone problems. It is often raised in pregnancy due
to production of ALP by the placenta.

A raised ALP is consistent with biliary obstruction when there is also

right upper quadrant pain or jaundice.

Raised alkaline phosphatase can also be caused by liver or bone

malignancy, primary biliary cirrhosis, Paget’s disease of the bone and
many other things.

Aminotransferases

Alanine aminotransferase (ALT) and aspartate aminotransferase

(AST) are enzymes produced in the liver. They are helpful as markers of
hepatocellular injury (damage to the liver cells).

In patients with cholestasis (e.g., due to gallstones), ALT and AST can
increase slightly, with a higher rise in ALP (“an obstructive picture”).

If ALT and AST are high compared with the ALP level, this indicates a
problem inside the liver with hepatocellular injury (“a hepatitic picture”).

Ultrasound

An ultrasound scan is a useful first-line investigation for symptoms of

gallstone disease, for example, abdominal pain, right upper quadrant pain
and jaundice. It is the most sensitive initial imaging test for gallstones (CT
scans are not good at identifying gallstones or biliary disease).

Ultrasound is limited by the patient’s weight, gaseous bowel

obstructing the view and discomfort from the probe.
 Ultrasound Findings

Ultrasound can be helpful in identifying:

• Gallstones in the gallbladder
• Gallstones in the ducts
• Bile duct dilatation (normally less than 6mm diameter)
• Acute cholecystitis (thickened gallbladder wall, stones or sludge in
gallbladder and fluid around the gallbladder)
• The pancreas and pancreatic duct

Magnetic Resonance Cholangio-Pancreatography

A magnetic resonance cholangio-pancreatography (MRCP) is an

MRI scan with a specific protocol that produces a detailed image of the
biliary system. It is very sensitive and specific for biliary tree disease,
such as stones in the bile duct and malignancy.

MRCP is used in a number of scenarios for gaining a detailed picture

of the biliary system, such as identifying biliary strictures or congenital
abnormalities.

With gallstone disease, MRCP is typically used to investigate further if

the ultrasound scan does not show stones in the duct, but there is bile
duct dilatation or raised bilirubin suggestive of obstruction.

Endoscopic Retrograde Cholangio-Pancreatography

An endoscopic retrograde cholangio-pancreatography (ERCP)

involves inserting an endoscope down the oesophagus, past the
stomach, to the duodenum and the opening of the common bile duct (the
sphincter of Oddi). This gives the operator access to the biliary system.
The main indication for ERCP is to clear stones in the bile ducts.

ERCP allows the operator to:

• Inject contrast and take x-rays to visualise the biliary system and
diagnose pathology (e.g., stones or strictures)
• Perform a sphincterotomy on the sphincter of Oddi if it is
dysfunctional (blocking flow)
• Clear stones from the ducts
 • Insert stents to improve bile duct drainage (e.g., with strictures or
tumours)
• Take biopsies of tumours

Key complications of ERCP are:

• Excessive bleeding
• Cholangitis (infection in the bile ducts)
• Pancreatitis

CT Scans

CT scans are less useful for looking at the biliary system and for
gallstones. They may be used to look for differential diagnoses (e.g.,
pancreatic head tumour) and complications such as perforation and
abscesses.

Management

Asymptomatic patients with gallstones may be treated conservatively,

with no intervention required.

Patients with symptoms or complications of gallstones are treated with

cholecystectomy, which is surgical removal of the gallbladder (provided
they are fit for surgery).

Cholecystectomy

Cholecystectomy involves surgical removal of the gallbladder. It is

indicated where patients are symptomatic of gallstones, or the gallstones
are leading to complications (e.g., acute cholecystitis). Stones in the bile
ducts can be removed before (by ERCP) or during surgery.

Laparoscopic cholecystectomy (keyhole surgery) is preferred to

open cholecystectomy (with a right subcostal “Kocher” incision), as it
has less complications and a faster recovery.

Complications of cholecystectomy include:

• Bleeding, infection, pain and scars
• Damage to the bile duct including leakage and strictures
 • Stones left in the bile duct
• Damage to the bowel, blood vessels or other organs
• Anaesthetic risks
• Venous thromboembolism (deep vein thrombosis or pulmonary
embolism)
• Post-cholecystectomy syndrome

Post-cholecystectomy syndrome involves a group of non-specific

symptoms that can occur after a cholecystectomy. They may be attributed
to changes in the bile flow after removal of the gallbladder. Symptoms
often improve with time. Symptoms include:
• Diarrhoea
• Indigestion
• Epigastric or right upper quadrant pain and discomfort
• Nausea
• Intolerance of fatty foods
• Flatulence
 Acute Cholecystitis
Acute cholecystitis refers to inflammation of the gallbladder, which is
caused by a blockage of the cystic duct preventing the gallbladder from
draining. It is a key complication of gallstones, and the majority of cases
(around 95%) are caused by gallstones (calculous cholecystitis).
Gallstones may be trapped in the neck of the gallbladder or in the
cystic duct.

In a small number of cases, the dysfunction in gallbladder emptying is

caused by something other than gallstones (acalculous cholecystitis).
One scenario where this may occur is in patients on total parental
nutrition or having long periods of fasting (for example in ICU for other
serious conditions), where the gallbladder is not being stimulated by food
to regularly empty, resulting in a build-up of pressure.

Presentation

The main presenting symptom of cholecystitis is pain in the right

upper quadrant (RUQ). This may radiate to the right shoulder.

Other features include:

• Fever
• Nausea
• Vomiting
• Tachycardia (fast heart rate) and tachypnoea (raised respiratory
rate)
• Right upper quadrant tenderness
• Murphy’s sign
• Raised inflammatory markers and white blood cells

Murphy’s sign is suggestive of acute cholecystitis:

• Place a hand in RUQ and apply pressure
• Ask the patient to take a deep breath in
• The gallbladder will move downwards during inspiration and come
in contact with your hand
 • Stimulation of the inflamed gallbladder results in acute pain and
sudden stopping of inspiration

Imaging

The first step is an abdominal ultrasound scan. Signs of acute

cholecystitis on ultrasound are:
• Thickened gallbladder wall
• Stones or sludge in gallbladder
• Fluid around the gallbladder

Magnetic resonance cholangiopancreatography (MRCP) may be

used to visualise the biliary tree in more detail if a common bile duct stone
is suspected but not seen on an ultrasound scan (e.g., bile duct dilatation
or raised bilirubin).

Management

Patients with suspected acute cholecystitis need emergency

admission for investigations and management.

Conservative management involves:

• Nil by mouth
• IV fluids
• Antibiotics (as per local guidelines)
• NG tube if required for vomiting

Endoscopic retrograde cholangio-pancreatography (ERCP) can

be used to remove stones trapped in the common bile duct.

Cholecystectomy (removal of the gallbladder) is usually be

performed during the acute admission, within 72 hours of symptoms. In
some cases, it may be delayed for 6-8 weeks after the acute episode to
allow the inflammation to settle.

Complications

• Sepsis
• Gallbladder empyema
 • Gangrenous gallbladder
• Perforation

Gallbladder Empyema

Gallbladder empyema refers to infected tissue and pus collecting in

the gallbladder. Management involves IV antibiotics and one of two main
options:
• Cholecystectomy (to remove the gallbladder)
• Cholecystostomy (inserting a drain into the gallbladder to allow
the infected contents to drain)
 Acute Cholangitis
Acute cholangitis is infection and inflammation in the bile ducts. It is a
surgical emergency and has a high mortality due to sepsis and
septicaemia.

There are two main causes of acute cholangitis:

• Obstruction in the bile ducts stopping bile flow (i.e., gallstones in
the common bile duct)
• Infection introduced during an ERCP procedure

The most common organisms are:

1. Escherichia coli
2. Klebsiella species
3. Enterococcus species

Charcot’s Triad

Acute cholangitis presents with Charcot’s triad:

• Right upper quadrant pain
• Fever
• Jaundice (raised bilirubin)

TOM TIP: It is worth remembering Charcot’s triad. If you see a

patient in your exams with fever, raised bilirubin and right upper
quadrant pain, you know the diagnosis is acute cholangitis.

Management

Patients with suspected acute cholangitis need emergency admission

for investigations and management.

Patients need acute management of sepsis and acute abdomen,

including:
• Nil by mouth
• IV fluids
 • Blood cultures
• IV antibiotics (as per local guidelines)
• Involvement of seniors and potentially HDU or ICU

Imaging to diagnose common bile duct (CBD) stones and

cholangitis (from least to most sensitive) are:
• Abdominal ultrasound scan
• CT scan
• Magnetic resonance cholangio-pancreatography (MRCP)
• Endoscopic ultrasound

An endoscopic retrograde cholangio-pancreatography (ERCP) is

required to remove stones blocking the bile duct. It involves inserting an
endoscope down the oesophagus, past the stomach, to the duodenum
and the opening of the common bile duct (the sphincter of Oddi). This
gives the operator access to the biliary system. A number of procedures
can be performed during an ERCP:
• Cholangio-pancreatography: retrograde injection of contrast into
the duct through the sphincter of Oddi and x-ray images to visualise
biliary system
• Sphincterotomy: making a cut in the sphincter to dilate it and
allow stone removal
• Stone removal: a basket can be inserted and pulled through the
common bile duct to remove stones
• Balloon dilatation: a balloon can be inserted and inflated to treat
strictures
• Biliary stenting: a stent can be inserted to maintain a patent bile
duct (for strictures or tumours)
• Biopsy: a small biopsy can be taken to diagnose obstructing
lesions

Percutaneous transhepatic cholangiogram (PTC) involves

radiologically guided insertion of a drain through the skin and liver, into
the bile ducts. The drain relieves the immediate obstruction. A stent can
be inserted to give longer-lasting relief of obstruction. This is an option for
patients that are less suitable for ERCP, or where ERCP has failed.
 Cholangiocarcinoma
Cholangiocarcinoma is a type of cancer that originates in the bile
ducts. The majority are adenocarcinomas. It may affect the bile ducts
inside the liver (intrahepatic ducts) or outside the liver (extrahepatic
ducts). The most common site is in the perihilar region, where the right
and left hepatic duct have joined to become the common hepatic duct,
just after leaving the liver.

Key risk factors include:

• Primary sclerosing cholangitis
• Liver flukes (a parasitic infection)

TOM TIP: Patients with ulcerative colitis are at risk of developing

primary sclerosing cholangitis. Patients that have primary
sclerosing cholangitis are at risk of developing cholangiocarcinoma
(10-20%). Primary sclerosing cholangitis is the key risk factor for
cholangiocarcinoma worth remembering for your exams. The other
notable cause is parasitic infection with liver flukes, which are found
in various parts of Southeast Asia and Europe.

Presentation

Obstructive jaundice is the key presenting feature to remember.

Obstructive jaundice is also associated with:
• Pale stools
• Dark urine
• Generalised itching

Other non-specific signs and symptoms include:

• Unexplained weight loss
• Right upper quadrant pain
• Palpable gallbladder (swelling due to an obstruction in the duct
distal to the gallbladder)
• Hepatomegaly
 Courvoisier's law states that a palpable gallbladder along with
jaundice is unlikely to be gallstones. The cause is usually
cholangiocarcinoma or pancreatic cancer.

TOM TIP: Painless jaundice should make you think of

cholangiocarcinoma or cancer of the head of the pancreas.
Pancreatic cancer is more common, so this is likely the answer in
your exams.

Investigations

Diagnosis is based on imaging (CT or MRI) plus histology from a

biopsy.

Staging CT scan involves a full CT thorax, abdomen and pelvis (CT

TAP). This is used to look for metastasis and other cancers.

CA 19-9 (carbohydrate antigen) is a tumour marker that may be

raised in cholangiocarcinoma. It is also raised in pancreatic cancer and a
number of other malignant and non-malignant conditions.

Magnetic resonance cholangio-pancreatography (MRCP) may be

used to visualise the biliary system in detail to assess the obstruction.

Endoscopic retrograde cholangio-pancreatography (ERCP) can

be used to put a stent in and relieve the obstruction, and also obtain a
biopsy from the tumour.

Management

Management will be decided at a multidisciplinary team (MDT)

meeting.

Curative surgery may be possible in early cases. It may be combined

with radiotherapy and chemotherapy.

In most cases, curative surgery is not possible. Palliative treatment

may involve:
• Stents inserted to relieve the biliary obstruction
• Surgery to improve symptoms (e.g., bypassing the biliary
obstruction)
• Palliative chemotherapy
• Palliative radiotherapy
• End of life care with symptom control
 Pancreatic Cancer
Pancreatic cancer is often diagnosed late and has a very poor
prognosis. The vast majority are adenocarcinomas, and most occur in
the head of the pancreas (as opposed to the body and tail). Once a
tumour in the head of the pancreas grows large enough it can compress
the bile ducts, resulting in obstructive jaundice.

Pancreatic cancers tend to spread and metastasise early, particularly

to the liver, then to the peritoneum, lungs and bones. The average
survival, when diagnosed with advanced disease, is around 6 months.

When caught early, the cancer is isolated to the pancreas and surgery
is possible, the 5-year survival is still around 25% or less.

Presentation

Painless obstructive jaundice is a key presenting feature that

should make you immediately consider pancreatic cancer (the key
differential is cholangiocarcinoma). This occurs when a tumour at the
head of the pancreas compresses the bile ducts, blocking the flow of bile
out of the liver. It presents with:
• Yellow skin and sclera
 • Pale stools
• Dark urine
• Generalised itching

The other presenting features for pancreatic cancer can be vague:

• Non-specific upper abdominal or back pain
• Unintentional weight loss
• Palpable mass in the epigastric region
• Change in bowel habit
• Nausea or vomiting
• New‑onset diabetes or worsening of type 2 diabetes

TOM TIP: It is worth noting that a new onset of diabetes, or a

rapid worsening of glycaemic control with type 2 diabetes, can be a
sign of pancreatic cancer. Keep pancreatic cancer in mind if a
patient in your exams or practice has worsening glycaemic control
despite good lifestyle measures and medication.

Referral

The NICE guidelines on suspected cancer (updated January 2021)

give the criteria for when to refer for suspected pancreatic cancer:
• Over 40 with jaundice - referred on a two week wait referral
• Over 60 with weight loss plus an additional symptom (see below) -
referred for a direct access CT abdomen

The NICE guidelines suggest a GP referral for a direct access CT

abdomen (or ultrasound if not available) to assess for pancreatic cancer
if a patient over 60 has weight loss plus any of:

• Diarrhoea
• Back pain
• Abdominal pain
• Nausea
• Vomiting
• Constipation
• New‑onset diabetes
 TOM TIP: As far as I am aware, suspected pancreatic cancer is
the only scenario where GPs can refer directly for a CT scan.
Whenever guidelines and clinical practice have notable exceptions
like this it is worth taking note of, as these make good facts for
examiners to test your knowledge on.

Named Signs

Courvoisier's law states that a palpable gallbladder along with

jaundice is unlikely to be gallstones. The cause is usually
cholangiocarcinoma or pancreatic cancer.

Trousseau’s sign of malignancy refers to migratory

thrombophlebitis as a sign of malignancy, particularly pancreatic
adenocarcinoma. Thrombophlebitis is where blood vessels become
inflamed with an associated blood clot (thrombus) in that area. Migratory
refers to the thrombophlebitis reoccurring in different locations over time.

Investigations

Diagnosis is based on imaging (usually CT scan) plus histology from

a biopsy.

Staging CT scan involves a full CT thorax, abdomen and pelvis (CT

TAP). This is used to look for metastasis and other cancers.

CA 19-9 (carbohydrate antigen) is a tumour marker that may be

raised in pancreatic cancer. It is also raised in cholangiocarcinoma and a
number of other malignant and non-malignant conditions.

Magnetic resonance cholangio-pancreatography (MRCP) may be

used to assess the biliary system in detail to assess the obstruction.

Endoscopic retrograde cholangio-pancreatography (ERCP) can

be used to put a stent in and relieve the obstruction, and also obtain a
biopsy from the tumour.

Biopsy may be taken through the skin (percutaneous) under

ultrasound or CT guidance, or during an endoscopy under ultrasound
guidance.

Management

Management will be decided at a hepatobiliary (HPB) MDT meeting.

Surgery to remove the tumour is more likely to be considered with

small tumours isolated in the head of the pancreas (about 10% of cases).
There are a number of surgical options depending on the location of the
tumour:
• Total pancreatectomy
• Distal pancreatectomy
• Pylorus-preserving pancreaticoduodenectomy (PPPD)
(modified Whipple procedure)
• Radical pancreaticoduodenectomy (Whipple procedure)

In most cases, curative surgery is not possible. Palliative treatment

may involve:
• Stents inserted to relieve the biliary obstruction
• Surgery to improve symptoms (e.g., bypassing the biliary
obstruction)
• Palliative chemotherapy (to improve symptoms and extend life)
• Palliative radiotherapy (to improve symptoms and extend life)
• End of life care with symptom control

Whipple Procedure

A Whipple procedure (pancreaticoduodenectomy) is a surgical

operation to remove a tumour of the head of the pancreas that has not
spread. A Whipple procedure is a massive operation so patients need to
be in good baseline health. It involves the removal of the:

• Head of the pancreas

• Pylorus of the stomach
• Duodenum
• Gallbladder
• Bile duct
• Relevant lymph nodes
 A modified Whipple procedure involves leaving the pylorus in place.
It is also known as a pylorus-preserving pancreaticoduodenectomy
(PPPD).
 Pancreatitis
Pancreatitis refers to inflammation of the pancreas. It can be
categorised as acute pancreatitis or chronic pancreatitis. This section
relates mainly to acute pancreatitis.

Acute pancreatitis presents with a rapid onset of inflammation and

symptoms. After an episode of acute pancreatitis, normal function usually
returns.

Chronic pancreatitis involves longer-term inflammation and

symptoms with a progressive and permanent deterioration in pancreatic
function.

Causes

The three key causes of pancreatitis to remember are:

• Gallstones
• Alcohol
• Post-ERCP

Gallstone pancreatitis is caused by gallstones getting trapped at the

end of the biliary system (ampulla of Vater), blocking the flow of bile and
pancreatic juice into the duodenum. The reflux of bile into the pancreatic
duct, and the prevention of pancreatic juice containing enzymes from
being secreted, results in inflammation in the pancreas. Gallstone
pancreatitis is more common in women and older patients.

Alcohol is directly toxic to pancreatic cells, resulting in inflammation.

Alcohol-induced pancreatitis is more common in men and younger
patients.

I GET SMASHED is a popular mnemonic for remembering a long list

of causes of pancreatitis:
• I - Idiopathic
• G - Gallstones
• E - Ethanol (alcohol consumption)
 • T - Trauma
• S - Steroids
• M - Mumps
• A - Autoimmune
• S - Scorpion sting (the one everyone remembers)
• H - Hyperlipidaemia
• E - ERCP
• D - Drugs (furosemide, thiazide diuretics and azathioprine)

Presentation

Acute pancreatitis typically presents with an acute onset of:

• Severe epigastric pain
• Radiating through to the back
• Associated vomiting
• Abdominal tenderness
• Systemically unwell (e.g., low-grade fever and tachycardia)

Acute pancreatitis is a clinical diagnosis, based mainly on the

presenting features and the amylase level.

Investigations

Initial investigations are required as with any presentation of an acute

abdomen. Importantly these need to include the blood tests required for
calculating the Glasgow score:
• FBC (for white cell count)
• U&E (for urea)
• LFT (for transaminases and albumin)
• Calcium
• ABG (for PaO2 and blood glucose)

Amylase is raised more than 3 times the upper limit of normal in acute
pancreatitis. In chronic pancreatitis it may not rise because the pancreas
has reduced function.

C-reactive protein (CRP) can be used to monitor the level of

inflammation.
 Ultrasound is the initial investigation of choice in assessing for
gallstones.

CT abdomen can assess for complications of pancreatitis (such as

necrosis, abscesses and fluid collections). It is not usually required unless
complications are suspected (e.g., the patient is becoming more unwell).

Glasgow Score

The Glasgow score is used to assess the severity of pancreatitis. It

gives a numerical score based on how many of the key criteria are
present:
• 0 or 1 - mild pancreatitis
• 2 - moderate pancreatitis
• 3 or more - severe pancreatitis

The criteria for the Glasgow score can be remembered using the
PANCREAS mnemonic (1 point for each answer):
• P – Pa02 < 8 KPa
• A – Age > 55
• N – Neutrophils (WBC > 15)
• C – Calcium < 2
• R – uRea >16
• E – Enzymes (LDH > 600 or AST/ALT >200)
• A – Albumin < 32
• S – Sugar (Glucose >10)

Management of Acute Pancreatitis

Patients with acute pancreatitis can become very unwell rapidly. They
require admission for supportive management. Moderate or severe cases
should be considered for management in the high dependency unit
(HDU) or intensive care unit (ICU).

Management involves:
• Initial resuscitation (ABCDE approach)
• IV fluids
• Nil by mouth
 • Analgesia
• Careful monitoring
• Treatment of gallstones in gallstone pancreatitis (ERCP /
cholecystectomy)
• Antibiotics if there is evidence of a specific infection (e.g., abscess
or infected necrotic area)
• Treatment of complications (e.g., endoscopic or percutaneous
drainage of large collections)

Most patients will improve within 3-7 days.

Complications of Acute Pancreatitis

• Necrosis of the pancreas

• Infection in a necrotic area
• Abscess formation
• Acute peripancreatic fluid collections
• Pseudocysts (collections of pancreatic juice) can develop 4 weeks
after acute pancreatitis
• Chronic pancreatitis

Chronic Pancreatitis

Chronic pancreatitis refers to chronic inflammation in the pancreas. It

results in fibrosis and reduced function of the pancreatic tissue. Alcohol
is the most common cause. It presents with similar symptoms to acute
pancreatitis, but generally less intense and longer-lasting.

Key complications are:

• Chronic epigastric pain
• Loss of exocrine function, resulting in a lack of pancreatic
enzymes (particularly lipase) secreted into the GI tract
• Loss of endocrine function, resulting in a lack of insulin, leading
to diabetes
• Damage and strictures to the duct system, resulting in obstruction
of the excretion of pancreatic juice and bile
• Formation of pseudocysts or abscesses
 Management of Chronic Pancreatitis

Abstinence from alcohol and smoking is important in managing

symptoms and complications.

Analgesia can be used to manage the pain, although pain can be

severe and difficult to manage.

Replacement pancreatic enzymes (Creon) may be required if there

is a loss of pancreatic enzymes (i.e., lipase). Otherwise, a lack of
enzymes leads to malabsorption of fat, greasy stools (steatorrhoea), and
deficiency in fat-soluble vitamins.

Subcutaneous insulin regimes may be required to treat diabetes.

ERCP with stenting can be used to treat strictures and obstruction of

the biliary system and pancreatic duct.

Surgery may be required in specialist centres to treat:

• Severe chronic pain (by draining the ducts and removing inflamed
pancreatic tissue)
• Obstruction of the biliary system and pancreatic duct
• Pseudocysts
• Abscesses
 Liver Transplant
The most obvious source for a liver is from a healthy person who has
just died. When an entire liver is transplanted from a deceased donor to a
recipient it is known as an orthotopic transplant. This translates as
straight (ortho-) in place (-topic).

The liver can regenerate as an organ. Therefore, it is possible to take

a portion of the organ from a living donor, transplant it into a patient and
have both regenerate to become two fully functioning organs. This is
known as a living donor transplant.

It is also possible to split the organ of a deceased person into two and
transplant it into two patients and have them regenerate to their normal
size in each recipient. This is known as split donation.

Indications

Indications for liver transplant can be split into two categories: acute
liver failure or chronic liver failure. They may also be used in specific
cases of hepatocellular carcinoma.

Acute liver failure usually requires an immediate liver transplant, and

these patients are placed on the top of the transplant list. The most
common causes are acute viral hepatitis and paracetamol overdose.

Chronic liver failure patients can wait longer for their liver transplant
and are put on a standard transplant list. It is normal for it to take around 5
months for a liver to become available.

Factors Suggesting Unsuitability for Liver

Transplantation

• Significant co-morbidities (e.g., severe kidney or heart disease)

• Excessive weight loss and malnutrition
• Active hepatitis B, hepatitis C or other infection
 • End-stage HIV
• Active alcohol use (generally 6 months of abstinence is required)

Surgery

The liver transplant surgery is carried out in a specialist transplant

centre. It involves a “rooftop” or “Mercedes Benz" incision along the
lower costal margin for open surgery. The liver is mobilised away from the
other tissues and excised. The new liver, biliary system and blood supply
is then implanted and connected.

Post-Transplantation Care

Patients will require lifelong immunosuppression (e.g., steroids,

azathioprine and tacrolimus) and careful monitoring of these drugs. They
are required to follow lifestyle advice and require monitoring and
treatment for complications:
• Avoid alcohol and smoking
• Treating opportunistic infections
• Monitoring for disease recurrence (e.g., of hepatitis or primary
biliary cirrhosis)
• Monitoring for cancer, as there is a significantly higher risk in
immunosuppressed patients

Monitoring for evidence of transplant rejection:

• Abnormal LFTs
• Fatigue
• Fever
• Jaundice
 Urology
Obstructive Uropathy
Urinary Catheters
Benign Prostatic Hyperplasia
Prostatitis
Prostate Cancer
Epididymo-orchitis
Testicular Torsion
Scrotal Lumps
Testicular Cancer
Lower Urinary Tract Infections
Pyelonephritis
Interstitial Cystitis
Bladder Cancer
Kidney Stones
Renal Cell Carcinoma
Renal Transplant
 Obstructive Uropathy
The term obstructive uropathy refers to a blockage preventing urine
flow through the ureters, bladder and urethra. This blockage causes a
build-up of urine and back-pressure up to the kidneys, resulting in
impaired kidney function.

Anatomy of the Urinary Tract

The key structures of the urinary tract are the:

• Kidneys
• Ureters
• Bladder (with the detrusor muscle)
• Urethra
• Internal urethral sphincter (smooth muscle under autonomic
control)
• Prostate (in males)
• External urethral sphincter (skeletal muscle under voluntary
control)
It is worth being familiar with the basic anatomy of the kidney.

From the outside in, the basic structures of the kidney are the:
• Cortex
• Medulla
• Pyramids and columns
• Major and minor calyx (pleural: calyces)
• Renal pelvis
• Pelviureteric junction (PUJ)
• Ureter
 Obstructive Uropathy

Obstruction leads to back-pressure in the urinary system, causing

areas proximal to the site of obstruction to become swollen with urine. For
example, obstruction at the opening of the ureters in the bladder, from a
bladder tumour, will result in swelling of the ureter and kidney on that
side. Swelling of the kidney is known as hydronephrosis.
 Vesicoureteral reflux (VUR) refers to urine refluxing from the bladder
back into the ureters.

When obstructive uropathy leads to an acute reduction in kidney

function, it is referred to as a “post-renal” acute kidney injury (AKI).
This is different from “pre-renal” AKI, which is caused by hypoperfusion
of the kidneys (e.g., due to dehydration, sepsis or acute blood loss), and
“renal” AKI, which refers to damage within the kidney itself (e.g., due to
glomerulonephritis or nephrotoxic medications).
 TOM TIP: Whenever someone asks you the cause of renal
impairment, always answer: "the causes are pre-renal, renal or post-
renal". This will impress them and allow you to think through the
causes more logically.

Presentation

An upper urinary tract obstruction (i.e., in the ureters) presents with:

• Loin to groin or flank pain on the affected side (due to stretching
and irritation of the ureter and kidney)
• Reduced or no urine output
• Non-specific systemic symptoms, such as vomiting
• Impaired renal function on blood tests (i.e., raised creatinine)

Lower urinary tract obstruction (i.e., in the bladder or urethra) presents

with:
• Difficulty or inability to pass urine (e.g., poor flow, difficulty initiating
urination or terminal dribbling)
• Urinary retention, with an increasingly full bladder
• Impaired renal function on blood tests (i.e., raised creatinine)

An ultrasound of the kidneys, ureters and bladder can be helpful in

diagnosing obstructive uropathy.

TOM TIP: “Loin” is a vague term that can be confusing and does
not describe a specific location. Sometimes “loin” is used to
describe the sides of the body between the lower ribs and pelvis,
although “flank” is also used for the same area. “Loin” is also used
to describe the side of the lower back, where the kidneys are
situated; as well as the lumbar region of the back, the groin and the
area around the hips.

“Loin to groin” pain usually refers to pain that circles from the
kidney area at the back, round the sides and down into the groin.
“Loin to groin” pain is a sign of pathology in the ureter and kidney
on that side, such as kidney stones or pyelonephritis.

The “renal angle”, also called the “costovertebral angle”, refers

to the angle formed by the twelfth rib and vertebral column at the
back. The lower part of the kidneys are at the renal angle.
Tenderness in the renal angle suggests kidney pathology.

Common Causes

Upper urinary tract obstruction:

• Kidney stones
• Tumours pressing on the ureters
• Ureter strictures (due to scar tissue narrowing the tube)
• Retroperitoneal fibrosis (the development of scar tissue in the
retroperitoneal space)
• Bladder cancer (blocking the ureteral openings to the bladder)
• Ureterocele (ballooning of the most distal portion of the ureter - this
is usually congenital)

Lower urinary tract obstruction:

• Benign prostatic hyperplasia (benign enlarged prostate)
• Prostate cancer
• Bladder cancer (blocking the neck of the bladder)
• Urethral strictures (due to scar tissue)
• Neurogenic bladder

Neurogenic Bladder

Neurogenic bladder refers to abnormal function of the nerves

innervating the bladder and urethra. It can result in overactivity or
underactivity in the detrusor muscle of the bladder and the sphincter
muscles of the urethra.
Key causes are:

• Multiple sclerosis
• Diabetes
• Stroke
• Parkinson's disease
• Brain or spinal cord injury
• Spina bifida

Neurogenic bladder can result in a variety of problems, including:

• Urge incontinence
 • Increased bladder pressure
• Obstructive uropathy

Management of Obstructive Uropathy

Management involves removing or bypassing the obstruction.

A nephrostomy may be used to bypass an obstruction in the upper

urinary tract (e.g., a ureteral stone). A nephrostomy involves surgically
inserting a thin tube through the skin at the back, through the kidney and
into the ureter. This tube allows urine to drain out of the body, into a
catheter bag.

A urethral or suprapubic catheter may be used to bypass an

obstruction in the lower urinary tract (e.g., a urethral stricture or prostatic
hyperplasia). A urethral catheter is a tube, inserted through the urethra,
into the bladder. A suprapubic catheter is a tube, inserted through the
skin just above the pubic bone, directly into the bladder.

Complications of Obstructive Uropathy

• Pain
• Acute kidney injury (post-renal)
• Chronic kidney disease
• Infection (from bacteria tracking up the urinary tract into areas of
stagnated urine)
• Hydronephrosis (swelling of the renal pelvis and calyces in the
kidney)
• Urinary retention and bladder distention
• Overflow incontinence of urine

Hydronephrosis

Hydronephrosis is swelling of the renal pelvis and calyces in the

kidney. This occurs due to obstruction of the urinary tract, leading to back-
pressure into the kidneys.

Idiopathic hydronephrosis is the result of a narrowing at

the pelviureteric junction (PUJ) - the site where the renal pelvis
becomes the ureter. This narrowing may be congenital or develop later. It
can be treated with an operation to correct the narrowing and restructure
the renal pelvis (pyeloplasty).

Typical presenting features of hydronephrosis are vague renal angle

pain and a mass in the kidney area. It may be seen on an ultrasound, CT
scan or intravenous urogram (x-ray with IV contrast collecting in the
urinary tract).

Treatment of hydronephrosis involves treating the underlying cause. If

required, pressure can be relieved with either:
• Percutaneous nephrostomy - a tube inserted under radiological
guidance through the skin and kidney into the ureter, which drains
urine into a catheter bag
• Antegrade ureteric stent - a stent inserted under radiological
guidance through the kidney into the ureter, which keeps the ureter
patent and relieves the obstruction
 Urinary Catheters
Urinary catheters are inserted into the bladder to passively drain urine.
The urine drains through a tube into a catheter bag. They may be used
short term or long term, depending on the indication.

When urinary catheters are left in, a balloon on the end of the catheter
is inflated inside the bladder with sterile water (usually 10mls), preventing
the catheter from falling out.

Indications

The reasons for inserting a urinary catheter include:

• Urinary retention due to a lower urinary tract obstruction (e.g., an
enlarged prostate)
• Neurogenic bladder (e.g., intermittent self-catheterisation in
multiple sclerosis)
• Surgery (during and after)
• Output monitoring in acutely unwell patients (e.g., sepsis or
intensive care)
• Bladder irrigation (e.g., to wash out blood clots in the bladder)
• Delivery of medications (e.g., chemotherapy to treat bladder
cancer)

A bladder scanner can be used to measure the volume of urine in the

bladder. A post-void bladder scan (measured after the patient attempts
to empty their bladder) can indicate the need for a catheter (e.g., more
than 500mls).

TOM TIP: A common presentation requiring catheterisation is an

older man presenting acutely with urinary retention due to an
enlarged prostate. Typical management involves inserting a
catheter, starting tamsulosin (an alpha-blocker) and discharging the
patient to have a trial without a catheter (TWOC) in the community. It
is worth remembering tamsulosin for your exams, as they may give
you this scenario and ask what medication should be started. The
key side effect to remember is postural hypotension, leading to
dizziness on standing or falls.

Types of Catheter

Urethral catheters are inserted through the urethra into the bladder.
There are various types:
• Intermittent catheters - simple catheters used to drain urine, then
immediately removed
• Foley catheter (two-way catheter) - the "standard" catheter with
an inflatable balloon to hold it in place
• Coudé tip catheter - has a curved tip to help navigate it past an
obstruction during insertion
• Three-way catheter - has three tubes used for inflating the
balloon, injecting irrigation and drainage

Suprapubic catheters are inserted through the abdomen into the

bladder, just above the pubic symphysis, under local anaesthetic. An
inflated balloon holds them in place in the same way as a urethral
catheter. When used long term, they can be easily replaced at regular
intervals by an appropriately trained person.

TOM TIP: The catheter you will see most often on the wards and
in OSCEs is the Foley catheter (two-way catheter). It might not be
possible to insert a Foley catheter into a man with acute urinary
retention due to an enlarged prostate. If using a Foley catheter fails,
it is worth giving a Coudé tip catheter a try, as the slightly rigid
curved tip can make bypassing an obstruction much easier. One of
the most rewarding jobs as a junior doctor is inserting a catheter for
someone in acute urinary retention, where you can almost
immediately relieve a patient's distress. Always replace the foreskin
after inserting a catheter (risk of paraphimosis)!

Trial Without Catheter

A trial without a catheter (TWOC) involves removing a urethral

catheter to see if a patient can manage without it. After the catheter is
removed, the urine output is monitored, and a bladder scanner is used to
make sure there is minimal residual urine left in the bladder. They may
"fail" the TWOC, in which case another catheter is inserted.

Catheter-Associated Urinary Tract Infections

Infections are a key complication of urinary catheters. The longer the

catheter is in place, the more likely bacteria are to grow in the urine. A
sample of urine should be taken directly from the catheter or sample port
using an aseptic technique (not from the catheter bag as this may be
contaminated).

There are NICE guidelines on catheter-associated UTIs from 2018,

see the full guidelines when treating patients.

Patients without symptoms do not generally require antibiotics for

bacteria in the urine (bacteriuria).

Patients with symptoms require treatment with 7 days of antibiotics.

Depending on the severity of symptoms, this may be with oral antibiotics
or require admission to hospital and IV antibiotics. The catheter should be
changed as soon as possible (but not delaying antibiotics).
 Benign Prostatic Hyperplasia
Benign prostatic hyperplasia (BPH) is a very common condition
affecting men in older age (usually over 50 years). It is caused by
hyperplasia of the stromal and epithelial cells of the prostate. It usually
presents with lower urinary tract symptoms.

Lower Urinary Tract Symptoms

There are typical lower urinary tract symptoms (LUTS) that occur
with prostate pathology:
• Hesitancy - difficult starting and maintaining the flow of urine
• Weak flow
• Urgency - a sudden pressing urge to pass urine
• Frequency - needing to pass urine often, usually with small
amounts
• Intermittency - flow that starts, stops and varies in rate
• Straining to pass urine
• Terminal dribbling - dribbling after finishing urination
 • Incomplete emptying - not being able to fully empty the bladder,
with chronic retention
• Nocturia - having to wake to pass urine multiple times at night

The international prostate symptom score (IPSS) is a scoring

system that can be used to assess the severity of lower urinary tract
symptoms.

Assessment

The initial assessment of men presenting with LUTS involves:

• Digital rectal examination (prostate exam) to assess the size,
shape and characteristics of the prostate
• Abdominal examination to assess for a palpable bladder and
other abnormalities
• Urinary frequency volume chart, recording 3 days of fluid intake
and output
• Urine dipstick to assess for infection, haematuria (e.g., due to
bladder cancer) and other pathology
• Prostate-specific antigen (PSA) for prostate cancer, depending
on the patient preference

Prostate-specific antigen (PSA) testing is known to be unreliable,

with a high rate of false positives (75%) and false negatives (15%).
False positive results may lead to further investigations, including
invasive prostate biopsies, which have complications and may be
unnecessary. False negatives may lead to inappropriate reassurance.
Therefore, it is essential to counsel patients to make an informed decision
about whether to have the test.

Common causes of a raised PSA are:

• Prostate cancer
• Benign prostatic hyperplasia
• Prostatitis
• Urinary tract infections
• Vigorous exercise (notably cycling)
• Recent ejaculation or prostate stimulation
 Prostate Examination

• A benign prostate feels smooth, symmetrical and slightly soft, with

a maintained central sulcus
• A cancerous prostate may feel firm/hard, asymmetrical, craggy or
irregular, with loss of the central sulcus

TOM TIP: When you first start performing any intimate

examination, there is a temptation to rush. It is natural to want to
reduce the discomfort of the patient and get it over with quickly. It is
important to take your time and adequately assess the prostate,
feeling for any abnormal area, asymmetry or tenderness. If you rush,
you are more likely to miss something. The same is true of breast,
vaginal and testicular examinations.

Management

Patients with mild and manageable symptoms may not require

interventions.

The medical options are:

• Alpha-blockers (e.g., tamsulosin) relax smooth muscle, giving a
rapid improvement in symptoms
• 5-alpha reductase inhibitors (e.g., finasteride) gradually reduce
the size of the prostate

The general idea is that alpha-blockers are used to treat immediate

symptoms, and 5-alpha reductase inhibitors are used to treat
enlargement of the prostate. They may be used together where patients
have significant symptoms and enlargement of the prostate.

5-alpha reductase converts testosterone

to dihydrotestosterone (DHT), which is a more potent androgen
hormone. Inhibitors of 5-alpha reductase (i.e., finasteride) reduce DHT in
the tissues, including the prostate, leading to a reduction in prostate size.
It takes up to 6 months of treatment for the effects to result in an
improvement in symptoms.

The surgical options are:

 • Transurethral resection of the prostate (TURP)
• Transurethral electrovaporisation of the prostate
(TEVAP/TUVP)
• Holmium laser enucleation of the prostate (HoLEP)
• Open prostatectomy via an abdominal or perineal incision

TOM TIP: The notable side effect of alpha-blockers like

tamsulosin is postural hypotension. If an older man presents with
lightheadedness on standing or falls, check whether they are on
tamsulosin and check their lying and standing blood pressure. The
most common side effect of finasteride is sexual dysfunction (due
to reduced androgen activity).

Transurethral Resection of the Prostate

Transurethral resection of the prostate (TURP) is the most common

surgical treatment of BPH. It involves removing part of the prostate from
inside the urethra. A resectoscope is inserted into the urethra, and
prostate tissue is removed using a diathermy loop. The aim is to create
a more expansive space for urine to flow through, thereby improving
symptoms.

Major complications:
• Bleeding
• Infection
• Urinary incontinence
• Erectile dysfunction
• Retrograde ejaculation (semen goes backwards and is not
produced from the urethra)
• Urethral strictures
• Failure to resolve symptoms

Other Surgical Options

Transurethral electrovaporisation of the prostate (TEVAP / TUVP)

involves inserting a resectoscope into the urethra. A rollerball electrode
is then rolled across the prostate, vaporising prostate tissue and creating
a more expansive space for urine flow.
 Holmium laser enucleation of the prostate (HoLEP) also involves
inserting a resectoscope into the urethra. A laser is then used to remove
prostate tissue, creating a more expansive space for urine flow.

Open prostatectomy involves an open procedure to remove the

prostate. An abdominal or perineal incision can be used to access the
prostate. Open surgery is less commonly used as it carries an increased
risk of complications, a more extended hospital stay and longer recovery
than other surgical procedures.
 Prostatitis
Prostatitis refers to inflammation of the prostate. It can be classed as:
• Acute bacterial prostatitis - acute infection in the prostate,
presenting with a more rapid onset of symptoms
• Chronic prostatitis - symptoms lasting for at least 3 months

Chronic prostatitis may be sub-divided into:

• Chronic prostatitis or chronic pelvic pain syndrome (no
infection)
• Chronic bacterial prostatitis (infection)

The cause of inflammation and pain in chronic prostatitis is unclear. It

may be initially triggered by an infection, with inflammation persisting after
the infection has resolved.

Presentation

Chronic prostatitis presents with at least 3 months of:

• Pelvic pain, which may affect the perineum, testicles, scrotum,
penis, rectum, groin, lower back or suprapubic area
• Lower urinary tract symptoms, such as dysuria, hesitancy,
frequency and retention
• Sexual dysfunction, such as erectile dysfunction, pain on
ejaculation and haematospermia (blood in the semen)
• Pain with bowel movements
• Tender and enlarged prostate on examination (although
examination may be normal)

Acute bacterial prostatitis involves with a more acute presentation

of similar symptoms to chronic prostatitis. There may also be systemic
symptoms of infection, such as:

• Fever
• Myalgia (muscle aches)
• Nausea
 • Fatigue
• Sepsis

National Institute of Health Chronic Prostatitis Symptom

Index

The National Institute of Health has an online scoring tool

for chronic prostatitis. It can be used to assess the severity of the
symptoms and their impact on quality of life. It can also be used to track
symptoms over time.

Investigations

Urine dipstick testing can confirm evidence of infection.

Urine microscopy, culture and sensitivities (MC&S) can identify

the causative organism and the antibiotic sensitivities.

Chlamydia and gonorrhoea NAAT testing on a first pass urine, if

sexually transmitted infection is considered.

Management

Management of acute bacterial prostatitis:

• Hospital admission for systemically unwell or septic patients (for
bloods, blood cultures and IV antibiotics)
• Oral antibiotics, typically for 2-4 weeks (e.g., ciprofloxacin,
ofloxacin or trimethoprim)
• Analgesia (paracetamol or NSAIDs)
• Laxatives for pain during bowel movements

Management of chronic prostatitis (adapted from NICE CKS, updated

2019):
• Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with
rapid improvement in symptoms
• Analgesia (paracetamol or NSAIDs)
• Psychological treatment, where indicated (e.g., cognitive
behavioural therapy and antidepressants)
 • Antibiotics if less than 6 months of symptoms or a history of
infection (e.g., trimethoprim or doxycycline for 4-6 weeks)
• Laxatives for pain during bowel movements

Complications

The complications of acute bacterial prostatitis are:

• Sepsis
• Prostate abscess (may be felt as a fluctuant mass and requires
surgical drainage)
• Acute urinary retention
• Chronic prostatitis
 Prostate Cancer
Prostate cancer is the most common cancer in men. It varies in how
aggressive it is, and many prostate cancers are very slow-growing and do
not cause death. Advanced prostate cancer most commonly spreads to
the lymph nodes and bones. Prostate cancer is almost always
androgen-dependent, meaning it relies on androgen hormones (e.g.,
testosterone) to grow. The majority are adenocarcinomas and grow in
the peripheral zone of the prostate.

There is a challenge with prostate cancer, as the ideal situation is to:

• Find and treat clinically significant prostate cancers early
• Avoid picking up cancers that would not turn out to be clinically
significant (to avoid unnecessary investigations, treatments and
stress)

The key risk factors for prostate cancer are:

• Increasing age
• Family history
• Black African or Caribbean origin
• Tall stature
• Anabolic steroids

Presentation

Prostate cancer may be asymptomatic. It may also present with

lower urinary tract symptoms (LUTS), similar to benign enlargement of
the prostate. These symptoms include hesitancy, frequency, weak flow,
terminal dribbling and nocturia.

Other symptoms include:

• Haematuria
• Erectile dysfunction
• Symptoms of advanced disease or metastasis (e.g., weight loss,
bone pain or cauda equina syndrome)
 Prostate-Specific Antigen

The epithelial cells of the prostate produce prostate-specific

antigen (PSA). PSA is a glycoprotein that is secreted in the semen, with
a small amount entering the blood. Its enzymatic activity helps thin the
semen into a liquid consistency after ejaculation. It is specific to the
prostate, meaning it is not produced anywhere else in the body. A raised
level can be an indicator of prostate cancer.

Prostate-specific antigen testing may lead to the early detection of

prostate cancer, potentially leading to effective treatment and preventing
significant problems. However, research has failed to show that the
benefits of using PSA for screening outweigh the risks. In the UK, men
over 50 can request a PSA test if they would like one.

PSA testing is unreliable, with a high rate of false positives (75%) and
false negatives (15%).

Common causes of a raised PSA are:

• Prostate cancer
• Benign prostatic hyperplasia
• Prostatitis
• Urinary tract infections
• Vigorous exercise (notably cycling)
• Recent ejaculation or prostate stimulation

False positives may lead to further investigations, including invasive

prostate biopsies, which have complications and may be unnecessary.
Additionally, it may lead to the unnecessary diagnosis and treatment of
prostate cancer that would never have caused problems (the patient
would have died of other causes before experiencing any adverse effects
of the prostate cancer).

False negatives may lead to false reassurance.

TOM TIP: Counselling a patient about whether to have a PSA test

is a common OSCE scenario. They are trying to test whether you
understand the concept and implications of false positives and false
negatives, and whether you can explain this to a patient to allow
them to make an informed decision for themselves.

Prostate Examination

A prostate examination is performed during a digital rectal

examination.

A benign prostate feels smooth, symmetrical and slightly soft, with a

maintained central sulcus (the dip in the middle between the right and
left lobe). There may be generalised enlargement in prostatic
hyperplasia.

An infected or inflamed prostate (prostatitis) may be enlarged,

tender and warm.

A cancerous prostate may feel firm or hard, asymmetrical, craggy or

irregular, with loss of the central sulcus. There may be a hard nodule. Any
of these features can indicate prostate cancer and warrant further
investigation. In primary care, these findings require a two week wait
urgent cancer referral to urology.

Multiparametric MRI

Multiparametric MRI of the prostate is now the usual first-line

investigation for suspected localised prostate cancer. The results are
reported on a Likert scale, scored as:

• 1 - very low suspicion

• 2 - low suspicion
• 3 - equivocal
• 4 - probable cancer
• 5 - definite cancer

Prostate Biopsy

Prostate biopsy is the next step in establishing a diagnosis. The

decision to perform a biopsy depends on the MRI findings (e.g., Likert 3 or
above) and the clinical suspicion (i.e., examination and PSA results).
 Prostate biopsy carries a risk of false-negative results if the biopsy
misses the cancerous area. Multiple needles are used to take samples
from different areas of the prostate. The MRI scan results can guide the
biopsy to decide the best target for the needles.

There are two options for prostate biopsy:

• Transrectal ultrasound-guided biopsy (TRUS)
• Transperineal biopsy

Transrectal ultrasound-guided biopsy involves an ultrasound probe

inserted into the rectum, which provides a good indication of the size and
shape of the prostate. Guided biopsies are taken through the wall of the
rectum, into the prostate.

Transperineal biopsy involves needles inserted through the

perineum, usually under local anaesthetic.

The main risks of a prostate biopsy are:

• Pain (particularly lower abdominal, rectal or perineal pain)
• Bleeding (blood in the stools, urine or semen)
• Infection
• Urinary retention due to short term swelling of the prostate
• Erectile dysfunction (rare)

Isotope Bone Scan

An isotope bone scan (also called a radionuclide scan or bone

scintigraphy) can be used to look for bony metastasis.

A radioactive isotope is given by intravenous injection, followed by a

short wait (2-3 hours) to allow the bones to take up the isotope. A gamma
camera is used to take pictures of the entire skeleton. Metastatic bone
lesions take up more of the isotope, making them stand out on the scan.

Gleason Grading System

The Gleason grading system is based on the histology from the

prostate biopsies. It is specific to prostate cancer and helps to determine
what treatment is most appropriate. The greater the Gleason score, the
more poorly differentiated the tumour is (the cells have mutated further
from normal prostate tissue) and the worse the prognosis is. The tissue
samples are graded 1 (closest to normal) to 5 (most abnormal).

The Gleason score will be made up of two numbers added together

for the total score (for example, 3 + 4 = 7):
• The first number is the grade of the most prevalent pattern in the
biopsy
• The second number is the grade of the second most prevalent
pattern in the biopsy

A Gleason score of:

• 6 is considered low risk
• 7 is intermediate risk (3 + 4 is lower risk than 4 + 3)
• 8 or above is deemed to be high risk

TNM Staging for Prostate Cancer

The TNM staging system can be used for prostate cancer, rating the
T (tumour), N (lymph nodes) and M (metastasis).

T for Tumour:
• TX – unable to assess size
• T1 – too small to be felt on examination or seen on scans
• T2 – contained within the prostate
• T3 – extends out of the prostate
• T4 – spread to nearby organs

N for Nodes:
• NX – unable to assess nodes
• N0 – no nodal spread
• N1 – spread to lymph nodes

M for Metastasis:
• M0 – no metastasis
• M1 – metastasis

Management
 Management of any cancer is guided by a multidisciplinary team
(MDT) meeting to decide the best course of action for the individual
patient.

Depending on the grade and stage of prostate cancer, treatment can

involve:
• Surveillance or watchful waiting in early prostate cancer
• External beam radiotherapy directed at the prostate
• Brachytherapy
• Hormone therapy
• Surgery

A key complication of external beam

radiotherapy is proctitis (inflammation in the rectum) caused by
radiation affecting the rectum. Proctitis can cause pain, altered bowel
habit, rectal bleeding and discharge. Prednisolone suppositories can help
reduce inflammation.

Brachytherapy involves implanting radioactive metal “seeds” into the

prostate. These deliver continuous, targeted radiotherapy to the prostate.
The radiation can cause inflammation in nearby organs, such as the
bladder (cystitis) or rectum (proctitis). Other side effects include erectile
dysfunction, incontinence and increased risk of bladder or rectal cancer.

Hormone therapy aims to reduce the level of androgens (e.g.,

testosterone) that stimulate the cancer to grow. They are usually either
used in combination with radiotherapy, or alone in advanced disease
where cure is not possible. The options are:
• Androgen-receptor blockers such as bicalutamide
• GnRH agonists such as goserelin (Zoladex) or leuprorelin
(Prostap)
• Bilateral orchidectomy to remove the testicles (rarely used)

Side effects of hormone therapy include:

• Hot flushes
• Sexual dysfunction
• Gynaecomastia
• Fatigue
 • Osteoporosis

Radical prostatectomy involves a surgical operation to remove the

entire prostate. The aim is to cure prostate cancer confined to the
prostate. Key complications are erectile dysfunction and urinary
incontinence.
 Epididymo-orchitis
Epididymitis is inflammation of the epididymis. Orchitis is inflammation
of a testicle. Epididymo-orchitis is usually the result of infection in the
epididymis and testicle on one side.

Basic Anatomy

At the back of each testicle is the epididymis. Sperm are released

from the testicle, into the head of the epididymis, connected at the top of
the testicle. The sperm travel through the head, then body, then tail of
the epididymis. Sperm mature and are stored in the epididymis. The
epididymis drains into the vas deferens.

Causes
 • Escherichia coli (E. coli)
• Chlamydia trachomatis
• Neisseria gonorrhoea
• Mumps

TOM TIP: Think of mumps in patients with parotid gland

swelling and orchitis. Mumps tends only to affect the testicle,
sparing the epididymis. It can also cause pancreatitis.

Presentation

Epididymo-orchitis typically presents with a gradual onset, over

minutes to hours, of unilateral:
• Testicular pain
• Dragging or heavy sensation
• Swelling of the testicle and epididymis
• Tenderness on palpation, particularly over epididymis
• Urethral discharge (think of chlamydia or gonorrhoea)
• Systemic symptoms such as fever and potentially sepsis

The key differential diagnosis for epididymo-orchitis is testicular

torsion. Testicular torsion is a urological emergency that requires rapid
treatment to avoid the testicle dying. Both present similarly, with acute
onset of pain in one testicle. If there is any doubt, treat it as testicular
torsion until proven otherwise.

Diagnosis

The key with epididymo-orchitis is to distinguish whether the cause is

likely to be an enteric organism (e.g., E. coli) or a sexually transmitted
organism (e.g., chlamydia or gonorrhoea). The features that make a
sexually transmitted organism more likely are (as per NICE CKS 2020):
• Age under 35
• Increased number of sexual partners in the last 12 months
• Discharge from the urethra

Investigations to help establish the diagnosis are:

• Urine microscopy, culture and sensitivity (MC&S)
• Chlamydia and gonorrhoea NAAT testing on a first pass urine
 • Charcoal swab of purulent urethral discharge for gonorrhoea
culture and sensitivities
• Saliva swap for PCR testing for mumps, if suspected
• Serum antibodies for mumps, if suspected (IgM - acute infection,
IgG - previous infection or vaccination)
• Ultrasound may be used to assess for torsion or tumours

Management

Acutely very unwell or septic patients are admitted to hospital for

treatment (IV antibiotics).

Patients at high risk of sexually transmitted infections should be

referred urgently to genitourinary medicine (GUM) for assessment and
treatment.

Local guidelines guide the choice of antibiotic.

For patients that are at a low risk of STIs, a typical choice is:
• Ofloxacin (usually first-line) for 14 days

Alternatives:

• Levofloxacin
• Ciprofloxacin
• Doxycycline
• Co-amoxiclav

Additional measures:

• Analgesia
• Supportive underwear
• Reduced physical activity
• Abstinence from intercourse

TOM TIP: Quinolone antibiotics such as ofloxacin, levofloxacin

and ciprofloxacin are powerful broad-spectrum antibiotics, often
used for urinary tract infections, pyelonephritis, epididymo-orchitis
and prostatitis. They give excellent gram-negative cover. It is worth
remembering two critical side effects, as these may be tested in
exams and are essential to inform patients about:
• Tendon damage and tendon rupture, notably in the Achilles
tendon
• Lower seizure threshold (caution in patients with epilepsy)

Complications

Epididymo-orchitis can lead to:

• Chronic pain
• Chronic epididymitis
• Testicular atrophy
• Sub-fertility or infertility
• Scrotal abscess
 Testicular Torsion
Testicular torsion refers to twisting of the spermatic cord with rotation
of the testicle. It is a urological emergency. A delay in treatment
increases the risk of ischaemia and necrosis of the testicle, leading to
sub-fertility or infertility.

The typical patient in exams is a teenage boy, but it can occur at any
age.

There may be a history of recurrent symptoms in patients where there

is intermittent testicular torsion.

Presentation

Testicular torsion is often triggered by activity, such as playing sports.

Ask what the patient was doing at the time when the pain started.

It presents with a rapid onset of unilateral testicular pain, and may

be associated with abdominal pain and vomiting. Sometimes abdominal
pain is the only symptom in boys, and testicular examination to exclude
torsion is essential.

Examination findings are:

• Firm swollen testicle
• Elevated (retracted) testicle
• Absent cremasteric reflex
• Abnormal testicular lie (often horizontal)
• Rotation, so that the epididymis is not in the normal posterior
position

If in doubt, or if there is any suspicion of torsion, get an immediate

senior urology opinion.

Bell-Clapper Deformity

A bell-clapper deformity is one of the causes of testicular torsion.

 Normally, the testicle is fixed posteriorly to the tunica vaginalis.
A bell-clapper deformity is where the fixation between the testicle and
the tunica vaginalis is absent. The testicle hangs in a horizontal position
(like a bell-clapper) instead of the typical more vertical position. It is also
able to rotate within the tunica vaginalis, twisting at the spermatic cord. As
it rotates, it twists the vessels and cuts off the blood supply.

Management

Testicular torsion is a urological emergency, and there is an urgent

requirement for treatment. Any delay in treatment will prolong the
ischaemia and reduce the chances of saving the testicle.

The management of testicular torsion involves:

• Nil by mouth, in preparation for surgery
• Analgesia as required
• Urgent senior urology assessment
• Surgical exploration of the scrotum
• Orchiopexy (correcting the position of the testicles and fixing them
in place)
 • Orchidectomy (removing the testicle) if the surgery is delayed or
there is necrosis

A scrotal ultrasound can confirm the diagnosis. However, any

investigation that will delay the patient going to theatre for treatment is not
recommended. Ultrasound can show the whirlpool sign, with a spiral
appearance to the spermatic cord and blood vessels.
 Scrotal Lumps
The key causes of scrotal or testicular lumps are:
• Hydrocele
• Varicocele
• Epididymal cyst
• Testicular cancer
• Epididymo-orchitis
• Inguinal hernia
• Testicular torsion

Hydrocele

A hydrocele is a collection of fluid within the tunica vaginalis that

surrounds the testes. They are usually painless and present with a soft
scrotal swelling. The tunica vaginalis is a sealed pouch of membrane
that surrounds the testes. Originally the tunica vaginalis is part of
the peritoneal membrane. During the development of the fetus, it
becomes separated from the peritoneal membrane and remains in the
scrotum, partially covering each testicle.
 Examination findings with a hydrocele are:
• The testicle is palpable within the hydrocele
• Soft, fluctuant and may be large
• Irreducible and has no bowel sounds (distinguishing it from a
hernia)
• Transilluminated by shining torch through the skin, into the fluid
(the testicle floats within the fluid)

Hydroceles can be idiopathic, with no apparent cause, or secondary

to:
• Testicular cancer
• Testicular torsion
• Epididymo-orchitis
• Trauma

Management involves excluding serious causes (e.g., cancer).

Idiopathic hydroceles may be managed conservatively. Surgery,
aspiration or sclerotherapy may be required in large or symptomatic
cases.

Varicocele

A varicocele occurs where the veins in the pampiniform plexus

become swollen. They are common, affecting around 15% of men. They
can cause impaired fertility, probably due to disrupting the temperature in
the affected testicle. They may result in testicular atrophy, reducing the
size and function of the testicle.

The pampiniform plexus is a venous plexus, which is found in the

spermatic cord and drains the testes. The pampiniform plexus drains
into the testicular vein. It plays a role in regulating the temperature of
blood entering the testes by absorbing heat from the nearby testicular
artery. The testicles need to be at an optimum temperature for producing
sperm.
 Varicoceles are the result of increased resistance in the testicular
vein. Incompetent valves in the testicular vein allow blood to flow back
from the testicular vein into the pampiniform plexus.

The right testicular vein drains directly into the inferior vena cava.
The left testicular vein drains into the left renal vein. Most varicoceles
(90%) occur on the left due to increased resistance in the left testicular
vein. A left-sided varicocele can indicate an obstruction of the left
testicular vein caused by a renal cell carcinoma.

Varicoceles may present with:

• Throbbing/dull pain or discomfort, worse on standing
• A dragging sensation
• Sub-fertility or infertility

Examination findings are:

• A scrotal mass that feels like a “bag of worms”
• More prominent on standing
• Disappears when lying down
• Asymmetry in testicular size if the varicocele has affected the
growth of the testicle

Varicoceles that do not disappear when lying down should raise

concerns about a retroperitoneal tumour obstructing the drainage of the
renal vein. These warrant an urgent referral to urology for further
investigation.

Investigations to consider are:

• Ultrasound with Doppler imaging can be used to confirm the
diagnosis
• Semen analysis if there are concerns about fertility
• Hormonal tests (e.g., FSH and testosterone) if there are concerns
about function

Uncomplicated cases can be managed conservatively.

Surgery or endovascular embolisation may be indicated for pain,

testicular atrophy or infertility.
 Epididymal Cysts

Epididymal cysts occur at the head of the epididymis (at the top of the
testicle). A cyst is a fluid-filled sac. An epididymal cyst that contains
sperm is called a spermatocele. Management of epididymal cysts and
spermatoceles is identical.

Epididymal cysts are very common in adults, occurring in around 30%

of men. Most cases are asymptomatic. Patients may present having felt a
lump, or they may be found incidentally on an ultrasound arranged for
another indication.

Examination findings are:

• A soft, round lump
• Typically at the top of the testicle
• Associated with the epididymis
 • Separate from the testicle
• May be able to transilluminate large cysts (appearing separate from
the testicle)

Usually, they are entirely harmless and are not associated with
infertility or cancer. Occasionally, they may cause pain or discomfort, and
removal may be considered. Exceptionally rarely, there may be torsion of
the cyst, causing acute pain and swelling.
 Testicular Cancer
Testicular cancer arises from the germ cells in the testes. Germ cells
are cells that produce gametes (sperm in males). There are other, rare
tumours in the testes, such as non-germ cell tumours and secondary
metastases.

Testicular cancer is more common in younger men, with the highest

incidence between 15 and 35 years.

Testicular cancer can be divided into two types:

• Seminomas
• Non-seminomas (mostly teratomas)

Risk Factors

• Undescended testes
• Male infertility
• Family history
• Increased height

Presentation

The typical presentation is a painless lump on the testicle.

Occasionally it can present with testicular pain.

The lump will be:

• Non-tender (or even reduced sensation)

• Arising from testicle
• Hard
• Irregular
• Not fluctuant
• No transillumination

Rarely, gynaecomastia (breast enlargement) can be a presentation

of testicular cancer, particularly a rare type of tumour called a Leydig cell
tumour. About 2% of patients presenting with gynaecomastia have a
testicular tumour.

Investigations

Scrotal ultrasound is the usual initial investigation to confirm the

diagnosis.

Tumour markers for testicular cancer are:

• Alpha-fetoprotein - may be raised in teratomas (not in pure
seminomas)
• Beta-hCG - may be raised in both teratomas and seminomas
• Lactate dehydrogenase (LDH) is a very non-specific tumour
marker

A staging CT scan can be used to look for areas of spread and to

stage the cancer.

Royal Marsden Staging System

Testicular cancer is staged with the Royal Marsden staging system:

• Stage 1 - isolated to the testicle
• Stage 2 - spread to the retroperitoneal lymph nodes
• Stage 3 - spread to the lymph nodes above the diaphragm
• Stage 4 - metastasised to other organs

Metastasis

The common places for testicular cancer to metastasise to are:

• Lymphatics
• Lungs
• Liver
• Brain

Management

Management of any cancer is guided by a multidisciplinary team

(MDT) meeting to decide the best course of action for the individual
patient.
 Depending on the grade and stage of testicular cancer, treatment can
involve:
• Surgery to remove the affected testicle (radical orchidectomy) - a
prosthesis can be inserted
• Chemotherapy
• Radiotherapy
• Sperm banking to save sperm for future use, as treatment may
cause infertility

Long term side effects of treatment are particularly significant, as most

patients are young and expected to live many years after treatment of
testicular cancer. Side effects include:
• Infertility
• Hypogonadism (testosterone replacement may be required)
• Peripheral neuropathy
• Hearing loss
• Lasting kidney, liver or heart damage
• Increased risk of cancer in the future

Prognosis

The prognosis for early testicular cancer is good, with a greater than
90% cure rate. Metastatic disease is also often curable. Seminomas have
a slightly better prognosis than non-seminomas.

Patients will require follow-up to monitor for reoccurrence. This usually

involves monitoring tumour markers, and may include imaging such
as CT scans or chest x-rays.
 Lower Urinary Tract Infections
Lower urinary tract infections (UTIs) involve infection in the
bladder, causing cystitis (inflammation of the bladder). They can spread
up to the kidneys and cause pyelonephritis. Urinary tract infections are
far more common in women, where the urethra is much shorter, making it
easier for bacteria to get into the bladder.

The primary source of bacteria for urinary tract infections is from the
faeces. Normal intestinal bacteria, such as E. coli, can easily make the
short journey to the urethral opening from the anus. Sexual activity is a
crucial method for spreading bacteria around the perineum. Incontinence
or poor hygiene can also contribute to the development of UTIs.

Urinary catheters are a key source of infection, and catheter-

associated urinary tract infections tend to be more significant and
challenging to treat.

Presentation
Lower urinary tract infections present with:
• Dysuria (pain, stinging or burning when passing urine)
• Suprapubic pain or discomfort
• Frequency
• Urgency
• Incontinence
• Haematuria
• Cloudy or foul smelling urine
• Confusion is commonly the only symptom in older and frail patients

TOM TIP: It is important to distinguish between patients with a

lower urinary tract infection and those with pyelonephritis.
Pyelonephritis is generally a more serious condition with significant
complications, including sepsis and kidney scarring. Suspect
pyelonephritis in patients with:
• Fever
• Loin/back pain
 • Nausea/vomiting
• Renal angle tenderness on examination

Urine Dipstick

Nitrites – gram-negative bacteria (such as E. coli) break

down nitrates, a normal waste product in urine, into nitrites. The
presence of nitrites suggest bacteria in the urine.

Leukocytes are white blood cells. It is normal to have a small

number of leukocytes in the urine, but a significant rise can result from an
infection or other cause of inflammation. Leukocyte esterase is tested on
a urine dipstick, which is a product of leukocytes and indicates the
number of leukocytes in the urine.

Red blood cells in the urine indicate blood. Microscopic

haematuria is where blood is identified on a urine dipstick but not seen
when looking at the sample. Macroscopic haematuria is where blood is
visible in the urine. Haematuria is a common sign of infection but can also
be present with other causes, such as bladder cancer or nephritis.

Nitrites are a better indication of infection than leukocytes. The NICE

clinical knowledge summaries (2020) suggest that the presence
of nitrites or leukocytes plus red blood cells indicate that the patient is
likely to have a UTI.

If only nitrites are present, it is worth treating as a UTI. If

only leukocytes are present, the patient should not be treated for a UTI
unless there is clinical evidence they have one. If both are present, the
patient requires treatment for a UTI.

A midstream urine (MSU) sample sent for microscopy, culture and

sensitivity testing will determine the infective organism and the antibiotics
that will be effective in treatment. Not all patients with an uncomplicated
UTI require an MSU. An MSU is important in:
• Pregnant patients
• Patients with recurrent UTIs
• Atypical symptoms
• When symptoms do not improve with antibiotics
 Causes

The most common cause of UTI is Escherichia coli. E. coli are gram-
negative, anaerobic, rod-shaped bacteria that are part of the normal
lower intestinal microbiome. It is found in faeces and can easily spread to
the bladder.

Other causes:
• Klebsiella pneumoniae (gram-negative anaerobic rod-shaped
bacteria)
• Enterococcus
• Pseudomonas aeruginosa
• Staphylococcus saprophyticus
• Candida albicans (fungal)

Antibiotics Choice

Follow local guidelines. An appropriate initial antibiotic in the

community would be:
• Nitrofurantoin (avoided in patients with an eGFR <45)
• Trimethoprim (often associated with high rates of bacterial
resistance)

Alternatives:

• Pivmecillinam
• Amoxicillin
• Cefalexin

Duration of Antibiotics

• 3 days of antibiotics for simple lower urinary tract infections in

women
• 5-10 days of antibiotics for immunosuppressed women, abnormal
anatomy or impaired kidney function
• 7 days of antibiotics for men, pregnant women or catheter-related
UTIs
 It is worth noting that NICE recommend changing the catheter when
someone is diagnosed with a catheter-related urinary tract infection.

Pregnancy

Urinary tract infections in pregnancy increase the risk

of pyelonephritis, premature rupture of membranes and pre-term
labour.

Management in Pregnancy

Urinary tract infection in pregnancy requires 7 days of antibiotics. All

women should have an MSU for microscopy, culture and sensitivity
testing.

The antibiotic options are:

• Nitrofurantoin (avoided in the third trimester)
• Amoxicillin (only after sensitivities are known)
• Cefalexin

Nitrofurantoin needs to be avoided in the third trimester as there is

a risk of neonatal haemolysis (destruction of the neonatal red blood
cells).

Trimethoprim needs to be avoided in the first trimester as it works

as a folate antagonist. Folate is essential in early pregnancy for the
normal development of the fetus. Trimethoprim in early pregnancy can
cause congenital malformations, particularly neural tube defects (e.g.,
spina bifida). It is not known to be harmful later in pregnancy but is
generally avoided unless necessary.
 Pyelonephritis
Pyelonephritis refers to inflammation of the kidney resulting from
bacterial infection. The inflammation affects the renal pelvis (join
between kidney and ureter) and parenchyma (tissue).

Risk factors for pyelonephritis are:

• Female sex
• Structural urological abnormalities
• Vesico-ureteric reflux (urine refluxing from the bladder to the
ureters - usually in children)
• Pregnancy
• Diabetes

Causes

Escherichia coli is the most common cause, as with lower urinary

tract infections. E. coli are gram-negative, anaerobic, rod-shaped
bacteria that are part of the normal lower intestinal microbiome. It is
found in faeces and can easily spread to the bladder.

Other causes:
• Klebsiella pneumoniae (gram-negative anaerobic rod-shaped
bacteria)
• Enterococcus
• Pseudomonas aeruginosa
• Staphylococcus saprophyticus
• Candida albicans (fungal)

Presentation

Diagnosis can be made clinically with a history and examination.

Patients have a similar presentation to lower urinary tract infections

(i.e., dysuria, suprapubic discomfort and increased frequency) plus the
additional triad of symptoms:
 • Fever
• Loin or back pain (bilateral or unilateral)
• Nausea / vomiting

Patients may also have:

• Systemic illness
• Loss of appetite
• Haematuria
• Renal angle tenderness on examination

Investigations

Urine dipstick will show signs of infection, including nitrites,

leukocytes and blood.

Midstream urine (MSU) for microscopy, culture and sensitivity

testing is essential to establish the causative organism. The sample
should ideally be collected before starting antibiotics.

Blood tests will show raised white blood cells and raised
inflammatory markers (e.g., CRP).

Imaging may be used to exclude other pathology, such as kidney

stones or abscesses. This could be an ultrasound or CT scan.

Management of Pyelonephritis

Referral to hospital is required if there are features of sepsis or if it is

not safe to manage them in the community.

NICE guidelines (2018) recommend the following first-line antibiotics

for 7-10 days when treating pyelonephritis in the community:
• Cefalexin
• Co-amoxiclav (if culture results are available)
• Trimethoprim (if culture results are available)
• Ciprofloxacin (keep tendon damage and lower seizure threshold in
mind)
 Patients admitted to hospital with sepsis require the sepsis six; with
three tests and three treatments.

Three tests:
• Blood lactate level
• Blood cultures
• Urine output monitoring

Three treatments:
• Oxygen to maintain oxygen saturations of 94-98% (or 88-92% in
COPD)
• Empirical broad-spectrum IV antibiotics (according to local
guidelines)
• IV fluids

Two things to keep in mind with patients that have significant

symptoms or do not respond well to treatment are:
• Renal abscess
• Kidney stone obstructing the ureter, causing pyelonephritis

Chronic Pyelonephritis

Chronic pyelonephritis presents with recurrent episodes of infection in

the kidneys. Recurrent infections lead to scarring of the renal
parenchyma, leading to chronic kidney disease (CKD). This can
progress to end-stage renal failure.

Dimercaptosuccinic acid (DMSA) scans involve

injecting radiolabeled DMSA, which builds up in healthy kidney tissue.
When imaged using gamma cameras, it indicates scarring or damage in
areas that do not take up the DMSA. They are used in recurrent
pyelonephritis to assess for renal damage.
 Interstitial Cystitis
Interstitial cystitis is a chronic condition causing inflammation in the
bladder, resulting in lower urinary tract symptoms and suprapubic pain. It
is also called bladder pain syndrome and hypersensitive bladder
syndrome.

There is no simple explanation for the symptoms, and the

pathophysiology is likely a complex combination of various factors,
including dysfunction of the blood vessels, nerves, immune system and
epithelium.

It is much more common in women than men. It can have a significant

impact on quality of life and mental health.

Presentation

The symptoms are similar to a lower urinary tract infection, but are
more persistent.

The typical presentation is with more than 6 weeks of:

• Suprapubic pain, worse with a full bladder and often relieved by
emptying the bladder
• Frequency of urination
• Urgency of urination
• Symptoms may be worse during menstruation

Investigations

Other causes of symptoms need to be excluded, with:

• Urinalysis for urinary tract infections
• Swabs for sexually transmitted infections
• Cystoscopy for bladder cancer
• Prostate examination for prostatitis, hypertrophy or cancer

Hunner lesions, seen during cystoscopy, are a finding in 5-20% of

patients with interstitial cystitis. These are red, inflamed patches of the
bladder mucosa associated with small blood vessels.

Granulations are another finding during cystoscopy in patients with

interstitial cystitis. These are tiny haemorrhages on the bladder wall.

Management

Interstitial cystitis can be difficult to manage. Symptoms are often

resistant to treatment and persist long-term, having a significant impact
on quality of life.

Supportive management is used initially:

• Diet changes such as avoiding alcohol, caffeine and tomatoes
• Stopping smoking
• Pelvic floor exercises
• Bladder retraining
• Cognitive behavioural therapy
• Transcutaneous electrical nerve stimulation (TENS)

Oral medications may be helpful, including;

• Analgesia
• Antihistamines
• Anticholinergic medications (e.g., solifenacin or oxybutynin)
• Mirebegron (beta-3-adrenergic-receptor agonist)
• Cimetidine (histamine-2-receptor antagonist)
• Pentosan polysulfate sodium
• Ciclosporin (an immunosuppressant)

Intravesical medication may be helpful, given directly into the

bladder:
• Lidocaine
• Pentosan polysulfate sodium
• Hyaluronic acid
• Chondroitin sulphate

Hydrodistention involves filling the bladder with water, to high

pressure, during a cystoscopy. It requires a general anaesthetic. This can
give a temporary (3-6 month) improvement in symptoms.
 Surgical procedures may be used, including:
• Cauterisation of Hunner lesions during cystoscopy
• Butulinum toxin injections during cystoscopy
• Neuromodulation with an implanted electrical nerve stimulator
• Augmentation of the bladder, using a section of ileum, to increase
the capacity (ileocystoplasty)
• Cystectomy (removal of the bladder)

TOM TIP: Interstitial cystitis is a complex condition with complex

treatments. You certainly don’t need to remember all the treatments,
and they are unlikely to be tested in medical school exams. Just
keep it in mind as a differential diagnosis and be generally aware of
the investigations (including cystoscopy) and treatment options.
 Bladder Cancer
Cancer in the bladder arises from the endothelial lining (urothelium).
The majority are superficial (not invading the muscle) at presentation.

Risk Factors

Smoking and increased age are the main risk factors for bladder
cancer.

Aromatic amines are worth noting as a carcinogen that causes

bladder cancer. Aromatic amines were used in
the dye and rubber industries but have been heavily regulated or banned
for many years. They are also found in cigarette smoke and seem to be
the reason smoking causes bladder cancer.

Schistosomiasis causes squamous cell carcinoma of the bladder

in countries with a high prevalence of the infection.

TOM TIP: The typical presentation to look out for in your exams is
a retired dye factory worker with painless haematuria. Whenever an
exam question mentions a patient’s occupation, it is almost
certainly relevant and will tell you the diagnosis. Dye factory
workers get transitional cell carcinoma of the bladder. Patients with
asbestos exposure get mesothelioma. Outdoor workers with
significant sun exposure get skin cancer.

Types

• Transitional cell carcinoma (90%)

• Squamous cell carcinoma (5% - higher in areas of
schistosomiasis)
• Rarer causes are adenocarcinoma (2%), sarcoma and small-cell
carcinoma

Presentation
 Painless haematuria is the symptom to remember for your exams.

The NICE guidelines on recognising cancer (updated January 2021)

advises a two week wait referral for:
• Aged over 45 with unexplained visible haematuria, either without
a UTI or persisting after treatment for a UTI
• Aged over 60 with microscopic haematuria (not visible but
positive on a urine dipstick) PLUS:
• Dysuria or;
• Raised white blood cells on a full blood count

The NICE guidelines also recommend considering a non-urgent

referral in people over 60 with recurrent unexplained UTIs.

Diagnosis

Cystoscopy (a camera inserted through the urethra into the bladder)

can be used to visualise bladder cancers. The cystoscope can be rigid or
flexible. Cystoscopy can be performed under local or general
anaesthetic.

Staging

The TNM staging system is used for bladder cancer, rating the T
(tumour), N (lymph node) and M (metastasis) stages.

There is a clear distinction between:

• Non-muscle-invasive bladder cancer (not invading the muscle
layer of the bladder)
• Muscle-invasive bladder cancer (invading the muscle and
beyond)

Non-muscle-invasive bladder cancer includes:

• Tis/carcinoma in situ: cancer cells only affect the urothelium and
are flat
• Ta: cancer only affecting the urothelium and projecting into the
bladder
• T1: cancer invading the connective tissue layer beyond the
urothelium, but not the muscle layer
 Invasive bladder cancer includes T2 - 4 and any lymph node or
metastatic spread.

Treatment Options

Management of any cancer is guided by a multidisciplinary team

(MDT) meeting to decide the best course of action for the individual
patient.

Transurethral resection of bladder tumour (TURBT) may be used

for non-muscle-invasive bladder cancer. This involves removing the
bladder tumour during a cystoscopy procedure.

Intravesical chemotherapy (chemotherapy given into the bladder

through a catheter) is often used after a TURBT procedure to reduce the
risk of recurrence.

Intravesical Bacillus Calmette-Guérin (BCG) may be used as a

form of immunotherapy. Giving the BCG vaccine (the same one as for
tuberculosis) into the bladder is thought to stimulate the immune system,
which in turn attacks the bladder tumours.

Radical cystectomy involves the removal of the entire bladder.

Following removal of the bladder, there are several options for draining
urine:
• Urostomy with an ileal conduit (most common)
• Continent urinary diversion
• Neobladder reconstruction
• Ureterosigmoidostomy

Chemotherapy and radiotherapy may also be used.

Urostomy

A urostomy is used to drain urine from the kidney, bypassing the

ureters, bladder and urethra. This is the most common and popular
solution after cystectomy.
 Forming a urostomy involves creating an ileal conduit. A section of
the ileum (15-20cm) is removed, and an end-to-end anastomosis is
created so that the bowel is continuous. The ends of the ureters are
anastomosed to the separated section of the ileum. The other end of this
section of the ileum forms a stoma on the skin, draining urine into a
urostomy bag. Urine drains from the kidneys to the ureters, then the
separated section of ileum (the conduit), then out of the urostomy.

Urostomy bags need to fit tightly around the urostomy to avoid urine
coming in contact with the skin. Urine in contact with the skin will cause
irritation and skin damage.

Continent Urinary Diversion

A continent urinary diversion involves creating a pouch inside the

abdomen from a section of the ileum, with the ureters connected. This
pouch fills with urine. A thin tube is connected between a stoma on the
skin and the internal pouch. Urine does not drain from the stoma (unlike a
urostomy), and the patient needs to intermittently insert a catheter into the
stoma to drain urine from the pouch.

Neobladder Reconstruction

Bladder reconstruction involves creating a new bladder from a section

of the ileum. This is connected to both the ureters and the urethra and
functions similarly to a normal bladder. It may require intermittent
catheterisation and bladder washouts to clear secretions from the small
bowel tissue.

Ureterosigmoidostomy

A ureterosigmoidostomy involves attaching the ureters directly to the

sigmoid colon. Urine drains into and collects in the sigmoid colon.
Techniques are used to prevent urine refluxing into the ureters or back
through the large bowel. The rectum may be expanded to create a recto
sigmoid pouch (called a Mainz II procedure) to create a larger space for
urine to collect. The patient can then drain the urine by relaxing the anal
sphincter in the same way they open their bowels.

This was previously used more often but is very rarely done now. It is
associated with infection in the kidneys, electrolyte imbalances and
secondary cancer at the anastomosis (join) between the ureters and
sigmoid colon.
 Kidney Stones
Renal stones are also referred to as renal
calculi, urolithiasis and nephrolithiasis. They are hard stones that form
in the renal pelvis, where the urine collects before travelling down the
ureters. They may be asymptomatic until they irritate or get stuck in the
ureters. They might get stuck at any point along the ureters, but
commonly at the vesico-ureteric junction.
 Two key complications are:
• Obstruction leading to acute kidney injury
• Infection with obstructive pyelonephritis

Types

Calcium-based stones are the most common type of kidney stone

(about 80%). Having a raised serum calcium (hypercalcaemia) and a
low urine output are key risk factors for calcium collecting into a stone.
There are two types of calcium stones:
• Calcium oxalate (more common)
• Calcium phosphate

Other types of kidney stones include:

• Uric acid - these are not visible on x-ray
• Struvite - produced by bacteria (associated with infection)
• Cystine - associated with cystinuria, an autosomal recessive
disease

Staghorn Calculus

A staghorn calculus is where the stone forms in the shape of the renal
pelvis, giving it a similar appearance to the antlers of a deer stag. The
body sits in the renal pelvis with horns extending into the renal calyces.
They may be seen on plain x-ray films.

Most commonly, this occurs with stones made of struvite. In recurrent

upper urinary tract infections, the bacteria can hydrolyse the urea in urine
to ammonia, creating the solid struvite.

Presentation

Renal stones may be asymptomatic and never cause an issue.

Renal colic is the presenting complaint in symptomatic kidney stones.

Renal colic is:
• Unilateral loin to groin pain that can be excruciating (“worse than
childbirth”)
• Colicky (fluctuating in severity) as the stone moves and settles

Patients often move restlessly due to the pain.

There may also be:

• Haematuria
• Nausea or vomiting
• Reduced urine output
• Symptoms of sepsis, if infection is present

Investigations

Urine dipstick usually shows haematuria in cases of kidney stones.

A normal urine dipstick does not exclude stones. Urine dipsticks are also
helpful to exclude infection.

Blood tests help establish signs of infection and also kidney function.
Checking the serum calcium helps identify hypercalcaemia that may have
caused the kidney stone.

An abdominal x-ray can show calcium-based stones, but uric acid

stones will not show up (they are radiolucent).

Non-contrast computer tomography (CT) of the kidneys, ureters

and bladder (CT KUB) is the initial investigation of choice for diagnosing
kidney stones. The NICE guidelines (2019) recommend a CT KUB within
24 hours of the presentation.
 Ultrasound of the kidneys, ureters and bladder (ultrasound KUB)
is a less preferred alternative to CT scan. A negative result does not
exclude kidney stones. It is less effective at identifying kidney stones but
is helpful in pregnant women and children.

Stones can be analysed to determine the type, which can help

establish the cause and reduce the risk of recurrence.

TOM TIP: Remember hypercalcaemia as a cause of kidney

stones. You can remember the presentation of hypercalcaemia with
the mnemonic “renal stones, painful bones, abdominal groans and
psychiatric moans”. The three causes to remember are calcium
supplementation, hyperparathyroidism and cancer (e.g., myeloma,
breast or lung cancer).

Management

NSAIDs are the most effective type of analgesia, for example,

intramuscular or rectal diclofenac. IV paracetamol is an alternative,
where NSAIDs are not suitable. Opiates are not very helpful for pain
management and are not routinely used.

Antiemetics are used for nausea and vomiting (e.g., metoclopramide,

prochlorperazine or cyclizine).

Antibiotics are required if infection is present.

Watchful waiting is usually used in stones less than 5mm, as there is

a 50-80% chance they will pass without any interventions. It may also be
suitable for patients with stones 5-10mm, depending on individual factors.
It can take several weeks for the stone to pass.

Tamsulosin (an alpha-blocker) can be used to help aid the

spontaneous passage of stones.

Surgical interventions are required in large stones (10mm or more),

stones that do not pass spontaneously or where there is complete
obstruction or infection.
 Surgical Interventions

Extracorporeal shock wave lithotripsy (ESWL):

ESWL involves an external machine that generates shock waves and
directs them at the stone under x-ray guidance. The shockwaves break
the stone into smaller parts to make them easier to pass.

Ureteroscopy and laser lithotripsy:

A camera is inserted via the urethra, bladder and ureter, and the stone
is identified. It is then broken up using targeted lasers, making the smaller
parts easier to pass.

Percutaneous nephrolithotomy (PCNL):

PCNL is performed in theatres under a general anaesthetic. A
nephroscope (small camera on a stick) is inserted via a small incision at
the patient’s back. The scope is inserted through the kidney to assess the
ureter. Stones can be broken into smaller pieces and removed. A
nephrostomy tube may be left in place after the procedure to help drain
the kidney.

Open surgery:
Open surgery can be used to access the kidneys and remove the
stones. This is rarely needed as other, less invasive, methods are usually
effective.

Recurrent Stones

One episode of kidney stones predisposes patients to further

episodes. NICE guidelines (2019) recommend advising patients to:
• Increase oral fluid intake (2.5 - 3 litres per day)
• Add fresh lemon juice to water (citric acid binds to urinary calcium
reducing the formation of stones)
• Avoid carbonated drinks (cola drinks contain phosphoric acid,
which promotes calcium oxalate formation)
• Reduce dietary salt intake (less than 6g per day)
• Maintain a normal calcium intake (low dietary calcium might
increase the risk of kidney stones)

Other common recommendations include:

 • For calcium stones - reduce the intake of oxalate-rich foods (e.g.,
spinach, beetroot, nuts, rhubarb and black tea)
• For uric acid stones - reduce the intake of purine-rich foods (e.g.,
kidney, liver, anchovies, sardines and spinach)
• Limit dietary protein

Two medications that may be used to reduce the risk of recurrence

are:
• Potassium citrate in patients with calcium oxalate stones and
raised urinary calcium
• Thiazide diuretics (e.g., indapamide) in patients with calcium
oxalate stones and raised urinary calcium
 Renal Cell Carcinoma
Renal cell carcinoma (RCC) is the most common type of kidney
tumour. It is a type of adenocarcinoma that arises from the renal tubules.
The classic triad of presenting features is haematuria, flank pain and a
palpable mass.

Types of Renal Cell Carcinoma

There are several subtypes of renal cell adenocarcinoma, the three

most common being:
• Clear cell (around 80%)
• Papillary (around 15%)
• Chromophobe (around 5%)

Wilms' tumour is a specific type of tumour affecting the kidney in

children, typically under 5 years.

Risk Factors

• Smoking
• Obesity
• Hypertension
• End-stage renal failure
• Von Hippel-Lindau disease
• Tuberous sclerosis

Presentation

Renal cell carcinoma may be asymptomatic, but may present with:

• Haematuria
• Vague loin pain
• Non-specific symptoms of cancer (e.g., weight loss, fatigue,
anorexia and night sweats)
• Palpable renal mass on examination
 The NICE guidelines on recognising cancer (updated January 2021)
advise a two week wait referral for those:
• Aged over 45 with unexplained visible haematuria, either without
a UTI or persisting after treatment for a UTI

Spread

Renal cell carcinoma tends to spread to the tissues around the kidney,
within Gerota’s fascia. It often spreads to the renal vein, then to the
inferior vena cava.

“Cannonball metastases” in the lungs are a classic feature of

metastatic renal cell carcinoma. These appear as clearly-defined circular
opacities scattered throughout the lung fields on a chest x-ray.

TOM TIP: Remember cannonball metastases as originating from

a renal cell carcinoma. It is worth looking at some images of
cannonball metastases. They are an exam favourite and an easy
question to get right if you know the answer. They can also appear
with choriocarcinoma (cancer in the placenta) and, less commonly,
with prostate, bladder and endometrial cancer.

Paraneoplastic Features

Renal cell carcinoma is associated with several paraneoplastic

syndromes:
• Polycythaemia - due to secretion of unregulated erythropoietin
• Hypercalcaemia - due to secretion of a hormone that mimics the
action of parathyroid hormone
• Hypertension - due to various factors, including increased renin
secretion, polycythaemia and physical compression
• Stauffer’s syndrome - abnormal liver function tests (raised ALT,
AST, ALP and bilirubin) without liver metastasis

Hypercalcaemia can also be caused by bony metastases.

Staging

A CT thorax, abdomen and pelvis is used to stage the cancer.

 The TNM staging system is the most common staging system for
renal cell carcinoma, rating the T (tumour), N (lymph node) and M
(metastasis) stages.

There is also a number staging system specific to renal cell

carcinoma:
• Stage 1: Less than 7cm and confined to the kidney
• Stage 2: Bigger than 7cm but confined to the kidney
• Stage 3: Local spread to nearby tissues or veins, but not beyond
Gerota’s fascia
• Stage 4: Spread beyond Gerota’s fascia, including metastases

Management

Management of any cancer is guided by a multidisciplinary team

(MDT) meeting to decide the best course of action for the individual
patient.

Surgery to remove the tumour is the first-line, where possible. This

may involve:
• Partial nephrectomy (removing part of the kidney)
• Radical nephrectomy (removing the entire kidney plus the
surrounding tissue, lymph nodes and possibly the adrenal gland)

Where patients are not suitable for surgery, less invasive procedures
can be used to treat the cancer:
• Arterial embolisation, cutting off the blood supply to the affected
kidney
• Percutaneous cryotherapy, injecting liquid nitrogen to freeze and
kill the tumour cells
• Radiofrequency ablation, putting a needle into the tumour and
using an electrical current to kill the tumour cells

Chemotherapy and radiotherapy may also be used.

 Renal Transplant
A renal transplant is where a kidney is transplanted into a patient
with end-stage renal failure. It typically adds 10 years to life compared
with just using dialysis, and also significantly improves quality of life.

Donor Matching

Patient and donor kidneys are matched based on the human

leukocyte antigen (HLA) type A, B and C on chromosome 6. They do
not have to match fully, but the closer the match, the less likely there is to
be organ rejection and the better the outcomes. Recipients can receive
treatment to desensitise them to the donor HLA in preparation for a
transplant from a living donor.

Procedure

The patient’s own kidneys are left in place. The donor kidney blood
vessels are connected (anastomosed) with the pelvic vessels, usually
the external iliac vessels. The ureter of the donor kidney is
anastomosed directly with the bladder. The donor kidney is placed
anteriorly in the abdomen and can usually be palpated in the iliac fossa
area. A “hockey stick” incision is typically used, and there will be a
“hockey stick” scar.
 After The Renal Transplant

The new kidney will start functioning immediately.

Patients will require life-long immunosuppression to reduce the risk

of transplant rejection. The usual regime is:
• Tacrolimus
• Mycophenolate
• Prednisolone

Other possible immunosuppressants:

• Cyclosporine
• Sirolimus
• Azathioprine

TOM TIP: When examining a patient with a renal transplant, you

can look particularly clever by looking for the side effects of
particular immunosuppressant medications.
• Immunosuppressants often cause seborrhoeic warts and skin
cancers (look for scars from skin cancer removal)
 • Tacrolimus causes a tremor
• Cyclosporine causes gum hypertrophy
• Steroids cause features of Cushing’s syndrome

Complications

Complications relating to the transplant:

• Transplant rejection (hyperacute, acute or chronic)
• Transplant failure
• Electrolyte imbalances

Complications related to immunosuppressants:

• Ischaemic heart disease
• Type 2 diabetes (steroids)
• Infections are more likely, more severe and may involve unusual
pathogens
• Non-Hodgkin lymphoma
• Skin cancer (particularly squamous cell carcinoma)

Unusual infections can occur secondary to immunosuppressant

medication, such as:
• Pneumocystis jiroveci pneumonia (PCP/PJP)
• Cytomegalovirus (CMV)
• Tuberculosis (TB)
 Vascular Surgery
Peripheral Arterial Disease
Deep Vein Thrombosis
Varicose Veins
Chronic Venous Insufficiency
Leg Ulcers
Lymphoedema
Abdominal Aortic Aneurysm
Aortic Dissection
Carotid Artery Stenosis
Buerger Disease
 Peripheral Arterial Disease
Peripheral arterial disease (PAD) refers to the narrowing of the
arteries supplying the limbs and periphery, reducing the blood supply to
these areas. It usually refers to the lower limbs, resulting in symptoms
of claudication.

Intermittent claudication is a symptom of ischaemia in a limb,

occurring during exertion and relieved by rest. It is typically a crampy,
achy pain in the calf, thigh or buttock muscles associated with muscle
fatigue when walking beyond a certain intensity.

Critical limb ischaemia is the end-stage of peripheral arterial

disease, where there is an inadequate supply of blood to a limb to allow it
to function normally at rest. The features are pain at rest, non-healing
ulcers and gangrene. There is a significant risk of losing the limb.

Acute limb ischaemia refers to a rapid onset of ischaemia in a limb.

Typically, this is due to a thrombus (clot) blocking the arterial supply of a
distal limb, similar to a thrombus blocking a coronary artery in myocardial
infarction.

Ischaemia refers to an inadequate oxygen supply to the tissues due

to reduced blood supply.

Necrosis refers to the death of tissue.

Gangrene refers to the death of the tissue, specifically due to an

inadequate blood supply.

Atherosclerosis

Athero- refers to soft or porridge-like and -sclerosis refers to

hardening. Atherosclerosis is a combination of atheromas (fatty
deposits in the artery walls) and sclerosis (the process of hardening or
stiffening of the blood vessel walls). Atherosclerosis affects the medium
and large arteries. It is caused by chronic inflammation and activation
of the immune system in the artery wall. Lipids are deposited in the
artery wall, followed by the development of fibrous atheromatous
plaques.

These plaques cause:

• Stiffening of the artery walls, leading to hypertension (raised
blood pressure) and strain on the heart (whilst trying to pump blood
against increased resistance)
• Stenosis, leading to reduced blood flow (e.g., in angina)
• Plaque rupture, resulting in a thrombus that can block a distal
vessel and cause ischaemia (e.g., in acute coronary syndrome)

Atherosclerosis Risk Factors

It is important to break these down into modifiable and non-

modifiable risk factors. We can do nothing about non-modifiable risk
factors, but we can do something about modifiable ones.

Non-modifiable risk factors:

• Older age
• Family history
• Male

Modifiable risk factors:

• Smoking
• Alcohol consumption
• Poor diet (high in sugar and trans-fat and low in fruit, vegetables
and omega 3s)
• Low exercise / sedentary lifestyle
• Obesity
• Poor sleep
• Stress

Medical Co-Morbidities

Medical co-morbidities increase the risk of atherosclerosis and should

be carefully managed to minimise the risk:
• Diabetes
• Hypertension
 • Chronic kidney disease
• Inflammatory conditions such as rheumatoid arthritis
• Atypical antipsychotic medications

TOM TIP: Think about risk factors when taking a history from
someone with suspected atherosclerotic disease (such as someone
presenting with intermittent claudication). Ask about their exercise,
diet, past medical history, family history, occupation, smoking,
alcohol intake and medications. This will help you perform well in
exams and when presenting to seniors.

End Results of Atherosclerosis

• Angina
• Myocardial infarction
• Transient ischaemic attack
• Stroke
• Peripheral arterial disease
• Chronic mesenteric ischaemia

Intermittent Claudication

Peripheral arterial disease presents with intermittent claudication.

Patients describe a “crampy” type pain that predictably occurs after
walking a certain distance. After stopping and resting, the pain will
disappear. The most common location is the calf muscles, but it can also
affect the thighs and buttocks.

Critical Limb Ischaemia

The features of critical limb ischaemia can be remembered with the

“6 P’s” mnemonic:
• P - Pain
• P - Pallor
• P - Pulseless
• P - Paralysis
• P - Paraesthesia (an abnormal sensation or “pins and needles”)
• P - Perishingly cold
 Critical limb ischaemia typically causes burning pain. It is worse at
night when the leg is raised, as gravity no longer helps pull blood into the
foot.

Leriche Syndrome

Leriche syndrome occurs with occlusion in the distal aorta or proximal

common iliac artery. There is a triad of:
• Thigh/buttock claudication
• Absent femoral pulses
• Male impotence

Signs on Examination

Look for risk factors:

• Tar staining on the fingers
• Xanthomata (yellow cholesterol deposits on the skin)

Looks for signs of cardiovascular disease:

• Missing limbs or digits after previous amputations
• Midline sternotomy scar (previous CABG)
• A scar on the inner calf for saphenous vein harvesting (previous
CABG)
• Focal weakness suggestive of a previous stroke

The peripheral pulses may be weak on palpation. Palpable pulses

throughout the body are the:
• Radial
• Brachial
• Carotid
• Abdominal aorta
• Femoral
• Popliteal
• Posterior tibial
• Dorsalis pedis

You can use a hand-held Doppler to accurately assess the pulses

when they are difficult to palpate.
 Signs of arterial disease on inspection are:
• Skin pallor
• Cyanosis
• Dependent rubor (a deep red colour when the limb is lower than the
rest of the body)
• Muscle wasting
• Hair loss
• Ulcers
• Poor wound healing
• Gangrene (breakdown of skin and a dark red/black change in
colouration)

On examination, there may be:

• Reduced skin temperature
• Reduce sensation
• Prolonged capillary refill time (more than 2 seconds)
• Changes during Buerger’s test

Buerger’s Test

Buerger’s test is used to assess for peripheral arterial disease in the

leg. There are two parts to the test.

The first part involves the patient lying on their back (supine). Lift the
patient’s legs to an angle of 45 degrees at the hip, one at a time. Hold
them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial
supply is not adequate to overcome gravity, suggesting peripheral arterial
disease. Buerger’s angle refers to the angle at which the leg turns pale
due to inadequate blood supply. For example, a Buerger’s angle of 30
degrees means that the legs go pale when lifted to 30 degrees.

The second part involves sitting the patient up with their legs hanging
over the side of the bed. Blood will flow back into the legs assisted by
gravity. In a healthy patient, the legs will remain a normal pink colour. In a
patient with peripheral arterial disease, they will go:
• Blue initially, as the ischaemic tissue deoxygenates the blood
• Dark red after a short time, due to vasodilation in response to the
waste products of anaerobic respiration
 The dark red colour is referred to as rubor.

Leg Ulcers

Leg ulcers indicate the skin and tissues are struggling to heal due to
impaired blood flow. Some features help you distinguish between arterial
and venous ulcers.

Arterial ulcers are caused by ischaemia secondary to an inadequate

blood supply. Typically, arterial ulcers:
• Are smaller than venous ulcers
• Are deeper than venous ulcers
• Have well defined borders
• Have a “punched-out” appearance
• Occur peripherally (e.g., on the toes)
• Have reduced bleeding
• Are painful

Venous ulcers are caused by impaired drainage and pooling of blood

in the legs. Typically, venous ulcers:
• Occur after a minor injury to the leg
• Are larger than arterial ulcers
• Are more superficial than arterial ulcers
• Have irregular, gently sloping borders
• Affect the gaiter area of the leg (from the mid-calf down to the
ankle)
• Are less painful than arterial ulcers
• Occur with other signs of chronic venous insufficiency (e.g.,
haemosiderin staining and venous eczema)

Investigations

• Ankle-brachial pressure index (ABPI)

• Duplex ultrasound - ultrasound that shows the speed and volume
of blood flow
• Angiography (CT or MRI) - using contrast to highlight the arterial
circulation
 Ankle-Brachial Pressure Index

Ankle-brachial pressure index (ABPI) is the ratio of the systolic blood

pressure (SBP) in the ankle (around the lower calf) compared with the
systolic blood pressure in the arm. These readings are taken manually
using a Doppler probe. For example, an ankle SBP of 80 and an arm SBP
of 100 gives a ratio of 0.8 (80/100).

Results:
• 0.9 - 1.3 is normal
• 0.6 - 0.9 indicates mild peripheral arterial disease
• 0.3 - 0.6 indicates moderate to severe peripheral arterial disease
• Less than 0.3 indicates severe disease to critical ischaemic

An ABPI above 1.3 can indicate calcification of the arteries, making

them difficult to compress. This is more common in diabetic patients.

Management of Intermittent Claudication

Lifestyle changes are required to manage modifiable risk factors

(e.g., stop smoking). Optimise medical treatment of co-morbidities (such
as hypertension and diabetes).

Exercise training involves a structured and supervised program of

regularly walking to the point of near-maximal claudication and pain, then
resting and repeating.

Medical treatments:
• Atorvastatin 80mg
• Clopidogrel 75mg once daily (aspirin if clopidogrel is unsuitable)
• Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a
peripheral vasodilator)

Surgical options:
• Endovascular angioplasty and stenting
• Endarterectomy - cutting the vessel open and removing the
atheromatous plaque
• Bypass surgery - using a graft to bypass the blockage
 Endovascular angioplasty and stenting involves inserting a
catheter through the arterial system under x-ray guidance. At the site of
the stenosis, a balloon is inflated to create space in the lumen. A stent is
inserted to keep the artery open. Endovascular treatments have lower
risks but might not be suitable for more extensive disease.

Management of Critical Limb Ischaemia

Patients with critical limb ischaemia require urgent referral to the

vascular team. They require analgesia to manage the pain.

Urgent revascularisation can be achieved by:

• Endovascular angioplasty and stenting
• Endarterectomy
• Bypass surgery
• Amputation of the limb if it is not possible to restore the blood
supply

Management of Acute Limb Ischaemia

Patients with acute limb ischaemia need an urgent referral to the on-
call vascular team for assessment.

Management options include:

• Endovascular thrombolysis - inserting a catheter through the
arterial system to apply thrombolysis directly into the clot
• Endovascular thrombectomy - inserting a catheter through the
arterial system and removing the thrombus by aspiration or
mechanical devices
• Surgical thrombectomy - cutting open the vessel and removing
the thrombus
• Endarterectomy
• Bypass surgery
• Amputation of the limb if it is not possible to restore the blood
supply
 Deep Vein Thrombosis
Venous thromboembolism (VTE) is a common and potentially fatal
condition. It involves a blood clot (thrombus) developing in the
circulation. This usually occurs secondary to stagnation of blood and
hyper-coagulable states. When a thrombus develops in the venous
circulation, it is called a deep vein thrombosis (DVT).

Once a thrombus has developed, it can travel (embolise) from the

deep veins, through the right side of the heart and into the lungs, where it
becomes lodged in the pulmonary arteries. This blocks blood flow to
areas of the lungs and is called a pulmonary embolism (PE).

If the patient has a hole in their heart (for example, an atrial septal
defect), the blood clot can pass through to the left side of the heart and
into the systemic circulation. If it travels to the brain, it can cause a large
stroke.

Risk Factors

There are several factors that can put patients at higher risk of
developing a DVT or PE. In many of these situations (e.g., surgery), we
give patients prophylactic treatment to prevent VTE.
• Immobility
• Recent surgery
• Long haul travel
• Pregnancy
• Hormone therapy with oestrogen (combined oral contraceptive pill
and hormone replacement therapy)
• Malignancy
• Polycythaemia
• Systemic lupus erythematosus
• Thrombophilia

TOM TIP: In your exams, when a patient presents with possible

features of a DVT or PE, ask about risk factors such as periods of
immobility, surgery and long haul flights to score extra points.

Thrombophilias

Thrombophilias are conditions that predispose patients to develop

blood clots. There are a large number of these:
• Antiphospholipid syndrome
• Factor V Leiden
• Antithrombin deficiency
• Protein C or S deficiency
• Hyperhomocysteinaemia
• Prothombin gene variant
• Activated protein C resistance

TOM TIP: If you remember one cause of recurrent venous

thromboembolism, remember antiphospholipid syndrome. The
common association you may come across in exams is recurrent
miscarriage. The diagnosis can be made with a blood test for
antiphospholipid antibodies.

VTE Prophylaxis

Every patient admitted to hospital should be assessed for their risk of

venous thromboembolism (VTE). If they are at increased risk of VTE,
they should receive prophylaxis unless contraindicated. Prophylaxis is
usually with a low molecular weight heparin, such as enoxaparin.
Contraindications include active bleeding or existing anticoagulation with
warfarin or a DOAC.

Anti-embolic compression stockings are also used, unless

contraindicated. The main contraindication for compression stockings is
significant peripheral arterial disease.

DVT Presentation

DVTs are almost always unilateral. Bilateral DVT is rare and bilateral
symptoms are more likely due to an alternative diagnosis such as
chronic venous insufficiency or heart failure. DVTs can present with:
• Calf or leg swelling
 • Dilated superficial veins
• Tenderness to the calf (particularly over the site of the deep veins)
• Oedema
• Colour changes to the leg

To examine for leg swelling, measure the circumference of the calf

10cm below the tibial tuberosity. More than 3cm difference between
calves is significant.

Always ask questions and examine with the suspicion of a potential

pulmonary embolism as well.

Wells Score

The Wells score predicts the risk of a patient presenting with

symptoms having a DVT or PE. It includes risk factors such as recent
surgery and clinical findings such as unilateral calf swelling 3cm greater
than the other leg.

Diagnosis

D-dimer is a sensitive (95%), but not specific, blood test for VTE.
This makes it helpful in excluding VTE where there is a low suspicion. It
is almost always raised if there is a DVT; however other conditions can
also cause a raised d-dimer:
• Pneumonia
• Malignancy
• Heart failure
• Surgery
• Pregnancy

Doppler ultrasound of the leg is required to diagnose deep vein

thrombosis. NICE recommends repeating negative ultrasound scans after
6-8 days if the patient has a positive D-dimer and the Wells
score suggest a DVT is likely.

Pulmonary embolism can be diagnosed with a CT pulmonary

angiogram (CTPA) or ventilation-perfusion (VQ) scan. CTPA is usually
preferred, unless the patient has significant kidney impairment or a
contrast allergy.

Initial Management

The initial management for a suspected or confirmed DVT or PE is

with anticoagulation. In most patients, NICE (2020) recommend treatment
dose apixaban or rivaroxaban. This should be started immediately in
patients where a DVT or PE is suspected and there is a delay in getting a
scan to confirm the diagnosis.

The NICE guidelines (2020) recommend considering catheter-

directed thrombolysis in patients with a symptomatic iliofemoral DVT
and symptoms lasting less than 14 days. This involves inserting a
catheter under x-ray guidance through the venous system to apply
thrombolysis directly into the clot.

Long Term Anticoagulation

The options for long term anticoagulation in VTE are a DOAC,

warfarin or LMWH.

DOACs are oral anticoagulants that do not require monitoring. They

were called “novel oral anticoagulants” (NOACs), but this has been
changed to "direct-acting oral anticoagulants” (DOACs). Options are
apixaban, rivaroxaban, edoxaban and dabigatran. They are suitable
for most patients, including patients with cancer.

Warfarin is a vitamin K antagonist. The target INR for warfarin is

between 2 and 3 when treating DVTs and PEs. It is the first-line in patients
with antiphospholipid syndrome (who also require initial concurrent
treatment with LMWH).

Low molecular weight heparin (LMWH) is the first-line anticoagulant

in pregnancy.

Continue anticoagulation for:

• 3 months if there is a reversible cause (then review)
 • Beyond 3 months if the cause is unclear, there is recurrent VTE,
or there is an irreversible underlying cause such as thrombophilia
(often 6 months in practice)
• 3-6 months in active cancer (then review)

Inferior Vena Cava Filter

Inferior vena cava filters are devices inserted into the inferior vena
cava, designed to filter the blood and catch any blood clots travelling from
the venous system, towards the heart and lungs. They act as a sieve,
allowing blood to flow through whilst stopping larger blood clots. They are
used in unusual cases of patients with recurrent PEs or those that are
unsuitable for anticoagulation.

Investigating Unprovoked DVT

When patients have their first VTE without a clear cause, the NICE
guidelines from 2020 recommend reviewing the medical history, baseline
blood results and physical examination for evidence of cancer. The
previous 2012 guidelines recommended routinely considering
investigations such as a chest x-ray and CT abdomen-pelvis, although
this is no longer recommended (unless the history and examination
findings warrant further investigations).

In patients with an unprovoked DVT or PE that are not going to

continue anticoagulation (they have finished 3-6 months of treatment and
are due to stop), NICE recommend considering testing for:
• Antiphospholipid syndrome (check antiphospholipid
antibodies)
• Hereditary thrombophilias (only if they have a first-degree
relative also affected by a DVT or PE)
 Varicose Veins
Varicose veins are distended superficial veins measuring more than
3mm in diameter, usually affecting the legs.

Reticular veins are dilated blood vessels in the skin measuring 1-

3mm in diameter.

Telangiectasia refers to dilated blood vessels in the skin measuring

less than 1mm in diameter. They are also known as spider veins or
thread veins.

Development

Veins contain valves that only allow blood to flow in one direction,
towards the heart. In the legs, as the muscles contract, they squeeze
blood upwards against gravity. The valves prevent gravity from pulling the
blood back into the feet. When the valves become incompetent, the blood
is drawn downwards by gravity and pools in the veins and feet.

The deep and superficial veins are connected by vessels called the
perforating veins (or perforators), which allow blood to flow from the
superficial veins to the deep veins. When the valves are incompetent in
these perforators, blood flows from the deep veins back into the
superficial veins and overloads them. This leads to dilatation and
engorgement of the superficial veins, forming varicose veins.
 Chronic Venous Insufficiency

When blood pools in the distal veins, the pressure causes the veins to
leak small amounts of blood into the nearby tissues. The haemoglobin in
this leaked blood breaks down to haemosiderin, which is deposited
around the shins in the legs. This gives a brown discolouration to the
lower legs. This is known as haemosiderin staining.

Pooling of blood in the distal tissues results in inflammation. The skin

becomes dry and inflamed, referred to as venous eczema.

The skin and soft tissues become fibrotic and tight, causing the lower
legs to become narrow and hard. This is referred to as
lipodermatosclerosis.

Risk Factors

• Increasing age
• Family history
• Female
 • Pregnancy
• Obesity
• Prolonged standing (e.g., occupations involving standing for long
periods)
• Deep vein thrombosis (causing damage to the valves)

Presentation

Varicose veins present with engorged and dilated superficial leg veins.
They may be asymptomatic or have symptoms of:
• Heavy or dragging sensation in the legs
• Aching
• Itching
• Burning
• Oedema
• Muscle cramps
• Restless legs

Patients may also have signs and symptoms of chronic venous

insufficiency (e.g., skin changes and ulcers).

Special Tests

Tap test - apply pressure to the saphenofemoral junction (SFJ) and

tap the distal varicose vein, feeling for a thrill at the SFJ. A thrill suggests
incompetent valves between the varicose vein and the SFJ.

Cough test - apply pressure to the SFJ and ask the patient to cough,
feeling for thrills at the SFJ. A thrill suggests a dilated vein at the SFJ
(called saphenous varix).

Trendelenburg’s test - with the patient lying down, lift the affected leg
to drain the veins completely. Then apply a tourniquet to the thigh and
stand the patient up. The tourniquet should prevent the varicose veins
from reappearing if it is placed distally to the incompetent valve. If the
varicose veins appear, the incompetent valve is below the level of the
tourniquet. Repeat the test with the tourniquet at different levels to assess
the location of the incompetent valves.
 Perthes test - apply a tourniquet to the thigh and ask the patient to
pump their calf muscles by performing heel raises whilst standing. If the
superficial veins disappear, the deep veins are functioning. Increased
dilation of the superficial veins indicates a problem in the deep veins,
such as deep vein thrombosis.

Duplex ultrasound can be used to assess the extent of varicose

veins. It is an ultrasound that shows the speed and volume of blood flow.

Management

Varicose veins in pregnancy often improve after delivery.

Simple treatment measures include:

• Weight loss if appropriate
• Staying physically active
• Keeping the leg elevated when possible to help drainage
• Compression stockings (exclude arterial disease first with an ankle-
brachial pressure index)

Surgical options:
• Endothermal ablation - inserting a catheter into the vein to apply
radiofrequency ablation
• Sclerotherapy - injecting the vein with an irritant foam that causes
closure of the vein
• Stripping - the veins are ligated and pulled out of the leg

Complications

• Prolonged and heavy bleeding after trauma

• Superficial thrombophlebitis (thrombosis and inflammation in the
superficial veins)
• Deep vein thrombosis
• All the issues of chronic venous insufficiency (e.g., skin changes
and ulcers)
 Chronic Venous Insufficiency
Chronic venous insufficiency occurs when blood does not efficiently
drain from the legs back to the heart. Usually, this is the result of damage
to the valves inside the veins. This damage may occur with age,
immobility, obesity, prolonged standing or after a deep vein thrombosis. It
is often associated with varicose veins.

The valves are responsible for ensuring blood flows in one direction as
the leg muscles contract and squeeze the veins. When the valves are
damaged, the pumping effect of the leg muscles becomes less effective in
draining blood towards the heart. Blood pools in the veins of the legs,
causing venous hypertension.

Chronic pooling of blood in the legs leads to skin changes. The area
between the top of the foot and the bottom of the calf muscle is the area
most affected by these changes. This is known as the gaiter area.
 Haemosiderin staining is a red/brown discolouration caused by
haemoglobin leaking into the skin.
 Venous eczema (or varicose eczema) is dry, itchy, flaky, scaly, red,
cracked skin. These eczema-like changes are caused by a chronic
inflammatory response in the skin.

Lipodermatosclerosis is hardening and tightening of the skin and

tissue beneath the skin. Chronic inflammation causes the subcutaneous
tissue to become fibrotic (turning to scar tissue). Inflammation of the
subcutaneous fat is called panniculitis. The narrowing of the lower legs
causes the typical “inverted champagne bottle” appearance.

Atrophie blanche refers to patches of smooth, porcelain-white scar

tissue on the skin, often surrounded by hyperpigmentation.

As well as the skin changes above, chronic venous insufficiency can

lead to:
• Cellulitis
• Poor healing after injury
• Skin ulcers
• Pain

TOM TIP: Chronic venous changes are very common in older

patients. It is very easy to find patients with these skin changes to
use in OSCE examinations, so it is worth getting familiar with their
appearance and confidently presenting your examination findings.
These changes are often misdiagnosed as cellulitis, and patients are
given a course of antibiotics. The broken skin does leave patients
prone to skin infections, so this does need to be considered,
although keep in mind that “bilateral cellulitis” is quite unusual, and
chronic skin changes related to venous insufficiency will not
resolve with antibiotics.

Management

Management involves:
• Keeping the skin healthy
• Improving venous drainage to the legs
• Managing complications

The skin is kept healthy by:

 • Monitoring skin health and avoiding skin damage
• Regular use of emollients (e.g., diprobase, oilatum, cetraben or
doublebase)
• Topical steroids to treat flares of venous eczema
• Very potent topical steroids to treat flares of lipodermatosclerosis

Improving venous drainage to the legs involves:

• Weight loss if obese
• Keeping active
• Keeping the legs elevated when resting
• Compression stockings (exclude arterial disease first with an ankle-
brachial pressure index)

Management of complications involves:

• Antibiotics for infection
• Analgesia for pain
• Wound care for ulceration
 Leg Ulcers
Leg ulcers are wounds or breaks in the skin that do not heal or heal
slowly due to underlying pathology. They have the potential to get
progressively larger and become more difficult to heal over time. There
are four common types of skin ulcers:
• Venous ulcers
• Arterial ulcers
• Diabetic foot ulcers
• Pressure ulcers

This section mainly covers arterial and venous ulcers. Arterial

ulcers result from insufficient blood supply to the skin due to peripheral
arterial disease. Venous ulcers occur due to the pooling of blood and
waste products in the skin secondary to venous insufficiency. Mixed
ulcers are a combination of arterial and venous disease causing the
ulcer.

Other Types of Ulcers

Diabetic foot ulcers are more common in patients with diabetic

neuropathy. Patients who have lost the sensation in their feet are less
likely to realise they have injured their feet or have poorly fitting shoes.
Additionally, damage to both the small and large blood vessels impairs
the blood supply and wound healing. Raised blood sugar, immune system
changes and autonomic neuropathy also contribute to ulceration and poor
healing. Osteomyelitis (infection in the bone) is an important
complication.

Pressure ulcers typically occur in patients with reduced mobility,

where prolonged pressure on particular areas (e.g., the sacrum whilst
sitting) lead to the skin breaking down. This happens due to a
combination of reduced blood supply and localised ischaemia, reduced
lymph drainage and an abnormal change in shape (deformation) of the
tissues under pressure. Extensive effort should be taken to prevent
pressure ulcers, including individual risk assessments, regular
repositioning, special inflating mattresses, regular skin checks and
protective dressings and creams. The Waterlow Score is a commonly
used risk assessment tool for estimating an individual patient’s risk of
developing a pressure ulcer.

Arterial Versus Venous Ulcers

Some features help you distinguish between arterial and venous

ulcers.

Typically, arterial ulcers:

• Occur distally, affecting the toes or dorsum of the foot
• Are associated with peripheral arterial disease, with absent pulses,
pallor and intermittent claudication
• Are smaller than venous ulcers
• Are deeper than venous ulcers
• Have well defined borders
• Have a “punched-out” appearance
• Are pale colour due to poor blood supply
• Are less likely to bleed
• Are painful
• Have pain worse at night (when lying horizontally)
• Have pain is worse on elevating and improved by lowering the leg
(gravity helps the circulation)

Typically, venous ulcers:

• Occur in the gaiter area (between the top of the foot and bottom of
the calf muscle)
• Are associated with chronic venous changes, such as
hyperpigmentation, venous eczema and lipodermatosclerosis
• Occur after a minor injury to the leg
• Are larger than arterial ulcers
• Are more superficial than arterial ulcers
• Have irregular, gently sloping border
• Are more likely to bleed
• Are less painful than arterial ulcers
• Have pain relieved by elevation and worse on lowering the leg
 Investigations

Ankle-brachial pressure index (ABPI) is used to assess for arterial

disease. This is required in both arterial and venous ulcers.

Blood tests may help assess for infection (FBC and CRP) and co-
morbidities (HbA1c for diabetes, FBC for anaemia and albumin for
malnutrition).

Skin swabs (charcoal swabs) may be helpful where infection is

suspected, to determine the causative organism.

Skin biopsy may be required in patients where skin cancer (e.g.,

squamous cell carcinoma) is suspected as a differential diagnosis. This
will require a two week wait referral to dermatology.

Management of Arterial Ulcers

The management of arterial ulcers is the same as peripheral arterial

disease, with an urgent referral to vascular to consider surgical
revascularisation. If the underlying arterial disease is effectively treated,
the ulcer should heal rapidly. Debridement and compression are not used
in arterial ulcers.

Management of Venous Ulcers

The management here is based on the NICE CKS (updated January

2021). Patients may require referral to:
• Vascular surgery where mixed or arterial ulcers are suspected
• Tissue viability / specialist leg ulcer clinics in complex or non-
healing ulcers
• Dermatology where an alternative diagnosis is suspected, such as
skin cancer
• Pain clinics if the pain is difficult to manage
• Diabetic ulcer services (for patients with diabetic ulcers)

Patients require input from experienced nurses, such as the district

nurses or tissue viability nurses. Good wound care involves:
• Cleaning the wound
 • Debridement (removing dead tissue)
• Dressing the wound

Compression therapy is used to treat venous ulcers (after arterial

disease is excluded with an ABPI).

Pentoxifylline (taken orally) can improve healing in venous ulcers

(but is not licensed).

Antibiotics are used to treat infection.

Analgesia is used to manage pain (avoid NSAIDs as they can worsen

the condition).
 Lymphoedema
Lymphoedema is a chronic condition caused by impaired lymphatic
drainage of an area.

The lymphatic system is responsible for draining excess fluid from the
tissues. The tissues in areas affected by an impaired lymphatic system
become swollen with excess, protein-rich fluid (lymphoedema).

The lymphatic system also plays an important role in the immune

system. Areas of lymphoedema are prone to infection.

Primary lymphoedema is a rare, genetic condition, which usually

presents before aged 30. It is a result of faulty development of the
lymphatic system.

Secondary lymphoedema is due to a separate condition that affects

the lymphatic system. The most common example is when patients
develop lymphoedema after breast cancer surgery, due to the removal
of axillary lymph nodes in the armpit.

Lipoedema is an important differential diagnosis, where there is an

abnormal build-up of fat tissue in the limbs, often the legs. The feet are
spared in lipoedema, unlike lymphoedema. This affects women more
often than men. It can cause pain, psychological distress and significantly
affect the patient’s quality of life.

Assessment

Stemmer’s sign can be used to assess for lymphoedema. The skin at

the bottom of the second toe or middle finger is gently pinched together
using two fingers. If it is possible to lift and “tent” the skin, Stemmer’s sign
is negative. If it is not possible to pinch the skin together, lift and “tent” it,
Stemmer’s sign is positive, suggesting lymphoedema.

Limb volume can be calculated using:

• Circumferential measurements at various points along the limb
 • Water displacement (putting the limb into water and measuring
the volume of water displaced)
• Perometry (a square frame with perpendicular light beams is
moved along the limb, measuring the outline and volume)

Bioelectric impedance spectrometry can be used to measure the

volume of fluid collected in the limb. Electrodes are placed on the limb,
and an electrical current is passed through the limb, between the
electrodes. The resistance to electrical flow through the tissues estimates
the volume of lymph fluid in the tissues.

Lymphoscintigraphy is a type of nuclear medicine scan. A

radioactive tracer is injected into the skin, and gamma cameras
(scintigraphy) are used to assess the structure of the lymphatic system.

Management

A specialist lymphoedema service manages patients with

lymphoedema.

Non-surgical treatment options include:

• Massage techniques to manually drain the lymphatic system
(manual lymphatic drainage)
• Compression bandages
• Specific lymphoedema exercises to improve lymph drainage
• Weight loss if overweight
• Good skin care

Lymphaticovenular anastomosis is a surgical procedure that

involves attaching lymphatic vessels to nearby veins, allowing the
lymphatic vessel to drain directly into the venous system. This and other
surgical procedures are occasionally used where other treatments fail.

Antibiotics are required if cellulitis (infection in the skin) develops.

Cognitive behavioural therapy and antidepressants can be used to

manage the psychological impact of having lymphoedema.
 TOM TIP: Avoid taking blood, inserting a cannula, giving
injections or performing a blood pressure reading in a limb with
lymphoedema.

Lymphatic Filariasis

Lymphatic filariasis is an infectious disease caused by parasitic

worms spread by mosquitos. The worms live in the lymphatic system
where they can cause damage, leading to severe lymphoedema. This
severe lymphoedema is associated with thickening and fibrosis of the
skin and tissues, and is referred to as elephantiasis. It is most common
in the tropics of Africa and Asia.
 Abdominal Aortic Aneurysm
Abdominal aortic aneurysm (AAA) refers to dilation of the abdominal
aorta, with a diameter of more than 3cm. Often the first time patients
become aware of an aneurysm is when it ruptures, causing life-
threatening bleeding into the abdominal cavity. The mortality of a ruptured
AAA is around 80%.

Risk Factors
 • Men are affected significantly more often and at a younger age
• Increased age
• Smoking
• Hypertension
• Family history
• Existing cardiovascular disease

Screening

All men in England are offered a screening ultrasound scan at age

65 to detect asymptomatic AAA. Early detection of an AAA means
preventative measures can stop it from expanding further or rupturing.

Women are not routinely offered screening, as they are at much lower
risk. The NICE guidelines (2020) say a routine ultrasound can be
considered in women aged over 70 with risk factors such as existing
cardiovascular disease, COPD, family history, hypertension,
hyperlipidaemia or smoking.

Patients with an aorta diameter above 3cm are referred to a vascular

team (urgently if more than 5.5cm).

Presentation

Most patients with an AAA are asymptomatic. It may be discovered on

routine screening or when it ruptures.

Other ways it can present include:

• Non-specific abdominal pain
• Pulsatile and expansile mass in the abdomen when palpated with
both hands
• As an incidental finding on an abdominal x-ray, ultrasound or CT
scan

Diagnosis

Ultrasound is the usual initial investigation for establishing the

diagnosis.
 CT angiogram gives a more detailed picture of the aneurysm and
helps guide elective surgery to repair the aneurysm.

Classification

The severity of the aortic aneurysm depends on the diameter:

• Normal: less than 3cm
• Small aneurysm: 3 - 4.4cm
• Medium aneurysm: 4.5 - 5.4cm
• Large aneurysm: above 5.5cm

Management

The risk of progression of an AAA can be reduced by treating

reversible risk factors:
• Stop smoking
• Healthy diet and exercise
• Optimising the management of hypertension, diabetes and
hyperlipidaemia

The Public Health England (updated 2017) screening and surveillance

programme recommends follow up scans:
• Yearly for patients with aneurysms 3-4.4cm
• 3 monthly for patients with aneurysms 4.5-5.4cm

The NICE guidelines (2020) recommend elective repair for patients

with any of:
• Symptomatic aneurysm
• Diameter growing more than 1cm per year
• Diameter above 5.5cm

Elective surgical repair involves inserting an artificial “graft” into the

section of the aorta affected by the aneurysm. There are two methods for
inserting the graft:
• Open repair via a laparotomy
• Endovascular aneurysm repair (EVAR) using a stent inserted via
the femoral arteries

Gov.uk (April 2021) advise that patients must:

 • Inform the DVLA if they have an aneurysm above 6cm
• Stop driving if it is above 6.5cm
• Stricter rules apply to drivers of heavy vehicles (e.g., bus or lorry
drivers)

Ruptured AAA

The risk of rupture increases with the diameter of the aneurysm

(roughly 5% for 5cm and 40% for 8 cm aneurysms). Ruptured AAA has an
extremely high mortality (around 80%).

A ruptured aortic aneurysm presents with:

• Severe abdominal pain that may radiate to the back or groin
• Haemodynamic instability (hypotension and tachycardia)
• Pulsatile and expansile mass in the abdomen
• Collapse
• Loss of consciousness

An abdominal aortic aneurysm is a surgical emergency requiring

immediate involvement of experienced seniors, vascular surgeons,
anaesthetists and theatre teams.

Permissive hypotension refers to the strategy of aiming for a lower

than normal blood pressure when performing fluid resuscitation. The
theory is that increasing the blood pressure may increase blood loss.

Haemodynamically unstable patients with a suspected AAA should

be transferred directly to theatre. Surgical repair should not be delayed
by getting imaging to confirm the diagnosis.

CT angiogram can be used to diagnose or exclude ruptured AAA in

haemodynamically stable patients.

In patients with co-morbidities that make the prognosis with surgery

very poor, a discussion needs to be had with senior doctors, the patient
and their family about palliative care.
 Aortic Dissection
Aortic dissection refers to when a break or tear forms in the inner layer
of the aorta, allowing blood to flow between the layers of the wall of the
aorta. There are three layers to the aorta, the intima, media and
adventitia. With aortic dissection, blood enters between the intima and
media layers of the aorta. A false lumen full of blood is formed within the
wall of the aorta. Intramural refers to within the walls of the blood
vessel.

Classification

Aortic dissection most commonly affects the ascending aorta and

aortic arch but can affect any part of the aorta. The right lateral area of
the ascending aorta is the most common site of a tear of the intima layer,
as this is under the most stress from blood exiting the heart. There are
two classification systems.
 The Stanford system:
• Type A - affects the ascending aorta, before the brachiocephalic
artery
• Type B - affects the descending aorta, after the left subclavian
artery

The DeBakey system:

• Type I - begins in the ascending aorta and involves at least the
aortic arch, if not the whole aorta
• Type II - isolated to the ascending aorta
• Type IIIa - begins in the descending aorta and involves only the
section above the diaphragm
• Type IIIb - begins in the descending aorta and involves the aorta
below the diaphragm

Risk Factors

Aortic dissection shares the same risk factors as peripheral arterial

disease, such as age, male sex, smoking, hypertension, poor diet,
reduced physical activity and raised cholesterol.

Hypertension is a big risk factor. Dissection can be triggered by

events that temporarily cause a dramatic increase in blood pressure, such
as heavy weightlifting or the use of cocaine.

Conditions or procedures that affect the aorta increase the risk of a

dissection, such as:
• Bicuspid aortic valve
• Coarctation of the aorta
• Aortic valve replacement
• Coronary artery bypass graft (CABG)

Conditions that affect the connective tissues can also increase the risk
of a dissection, notably:
• Ehlers-Danlos syndrome
• Marfan’s syndrome

TOM TIP: For your exams, a man aged around 60 with a

background of hypertension, presenting with a sudden onset
tearing chest pain, has aortic dissection. Marfan’s and Ehlers-
Danlos syndrome are worth remembering as risk factors, as these
may be options on an MCQ exam.

Presentation

Aortic dissection can be difficult to spot. The diagnosis is often missed.

The typical presentation is a sudden onset, severe, “ripping” or

“tearing” chest pain. The pain may be in the anterior chest when the
ascending aorta is affected, or the back if the descending aorta is
affected. The pain may change location (migrate) over time. Some
patients with aortic dissection do not have chest pain.

Other features that may suggest aortic dissection are:

• Hypertension
• Differences in blood pressure between the arms (more than a
20mmHg difference is significant)
 • Radial pulse deficit (the radial pulse in one arm is decreased or
absent and does not match the apex beat)
• Diastolic murmur
• Focal neurological deficit (e.g., limb weakness or paraesthesia)
• Chest and abdominal pain
• Collapse (syncope)
• Hypotension as the dissection progresses

Diagnosis

An ECG and chest x-ray are often used to exclude other causes
(such as myocardial infarction), although they may be normal and falsely
reassuring. Myocardial infarction can occur in combination with aortic
dissection, and treatment of the myocardial infarction (e.g., thrombolysis)
can cause fatal progression of the aortic dissection.

Bedside ultrasound can be used as a rapid test in A&E to look for

aortic dissection.

CT angiogram is usually the initial investigation to confirm the

diagnosis and can generally be performed very quickly.

MRI angiogram provides greater detail and can help plan

management but often takes longer to get.

Management

Aortic dissection is a surgical emergency and needs immediate

involvement of experienced seniors, vascular surgeons, anaesthetists
and intensive care teams. There is a very high mortality.

Analgesia (e.g., morphine) is required to manage the pain.

Blood pressure and heart rate need to be well controlled to reduce

the stress on the aortic walls. This usually involves beta-blockers.

Surgical intervention from the vascular team will depend on the type
of aortic dissection.
 Type A may be treated with open surgery (midline sternotomy) to
remove the section of the aorta with the defect in the wall and replace it
with a synthetic graft. The aortic valve may need to be replaced during the
procedure.

Type B may be treated with thoracic endovascular aortic repair

(TEVAR), with a catheter inserted via the femoral artery, inserting a stent
graft into the affected section of the descending aorta. Complicated cases
may require open surgery.

Complications

There is a long list of complications. Some of the key ones to

remember are:
• Myocardial infarction
• Stroke
• Paraplegia (motor or sensory impairment in the legs)
• Cardiac tamponade
• Aortic valve regurgitation
• Death
 Carotid Artery Stenosis
Carotid artery stenosis refers to narrowing of the carotid arteries in
the neck, usually secondary to atherosclerosis. Plaques build up in the
carotid arteries, reducing the diameter of the lumen. There is a risk of
parts of the plaque breaking away and becoming an embolus, travelling
to the brain and causing an embolic stroke.

The risk factors for developing carotid artery stenosis are the same as
for atherosclerosis and arterial disease in other areas, such as age, male
sex, smoking, hypertension, poor diet, reduced physical activity and
raised cholesterol.

Patients with a transient ischaemic attack (TIA) or stroke are

investigated for carotid artery stenosis, usually with a carotid ultrasound.

Patients with carotid artery stenosis are very likely to have arterial
disease and atherosclerosis elsewhere. They are at high risk of coronary
artery disease and myocardial infarction.

Classification

The severity of aortic stenosis is categorised as:

• Mild - less than 50% reduction in diameter
• Moderate - 50 to 69% reduction in diameter
• Severe - 70% or more reduction in diameter

Presentation

Carotid artery stenosis is usually asymptomatic. Usually, it is

diagnosed after a TIA or stroke.

A carotid bruit may be heard on examination. This is a whooshing

sound heard with a stethoscope over the affected carotid artery, caused
by turbulent flow around the stenotic area during systole (contraction of
the heart).
 Diagnosis

Carotid ultrasound is usually the initial investigation to diagnose and

assess carotid artery stenosis.

CT or MRI angiogram may be used to assess the stenosis in more

detail before surgical interventions.

Management

Conservative management involves addressing modifiable risk factors

and medical therapy:
• Healthy diet and exercise
• Stop smoking
• Management of co-morbidities (e.g., hypertension and diabetes)
• Antiplatelet medications (e.g., aspirin, clopidogrel or ticagrelor)
• Lipid-lowering medications (e.g., atorvastatin)

Surgical interventions are considered where there is significant

stenosis. The options are:
• Carotid endarterectomy
• Angioplasty and stenting

Endarterectomy involves an incision in the neck, opening the carotid

artery and scraping out the plaque. This is the first-line treatment for most
patients requiring surgical intervention. A key complication of the
procedure is stroke (around 2%).

During endarterectomy, nearby nerves can be injured. This may be

temporary or permanent. Symptoms depend on the nerve:
• Facial nerve injury causes facial weakness (often the marginal
mandibular branch causing drooping of the lower lip)
• Glossopharyngeal nerve injury causes swallowing difficulties
• Recurrent laryngeal nerve (a branch of the vagus nerve) injury
causes a hoarse voice
• Hypoglossal nerve injury causes unilateral tongue paralysis

Angioplasty and stenting is an alternative to endarterectomy. This is

an endovascular procedure. A catheter is inserted into the femoral artery
in the groin, passed through the aorta under x-ray guidance, up to the
affected carotid artery. A balloon is inflated in the narrowed area to widen
the lumen (angioplasty), and a stent is left in place to keep it open
(stenting).
 Buerger Disease
Buerger disease is also known as thromboangiitis obliterans. It is
an inflammatory condition that causes thrombus formation in the
small and medium-sized blood vessels in the distal arterial system
(affecting the hands and feet).

Buerger disease typically affects men aged 25 - 35 and has a very

strong association with smoking.

Notable features (included in the diagnostic criteria) are:

• Younger than 50 years
• Not having risk factors for atherosclerosis, other than smoking

Presentation

The typical presenting feature is painful, blue discolouration to the

fingertips or tips of the toes. The pain is often worse at night. This may
progress to ulcers, gangrene and amputation.

Corkscrew collaterals are a typical finding on angiograms, where

new collateral vessels form to bypass the affected arteries.

Management

Completely stopping smoking is the main component of treatment.

This usually results in a significant improvement. Cutting down or using
nicotine replacement products does not seem to be adequate to improve
the condition.

Other specialist treatments may be considered, including intravenous

iloprost (a prostacyclin analogue that dilates blood vessels).

TOM TIP: The key presentation to remember for your exams is a

young male smoker with painful blue fingertips. The exam question
may ask the diagnosis (Buerger disease or thromboangiitis
obliterans) or ask the most important aspect of management
(completely stopping smoking).
 Cardiothoracic Surgery
Coronary Artery Bypass Graft
Prosthetic Valves
Congenital Cardiac Conditions
Pericardial Effusion
Thoracic Aortic Aneurysms
Lung Cancer
Pneumothorax
Heart and Lung Transplant
 Coronary Artery Bypass Graft
A coronary artery bypass graft (CABG) procedure involves using a
graft blood vessel taken from elsewhere in the body (usually the
saphenous vein) to bypass a blockage in a coronary artery. Depending
on the affected areas, this may involve one, two, three or even four
bypass grafts.

Coronary Anatomy

The left coronary artery (LCA) becomes the circumflex and left
anterior descending (LAD) arteries.
 The right coronary artery (RCA) curves around the right side and
under the heart and supplies the:
• Right atrium
• Right ventricle
• Inferior aspect of the left ventricle
• Posterior septal area

The circumflex artery curves around the top, left and back of the
heart and supplies the:
• Left atrium
• Posterior aspect of the left ventricle

The left anterior descending (LAD) travels down the middle of the
heart and supplies the:
• Anterior aspect of the left ventricle
• Anterior aspect of septum

Atherosclerosis

Athero- refers to soft or porridge-like and -sclerosis refers to

hardening. Atherosclerosis is a combination of atheromas (fatty
deposits in the artery walls) and sclerosis (the process of hardening or
stiffening of the blood vessel walls). Atherosclerosis affects the medium
and large arteries. It is caused by chronic inflammation and activation
of the immune system in the artery wall. Lipids are deposited in the
artery wall, followed by the development of fibrous atheromatous
plaques.

These plaques cause:

• Stiffening of the artery walls, leading to hypertension (raised
blood pressure) and strain on the heart (whilst trying to pump blood
against increased resistance)
• Stenosis, leading to reduced blood flow (e.g., in angina)
• Plaque rupture, resulting in a thrombus that can block a distal
vessel and cause ischaemia (e.g., in acute coronary syndrome)

Atherosclerosis Risk Factors

 It is important to break these down into modifiable and non-
modifiable risk factors. We cannot do anything about non-modifiable risk
factors, but we can do something about modifiable ones.

Non-modifiable risk factors:

• Older age
• Family history
• Male

Modifiable risk factors:

• Smoking
• Alcohol consumption
• Poor diet (high in sugar and trans-fat and low in fruit, vegetables
and omega 3s)
• Low exercise / sedentary lifestyle
• Obesity
• Poor sleep
• Stress

Medical Co-Morbidities

Medical co-morbidities increase the risk of atherosclerosis and should

be carefully managed to minimise the risk:
• Diabetes
• Hypertension
• Chronic kidney disease
• Inflammatory conditions such as rheumatoid arthritis
• Atypical antipsychotic medications

TOM TIP: Think about risk factors when taking a history from
someone with suspected atherosclerotic disease (such as someone
presenting with exertional chest pain). Ask about their exercise, diet,
past medical history, family history, occupation, smoking, alcohol
intake and medications. This will help you perform well in exams
and when presenting to seniors.

Complications of Atherosclerosis

• Angina
 • Myocardial infarction
• Transient ischaemic attack
• Stroke
• Peripheral arterial disease
• Chronic mesenteric ischaemia

TOM TIP: Patients with one type of arterial disease are likely to
have others. When a patient has symptoms of one type of arterial
disease (e.g., intermittent claudication), consider the risk of others
(e.g., coronary artery disease). Erectile dysfunction can often be the
first indication of arterial disease and should prompt you to
consider checking the lipid profile, blood pressure and Q-risk score
(which is the percentage risk that a patient will have a stroke or
myocardial infarction in the next 10 years).

Coronary Artery Disease

Narrowing (stenosis) of the coronary arteries due to atherosclerosis

may be asymptomatic, or present with:
• Angina (stable or unstable)
• Myocardial infarction

The options for management are:

• Medical management (secondary prevention with statins, aspirin,
beta-blockers and ACE inhibitors)
• Percutaneous coronary intervention (PCI) with coronary
angioplasty
• Coronary artery bypass graft

Cardiopulmonary Bypass

The bypass machine takes blood from the vena cava or right atrium,
pumps it through a machine that adds oxygen and removes carbon
dioxide from the blood, then pumps it back into the ascending aorta. This
way, blood bypasses the heart and lungs and is artificially oxygenated.
Heparin is used to prevent blood clotting. A clinical perfusionist is
responsible for operating and monitoring the cardiopulmonary bypass
equipment.
 Cardioplegia

During a coronary artery bypass graft procedure, the heart needs to

be still. Causing the heart to stop beating is called cardioplegia. The
heart is only stopped after the cardiopulmonary bypass is up and running.
A high potassium solution is delivered into the coronary circulation,
causing the heart to stop. Once the surgery is complete, cardioplegia is
stopped and the heart will spontaneously start
beating. Cardioversion or temporary pacing may be used to treat
arrhythmias that occur.

Coronary Artery Bypass Grafts

A separate blood vessel needs to be obtained to create a bypass. This

blood vessel is called a graft. The three main options for graft vessels
are:
• Saphenous vein (harvested from the inner leg)
• Internal thoracic artery, also known as the internal mammary
artery
• Radial artery
 The internal thoracic artery is a branch of the subclavian artery.
When the internal thoracic artery is used in a CABG, the proximal end
may be left attached to the subclavian artery. The distal end is separated
from any connections and then joined to the left anterior descending
artery. As a result, blood flows from the subclavian artery, through the
internal thoracic artery and into the left anterior descending artery.
Leaving it proximally attached to the original site, whilst changing where it
supplies, is described as a pedicled graft. The internal thoracic artery
can also be used as a free graft if required.

A free graft refers to a section of blood vessel that is entirely

separated from its original connections, before being reattached in a new
site for the bypass. During a coronary artery bypass procedure, the graft
vessel is attached directly to the ascending aorta, with the other end
attached to the coronary artery, distal to the stenosis (bypassing the
diseased portion of the artery). Blood flows from the ascending aorta,
through the graft and into the coronary artery.
 Vein grafts (i.e., from the saphenous vein) have a tendency to
become stenosed (narrowed) over time in a process called intimal
hyperplasia. The tunica intima layer in the vessel becomes thickened,
mostly due to increased pressure. Arterial grafts (e.g., radial or internal
thoracic) are less affected by this, so tend to make better grafts.

Recovery

After cardiothoracic surgery, patients have careful monitoring and

supportive care in the intensive care unit. They are usually discharged
after about a week. There is a slow recovery period with a gradual
increase in activity. In straightforward cases, patients make a full recovery
and resume full normal activities after 3 months.

Complications

The two most serious and notable complications are:

• Death (2-3% in straightforward cases)
• Stroke (1-5% in straightforward cases)

Other complications:
• Infection
• Acute kidney injury
• Cognitive impairment
• Myocardial infarction
• Atrial fibrillation
 Prosthetic Heart Valves
Severe pathology of the aortic or mitral valves may be an indication
for surgical replacement of that valve. Replacement of the tricuspid valve
is very rare.

Patients that have had a valve replacement will have a scar. Usually,
this will be a midline sternotomy scar straight down the middle of the
sternum, indicating a mitral or aortic valve replacement or a coronary
artery bypass graft (CABG). Less commonly a right-sided mini-
thoracotomy incision can be used for minimally invasive mitral valve
surgery.

Aortic Stenosis

Severe aortic stenosis is the most common valvular heart disease

you will encounter and the most common indication for valve replacement
surgery.

Aortic stenosis causes an ejection-systolic, high-pitched murmur

(high velocity of systole). This has a crescendo-decrescendo character
due to the speed of blood flow across the value during the different
periods of systole. Flow during systole is slowest at the very start and
end, and is fastest in the middle.

Other signs:
• The murmur radiates to the carotids as the turbulence continues
up into the neck
• Slow rising pulse and narrow pulse pressure
• Patients may complain of exertional syncope (lightheadedness
and fainting when exercising) due to difficulty maintaining a good
flow of blood to the brain

Causes:
• Idiopathic age-related calcification (by far the most common cause)
• Rheumatic heart disease
 Mitral Regurgitation

Mitral regurgitation is the second most common indication for valve

replacement.

Mitral regurgitation is when an incompetent mitral valve allows blood

to leak back through during systolic contraction of the left ventricle.
The leaking valve causes a reduced ejection fraction and a backlog of
blood waiting to be pumped through the left side of the heart, resulting in
congestive cardiac failure.

Mitral regurgitation causes a pan-systolic, high pitched “whistling”

murmur due to high-velocity blood flow through the leaky valve. The
murmur radiates to the left axilla. You may hear a third heart sound.

Causes:
• Idiopathic weakening of the valve with age
• Ischaemic heart disease
• Infective endocarditis
• Rheumatic heart disease
• Connective tissue disorders, such as Ehlers Danlos syndrome or
Marfan syndrome

Bioprosthetic Versus Mechanical

Valves can be either replaced by a bioprosthetic or a metallic

mechanical valve.

Bioprosthetic valves have a limited lifespan of around 10 years.

“Porcine” bioprosthetic valves come from a pig.

Mechanical valves have a good lifespan (well over 20 years) but

require lifelong anticoagulation with warfarin. The INR target range with
mechanical valves is 2.5 - 3.5 (this is higher than the 2 - 3 target for atrial
fibrillation).

Types of Mechanical Heart Valve

 Starr-Edwards valves feature a ball in a cage. The ball moves away
from the opening to let blood through, then moves back against the
opening to prevent blood from regurgitating through the valve. They were
very successful but are no longer used due to the high risk of thrombus
formation.

Tilting disc valves feature a single tilting disc.

St Jude valves consists of two tilting metal discs. The two discs mean
they are called bileaflet valves. Of the three mechanical valves listed, the
St Jude valve has the smallest risk of thrombus formation.

Mechanical Heart Valves

It is possible to hear a click when auscultating the heart sounds in a

patient with a mechanical valve:
• A click replaces S1 for metallic mitral valves
• A click replaces S2 for metallic aortic valves

There are three major complications of mechanical heart valves:

• Thrombus formation (blood stagnates and clots)
• Infective endocarditis (infection in the prosthesis)
• Haemolysis causing anaemia (blood gets churned up in the valve)

Transcatheter Aortic Valve Implantation

Transcatheter aortic valve implantation (TAVI) is a treatment for

severe aortic stenosis, usually in patients that are at high risk for an
open valve replacement operation. It involves local or general
anaesthetic, inserting a catheter into the femoral artery, feeding a wire
under x-ray guidance to the location of the aortic valve, inflating a
balloon to stretch the stenosed aortic valve and implanting a
bioprosthetic valve in the location of the aortic valve.

Long term outcomes for TAVI are still not clear as it is a relatively new
procedure. Therefore, in younger, fitter patients, open surgery is still the
first-line option.

Patients that have a TAVI do not typically require warfarin as the valve
is bioprosthetic.

Infective Endocarditis

This occurs in around 2.5% of patients having a surgical valve

replacement. The rate is slightly lower for TAVI at around 1.5%. Infective
endocarditis in a prosthetic valve has quite a high mortality of around
15%. This is usually caused by one of three gram-positive cocci
organisms:

• Staphylococcus
• Streptococcus
• Enterococcus
 Congenital Cardiac Conditions
Several congenital heart defects may present for the first time, or
worsen, in adulthood. The conditions covered here are:
• Atrial septal defects
• Ventricular septal defects
• Coarctation of the aorta

Other congenital heart conditions usually present and are managed in

infancy or childhood. They require follow up and monitoring, but the
defect is usually repaired by adulthood. These are discussed elsewhere
in the paediatrics content:
• Patent ductus arteriosus
• Tetralogy of Fallot
• Ebstein’s anomaly
• Transposition of the great arteries

An echocardiogram is the initial investigation of choice for

diagnosing congenital heart defects.

Cyanotic Heart Disease

Congenital heart disease can be divided into two categories: cyanotic

and acyanotic.

Cyanosis occurs when deoxygenated blood enters the systemic

circulation. Cyanotic heart disease occurs when blood
can bypass the pulmonary circulation and the lungs. This occurs
across a right-to-left shunt. A right-to-left shunt describes any defect
that allows blood to flow from the right side of the
heart (the deoxygenated blood returning from the body) to the left side
of the heart (the blood exiting the heart into the systemic circulation),
without travelling through the lungs to get oxygenated.

Heart defects that can cause a right-to-left shunt, and

therefore cyanotic heart disease, are:
 • Ventricular septal defect (VSD)
• Atrial septal defect (ASD)
• Patent ductus arteriosus (PDA)
• Transposition of the great arteries

Patients with a VSD, ASD or PDA are usually not cyanotic. This is
because the pressure in the left side of the heart is much greater than the
right side, and blood will flow from the area of high pressure to the area
of low pressure (left to right). This prevents a right-to-left shunt. If
the pulmonary pressure increases beyond the systemic pressure, blood
will start to flow from right to left across the defect, causing cyanosis.
This is called Eisenmenger syndrome.

Complications

The key complications of congenital heart disease are:

• Heart failure
• Arrhythmias
• Endocarditis
• Stroke
• Pulmonary hypertension
• Eisenmenger syndrome

Generally, the risks associated with congenital heart defects are much
higher during pregnancy. Women with congenital heart defects need to
be counselled by their specialist about the risks of pregnancy and require
careful monitoring throughout pregnancy.

Atrial Septal Defects

An atrial septal defect is a defect (a hole) in the septum (the wall)

between the two atria. This connects the right and left atria, allowing
blood to flow between them.
The types of atrial septal defect, from most to least common, are:
• Patent foramen ovale, where the foramen ovale fails to close
(although this is not strictly classified as an ASD)
• Ostium secondum, where the septum secondum fails to fully
close, leaving a hole in the wall
• Ostium primum, where the septum primum fails to fully close,
leaving a hole in the wall (this tends to lead to a atrioventricular
septal defect)
 An atrial septal defect leads to a shunt, with blood moving between
the two atria. Blood moves from the left atrium to the right atrium
because the pressure in the left atrium is higher than the pressure in the
right atrium. This means blood continues to flow to the pulmonary
vessels and lungs to get oxygenated and the patient does not become
cyanotic. However, the increased flow to the right side of the heart leads
to right-sided overload and right heart strain. This right-sided
overload can lead to right heart failure and pulmonary hypertension.

Eventually, pulmonary hypertension can lead to Eisenmenger

syndrome. This occurs because the pulmonary pressure exceeds the
systemic pressure, causing the shunt to reverse and become a right-to-
left shunt across the ASD. This causes blood to bypass the lungs,
resulting in the patient becoming cyanotic.

Presentation of Atrial Septal Defects

Atrial septal defects are often picked up on antenatal scans or

newborn examinations. It may be asymptomatic in childhood and present
in adulthood with:
• Dyspnoea (shortness of breath) secondary to pulmonary
hypertension and right-sided heart failure
• Stroke in the context of venous thromboembolism (see below)
• Atrial fibrillation or atrial flutter

TOM TIP: It is worth remembering atrial septal defects as a cause

of stroke in patients with a DVT. Normally, when patients have a DVT
and this becomes an embolus, the clot travels to the right side of the
heart, enters the lungs and becomes a pulmonary embolism. In
patients with an ASD the clot can travel from the right atrium to the
left atrium across the ASD. This means the clot can travel to the left
ventricle, aorta and up to the brain, causing a large stroke. An exam
question may feature a patient with a DVT that develops a large
stroke and the challenge is to identify that they have had a lifelong
asymptomatic ASD.

Atrial septal defects cause a mid-systolic, crescendo-

decrescendo murmur loudest at the upper left sternal border, with a
fixed split second heart sound. Splitting of the second heart sound can
be normal with inspiration. However, a “fixed split” second heart sound
means the split does not change with inspiration and expiration. This
occurs in an atrial septal defect because blood is flowing from the left
atrium into the right atrium across the atrial septal defect, increasing the
volume of blood that the right ventricle has to empty before the pulmonary
valve can close. Pulmonary valve closure is slightly delayed compared
with aortic valve closure. This does not vary with respiration.

Interestingly, there is a possible link between migraine with aura and

patent foramen ovale (PFO). However, patients with migraines are not
routinely screened for PFO. This is because the surgical management of
PFOs carry risks and it is not clear whether treatment for a PFO improves
symptoms of recurrent migraines.

Management of Atrial Septal Defects

In cases where the ASD is small and asymptomatic, watching and

waiting may be appropriate. ASDs can be corrected surgically using a
percutaneous transvenous catheter closure (via the femoral vein)
or open-heart surgery. Anticoagulants (such as aspirin, warfarin and
DOACs) are used to reduce the risk of clots and stroke in adults.

Ventricular Septal Defects

 A ventricular septal defect (VSD) is a hole in the septum (wall)
between the two ventricles. This can vary in size from tiny to the entire
septum, forming one large ventricle.

Congenital VSDs can occur in isolation but there are often underlying
genetic conditions associated with them (e.g., Down’s syndrome and
Turner’s syndrome).

Ventricular septal defects can also develop after myocardial

infarction, where there is damage to the ventricular septum due to
ischaemia.
 Similarly to atrial septal defects, VSDs usually feature a left-to-right
shunt. Over time this causes right-sided overload, right heart failure
and increased flow into the pulmonary vessels. Pulmonary
hypertension may progress to a right-to-left shunt, resulting in cyanosis
(Eisenmenger syndrome).

Presentation of Ventricular Septal Defects

Often VSDs are initially asymptomatic and patients can present as

late as adulthood. They may be picked up on antenatal scans or when a
murmur is heard during the newborn baby check.

Patients with a VSD typically have a pan-systolic murmur more

prominently heard at the left lower sternal border in the third and
fourth intercostal spaces. There may be a systolic thrill on palpation.

TOM TIP: When you hear a pan-systolic murmur it is worth giving

your top differential but also mentioning the other causes of this
type of murmur. The causes of a pan-systolic murmur are
ventricular septal defect, mitral regurgitation and tricuspid
regurgitation.

Management of Ventricular Septal Defects

VSDs can be corrected surgically using a transvenous catheter

closure via the femoral vein, or open-heart surgery.

There is an increased risk of infective endocarditis in patients with a

VSD. Antibiotic prophylaxis should be considered during surgical
procedures to reduce the risk of developing infective endocarditis.

Coarctation of the Aorta

 Coarctation of the aorta is a congenital condition where there is
a narrowing of the aortic arch, usually around the ductus arteriosus.
The severity of the coarctation (or narrowing) can vary from mild to
severe. It is often associated with an underlying genetic condition,
particularly Turner’s syndrome.

Coarctation of the aorta can reoccur later after previously being

treated in childhood.
 Narrowing of the aorta reduces the pressure of blood flowing to the
arteries that are distal to the narrowing. It increases the pressure in
areas proximal to the narrowing, such as the heart and the three
branches of the aorta arch (the brachiocephalic artery, the left
common carotid and the left subclavian artery).

Presentation of Coarctation of the Aorta

Coarctation may go undiagnosed until adulthood. Often the first sign in

adulthood is hypertension.

There may be a systolic murmur heard below the left clavicle (left
infraclavicular area) and below the left scapula.

Performing a four limb blood pressure will reveal high blood

pressure in the limbs supplied from arteries that branch off the aorta
before the narrowing and lower blood pressure in limbs that branch off
the aorta after the narrowing.

Additional signs may develop over time:

• Left ventricular heave due to left ventricular hypertrophy
• Underdeveloped left arm where there is reduced flow to the left
subclavian artery
• Underdevelopment of the legs

CT angiography gives a detailed picture of the structure and

narrowing in coarctation of the aorta.

Management of Coarctation of the Aorta

The severity of the coarctation varies between patients. In mild cases,

patients can live symptom-free until adulthood without requiring surgical
input. In severe cases, patients will require emergency surgery shortly
after birth.

In adulthood it can be treated with:

• Percutaneous balloon angioplasty (stretching the stenosis),
potentially with a stent inserted
• Open surgical repair
Patients also need medical management of hypertension.
 Pericardial Effusion
Pericardial effusion is where excess fluid collects within the
pericardial sac. Pericardial effusions can be acute or chronic. They can
fill the entire pericardial cavity or only a localised section.

The effusion can be made of:

• Transudates (low protein content)
• Exudates (associated with inflammation)
 • Blood
• Pus
• Gas (associated with bacterial infections)

Pathophysiology

There is a membrane that surrounds the heart called the pericardium

or pericardial sac. This has two layers with a small amount of fluid in
between (less than 50mls), providing lubrication. These layers separate
the heart from the rest of the contents of the mediastinum. Lubrication
between the two layers allows the heart to beat without generating too
much friction.

Between the two layers, there is a potential space, called the

pericardial cavity. The two layers are usually touching each other, which
is why it is only a potential space.

Pericardial effusion is when the potential space of the pericardial

cavity fills with fluid. This creates an inward pressure on the heart, making
it more difficult to expand during diastole (filling of the heart).

Pericardial tamponade (or cardiac tamponade) is where the

pericardial effusion is large enough to raise the intra-pericardial pressure.
This increased pressure squeezes the heart and affects its ability to
function. It leads to reduced filling of the heart during diastole, resulting in
decreased cardiac output during systole. This is an emergency requiring
rapid drainage of the pericardial effusion to relieve the pressure.

Causes

Increased venous pressure can reduce drainage from the

pericardial cavity, resulting in a transudative effusion. This may occur
in:
• Congestive heart failure
• Pulmonary hypertension

Exudative effusions may occur in any inflammatory process

affecting the pericardium (pericarditis), such as in:
 • Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr
virus and other viruses)
• Autoimmune and inflammatory conditions (e.g., systemic lupus
erythematosus and rheumatoid arthritis)
• Injury to the pericardium (e.g., after myocardial infarction, open
heart surgery or trauma)
• Uraemia (raised urea) secondary to renal impairment
• Cancer
• Medications (e.g., methotrexate)

Rupture of the heart or aorta can cause bleeding into the pericardial
cavity, resulting in a rapid-onset cardiac tamponade. Rupture may be the
result of:
• Myocardial infarction
• Trauma
• Aortic dissection (type A)

Presentation

The speed of onset of symptoms relates to how quickly the effusion

develops. A rapidly collecting effusion with cardiac tamponade can
quickly cause haemodynamic compromise and collapse.

Slowly developing, chronic effusions, may initially be asymptomatic.

As the pressure rises, symptoms can develop, which may include:
• Chest pain
• Shortness of breath
• A feeling of fullness in the chest
• Orthopnoea (shortness of breath on lying flat)

The effusion may compress surrounding structures, causing additional

symptoms:
• Phrenic nerve compression can cause hiccups
• Oesophageal compression may cause dysphagia (difficulty
swallowing)
• Recurrent laryngeal nerve compression may cause a hoarse
voice

Signs on examination include:

 • Quiet heart sounds
• Pulsus paradoxus (an abnormally large fall in blood pressure
during inspiration, notably when palpating the pulse)
• Hypotension
• Raised JVP
• Fever (with pericarditis)
• Pericardial rub (with pericarditis)

Diagnosis

An echocardiogram is the investigation of choice. It can be used to:

• Diagnose pericardial effusion
• Assess the size of the effusion
• Assess the effect on the heart function (haemodynamic effect)

Fluid analysis can be performed on the pericardial fluid to diagnose

the underlying cause, including:
• Protein content (to distinguish between transudative or exudative)
• Bacterial culture
• Viral PCR
• Cytology and tumour markers (for cancer)

Management

There are two components to treating a pericardial effusion:

• Treatment of the underlying cause (e.g., infection)
• Drainage of the effusion (where required)

Inflammatory causes (pericarditis) may be treated with:

• Aspirin
• NSAIDs
• Colchicine
• Steroids

There are two options for draining an effusion:

• Needle pericardiocentesis (echocardiogram guided)
• Surgical drainage
 A pericardial window is a surgical procedure where a portion of the
pericardium is removed, creating a “window” or fistula, that allows fluid
to drain from the pericardial cavity into the pleural cavity or the peritoneal
cavity.

Rarely, pericardiectomy (surgical removal of the pericardium) may

be performed in recurrent cases.
 Thoracic Aortic Aneurysm
A thoracic aortic aneurysm refers to the dilation of the thoracic aorta.
The most commonly affected area is the ascending aorta. The diameter
of the thoracic aorta varies depending on several factors (e.g., age and
body size), but is normally less than 4.5cm for the ascending and 3.5cm
for the descending thoracic aorta.
 The first time a patient may become aware of an aneurysm is when it
ruptures, causing life-threatening bleeding into the mediastinum cavity.
This has an extremely high mortality.

False Aneurysms
 There are three layers to the aorta: the intima, media and adventitia.

False aneurysms (or pseudoaneurysms) occur when the inner two

layers (intima and media) rupture and there is dilation of the vessel, with
the blood only being contained within the outer (adventitia) layer of the
aorta. This typically occurs after trauma, such as a road traffic accident. It
can also occur after surgery to the aorta or infection in the vessel.

True aneurysms are where the three layers of the aorta are intact but
dilated.

Risk Factors

• Men are affected significantly more often and at a younger age

than women
• Increased age
• Smoking
• Hypertension
• Family history
• Existing cardiovascular disease
• Marfan syndrome and other connective tissue disorders

Presentation
 Dilation of the thoracic aorta is often asymptomatic. It may be found
incidentally on investigations for other reasons, for example on a chest x-
ray, echocardiogram or CT scan.

An aneurysm may cause symptoms due to taking up space within the

mediastinum:
• Chest or back pain
• Trachea or left bronchus compression may cause cough,
shortness of breath and stridor
• Phrenic nerve compression may cause hiccups
• Oesophageal compression may cause dysphagia (difficulty
swallowing food)
• Recurrent laryngeal nerve compression may cause a hoarse
voice
 Diagnosis

The main investigations for diagnosis and assessment are:

• Echocardiogram
• CT or MRI angiogram

Management

The risk of progression of a thoracic aortic aneurysm can be reduced

by treating modifiable risk factors:
• Stop smoking
• Healthy diet and exercise
• Optimising the management of hypertension, diabetes and
hyperlipidaemia

Management options depend on individual patient factors and the

size. The larger the size of the aneurysm, the higher the risk of rupture.

The options are:

• Surveillance with regular imaging to monitor the size
• Thoracic endovascular aortic repair (TEVAR), with a catheter
inserted via the femoral artery inserting a stent graft into the affected
section of the aorta
• Open surgery (midline sternotomy) to remove the section of the
aorta with the defect in the wall and replace it with a synthetic graft

Complications

• Aortic dissection
• Ruptured aneurysm
• Aortic regurgitation (if the aortic valve is affected)

Ruptured Thoracic Aortic Aneurysm

The risk of rupture increases with the diameter of the aneurysm.

Rupture of a thoracic aortic aneurysm results in bleeding into the

mediastinum. There may be bleeding into the:
• Oesophagus, causing haematemesis (vomiting blood)
 • Airways or lungs, causing haemoptysis (coughing up blood)
• Pericardial cavity, causing cardiac tamponade (compression of
the heart)

A ruptured thoracic aortic aneurysm presents with:

• Severe chest pain or back pain
• Haemodynamic instability (hypotension and tachycardia)
• Collapse
• Death (often patients do not reach hospital)

Emergency open surgery is required, with replacement of the affected

section of the aorta with a synthetic graft.
 Lung Cancer
Lung cancer is the third most common cancer in the UK behind breast
and prostate cancer. Smoking is the biggest cause. Around 80% of lung
cancers are thought to be preventable.

Basic Anatomy

Air enters the lung through the trachea, which splits into the left main
bronchus and right main bronchus. These bronchi then split into lobar
bronchi, segmental bronchi, bronchioles, then alveoli. Bronchi is
pleural for bronchus.

The right lung has three lobes. The left lung has two lobes. The
heart is on the left, leaving less room for an extra lobe. Both lungs have
an oblique fissure separating the lobes. The right lung also has a
horizontal fissure. Fluid may be seen in the fissures in acute heart
failure and pulmonary oedema.
 There is a membrane that surrounds the lungs called the pleura.
There are two layers of this membrane, with a small amount of fluid
between them (less than 20mls). These layers separate the lungs from
the chest wall. Lubrication between the two layers allows the lungs to
expand and move without creating friction with the chest wall.

Between the two layers, there is a potential space, called the pleural
cavity. The two layers are usually touching each other, which is why it is
only a potential space. There is negative pressure within the pleural
cavity, pulling the two layers of the pleura together. As the chest wall
expands, the negative pressure within the pleural cavity pulls the lungs
outwards with the chest wall, causing them to expand.

A pleural effusion is when the potential space of the pleural cavity

fills with excess fluid. This creates an inward pressure on the lungs,
reducing the lung volume. A pneumothorax is when air gets into the
pleural cavity.

Histology

The histological types of lung cancer can be broadly divided into:

• Small cell lung cancer (SCLC) (around 20%)
• Non-small cell lung cancer (around 80%)

Non-small cell lung cancer can be further divided into:

• Adenocarcinoma (around 40% of total lung cancers)
• Squamous cell carcinoma (around 20% of total lung cancers)
• Large-cell carcinoma (around 10% of total lung cancers)
• Other types (around 10% of total lung cancers)

Small cell lung cancer cells contain neurosecretory granules that

can release neuroendocrine hormones. This makes SCLC responsible
for multiple paraneoplastic syndromes.

Mesothelioma

Mesothelioma is a lung malignancy affecting the mesothelial cells of

the pleura. It is strongly linked to asbestos inhalation. There is a huge
latent period between exposure to asbestos and the development of
mesothelioma of up to 45 years. The prognosis is very poor.
Chemotherapy can improve survival, but it is essentially palliative.

Presentation

• Shortness of breath
• Cough
• Haemoptysis (coughing up blood)
• Finger clubbing
• Recurrent pneumonia
• Weight loss
• Lymphadenopathy - often supraclavicular nodes are the first to be
found on examination

Extrapulmonary Manifestations

Lung cancer is associated with a lot of extrapulmonary

manifestations and paraneoplastic syndromes. These are linked to
different types and distributions of lung cancer. Exam questions
commonly ask you to suggest the underlying cause of a paraneoplastic
syndrome. Sometimes they can be the first evidence of lung cancer in an
otherwise asymptomatic patient.

Recurrent laryngeal nerve palsy presents with a hoarse voice. It is

caused by a tumour pressing on or affecting the recurrent laryngeal nerve
as it passes through the mediastinum.

Phrenic nerve palsy, due to nerve compression, causes diaphragm

weakness and presents with shortness of breath.

Superior vena cava obstruction is a complication of lung cancer. It

is caused by direct compression of the tumour on the superior vena cava.
It presents with facial swelling, difficulty breathing and distended veins in
the neck and upper chest. Pemberton’s sign is where raising the hands
over the head causes facial congestion and cyanosis. This is a medical
emergency.

Horner’s syndrome is a triad of partial ptosis, anhidrosis and

miosis. It can be caused by a Pancoast tumour (tumour in the
pulmonary apex) pressing on the sympathetic ganglion.

Syndrome of inappropriate ADH (SIADH) can be caused by

ectopic ADH secreted by a small cell lung cancer. It presents with
hyponatraemia.

Cushing’s syndrome can be caused by ectopic ACTH secretion by

a small cell lung cancer.

Hypercalcaemia can be caused by ectopic parathyroid hormone

secreted by a squamous cell carcinoma.

Limbic encephalitis is a paraneoplastic syndrome where small cell

lung cancer causes the immune system to make antibodies to tissues in
the brain, specifically the limbic system, causing inflammation in these
areas. This causes symptoms such as short-term memory impairment,
hallucinations, confusion and seizures. It is associated with anti-Hu
antibodies.

Lambert-Eaton myasthenic syndrome can be caused by

antibodies produced by the immune system against small cell lung
cancer cells. These antibodies also target and damage voltage-gated
calcium channels sited on the presynaptic terminals in motor
neurones. This leads to weakness, particularly in the proximal muscles,
but can also affect the intraocular muscles causing diplopia (double
vision), levator muscles in the eyelid causing ptosis and pharyngeal
muscles causing slurred speech and dysphagia (difficulty swallowing).
Patients may also experience dry mouth, blurred vision, impotence and
dizziness due to autonomic dysfunction.

Referral Criteria

The NICE guidelines on suspected cancer (updated January 2021)

recommend offering a chest x-ray, carried out within 2 weeks, to
patients over 40 with:
• Clubbing
• Lymphadenopathy (supraclavicular or persistent abnormal
cervical nodes)
• Recurrent or persistent chest infections
 • Raised platelet count (thrombocytosis)
• Chest signs of lung cancer

TOM TIP: Remember two key examination findings that would

automatically indicate an urgent chest x-ray: finger clubbing and
supraclavicular lymphadenopathy. These are quick things to check
for and spotting them could lead to an early diagnosis, potentially
saving a patient’s life.

They also recommend considering a chest x-ray in patients over 40

years old who have:
• Two or more unexplained symptoms in patients that have never
smoked
• One or more unexplained symptoms in patients that have ever
smoked

The unexplained symptoms that the NICE guidelines list are:

• Cough
• Shortness of breath
• Fatigue
• Chest pain
• Weight loss
• Loss of appetite
 TOM TIP: It is worth noting that this is quite a vague list. It is very
common for patients to present with vague symptoms of fatigue or
shortness of breath, and your first thought might not be of lung
cancer. If a 60 year old ex-smoker presents feeling “tired all the
time”, with no other symptoms, these guidelines suggest
considering an urgent chest x-ray to exclude lung cancer. Doctors
often do a general examination and get a set of blood tests in
patients with this presentation, but don’t always consider getting a
chest x-ray.

Investigations

Chest x-ray is the first-line investigation in suspected lung cancer.

Findings suggesting cancer include:
• Hilar enlargement
• Peripheral opacity - a visible lesion in the lung field
• Pleural effusion - usually unilateral in cancer
• Collapse

Staging CT scan of chest, abdomen and pelvis is used to assess the

stage, lymph node involvement and presence of metastases. This should
be contrast-enhanced, using an injected contrast to give more detailed
information about different tissues.

PET-CT (positron emission tomography) scans involve injecting a

radioactive tracer (usually attached to glucose molecules) and taking
images using a combination of a CT scanner and a gamma-ray detector
to visualise how metabolically active various tissues are. They are useful
in identifying metastases by highlighting areas of increased metabolic
activity.

Bronchoscopy with endobronchial ultrasound (EBUS) involves

endoscopy with ultrasound equipment on the end of the scope. This
allows detailed assessment of the tumour and ultrasound-guided biopsy.

Histological diagnosis requires a biopsy to check the type of cells in

the tumour. This can be either by bronchoscopy or percutaneous
biopsy (through the skin).
 Treatment options

All treatments are discussed at an MDT meeting involving various

consultants and specialists, such as pathologists, surgeons, oncologists
and radiologists. This is to make a joint decision about the most suitable
options for the individual patient.

Surgery is offered first-line in non-small cell lung cancer to patients

that have disease isolated to a single area. The intention is to remove the
entire tumour and cure the cancer. See below for more detail on surgery.

Radiotherapy can also be curative in non-small cell lung cancer

when diagnosed early enough.

Chemotherapy can be offered in addition to surgery or radiotherapy

in certain patients to improve outcomes (adjuvant chemotherapy) or as
palliative treatment to improve survival and quality of life in later stages of
non-small cell lung cancer (palliative chemotherapy).

Treatment for small cell lung cancer is usually with chemotherapy

and radiotherapy. Prognosis is generally worse for small cell lung cancer
compared with non-small cell lung cancer.

Endobronchial treatment with stents or debulking can be used as

part of palliative treatment to relieve bronchial obstruction caused by lung
cancer.

Lung Cancer Surgery

There are several options for removing a lung tumour:

• Segmentectomy or wedge resection involves removing a
segment or wedge of lung (a portion of one lobe)
• Lobectomy involves removing the entire lung lobe containing the
tumour (the most common method)
• Pneumonectomy involves removing an entire lung

The types of surgery that can be used are:

• Thoracotomy - open surgery with an incision and separation of the
rib to access the thoracic cavity
 • Video-assisted thoracoscopic surgery (VATS) - minimally
invasive “keyhole” surgery
• Robotic surgery

Minimally invasive surgery (i.e., VATS or robotic surgery) is generally

preferred as it has a faster recovery and fewer complications.

There are three main thoracotomy incisions:

• Anterolateral thoracotomy with an incision around the front and
side
• Axillary thoracotomy with an incision in the axilla (armpit)
• Posterolateral thoracotomy with an incision around the back and
side (the most common approach to the thorax)

TOM TIP: If you see a patient with a thoracotomy scar in your

OSCEs, they are likely to have had a lobectomy, pneumonectomy or
lung volume reduction surgery for COPD. If they have no breath
sounds on that side, this indicates a pneumonectomy rather than a
lobectomy. If they have absent breath sound in a specific area on
the affected side (e.g., the upper zone), but breath sounds are
present in other areas, this indicates a lobectomy. Lobectomies and
pneumonectomies are usually used to treat lung cancer. In the past,
they were often used to treat tuberculosis, so keep this in mind in
older patients. If it is a cardiology examination and they have a right-
sided mini-thoracotomy incision, this is more likely to indicate
previous minimally invasive mitral valve surgery.

Chest Drains

A chest drain will be left in after thoracic surgery. The chest drain
allows air and fluid to exit the thoracic cavity and the lungs to expand. A
chest drain pump can be used to suck fluid and air out of the chest. They
are removed when they are no longer required to drain air or fluid.
 Pneumothorax
Pneumothorax occurs when air gets into the pleural space,
separating the lung from the chest wall. It can occur spontaneously, or
secondary to trauma, medical interventions (“iatrogenic”) or lung
pathology. The typical patient in exams is a tall, thin young man
presenting with sudden breathlessness and pleuritic chest pain, possibly
whilst playing sports.

Causes

• Spontaneous
• Trauma
• Iatrogenic, for example, due to lung biopsy, mechanical ventilation
or central line insertion
• Lung pathologies such as infection, asthma or COPD

Investigations

An erect chest x-ray is the investigation of choice for diagnosing a

simple pneumothorax. It shows an area between the lung tissue and the
chest wall where there are no lung markings. There will be a line
demarcating the edge of the lung where the lung markings end and the
pneumothorax begins.

Measuring the size of the pneumothorax on a chest x-ray can be

done according to the BTS guidelines from 2010. This involves
measuring horizontally from the lung edge to the inside of the chest wall
at the level of the hilum.

CT thorax can detect a pneumothorax that is too small to be seen on

a chest x-ray. It can also be used to accurately assess the size of the
pneumothorax.

Management
 The acute management here is based on the 2010 guidelines from the
British Thoracic Society. Always check the latest local and national
guidelines, and consult with seniors when managing patients.

No shortness of breath and less than a 2cm rim of air on the chest x-
ray:
• No treatment is required as it will spontaneously resolve
• Follow up in 2 - 4 weeks is recommended

Shortness of breath and/or more than a 2cm rim of air on the chest x-
ray:
• Aspiration followed by reassessment
• When aspiration fails twice, a chest drain is required

Unstable patients, bilateral or secondary pneumothoraces generally

require a chest drain.

Chest Drain

Chest drains are inserted in the “triangle of safety”. This triangle is

formed by the:
• 5th intercostal space (or the inferior nipple line)
• Midaxillary line (or the lateral edge of the latissimus dorsi)
• Anterior axillary line (or the lateral edge of the pectoralis major)
 The needle is inserted just above the rib to avoid the neurovascular
bundle that runs just below the rib. Once the chest drain is inserted,
obtain a chest x-ray to check the positioning.

The external end of the drain is placed underwater, creating a seal to

prevent air from flowing back through the drain, into the chest. Air can exit
the chest cavity and bubble through the water, but the water prevents air
from re-entering the drain and chest. During normal respiration, the water
in the drain will rise and fall due to changes in pressure in the chest
(described as “swinging”).
 When the chest drain is successfully treating the pneumothorax, air
will bubble through the fluid in the drain bottle. There will be swinging of
the water with respiration. On a repeat chest x-ray there will be re-
inflation of the lung. If these things do not occur, there may be a problem
with the drain, such as:
• Blocked or kinked tube
• Incorrect position in the chest
• Not properly connected to the bottle

Once the pneumothorax resolves, there should be no further bubbling

in the drain bottle. The swinging of the water with respiration will also
reduce.

Two key complications of chest drains are:

• Air leaks around the drain site (indicated by persistent bubbling of
fluid, particularly on coughing)
• Surgical emphysema (also known as subcutaneous
emphysema) is when air collects in the subcutaneous tissue

Surgical Management

Patients may require surgical interventions when:

• A chest drain fails to correct the pneumothorax
• There is a persistent air leak in the drain
• The pneumothorax reoccurs (recurrent pneumothorax)

Video-assisted thoracoscopic surgery (VATS) can be used to

correct a pneumothorax.

The surgical options are:

• Abrasive pleurodesis (using direct physical irritation of the pleura)
• Chemical pleurodesis (using chemicals, such as talc powder, to
irritate the pleura)
• Pleurectomy (removal of the pleura)

Pleurodesis involves creating an inflammatory reaction in the pleural

lining so that the pleura stick together and the pleural space becomes
sealed. This prevents further pneumothoraces from developing.

Tension Pneumothorax
 Tension pneumothorax is caused by trauma to the chest wall that
creates a one-way valve that lets air in but not out of the pleural space.
The one-way valve means that during inspiration, air is drawn into the
pleural space, and during expiration, the air is trapped in the pleural
space. Therefore, more air keeps getting drawn into the pleural space
with each breath and cannot escape. This is dangerous as it creates
pressure inside the thorax that will push the mediastinum across, kink
the big vessels in the mediastinum and cause cardiorespiratory arrest.

Signs of Tension Pneumothorax

• Tracheal deviation away from side of the pneumothorax

• Reduced air entry on the affected side
• Increased resonance to percussion on the affected side
• Tachycardia
• Hypotension

Management of Tension Pneumothorax

The management sentence you need to learn and recite in your

exams is: “Insert a large bore cannula into the second intercostal
space in the midclavicular line.”

If a tension pneumothorax is suspected do not wait for any

investigations. Once the pressure is relieved with a cannula then a chest
drain is required for definitive management.
 Heart and Lung Transplant
Heart and lung transplants will inevitably come from a recently
deceased donor. The demand for donor hearts and lungs outweighs the
supply.

Indications

The most common indiction for a heart transplant is congestive heart

failure, which can be secondary to:
• Ischaemic heart disease
• Cardiomyopathy
• Congenital heart disease

The most common indications for a lung transplant are:

• Chronic obstructive pulmonary disease (COPD)
• Pulmonary fibrosis
• Cystic fibrosis
• Pulmonary hypertension

Variations

There are several ways hearts and lungs can be transplanted:

• Single lung transplant
• Double lung transplant
• Heart transplant
• Heart-lung transplant

A double lung transplant can be performed as a bilateral single lung

transplant (one lung, then the other), or an “en bloc” transplant where
both lungs are implanted together. Bilateral single lung transplants are
generally preferred.

Incisions
 A lateral thoracotomy incision may be used for single lung
transplants.

A midline sternotomy incision may be used for heart transplants.

A clamshell incision may be used for bilateral lung transplants.

 Procedure

The time between the death of the donor and the transplant needs to
be as short as possible (under 6 hours). In the meantime, the organ is
cooled to reduce the damage during transportation. This is referred to as
the cold ischaemic time. Usually, the operation will begin before the
donated organ has arrived, so that the transplant can take place
immediately on arrival of the organ.

Heart or lung transplantation requires a cardiopulmonary bypass, to

bypass the circulation in the organs that will be removed and
transplanted. The bypass machine takes blood from the vena cava or
right atrium, pumps it through a machine that adds oxygen and removes
carbon dioxide from the blood, then pumps it back into the ascending
aorta. This way, blood bypasses the heart and lungs and is artificially
oxygenated. Heparin is used to prevent blood clotting. A clinical
perfusionist is responsible for operating and monitoring the
cardiopulmonary bypass equipment.

After a donor heart is implanted, the heart is reperfused with blood and
warmed. The treatment that prevents the heart from beating
(cardioplegia) is stopped. The heart will then spontaneously start
beating. Cardioversion or temporary pacing may be used to treat any
arrhythmias that occur.

Patients will be transferred to the intensive care unit after surgery.

Post Transplant

Organ rejection is a major risk with any organ transplant. Patients will
require life-long immunosuppression to reduce the risk of transplant
rejection.

Immunosuppressants have a long list of complications, particularly:

• Side effects of steroids (e.g., diabetes, osteoporosis and Cushing’s
syndrome)
• Severe or unusual infections
• Skin cancer
• Post-transplant lymphoproliferative disorder (a form of non-
Hodgkin lymphoma)

A key complication after a heart transplant is cardiac allograft

vasculopathy (CAV), which involves narrowing of the coronary arteries
in the donor heart. The donor heart is not innervated, meaning the patient
will not experience symptoms of ischaemia in the heart tissue. This
means they will not have any symptoms of angina or myocardial
infarction. Patients have regular follow up coronary angiograms to
monitor for this.

The key complications after a lung transplant are:

• Primary graft dysfunction (PGD), which usually occurs within 3
days, with acute pulmonary oedema, alveolar damage and hypoxia
• Bronchiolitis obliterans syndrome (BOS), which usually occurs
within 1 year, with damage to the bronchioles
• Dehiscence of the bronchial anastomosis, which causes air
leakage into the mediastinum and is life-threatening

Survival is approximately:
• 85% at 1 year for heart or lung transplants
• 75% at 5 years for heart transplants
• 50% at 5 years for lung transplants
 Breast Surgery
Breast Examination
Breast Lumps
Breast Pain
Gynaecomastia
Galactorrhea
Mammary Duct Ectasia
Intraductal Papilloma
Lactational Mastitis
Breast Abscess
Breast Cancer
 Breast Examination
Breast examination is a common intimate examination that appears in
OSCEs. It is also an essential skill in clinical practice, particularly in
primary care and surgery.

General Principles

• Explain the process and reason for the examination

• Obtain informed consent
• Have a chaperone present, explain their role and document this
(along with the full name of the chaperone)
• Allow the patient to get undressed and dressed in privacy
• Allow the patient to remain covered until just before the
examination
• Ask about any areas of pain
• Ask the patient to point out any abnormalities they have noticed
• Use your examination to teach the patient how to self examine

Inspection

Ask the patient to sit on the side of the bed so you can inspect the
breasts straight on, comparing both sides. Inspect the breasts in three
positions:
• Relaxed with arms by the sides
• Hands pressed into the hip (tensing muscles of the chest wall to
look for tethering)
• Hands placed behind the head

On inspection, look for:

• Asymmetry (size/shape)
• Scars
• Cosmetic augmentation (breast implants)
• Tethering, fixation or puckering of the overlying skin
• Nipple eversion/inversion
• Nipple discharge
 • Skin colour (e.g., erythema)
• Peau d’orange (“orange peel” skin)
• Paget’s disease of the nipple

Peau d’orange describes an irregular patch of skin, which may be

associated with inflammatory breast cancer. Blocked lymphatic drainage
from the affected skin area causes superficial oedema (fluid collecting in
the skin), making the skin thickened. The sweat ducts cause small
dimples within the oedematous skin, leading to a thickened and dimpled
appearance, similar to the surface of orange peel.

Paget’s disease of the nipple is an erythematous, scaly rash of the

nipple region, resembling eczema. It can be itchy, inflamed or ulcerated. It
may indicate underlying breast cancer and requires further investigation.

Palpation

Examine the patient with them sat back at 45 degrees. Ask them to put
their hand, on the side being examined, behind their head.
Use the flat of your fingers to palpate, gently pressing the breast tissue
down against the chest wall and rolling the tissue around to feel for any
irregularities or lumps. Use the other hand to support the breast, if
necessary.

Examine areas away from any abnormal or painful regions first. This
helps you note the patient’s normal breast tissue and reduces the
chances of missing other abnormalities.

There is no single best pattern for examining the breasts. Choose one
where you feel confident you will properly cover all areas.

Possible methods to choose from are:

• Vertical up-and-down lines (moving up and down across the breast)
• Quadrants (assessing each quadrant in turn)
• Spirals (starting at the nipple and circling outwards in a spiral)
• Radial / wedge / clock face (moving outward or inward between the
nipple and the outer areas of the breast, like the hands on a clock)
The important areas to cover are:
• The four quadrants of each breast (upper outer, upper inner,
lower outer and lower inner)
• Subareolar area (under the nipple)
• Tail of Spence (the extension between the breast and the axilla)
• Axilla (armpit)

Assessing a Lump

If you find a lump, the key features to assess and describe are:
 • Location
• Size
• Shape (round / oval / irregular)
• Consistency (soft / firm / hard / fluctuant)
• Margins (irregular / smooth)
• Mobile or fixed (tethered) to the skin or chest wall
• Tenderness (e.g., abscess)
• Skin colour (e.g., erythema indicating inflammation or infection)
• Nipple discharge (e.g., mammary duct ectasia or intraductal
papilloma)

Additional Steps

Examine the neck for cervical and supraclavicular

lymphadenopathy.

You can add additional examinations for areas of metastasis, such as

the lungs, liver and bones.

Triple assessment of a breast lump requires:

• Clinical assessment (history and examination)
• Imaging (ultrasound or mammography)
• Histology (fine needle aspiration or core biopsy)
 Breast Lumps
There are numerous causes of breast lumps, many of which are
benign. Any breast lump needs a thorough assessment to exclude breast
cancer.

Basic Breast Anatomy

The breasts sit in front of the chest wall, which contains the ribs and
pectoral muscles. Most of the breast is adipose (fatty) tissue.
The areola surrounds the nipple. Behind the nipple are the ducts, which
lead into the lobules, where breast milk is produced. Milk is secreted
through the ducts and out of openings on the nipple.
 Breast Cancer

The most significant differential of a breast lump is breast cancer.

Triple assessment of a breast lump is standard practice to exclude or

diagnose cancer. This involves:
• Clinical assessment (history and examination)
• Imaging (ultrasound or mammography)
• Histology (fine needle aspiration or core biopsy)

Clinical features that may suggest breast cancer are:

• Lumps that are hard, irregular, painless or fixed in place
• Lumps may be tethered to the skin or the chest wall
• Nipple retraction
• Skin dimpling or oedema (peau d’orange)

The NICE guidelines (updated January 2021) recommend a two week

wait referral for suspected breast cancer for:
• An unexplained breast lump in patients aged 30 or above
• Unilateral nipple changes in patients aged 50 or above (discharge,
retraction or other changes)

The NICE guidelines recommend also considering a two week wait

referral for:
• An unexplained lump in the axilla in patients aged 30 or above
• Skin changes suggestive of breast cancer

The NICE guidelines suggest considering non-urgent referral for

unexplained breast lumps in patients under 30 years.

Fibroadenoma

Fibroadenomas are common benign tumours of stromal/epithelial

breast duct tissue. They are typically small and mobile within the breast
tissue. They are sometimes called a "breast mouse”, as they move
around within the breast tissue.

They are more common in younger women, aged between 20 and 40

years. They respond to the female hormones (oestrogen and
progesterone), which is why they are more common in younger women
and often regress after menopause.

On examination, fibroadenomas are:

• Painless
• Smooth
• Round
• Well circumscribed (well-defined borders)
• Firm
• Mobile (moves freely under the skin and above the chest wall)
• Usually up to 3cm diameter

Fibroadenomas are not cancerous and are not usually associated with
an increased risk of developing breast cancer. Complex fibroadenomas
and a positive family history of breast cancer may indicate a higher risk.

Fibrocystic Breast Changes

Fibrocystic breast changes were previously called fibrocystic breast

disease. However, fibrocystic breast changes, and generalised lumpiness
to the breast, are considered a variation of normal and not a disease. The
connective tissues (stroma), ducts and lobules of the breast respond to
the female sex hormones (oestrogen and progesterone), becoming
fibrous (irregular and hard) and cystic (fluid-filled). These changes
fluctuate with the menstrual cycle.

It is a benign (non-cancerous) condition, although it can vary in

severity and significantly affect the patient’s quality of life if severe. It is
common in women of menstruating age. Symptoms often occur prior to
menstruation (within 10 days) and resolve once menstruation begins.
Symptoms usually improve or resolve after menopause.

Symptoms can affect different areas of the breast, or both breasts,

with:
• Lumpiness
• Breast pain or tenderness (mastalgia)
• Fluctuation of breast size
 Management of fibrocystic breast changes is to exclude cancer and
manage symptoms. Options to manage cyclical breast pain (mastalgia)
include:
• Wearing a supportive bra
• Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen
• Avoiding caffeine is commonly recommended
• Applying heat to the area
• Hormonal treatments (e.g., danazol and tamoxifen) under
specialist guidance

Breast Cysts

Breast cysts are benign, individual, fluid-filled lumps. They are the
most common cause of breast lumps and occur most often between ages
30 and 50, more so in the perimenopausal period. They can be painful and
may fluctuate in size over the menstrual cycle.

On examination, breast cysts are:

• Smooth
• Well-circumscribed
• Mobile
• Possibly fluctuant

Breasts cysts require further assessment to exclude cancer, with

imaging and potentially aspiration or excision. Aspiration can resolve
symptoms in patients with pain. Having a breast cyst may slightly
increase the risk of breast cancer.

Fat Necrosis

Fat necrosis causes a benign lump formed by localised degeneration

and scarring of fat tissue in the breast. It may be associated with an oil
cyst, containing liquid fat. Fat necrosis is commonly triggered by localised
trauma, radiotherapy or surgery, with an inflammatory reaction resulting in
fibrosis and necrosis (death) of the fat tissue. It does not increase the
risk of breast cancer.

On examination, fat necrosis can be:

• Painless
 • Firm
• Irregular
• Fixed in local structures
• There may be skin dimpling or nipple inversion

Ultrasound or mammogram can show a similar appearance to

breast cancer. Histology (by fine needle aspiration or core biopsy)
may be required to confirm the diagnosis and exclude breast cancer.

After excluding breast cancer, fat necrosis is usually treated

conservatively. It may resolve spontaneously with time. Surgical excision
may be used if required for symptoms.

Lipoma

Lipomas are benign tumours of fat (adipose) tissue. They can occur
almost anywhere on the body where there is adipose tissue, including the
breasts.

On examination, lipomas are typically:

• Soft
• Painless
• Mobile
• Do not cause skin changes

They are typically treated conservatively with reassurance.

Alternatively, they can be surgically removed.

Galactocele

Galactoceles occur in women that are lactating (producing breast

milk), often after stopping breastfeeding. They are breast milk filled cysts
that occur when the lactiferous duct is blocked, preventing the gland from
draining milk. They present with a firm, mobile, painless lump, usually
beneath the areola. They are benign and usually resolve without any
treatment. It is possible to drain them with a needle. Rarely, they can
become infected and require antibiotics.

Phyllodes tumour
 Phyllodes tumours are rare tumours of the connective tissue (stroma)
of the breast, occurring most often between ages 40 and 50. They are
large and fast-growing. They can be benign (~50%), borderline (~25%) or
malignant (~25%). Malignant phyllodes tumours can metastasise.

Treatment involves surgical removal of the tumour and the

surrounding tissue (“wide excision”). They can reoccur after removal.

Chemotherapy may be used in malignant or metastatic tumours.

 Breast Pain
Breast pain (mastalgia) is common. It can be:
• Cyclical - occurring at specific times of the menstrual cycle
• Non-cyclical - unrelated to the menstrual cycle

Pain is not typically considered a symptom of breast cancer. After a

proper assessment and without other features of breast cancer (e.g., a
lump or skin changes), patients with mastalgia can generally be
reassured.

Cyclical Breast Pain

Cyclical breast pain is more common and is related to hormonal

fluctuations during the menstrual cycle. The pain typically occurs during
the two weeks before menstruation (the luteal phase) and settles during
the menstrual period. There may be other symptoms of premenstrual
syndrome, such as low mood, bloating, fatigue and headaches.

Symptoms are typically:

• Bilateral and generalised

• Heaviness
• Aching

Non-Cyclical Breast Pain

Non-cyclical breast pain is more common in women aged 40 - 50

years. It is more likely to be localised than cyclical breast pain. Often no
cause is found. However, it may be caused by:
• Medications (e.g., hormonal contraceptive medications)
• Infection (e.g., mastitis)
• Pregnancy

The pain may not originate in the breast but instead come from:
• The chest wall (e.g., costochondritis)
• The skin (e.g., shingles or post-herpetic neuralgia)
 Diagnosis

A breast pain diary can help diagnose cyclical breast pain.

The three main things to exclude when someone presents with breast
pain are:
• Cancer (perform a thorough history and examination)
• Infection (mastitis)
• Pregnancy (perform a pregnancy test)

Management

Options to manage cyclical breast pain include:

• Wearing a supportive bra
• Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen
(oral or topical)
• Avoiding caffeine is commonly recommended
• Applying heat to the area
• Hormonal treatments (e.g., danazol and tamoxifen) under
specialist guidance
 Gynaecomastia
Gynaecomastia refers to the enlargement of the glandular breast
tissue in males. Male breast enlargement is relatively common,
particularly in adolescents and older men (aged over 50 years). It may
also be present in newborns due to circulating maternal hormones,
resolving as the maternal hormones are cleared.

Causes

Gynaecomastia is generally caused by a hormonal imbalance

between oestrogen and androgens (e.g., testosterone), with higher
oestrogen and lower androgen levels. Raised oestrogen stimulates breast
development, whilst androgens have an inhibitory effect on breast
development.

Prolactin is a hormone that also stimulates glandular breast tissue

development (as well as breast milk production). Therefore, raised
prolactin (hyperprolactinaemia) can cause gynaecomastia. It is worth
remembering that dopamine has an inhibitory effect on prolactin.
Dopamine antagonists (e.g., antipsychotic medications) block
dopamine production, which allows prolactin levels to rise and can cause
gynaecomastia and galactorrhea (breast milk production).

Gynaecomastia is idiopathic in many cases, meaning no cause is

found.

Gynaecomastia may be physiological in adolescents, where there

can be proportionally higher oestrogen levels around puberty. This
resolves after a few years, as the hormone levels balance.

Gynaecomastia can be caused by conditions that increase

oestrogen:
• Obesity (aromatase is an enzyme found in adipose tissue that
converts androgens to oestrogen)
 • Testicular cancer (oestrogen secretion from a Leydig cell
tumour)
• Liver cirrhosis and liver failure
• Hyperthyroidism
• Human chorionic gonadotrophin (hCG) secreting tumour,
notably small cell lung cancer

TOM TIP: It is worth remembering the link between

gynaecomastia and Leydig cell testicular tumours. About 2% of
patients presenting with gynaecomastia have a testicular tumour.
An examination question might describe a patient presenting with
gynaecomastia and ask what additional examination should be
performed. The answer will be a testicular examination. Also,
examine for signs of liver failure and hyperthyroidism.

Gynaecomastia can be caused by conditions that reduce

testosterone:
• Testosterone deficiency in older age
• Hypothalamus or pituitary conditions that reduce LH and FSH
levels (e.g., tumours, radiotherapy or surgery)
• Klinefelter syndrome (XXY sex chromosomes)
• Orchitis (inflammation of the testes, e.g., infection with mumps)
• Testicular damage (e.g., secondary to trauma or torsion)

There is a long list of medications and drugs that can cause

gynaecomastia:
• Anabolic steroids (raise oestrogen levels)
• Antipsychotics (increase prolactin levels)
• Digoxin (stimulates oestrogen receptors)
• Spironolactone (inhibits testosterone production and blocks
testosterone receptors)
• Gonadotrophin-releasing hormone (GnRH) agonists (e.g.,
goserelin used to treat prostate cancer)
• Opiates (e.g., illicit heroin use)
• Marijuana
• Alcohol
 TOM TIP: It is worth remembering spironolactone as a cause for
gynaecomastia, as this seems to come up in exams. It is also worth
remembering to ask about anabolic steroid use, as this is the most
common cause I have seen in young men in clinical practice. A large
proportion cases of gynaecomastia will be idiopathic.

Assessment

It is important to distinguish between gynaecomastia and breast

enlargement due to obesity (pseudogynaecomastia). On palpation, there
will be firm tissue behind the areolas in gynaecomastia, representing
growth of the glands and ducts. This is different to simple adipose (fat)
tissue, which is soft and more evenly distributed.

The next step is to try and establish the cause.

The key points to cover in the history are:

• Age of onset, duration and change over time
• Associated sexual dysfunction (indicating low testosterone)
• Any palpable breast lumps or skin changes (exclude breast cancer)
• Associated symptoms that may indicate the cause (e.g., testicular
lumps or symptoms of hyperthyroidism)
• Prescription medication (e.g., antipsychotics, spironolactone or
GnRH agonists)
• Use of anabolic steroids, illicit drugs or alcohol

The key points to cover in the examination are:

• True gynaecomastia versus simple adipose tissue
• Unilateral or bilateral
• Any palpable lumps, skin changes or lymphadenopathy (exclude
breast cancer)
• Body mass index (BMI)
• Testicular examination (e.g., lumps, atrophy or absence)
• Signs of testosterone deficiency (e.g., reduced body and pubic hair)
• Signs of liver disease (e.g., jaundice, hepatomegaly, spider naevi
and ascites)
• Signs of hyperthyroidism (e.g., sweating, tachycardia and weight
loss)
 Investigations

Investigations will be determined by the history and examination

findings. Simple gynaecomastia in an otherwise healthy adolescent may
be managed with watchful waiting. Unexplained rapid-onset
gynaecomastia in a 30 year old male with no apparent cause may require
in-depth investigations.

Blood tests:
• Renal profile (U&Es)
• Liver function tests (LFTs)
• Thyroid function tests (TFTs)
• Testosterone
• Sex hormone-binding globulin (SHBG)
• Oestrogen
• Prolactin (hyperprolactinaemia)
• Luteinising hormone (LH) and follicle-stimulating hormone
(FSH)
• Alpha-fetoprotein and beta-hCG (testicular cancer tumour
markers)
• Genetic karyotyping (if Klinefelter’s syndrome is suspected)

Imaging:
• Breast ultrasound (may help assess the extent of gynaecomastia)
• Mammogram (if cancer is suspected)
• Biopsy (if cancer is suspected)
• Testicular ultrasound (if cancer is suspected)
• Chest x-ray (if lung cancer is suspected)

Management

Management depends on the underlying cause. Gynaecomastia

almost always resolves with time in adolescents. Stopping a causative
drug (e.g., anabolic steroids or spironolactone) will usually resolve the
symptoms. Patients may be referred to the specialist breast clinic where
the cause is unclear or cancer is suspected.
 Treatment options in problematic cases (e.g., pain or psychological
distress) include:
• Tamoxifen (a selective oestrogen receptor modulator that reduces
the effects of oestrogen on the breast tissue)
• Surgery
 Galactorrhoea
Galactorrhoea refers to breast milk production not associated with
pregnancy or breastfeeding. Breast milk is produced in response to the
hormone prolactin.

Prolactin is produced in the anterior pituitary gland. It is also

produced in other organs, such as the breast and prostate. Prolactin also
regulates aspects of immune function and metabolism.

Dopamine blocks the secretion of prolactin. Therefore, dopamine

antagonists (i.e., antipsychotic medications) can result in raised
prolactin and galactorrhea. Dopamine agonists (e.g., bromocriptine or
cabergoline) can be used to suppress prolactin secretion.

Pregnancy and Breastfeeding

Milk production may start in small amounts during the second or third
trimester of pregnancy, and leaking can occur during that
time. Oestrogen and progesterone inhibit the secretion of prolactin. In
pregnancy, higher levels of oestrogen and progesterone inhibit breast
milk production.

Oxytocin stimulates breast milk excretion. Full milk production starts

shortly after birth in response to oxytocin release and a rapid drop in
oestrogen and progesterone.

Breast milk production will taper off and stop once breastfeeding
stops.

Hyperprolactinaemia

Galactorrhoea is usually associated with a raised prolactin level

(hyperprolactinaemia).

There is a long list of causes of hyperprolactinaemia, but the key

causes to remember are:
 • Idiopathic (no cause can be found)
• Prolactinomas (hormone-secreting pituitary tumours)
• Endocrine disorders, particularly hypothyroidism and
polycystic ovarian syndrome
• Medications, particularly dopamine antagonists (i.e.,
antipsychotic medications)

Prolactin suppresses gonadotropin-releasing hormone (GnRH) by

the hypothalamus, leading to reduced LH and FSH release. Therefore,
hyperprolactinaemia can also present with:
• Menstrual irregularities, particularly amenorrhoea (absent
periods)
• Reduced libido (low sex drive)
• Erectile dysfunction (in men)
• Gynaecomastia (in men)

Prolactinomas

Prolactinomas are tumours of the pituitary gland that secrete

excessive prolactin. This may be associated with multiple endocrine
neoplasia (MEN) type 1, an autosomal dominant genetic condition.

Prolactinomas can be:

• Microprolactinomas - smaller than 10 mm
• Macroprolactinomas - larger than 10 mm

Macroadenomas can have adverse effects relating to their size:

• Headaches
• Bitemporal hemianopia (loss of the outer visual fields in both
eyes)

The optic chiasm sits just above the pituitary gland. The optic
chiasm is the point where the optic nerves coming from the eyes cross
over to different sides of the head. Only the nerve fibres containing the
signal from the outer visual fields cross over, whereas the fibres from
the inner visual fields continue on the same side. A pituitary tumour of
sufficient size will start to press on the optic chiasm, where the nerves
cross, leading to a visual field defect, with loss of vision in the outer
visual fields in both eyes (the inner visual fields are spared). This is
called bitemporal hemianopia.

TOM TIP: It is worth properly understanding and remembering

bitemporal hemianopia, as it is commonly tested in exams. If you
find it a bit confusing, there is a Zero to Finals YouTube video
explaining it in detail. Remember to examine the visual fields in any
patient with symptoms that may be related to a pituitary tumour.

Non-Milk Discharge

Other conditions can cause nipple discharge that is not breast milk:
• Mammary duct ectasia
• Duct papilloma
• Pus from a breast abscess

Investigations

A pregnancy test is essential in women with childbearing potential

presenting with breast milk production.

Blood tests include:

• Serum prolactin
• Renal profile (U&Es)
• Liver function tests (LFTs)
• Thyroid function tests (TFTs)

An MRI scan is the investigation of choice for diagnosing pituitary

tumours.

Management

Management is targeted at the underlying cause.

Dopamine agonists (e.g., bromocriptine or cabergoline) can be

used to treat the symptoms of hyperprolactinaemia. They block prolactin
secretion and improve symptoms.
 Trans-sphenoidal surgical removal of the pituitary tumour is the
definitive treatment of hyperprolactinaemia secondary to a prolactinoma.
The pituitary gland and tumour are accessed and removed through the
nose and sphenoid bone.
 Mammary Duct Ectasia
Mammary duct ectasia is a benign condition where there is dilation of
the large ducts in the breasts. Ectasia means dilation. There is
inflammation in the ducts, leading to intermittent discharge from the
nipple. The discharge may be white, grey or green.

Mammary duct ectasia occurs most frequently in perimenopausal

women. Smoking is a significant risk factor.

Presentation

Mammary duct ectasia may present with:

• Nipple discharge
• Tenderness or pain
• Nipple retraction or inversion
• A breast lump (pressure on the lump may produce nipple
discharge)

It may be picked up incidentally on a mammogram, leading to further

assessment and investigations.

Diagnosis

The initial priority is to exclude breast cancer, as they can present in

similar ways. This involves triple assessment with:
• Clinical assessment (history and examination)
• Imaging (ultrasound, mammography and MRI)
• Histology (fine needle aspiration or core biopsy)

Microcalcifications are a key finding to remember on a

mammogram, although they are not specific to mammary duct ectasia.

Other investigations that may be performed are:

• Ductography - contrast is injected into an abnormal duct, and
mammograms are performed to visualise the duct
 • Nipple discharge cytology - examining the cells in a sample of
the nipple discharge
• Ductoscopy - inserting a tiny endoscope (camera) into the duct

Management

Mammary duct ectasia may resolve without any treatment. It is not

associated with an increased risk of cancer.

Management depends on the individual patient:

• Reassurance after excluding cancer may be all that is required
• Symptomatic management of mastalgia (supportive bra and warm
compresses)
• Antibiotics if infection is suspected or present
• Surgical excision of the affected duct (microdochectomy) may be
required in problematic cases
 Intraductal Papilloma
An intraductal papilloma is a warty lesion that grows within one of the
ducts in the breast. It is the result of the proliferation of epithelial cells.
The typical presentation is with clear or blood-stained nipple
discharge.

Intraductal papillomas are benign tumours; however, they can be

associated with atypical hyperplasia or breast cancer.

Presentation

Intraductal papillomas can occur at any age, but most often occur
between 35-55 years.

Intraductal papillomas are often asymptomatic. They may be picked

up incidentally on mammograms or ultrasound.

They may present with:

• Nipple discharge (clear or blood-stained)
• Tenderness or pain
• A palpable lump

Diagnosis

Patients require triple assessment with:

• Clinical assessment (history and examination)
• Imaging (ultrasound, mammography and MRI)
• Histology (usually by core biopsy or vacuum-assisted biopsy)

Ductography may also be used. This involves injecting contrast into

the abnormal duct and performing mammograms to visualise that duct.
The papilloma will be seen as an area that does not fill with contrast (a
“filling defect”).

Management
 Intraductal papillomas require complete surgical excision. After
removal, the tissue is examined for atypical hyperplasia or cancer that
may not have been picked up on the biopsy.
 Lactational Mastitis
Mastitis refers to inflammation of breast tissue and is a common
complication of breastfeeding. It can occur with or without associated
infection.

Mastitis can be caused by an obstruction in the ducts and the

accumulation of milk. Regularly expressing breast milk can help prevent it
from occurring.

Mastitis can also be caused by infection. Bacteria can enter at the

nipple and back-track into the ducts, causing infection and inflammation.
The most common bacterial cause is Staphylococcus aureus.

Presentation

Mastitis presents with:

• Breast pain and tenderness (unilateral)
• Erythema in a focal area of breast tissue
• Local warmth and inflammation
• Nipple discharge
• Fever

Management

Where mastitis is caused by blockage of the ducts, management is

conservative, with continued breastfeeding, expressing milk and breast
massage. Heat packs, warm showers and simple analgesia can help
symptoms.

When conservative management is not effective, or infection is

suspected (e.g., they have a fever), antibiotics should be
started. Flucloxacillin is the first line, or erythromycin when allergic to
penicillin. A sample of milk can be sent to the lab for culture and
sensitivities. Fluconazole may be used for
suspected candidal infections.
 Women should be encouraged to continue breastfeeding, even when
an infection is suspected. It will not harm the baby and will help to clear
the mastitis by encouraging flow. Where breastfeeding is difficult, or there
is milk left after feeding, they can express milk to empty the breast.

A breast abscess is a rare complication if mastitis is not adequately

treated. This may need surgical incision and drainage.

Candida of the Nipple

Candidal infection of the nipple can occur, often after a course of

antibiotics. This can lead to recurrent mastitis, as it causes cracked
skin on the nipple that creates an entrance for infection. It is associated
with oral thrush and candidal nappy rash in the infant.

Candida infection of the nipple may present with:

• Sore nipples bilaterally, particularly after feeding
• Nipple tenderness and itching
• Cracked, flaky or shiny areola
• Symptoms in the baby, such as white patches in the mouth and on
the tongue, or candidal nappy rash

Both the mother and baby need treatment, or it will reoccur. Treatment
is with:
• Topical miconazole 2% to the nipple, after each breastfeed
• Treatment for the baby (e.g., oral miconazole gel or nystatin)
 Breast Abscess
A breast abscess is a collection of pus within an area of the breast,
usually caused by a bacterial infection. This may be a:
• Lactational abscess (associated with breastfeeding)
• Non-lactational abscess (unrelated to breastfeeding)

Pus is a thick fluid produced by inflammation. It contains dead white

blood cells of the immune system and other waste from the fight against
the infection. When pus becomes trapped in a specific area and cannot
drain, an abscess will form and gradually increase in size.

Mastitis refers to inflammation of breast tissue. Often this is related

to breastfeeding (lactational mastitis), although it can be caused by
infection. Bacteria can enter at the nipple and back-track into the ducts,
causing infection and inflammation. Mastitis caused by infection may
precede the development of an abscess.

Smoking is a key risk factor for infective mastitis and breast

abscesses. Damage to the nipple (e.g., nipple eczema, candidal
infection or piercings) provides an entry point for bacteria.
Underlying breast disease (e.g., cancer) can affect the drainage of the
breast, predisposing to infection.

Causes

The most common causative bacteria are:

• Staphylococcus aureus (the most common)
• Streptococcal species
• Enterococcal species
• Anaerobic bacteria (such as Bacteroides species and anaerobic
streptococci)

TOM TIP: It is worth becoming familiar with the effective

antibiotics against different classes of bacteria. Staph aureus,
streptococcal and enterococcal bacteria are gram positive, meaning
that penicillins are likely to be effective. Flucloxacillin, in particular,
is used against staph aureus skin infections (this association is
worth remembering). However, anaerobic bacteria can also cause
breast abscesses, and simple penicillins (e.g., amoxicillin or
flucloxacillin) do not cover anaerobic bacteria. Co-amoxiclav
(amoxicillin plus clavulanic acid) covers anaerobes. Metronidazole
gives excellent anaerobic cover (also worth remembering), so it can
be added to the mix to cover anaerobes.

Presentation

The presentation of mastitis or breast abscesses is usually acute,

meaning the onset is within a few days.

Mastitis with infection in the breast tissue presents with breast

changes of:

• Nipple changes
• Purulent nipple discharge (pus from the nipple)
• Localised pain
• Tenderness
• Warmth
• Erythema (redness)
• Hardening of the skin or breast tissue
• Swelling

The key feature that suggests a breast abscess is a

swollen, fluctuant, tender lump within the breast. Fluctuance refers to
being able to move fluid around within the lump using pressure during
palpation. Where there is infection without an abscess, there can still be
hardness of the tissue, forming a lump, but it will not be fluctuant as it is
not filled with fluid (pus).

There may be generalised symptoms of infection, such as:

• Muscle aches
• Fatigue
• Fever
• Signs of sepsis (e.g., tachycardia, raised respiratory rate and
confusion)
 Management

The diagnosis of mastitis or a breast abscess can usually be made

clinically, with a history and examination.

The NICE clinical knowledge summaries (updated January 2021)

recommend different management for mastitis depending on whether it is
lactational or non-lactational.

Lactational mastitis caused by blockage of the ducts is managed

conservatively, with continued breastfeeding, expressing milk and
breast massage. Heat packs, warm showers and simple analgesia can
help symptoms. Antibiotics (flucloxacillin or erythromycin/clarithromycin
where there is penicillin allergy) are required where infection is suspected
or symptoms do not improve.

Management of non-lactational mastitis involves:

• Analgesia
• Antibiotics
• Treatment for the underlying cause (e.g., eczema or candidal
infection)

Antibiotics for non-lactational mastitis need to be broad-spectrum.

The NICE clinical knowledge summaries (updated January 2021)
recommend either:
• Co-amoxiclav
• Erythromycin/clarithromycin (macrolides) plus metronidazole
(to cover anaerobes)

Management of a breast abscess requires:

• Referral to the on-call surgical team in the hospital for
management
• Antibiotics
• Ultrasound (to confirm the diagnosis and exclude other pathology)
• Drainage (needle aspiration or surgical incision and drainage)
• Microscopy, culture and sensitivities of the drained fluid

Women who are breastfeeding are advised to continue breastfeeding

when they have mastitis or breast abscesses. They should regularly
express breast milk if feeding is too painful, then resume feeding when
possible. This is not harmful to the baby and is important in helping
resolve the mastitis or abscess.
 Breast Cancer
Breast cancer is the most common form of cancer in the UK. It mostly
affects women and is rare in men (about 1% of UK cases). Around 1 in 8
women will develop breast cancer in their lifetime.

Risk Factors

• Female (99% of breast cancers)

• Increased oestrogen exposure (earlier onset of periods and later
menopause)
• More dense breast tissue (more glandular tissue)
• Obesity
• Smoking
• Family history (first-degree relatives)

The combined contraceptive pill gives a small increase in the risk

of breast cancer, but the risk returns to normal ten years after stopping
the pill.

Hormone replacement therapy (HRT) increases the risk of breast

cancer, particularly combined HRT (containing both oestrogen and
progesterone).

Genetics

BRCA refers to the BReast CAncer gene. The BRCA genes are
tumour suppressor genes. Mutations in these genes lead to an
increased risk of breast cancer (as well as ovarian and other cancers).

The BRCA1 gene is on chromosome 17. In patients with a faulty

gene:
• Around 70% will develop breast cancer by aged 80
• Around 50% will develop ovarian cancer
• Also increased risk of bowel and prostate cancer
 The BRCA2 gene is on chromosome 13. In patients with a faulty
gene:
• Around 60% will develop breast cancer by aged 80
• Around 20% will develop ovarian cancer

There are other rarer genetic abnormalities associated with breast

cancer (e.g., TP53 and PTEN genes).

Types of Breast Cancer

Ductal Carcinoma In Situ (DCIS)

• Pre-cancerous or cancerous epithelial cells of the breast ducts
• Localised to a single area
• Often picked up by mammogram screening
• Potential to spread locally over years
• Potential to become an invasive breast cancer (around 30%)
• Good prognosis if full excised and adjuvant treatment is used

Lobular Carcinoma In Situ (LCIS)

• A pre-cancerous condition occurring typically in pre-menopausal
women
• Usually asymptomatic and undetectable on a mammogram
• Usually diagnosed incidentally on a breast biopsy
• Represents an increased risk of invasive breast cancer in the future
(around 30%)
• Often managed with close monitoring (e.g., 6 monthly examination
and yearly mammograms)

Invasive Ductal Carcinoma - NST

• NST means no special/specific type, where it is not more
specifically classified (e.g., medullary or mucinous)
• Also known as invasive breast carcinoma of no special/specific
type (NST)
• Originate in cells from the breast ducts
• 80% of invasive breast cancers fall into this category
• Can be seen on mammograms

Invasive Lobular Carcinomas (ILC)

• Around 10% of invasive breast cancers
 • Originate in cells from the breast lobules
• Not always visible on mammograms

Inflammatory Breast Cancer

• 1-3% of breast cancers
• Presents similarly to a breast abscess or mastitis
• Swollen, warm, tender breast with pitting skin (peau d’orange)
• Does not respond to antibiotics
• Worse prognosis than other breast cancers

Paget’s Disease of the Nipple

• Looks like eczema of the nipple/areolar
• Erythematous, scaly rash
• Indicates breast cancer involving the nipple
• May represent DCIS or invasive breast cancer
• Requires biopsy, staging and treatment, as with any other invasive
breast cancer

Rarer Types of Breast Cancer

• Medullary breast cancer
• Mucinous breast cancer
• Tubular breast cancer
• Multiple others

Breast Cancer Screening

The NHS breast cancer screening program offers a mammogram

every 3 years to women aged 50 - 70 years.

Screening aims to detect breast cancer early, which improves

outcomes. Roughly 1 in 100 women are diagnosed with breast cancer
after going for a mammogram.

There are some potential downsides to screening:

• Anxiety and stress
• Exposure to radiation, with a very small risk of causing breast
cancer
• Missing cancer, leading to false reassurance
 • Unnecessary further tests or treatment where findings would not
have otherwise caused harm

Generally, the benefits far outweigh the downsides and breast cancer
screening is recommended.

High-Risk Patients

There are different recommendations for screening patients with a

higher risk due to a family history of breast cancer. These are in the NICE
guidelines (2013, updated 2019).

There are specific criteria for a referral from primary care for patients
that may be at higher risk due to their family history. For example:
• A first-degree relative with breast cancer under 40 years
• A first-degree male relative with breast cancer
• A first-degree relative with bilateral breast cancer, first diagnosed
under 50 years
• Two first-degree relatives with breast cancer

Depending on their risk factors, they may be seen in a secondary

care breast clinic or a specialist genetic clinic.

Patients require genetic counselling and pre-test counselling

before performing genetic tests. This is to discuss the benefits and
drawbacks of genetic testing, such as the implications for family members
and offspring.

Annual mammogram screening is offered to women with increased

risk, between specific age ranges, depending on their level of risk
(potentially starting from aged 30, if high risk).

Chemoprevention may be offered for women at high risk, with:

• Tamoxifen if premenopausal
• Anastrozole if postmenopausal (except with severe osteoporosis)

Risk-reducing bilateral mastectomy or bilateral

oophorectomy (removing the ovaries) is an option for women at high
risk. This is suitable for only a small number of women and requires
significant counselling and weighing up the risks and benefits.

Presentation

Clinical features that may suggest breast cancer are:

• Lumps that are hard, irregular, painless or fixed in place
• Lumps may be tethered to the skin or the chest wall
• Nipple retraction
• Skin dimpling or oedema (peau d’orange)
• Lymphadenopathy, particularly in the axilla

Referral Criteria

The NICE guidelines (updated January 2021) recommend a two week

wait referral for suspected breast cancer for:
• An unexplained breast lump in patients aged 30 or above
• Unilateral nipple changes in patients aged 50 or above (discharge,
retraction or other changes)

The NICE guidelines recommend also considering a two week wait

referral for:
• An unexplained lump in the axilla in patients aged 30 or above
• Skin changes suggestive of breast cancer

The NICE guidelines suggest considering non-urgent referral for

unexplained breast lumps in patients under 30 years.

Triple Diagnostic Assessment

Once a patient has been referred for specialist services under a two
week wait referral for suspected cancer, they should initially receive a
triple diagnostic assessment comprising of:
• Clinical assessment (history and examination)
• Imaging (ultrasound or mammography)
• Biopsy (fine needle aspiration or core biopsy)

Imaging
 Younger women generally have more dense breasts with more
glandular tissue.

Ultrasound scans are typically used to assess lumps in younger

women (e.g., under 30 years). They are helpful in
distinguishing solid lumps (e.g., fibroadenoma or cancer)
from cystic (fluid-filled) lumps.

Mammograms are generally more effective in older women. They can

pick up calcifications missed by ultrasound.

MRI scans may be used:

• For screening in women at higher risk of developing breast cancer
(e.g., strong family history)
• To further assess the size and features of a tumour

Lymph Node Assessment

Women diagnosed with breast cancer require an assessment to see if

the cancer has spread to the lymph nodes. All women are offered
an ultrasound of the axilla (armpit) and ultrasound-guided biopsy of
any abnormal nodes.

A sentinel lymph node biopsy may be used during breast cancer

surgery where the initial ultrasound does not show anyone abnormal
nodes.

Sentinel Lymph Node Biopsy

Sentinel node biopsy is performed during breast surgery for cancer.

An isotope contrast and a blue dye are injected into the tumour area. The
contrast and dye travel through the lymphatics to the first lymph node (the
sentinel node). The first node in the drainage of the tumour area shows
up blue and on the isotope scanner. A biopsy can be performed on this
node, and if cancer cells are found, the lymph nodes can be removed.

Breast Cancer Receptors

 Breast cancer cells may have receptors that can be targeted with
breast cancer treatments. These receptors are tested for on samples of
the tumour and help guide treatment. There are three types of receptors:
• Oestrogen receptors (ER)
• Progesterone receptors (PR)
• Human epidermal growth factor (HER2)

Triple-negative breast cancer is where the breast cancer cells do

not express any of these three receptors. This carries a worse prognosis,
as it limits the treatment options for targeting the cancer.

Gene Expression Profiling

Gene expression profiling involves assessing which genes are

present within the breast cancer on a histology sample. This helps predict
the probability that the breast cancer will reoccur as a distant metastasis
(away from the original cancer site) within 10 years.

The NICE guidelines (2018) [DG34] recommend this for women with
early breast cancers that are ER positive but HER2 and lymph node
negative. It helps guide whether to give additional chemotherapy.

Metastasis

You can remember the notable locations that breast cancer

metastases occur using 2 Ls and 2 Bs:
• L - Lungs
• L - Liver
• B - Bones
• B - Brain

TOM TIP: Breast cancer can spread to any region of the body. In
patients with a metastatic tumour, regardless of where it is, the
primary could be breast cancer. This is worth remembering, as you
may be asked “where might this metastasis have originated” in an
exam or OSCE scenario. If the patient is female, answering “breast
cancer” will be a safe answer. The other cancer that can spread
practically anywhere, and may be less obvious, is melanoma (a type
of skin cancer).
 Staging

The first step in staging is triple assessment (clinical assessment,

imaging and biopsy). Additional investigations may be required to stage
the breast cancer:
• Lymph node assessment and biopsy
• MRI of the breast and axilla
• Liver ultrasound for liver metastasis
• CT of the thorax, abdomen and pelvis for lung, abdominal or pelvic
metastasis
• Isotope bone scan for bony metastasis

The TNM system is used to stage breast cancer. This grades the
tumour (T), nodes (N) and metastasis (M).

Multidisciplinary Team

All patients are discussed with the multidisciplinary team (MDT)

meeting for treatment planning:
• After the initial diagnosis
• After abnormal staging tests
• After further pathology and results
• After recurrence of the disease
• At any point where a treatment decision will be made

Surgery

Tumour Removal

The objective is to remove the cancer tissue along with a clear margin
of normal breast tissue. The options are:
• Breast-conserving surgery (e.g., wide local excision), usually
coupled with radiotherapy
• Mastectomy (removal of the whole breast), potentially with
immediate or delayed breast reconstruction

Axillary Clearance
 Removal of the axillary lymph nodes is offered to patients where
cancer cells are found in the nodes. Usually, the majority or all lymph
nodes are removed from the axilla. This increases the risk of chronic
lymphoedema in that arm.

Chronic Lymphoedema

Lymphoedema is a chronic condition caused by impaired lymphatic

drainage of an area. Lymphoedema can occur in an entire arm after
breast cancer surgery on that side, with removal of the axillary lymph
nodes from the armpit.

The lymphatic system is responsible for draining excess fluid from the
tissues. The tissues in areas affected by an impaired lymphatic system
become swollen with excess, protein-rich fluid (lymphoedema).

The lymphatic system also plays an important role in the immune

system. Areas of lymphoedema are prone to infection.

There are specialist lymphoedema services that can help manage

patients. Non-surgical treatment options include:
• Massage techniques to manually drain the lymphatic system
(manual lymphatic drainage)
• Compression bandages
• Specific lymphoedema exercises to improve lymph drainage
• Weight loss if overweight
• Good skin care

TOM TIP: It is important to remember that you should avoid

taking blood or inserting a cannula on the side of previous breast
cancer removal surgery. This is because there is a higher risk of
complications and infection due to the impaired lymphatic drainage
on that side.

Radiotherapy

Radiotherapy is usually used in patients with breast-conserving

surgery to reduce the risk of recurrence. High-dose radiation is delivered
from multiple angles to concentrate radiation on a targeted area. Patients
will have a course of radiotherapy after surgery, for example, with a
session of radiotherapy every day for 3 weeks.
Common radiotherapy side effects include:
• General fatigue from the radiation
• Local skin and tissue irritation and swelling
• Fibrosis of breast tissue
• Shrinking of breast tissue
• Long term skin colour changes (usually darker)

Chemotherapy

Oncologists will guide chemotherapy. Chemotherapy is used in one of

three scenarios:
• Neoadjuvant therapy - intended to shrink the tumour before
surgery
• Adjuvant chemotherapy - given after surgery to reduce
recurrence
• Treatment of metastatic or recurrent breast cancer

Hormone Treatment

Patients with oestrogen-receptor positive breast cancer are given

treatment that disrupts the oestrogen stimulating the breast cancer.

There are two main first-line options for this:

• Tamoxifen for premenopausal women
• Aromatase inhibitors for postmenopausal women (e.g.,
letrozole, anastrozole or exemestane)

Tamoxifen is a selective oestrogen receptor modulator (SERM). It

either blocks or stimulates oestrogen receptors, depending on the
location. It blocks oestrogen receptors in breast tissue, and stimulates
oestrogen receptors in the uterus and bones. This means it helps
prevent osteoporosis, but it does increase the risk of endometrial
cancer.

Aromatase is an enzyme found in fat (adipose) tissue that converts

androgens to oestrogen. After menopause, the action of aromatase in fat
tissue is the primary source of oestrogen. Aromatase inhibitors work by
blocking the creation of oestrogen in fat tissue.

Tamoxifen or an aromatase inhibitor are given for 5 - 10 years to

women with oestrogen-receptor positive breast cancer.

TOM TIP: It is worth committing tamoxifen and aromatase

inhibitors (e.g., letrozole) to memory, their relationship to
menopausal status and their basic mechanism of action. These are
good facts for examiners to test you on.

Other options for women with oestrogen-receptor positive breast

cancer, used in different circumstances, are:
• Fulvestrant (a selective oestrogen receptor downregulator)
• GnRH agonists (e.g., goserelin or leuprorelin)
• Ovarian surgery (i.e., oophorectomy to remove the ovaries)

Targeted Treatments

Trastuzumab (Herceptin) is a monoclonal antibody that targets the

HER2 receptor. It may be used in patients with HER2 positive breast
cancer. Notably, it can affect heart function; therefore, initial and close
monitoring of heart function is required.
Pertuzumab (Perjeta) is another monoclonal antibody that targets the
HER2 receptor. It may be used in patients with HER2 positive breast
cancer. This is used in combination with trastuzumab (Herceptin).

Neratinib (Nerlynx) is a tyrosine kinase inhibitor, reducing the growth

of breast cancers. It may be used in patients with HER2 positive breast
cancer.

Follow-up

The NICE guidelines (2018) recommend all patients treated for breast
cancer have surveillance mammograms yearly for 5 years (longer if they
are not yet old enough for the regular breast cancer screening program).

Patients treated for breast cancer are given an individual written care
plan, including details on:
 • Designated contacts
• Adjuvant treatment review dates
• Surveillance dates
• Advice on identifying recurrence
• Support service details

Reconstructive Surgery

Reconstructive surgery is offered to all patients having a mastectomy.

There are two options:
• Immediate reconstruction, done at the time of the mastectomy
• Delayed reconstruction, which can be delayed for months or
years after the initial mastectomy

There are several different methods for reconstructing the breasts.

The most suitable will depend on individual factors and preferences.

After breast-conserving surgery, reconstruction may not be required.

The standard options, if needed, are:
• Partial reconstruction (using a flap or fat tissue to fill the gap)
• Reduction and reshaping (removing tissue and reshaping both
breasts to match)

After mastectomy, the options for reconstruction include:

• Breast implants (inserting a synthetic implant)
• Flap reconstruction (using tissue from another part of the body to
reconstruct the breast)

Implants

Inserting an implant is a relatively simple procedure (compared with a

flap) with minimal scarring. It gives an acceptable appearance but can
feel less natural (e.g., cold, less mobile and static size and shape). There
can also be long-term problems, such as hardening, leakage and shape
change.

Latissimus Dorsi Flap

 The breast can be reconstructed using a portion of the latissimus dorsi
and the associated skin and fat tissue. The tissue is tunnelled under the
skin to the breast area.

“Pedicled” refers to keeping the original blood supply and moving the
tissue under the skin to a new location.

“Free flap” refers to cutting the tissue away completely and

transplanting it to a new location.
Transverse Rectus Abdominis Flap (TRAM Flap)

The breast can be reconstructed using a portion of the rectus

abdominis, blood supply and skin. This can be either as a pedicled flap
(tunnelled under the skin) or a free flap (transplanted). It poses a risk of
developing an abdominal hernia due to the weakened abdominal wall.

Deep Inferior Epigastric Perforator Flap (DIEP Flap)

The breast can be reconstructed using skin and subcutaneous fat

from the abdomen (no muscle) as a free flap. The deep inferior
epigastric artery, with the associated fat, skin and veins, is transplanted
from the abdomen to the breast. The vessels are attached to branches of
the internal mammary artery and vein. This is a complex procedure
involving microsurgery. There is less risk of an abdominal wall hernia than
with a TRAM flap, as the abdominal wall muscles are left intact.
 Ear, Nose and Throat
Hearing Loss
Audiometry
Presbycusis
Sudden Sensorineural Hearing Loss
Eustachian Tube Dysfunction
Otosclerosis
Otitis Media
Otitis Externa
Ear Wax
Tinnitus
Vertigo
Benign Paroxysmal Positional Vertigo
Vestibular Neuronitis
Labyrinthitis
Ménière's Disease
Acoustic Neuroma
Cholesteatoma
Facial Nerve Palsy
Nosebleeds
Sinusitis
Nasal Polyps
Obstructive Sleep Apnoea
Tonsillitis
Quinsy
Tonsillectomy
Neck Lumps
Head and Neck Cancer
Tongue Conditions
Mouth and Gum Conditions
 Hearing Loss
There are two main categories of hearing loss: conductive hearing
loss and sensorineural hearing loss.

Conductive hearing loss relates to a problem with sound travelling

from the environment to the inner ear. The sensory system may be
working correctly, but the sound is not reaching it. Putting earplugs in your
ears causes conductive hearing loss.

Sensorineural hearing loss is caused by a problem with the

sensory system or vestibulocochlear nerve in the inner ear.

Basic Ear Anatomy

There are three sections of the ear are:

• Outer ear
• Middle ear
• Inner ear

The basic structures, from outside in, are:

• The pinna is the external portion of the ear
• The external auditory canal is the tube into the ear
• The tympanic membrane is the eardrum
• The Eustachian tube connects the middle ear with the throat to
equalise pressure
• The malleus, incus and stapes are the small bones in the middle
ear that connect the tympanic membrane to the structures of the
inner ear
• The semicircular canals are responsible for sensing head
movement (the vestibular system)
• The cochlea is responsible for converting the sound vibration into
a nerve signal
• The vestibulocochlear nerve transmits nerve signals from the
semicircular canals and cochlea to the brain
 Presentation

Hearing loss may be gradual and insidious. Patients may present

because others have noticed they are not paying attention or missing
details of conversations. Sometimes patients can present with concerns
about dementia, when in fact, the issue is hearing loss.

Sudden onset hearing loss (over less than 72 hours) requires a

thorough assessment to establish the cause.

There may be associated symptoms alongside hearing loss, which

can give clues about the potential cause:
• Tinnitus (ringing in the ears)
• Vertigo (the sensation that the room is spinning)
• Pain (may indicate infection)
• Discharge (may indicate an outer or middle ear infection)
• Neurological symptoms

It is worth noting patients with hearing loss are more likely to develop
dementia, and treating the hearing loss (e.g., a hearing aid) may reduce
the risk.

Weber’s and Rinne’s Tests

Weber’s test and Rinne’s test are used to differentiate between

sensorineural and conductive hearing loss. A tuning fork is used to
perform both tests.

Weber’s Test

To perform Weber’s test:

• Strike the tuning fork to make it vibrate and hum (use the palm of
your hand or your knee - not the patient!)
• Place it in the centre of the patient’s forehead
• Ask the patient if they can hear the sound and which ear it is
loudest in
 A normal result is when the patient hears the sound equally in both
ears.

In sensorineural hearing loss, the sound will be louder in the

normal ear (quieter in the affected ear). The normal ear is better at
sensing the sound.

In conductive hearing loss, the sound will be louder in the affected

ear. This is because the affected ear “turns up the volume” and becomes
more sensitive, as sound has not been reaching that side as well due to
the conduction problem. When the tuning fork's vibration is transmitted
directly to the cochlea through the bones of the skull, rather than having
to travel through the ear canal and middle ear structures, the increased
sensitivity makes it sound louder in the affected ear.

TOM TIP: The way I remember which way round these tests are,
is to picture Spiderman shooting a web (Weber’s) right in the middle
of someone’s face.

Rinne’s Test

To perform Rinne’s test:

• Strike the tuning fork to make it vibrate and hum
• Place the flat end on the mastoid process (the bony lump behind
the ear) - this tests bone conduction
• Ask the patient to tell you when they can no longer hear the
humming noise
• When they can no longer hear the noise, remove the tuning fork
(still vibrating) and hover it 1cm from the same ear
• Ask the patient if they can hear the sound now - this tests air
conduction
• Repeat the process on the other side

A normal result is when the patient can hear the sound again when
bone conduction ceases and the tuning fork is moved next to the ear
rather than on the mastoid process. It is normal for air conduction to be
better (more sensitive) than bone conduction. This is referred to as
“Rinne’s positive”.
 An abnormal result (Rinne’s negative) is when bone conduction is
better than air conduction. The sound is not heard after removing the
tuning fork from the mastoid process and holding it near the ear canal.
This suggests a conductive cause for the hearing loss. Sound is
transmitted through the bones of the skull directly to the cochlea, meaning
bone conduction is intact. However, the sound is less able to travel
through the air, ear canal, tympanic membrane and middle ear to the
cochlea due to a conductive problem.

Causes Of Sensorineural Hearing Loss

The causes of adult-onset sensorineural hearing loss are:

• Sudden sensorineural hearing loss (over less than 72 hours)
• Presbycusis (age-related)
• Noise exposure
• Ménière's disease
• Labyrinthitis
• Acoustic neuroma
• Neurological conditions (e.g., stroke, multiple sclerosis or brain
tumours)
• Infections (e.g., meningitis)
• Medications

There are a large number of medications that can cause sensorineural

hearing loss. Some of the more common and worth remembering are:
• Loop diuretics (e.g., furosemide)
• Aminoglycoside antibiotics (e.g., gentamicin)
• Chemotherapy drugs (e.g., cisplatin)

Causes Of Conductive Hearing Loss

The causes of adult-onset conductive hearing loss are:

• Ear wax
• Foreign body in the ear canal
• Infection (e.g., otitis media or otitis externa)
• Fluid in the middle ear (effusion)
• Eustachian tube dysfunction
• Perforated tympanic membrane
• Otosclerosis
• Cholesteatoma
• Exostoses (benign bone growths)
• Tumours
 Audiometry
Audiometry involves testing a patient’s hearing by playing a variety of
tones and volumes using headphones (air conduction) and a bone
conduction device (oscillator) that delivers sound directly to the bones of
the skull. Audiometry results are recorded on an audiogram.
Audiograms can help identify and differentiate conductive and
sensorineural hearing loss.

Audiogram

Audiograms are charts that document the volume at which patients

can hear different tones. The frequency in hertz (Hz) is plotted on the x-
axis, from low to high pitched. In decibels (dB), the volume is plotted on
the y-axis, from loud at the bottom to quiet at the top. The lower down the
chart, the higher the decibels and the louder the volume. The higher up
the y-axis, the more sensitive the hearing.

Hearing is tested to establish the quietest volume at which a patient

can hear each frequency. This level is plotted on the chart. The louder
the sound required for the patient to hear, the worse their hearing is and
the lower on the chart they will plot. For example, a 1000 Hz sound will be
played at various volumes until the patient can just about hear the sound.
If this tone is heard at 15 dB, a mark is made on the chart where 1000 Hz
meets 15 dB. If this sound can only be heard at 80 dB, a mark is made
where 1000 Hz meets 80 dB.

Hearing is tested in both ears separately. Both air and bone

conduction are tested independently. The following symbols are used to
mark each of these separate measurements:

• X - Left-sided air conduction

• ] - Left-sided bone conduction
• O - Right-sided air conduction
• [ - Right-sided bone conduction
 When a patient has normal hearing, all readings will be between 0
and 20 dB, at the top of the chart.

In patients with sensorineural hearing loss, both air and bone

conduction readings will be more than 20 dB, plotted below the 20 dB line
on the chart. This may affect only one side, one side more than the other
or both sides equally.
 In patients with conductive hearing loss, bone conduction readings
will be normal (between 0 and 20 dB). However, air conduction readings
will be greater than 20 dB, plotted below the 20 dB line on the chart. In
conductive hearing loss, sound can travel through bone, but is not
conducted through air due to pathology along the route into the ear.
 Both air and bone conduction readings will be more than 20 dB in
patients with mixed hearing loss. However, there will be a difference
of more than 15 dB between the two (bone conduction > air
conduction).
 Presbycusis
Presbycusis is described as age-related hearing loss. It is a type of
sensorineural hearing loss that occurs as people get older. It tends to
affect high-pitched sounds first and more markedly than lower-pitched
sounds. The hearing loss occurs gradually and symmetrically.

The causes of reduced hearing in presbycusis are complex. There are

several different mechanisms, including loss of the hair cells in the
cochlea, loss of neurones in the cochlea, atrophy of the stria
vascularis and reduced endolymphatic potential.

Risk Factors

• Age
• Male gender
• Family history
• Loud noise exposure
• Diabetes
• Hypertension
• Ototoxic medications
• Smoking

Exposure to loud noise over time is a key risk factor that can be
addressed to potentially prevent or reduce the extent of presbycusis.
Hearing protection should be worn in environments where there is
exposure to loud noises for prolonged periods to reduce the risk of
presbycusis, for example, in occupations such as woodworking or
construction.

Presentation

Hearing loss in presbycusis is gradual and insidious. The gradual

onset may mean patients do not notice the change in their hearing. The
loss of high-pitched sounds can make speech difficult to hear and
understand, particularly in loud environments. Male voices may be easier
to hear than female voices (due to the generally lower pitch). Patients
may present after others have noticed they are not paying attention or
missing details of conversations. Sometimes patients can present with
concerns about dementia, when in fact, the issue is hearing loss.

There may be associated tinnitus (ringing in the ears).

It is worth noting patients with hearing loss are more likely to develop
dementia, and treating the hearing loss (e.g., a hearing aid) may reduce
the risk.

Diagnosis

Audiometry is the investigation of choice for establishing the

diagnosis and extent of hearing loss. Presbycusis will give a
sensorineural pattern of hearing loss, with normal or near-normal hearing
at lower frequencies and worsening hearing loss at higher frequencies.

Management
 The effects of presbycusis cannot be reversed. Management involves
supporting the person to maintain normal functioning:
• Optimising the environment, for example, reducing the ambient
noise during conversations
• Hearing aids
• Cochlear implants (in patients where hearing aids are not sufficient)
 Sudden Sensorineural Hearing Loss
Sudden sensorineural hearing loss (SSNHL) is defined as hearing
loss over less than 72 hours, unexplained by other causes. This is
considered an otological emergency and requires an immediate referral
to the on-call ENT team. The diagnosis is made when someone rapidly
loses their hearing, and no conductive cause can be found.

With SSNHL, hearing loss is most often unilateral. It may be

permanent or resolve over days to weeks.

Conductive causes of rapid-onset hearing loss (not classed as

SSNHL) include:
• Ear wax (or something else blocking the canal)
• Infection (e.g., otitis media or otitis externa)
• Fluid in the middle ear (effusion)
• Eustachian tube dysfunction
• Perforated tympanic membrane

Causes

Most cases (90%) of SSNHL are idiopathic, meaning no specific

cause is found.

Other causes of SSNHL include:

• Infection (e.g., meningitis, HIV and mumps)
• Ménière's disease
• Ototoxic medications
• Multiple sclerosis
• Migraine
• Stroke
• Acoustic neuroma
• Cogan’s syndrome (a rare autoimmune condition causing
inflammation of the eyes and inner ear)

Investigations
 Audiometry is required to establish the diagnosis. A diagnosis of
SSNHL requires a loss of at least 30 decibels in three consecutive
frequencies on an audiogram.

MRI or CT head may be used if a stroke or acoustic neuroma are

being considered.

Management

The NICE clinical knowledge summaries (updated September 2019)

recommend an immediate referral to ENT for assessment within 24
hours for patients presenting with sudden sensorineural hearing loss
presenting within 30 days of onset.

Where an underlying cause is found (e.g., infection), treatment can be

directed at this.

Idiopathic SSNHL may be treated with steroids under the guidance

of the ENT team. Steroids may be:
• Oral
• Intra-tympanic (via an injection of steroid through the tympanic
membrane)
 Eustachian Tube Dysfunction
Eustachian tube dysfunction is when the tube between the middle ear
and throat is not functioning properly. The Eustachian tube is present
mainly to equalise the air pressure in the middle ear and drain fluid from
the middle ear.

When the Eustachian tube is not functioning correctly or becomes

blocked, the air pressure cannot equalise properly and fluid cannot drain
freely from the middle ear. The air pressure between the middle ear and
the environment can become unequal. The middle ear can fill with fluid.

Eustachian tube dysfunction may be related to a viral upper

respiratory tract infection (URTI), allergies (e.g., hayfever) or smoking.

Presentation
 Eustachian tube dysfunction may present with:
• Reduced or altered hearing
• Popping noises or sensations in the ear
• A fullness sensation in the ear
• Pain or discomfort
• Tinnitus

Symptoms tend to get worse when the external air pressure changes,
and the middle ear pressure cannot equalise to the outside pressure. This
may happen, for example, during air travel, climbing a mountain or scuba
diving.

Otoscopy may appear normal, but it is important to exclude other

causes (e.g., otitis media).

Investigations

Often Eustachian tube dysfunction gives a typical set of symptoms

and is associated with a clear cause, for example, a recent viral upper
respiratory tract infection or hayfever. In this situation, investigations are
not required as the symptoms will resolve with time or simple treatments.

With persistent, problematic or severe symptoms, investigations to

help establish the diagnosis and cause include:
• Tympanometry
• Audiometry
• Nasopharyngoscopy (an endoscopic camera through the nose to
the throat to inspect the Eustachian tube openings)
• CT scan to assess for structural pathology

Tympanometry

Tympanometry involves:
• Inserting a device into the external auditory canal (ear canal)
• Creating different air pressures in the canal
• Sending a sound in the direction of the tympanic membrane
• Measuring the amount of sound reflected back off the tympanic
membrane
 • Plotting a tympanogram (graph) of the amount of sound absorbed
(admittance) at different air pressures

The amount of sound absorbed by the tympanic membrane and

middle ear (not reflected back to the device) is known as the admittance.

Normally, sound is absorbed most effectively when the air pressure in

the ear canal is equal to the ambient air pressure. The ambient air
pressure is equal to the middle ear pressure in healthy ears.

When there is Eustachian tube dysfunction, the air pressure in

the middle ear may be lower than the ambient air pressure, because
new air cannot get in through the tympanic membrane to equalise the
pressures. As a result, the tympanogram will show a
peak admittance (most sound absorbed) with negative ear canal
pressures.

Management

Treatment options for Eustachian tube dysfunction include:

• No treatment, waiting for it to resolve spontaneously (e.g.,
recovering from the viral URTI)
• Valsalva manoeuvre (holding the nose and blowing into it to inflate
the Eustachian tube)
• Decongestant nasal sprays (short term only)
• Antihistamines and a steroid nasal spray for allergies or rhinitis
• Surgery may be required in severe or persistent cases

Otovent is an over the counter device where the patient blows into a
balloon using a single nostril, which can help inflate the Eustachian tube,
clear blockages and equalise pressure.

Surgery

There are three main surgical options:

• Treating other pathology that might be causing symptoms, for
example, adenoidectomy (removal of the adenoids)
• Grommets
• Balloon dilatation Eustachian tuboplasty
 Grommets are tiny tubes inserted into the tympanic membrane by
an ENT surgeon. This allows air or fluid from the middle ear to drain
through the tympanic membrane to the ear canal. Grommets are usually
inserted using a local anaesthetic. The procedure is relatively safe with
few complications. Grommets typically fall out within 18 months.

Balloon dilatation Eustachian tuboplasty involves inserting a

deflated balloon into the Eustachian tube, inflating the balloon for a short
period (i.e., 2 minutes) to stretch the Eustachian tube, then deflating and
removing it. This is usually done under general anaesthetic.
 Otosclerosis
Otosclerosis is a condition where there is remodelling of the small
bones in the middle ear, leading to conductive hearing loss. Oto- refers
to the ears, and -sclerosis means hardening. It usually presents before
the age of 40 years.

The development of otosclerosis is thought to result from a

combination of environmental and genetic factors, although the exact
mechanism is not understood. It can be inherited in an autosomal
dominant pattern. However, no specific genetic mutations have been
identified. It is more common in women.

Pathophysiology

The auditory ossicles are the tiny bones in the middle ear that
transmit sound vibrations from the tympanic membrane to the cochlea.
They are the malleus, incus and stapes. The stapes is connected to the
oval window (fenestra ovalis) of the cochlea, where it transmits
vibrations into the cochlea. The cochlea converts these vibrations into
sensory signals.

In patients with otosclerosis, these tiny bones in the middle are

affected by abnormal bone remodelling and formation. This mainly affects
the base of the stapes, where it attaches to the oval window, causing
stiffening and fixation and preventing it from transmitting sound
effectively. It causes conductive hearing loss.

Presentation

The typical presentation is a patient under 40 years presenting with

unilateral or bilateral:
• Hearing loss
• Tinnitus
 It tends to affect the hearing of lower-pitched sounds more than
higher-pitched sounds. Female speech may be easier to hear than male
speech (due to the generally higher pitch). This is the reverse of the
pattern seen in presbycusis.

Due to conductive hearing loss with intact sensory hearing, the patient
can experience their own voice as loud in comparison to the environment
(due to bone conduction of their voice). This can lead to them talking
quietly.

Examination

Otoscopy is normal.

Weber’s test is normal if the otosclerosis is bilateral, meaning that

when the tuning fork is applied to the centre of the forehead, they will hear
the sound equally in both ears. If the otosclerosis is unilateral or affects
one ear more than the other, the sound will be louder in the more affected
ear.

Rinne’s test will show conductive hearing loss. The sound will be
easily heard when the tuning fork is applied to the mastoid process (bone
conduction). When the patient stops being able to hear the sound during
bone conduction, and the tuning fork is removed from the mastoid
process and held close to the ear canal, they will not be able to hear the
sound (air conduction is worse than bone conduction).

Investigations

Audiometry is the initial investigation of choice. Otosclerosis will

show a conductive hearing loss pattern. Bone conduction readings
will be normal (between 0 and 20 dB). However, air conduction readings
will be greater than 20 dB, plotted below the 20 dB line on the chart.
Hearing loss tends to be greater at lower frequencies.

Tympanometry will show generally reduced admittance (absorption)

of sound. The tympanic membrane is stiff and non-compliant and does
not absorb sound, reflecting most of it back.
 High-resolution CT scans can detect bony changes associated with
otosclerosis, although they are not always required.

Management

The options for management are:

• Conservative, with the use of hearing aids
• Surgical (stapedectomy or stapedotomy)

Surgical management is generally successful and can potentially

restore hearing to normal. It involves lifting the tympanic membrane and
some of the surrounding skin out of the way to access the middle ear
through the ear canal.

Stapedectomy involves removing the entire stapes bone and

replacing it with a prosthesis. The prosthesis attaches to the oval window
and hooks around the incus, transmitting the sound from the incus to the
cochlea in the same way the stapes normally would.

Stapedotomy involves removing part of the stapes bone and leaving

the base of the stapes (the footplate) attached to the oval window. A
small hole is made in the base of the stapes for the prosthesis to enter. A
prosthesis is added to transmit sound from the incus to the cochlea.
 Otitis Media
Otitis media is the name given to an infection in the middle ear. The
middle ear is the space that sits between the tympanic
membrane (eardrum) and the inner ear. This is where the cochlea,
vestibular apparatus and nerves are found. Bacteria enter from the
back of the throat through the Eustachian tube. A viral upper
respiratory tract infection often precedes bacterial infection of the
middle ear.

Bacteria

The most common bacterial cause of otitis media is streptococcus

pneumoniae. This also commonly causes other ENT infections such
as rhino-sinusitis and tonsillitis.

Other common causes include:

• Haemophilus influenzae
• Moraxella catarrhalis
• Staphylococcus aureus

Presentation

Ear pain is the primary presenting feature of otitis media in adults.

It may also present with:

• Reduced hearing in the affected ear
• Feeling generally unwell, for example with fever and fatigue
• Symptoms of an upper airway infection such as cough, coryzal
symptoms and sore throat

When the infection affects the vestibular system, it can cause balance
issues and vertigo. When the tympanic membrane has perforated, there
may be discharge from the ear.

Examination
 An otoscope is used to visualise the tympanic membrane whilst
gently pulling the pinna up and backwards. It may be challenging to
visualise the tympanic membrane if there is significant discharge or wax
in the ear canal.

A normal tympanic membrane is “pearly-

grey”, translucent and slightly shiny. You should be able to visualise
the malleolus through the membrane. Look for a cone of light reflecting
the light of the otoscope.

Otitis media will give a bulging, red, inflamed looking membrane.

When there is a perforation, you may see discharge in the ear canal and a
hole in the tympanic membrane.

Management

Most otitis media cases will resolve without antibiotics within

around three days, sometimes up to a week. Antibiotics make little
difference to symptoms or complications. Complications
(mainly mastoiditis) are rare. Simple analgesia (e.g., paracetamol or
ibuprofen) can be used for pain and fever.

There are three options for prescribing antibiotics:

• Immediate antibiotics
• Delayed prescription
• No antibiotics

Consider immediate antibiotics at the initial presentation in patients

who have significant co-morbidities, are systemically unwell or are
immunocompromised.

Consider a delayed prescription that can be collected and used after

three days if symptoms have not improved or have worsened at any time.
This can be a helpful strategy in patients pressing for antibiotics or where
you suspect the symptoms might worsen.

The NICE clinical knowledge summaries (updated January 2021)

suggest:
• Amoxicillin for 5-7 days first-line
 • Clarithromycin (if penicillin allergic)
• Erythromycin (in pregnant women allergic to penicillin)

Always safety-net, offering education and advice to patients on when

to seek further medical attention.

Complications

• Otitis media with effusion

• Hearing loss (usually temporary)
• Perforated tympanic membrane (with pain, reduced hearing and
discharge)
• Labyrinthitis (causing dizziness or vertigo)
• Mastoiditis (rare)
• Abscess (rare)
• Facial nerve palsy (rare)
• Meningitis (rare)
 Otitis Externa
Otitis externa is inflammation of the skin in the external ear
canal. Oto- refers to ear, -itis refers to inflammation, and externa refers
to the external ear canal. The infection can be localised or diffuse. It can
spread to the external ear (pinna). It can be acute (less than three
weeks) or chronic (more than three weeks).

Otitis externa is sometimes called “swimmers ear”, as exposure to

water whilst swimming can lead to inflammation in the ear
canal. Trauma to the ear canal (e.g., from cotton buds or earplugs) is
another predisposing factor. Ear wax (cerumen) has a protective effect
against infection, and the removal of ear wax can increase the chances of
infection.

The inflammation in otitis externa may be caused by:

• Bacterial infection
• Fungal infection (e.g., aspergillus or candida)
• Eczema
• Seborrhoeic dermatitis
• Contact dermatitis

TOM TIP: Think about fungal infection in patients that have had
multiple courses of topical antibiotics. Antibiotics kill the “friendly
bacteria” that have a protective effect against fungal infections. This
is similar to how oral antibiotics can predispose people to develop
oral or vaginal candidiasis (thrush).

Bacterial Causes

The two most common bacterial causes of otitis externa are:

• Pseudomonas aeruginosa
• Staphylococcus aureus

TOM TIP: It is worth remembering Pseudomonas aeruginosa. It is

a gram-negative aerobic rod-shaped bacteria. It likes to grow in
moist, oxygenated environments. Other than causing otitis externa,
an important exam-related point to remember is that it can colonise
the lungs in patients with cystic fibrosis, significantly increasing
their morbidity and mortality. It is naturally resistant to many
antibiotics, making it very difficult to treat in children with cystic
fibrosis. It can be treated with aminoglycosides (e.g., gentamicin) or
quinolones (e.g., ciprofloxacin).

Presentation

The typical symptoms of otitis externa are:

• Ear pain
• Discharge
• Itchiness
• Conductive hearing loss (if the ear becomes blocked)

Examination can show:

• Erythema and swelling in the ear canal
• Tenderness of the ear canal
• Pus or discharge in the ear canal
• Lymphadenopathy (swollen lymph nodes) in the neck or around
the ear

The tympanic membrane may be obstructed by wax or discharge. It

may be red if the otitis externa extends to the tympanic membrane. If the
tympanic membrane is perforated, the discharge in the ear canal might be
from otitis media rather than otitis externa.

Diagnosis

The diagnosis can be made clinically with an examination of the ear

canal (otoscopy).

An ear swab can be used to identify the causative organism but is not
usually required.

Management
 Mild otitis externa may be treated with acetic acid 2% (available
over the counter as EarCalm). Acetic acid has an antifungal and
antibacterial effect. This can also be used prophylactically before and
after swimming in patients that are prone to otitis externa.

Moderate otitis externa is usually treated with a topical antibiotic

and steroid, for example:
• Neomycin, dexamethasone and acetic acid (e.g., Otomize spray)
• Neomycin and betamethasone
• Gentamicin and hydrocortisone
• Ciprofloxacin and dexamethasone

Aminoglycosides (e.g., gentamicin and neomycin) are potentially

ototoxic, rarely causing hearing loss if they get past the tympanic
membrane. Therefore, it is essential to exclude a perforated tympanic
membrane before using topical aminoglycosides in the ear. This can be
difficult if the patient has discharge, swelling or wax blocking the ear
canal. Patients with a blocked ear canal may need to be seen by ENT to
microsuction the debris from the canal and visualise the tympanic
membrane. They will also require a referral to ENT if the canal is so
blocked or swollen that topical treatments cannot reach the site of
infection.

Patients with severe or systemic symptoms may need oral

antibiotics (e.g., flucloxacillin or clarithromycin) or discussion with ENT
for admission and IV antibiotics.

An ear wick may be used if the canal is very swollen, and treatment
with ear drops or sprays is difficult. An ear wick is made of sponge or
gauze. They contain topical treatments for otitis externa (e.g., antibiotics
and steroids). Wicks are inserted into the ear canal and left there for a
period of time (e.g., 48 hours). As the swelling and inflammation settle, the
ear wick can be removed, and treatment can continue with drops or
sprays.

Fungal infections can be treated with clotrimazole ear drops.

TOM TIP: The treatment for otitis externa I have seen used most
often is Otomize ear spray, so this is probably the one to remember.
Always check the local antibiotic guidelines when prescribing
antibiotics, as they will vary in different hospitals and areas.

Malignant Otitis Externa

Malignant otitis externa is a severe and potentially life-threatening

form of otitis externa. The infection spreads to the bones surrounding the
ear canal and skull. It progresses to osteomyelitis of the temporal bone
of the skull.

Malignant otitis externa is usually related to underlying risk factors for

severe infection, such as:
• Diabetes
• Immunosuppressant medications (e.g., chemotherapy)
• HIV

Symptoms are generally more severe than otitis externa, with

persistent headache, severe pain and fever.

Granulation tissue at the junction between the bone and cartilage in

the ear canal (about halfway along) is a key finding that indicates
malignant otitis externa.

Malignant otitis externa requires emergency management, with:

• Admission to hospital under the ENT team
• IV antibiotics
• Imaging (e.g., CT or MRI head) to assess the extent of the
infection

It can lead to complications of:

• Facial nerve damage and palsy
• Other cranial nerve involvement (e.g., glossopharyngeal, vagus
or accessory nerves)
• Meningitis
• Intracranial thrombosis
• Death
 Ear Wax
Ear wax is also called cerumen. It is normally produced in small
amounts in the external ear canal. It is created from a combination of
secretions, dead skin cells and any substances that enter the ear. Ear
wax has a protective effect, helping to prevent infection in the ear canal.
In most people, ear wax does not cause any problems.

Impacted Ear Wax

Ear wax can build up and become impacted and stuck to the tympanic
membrane. This can result in:
• Conductive hearing loss
• Discomfort in the ear
• A feeling of fullness
• Pain
• Tinnitus

Ear wax can be seen on examination with an otoscope. It may

completely cover the tympanic membrane, preventing assessment of the
tympanic membrane and inner ear.

Management

In most cases, ear wax does not require any interventions. The ears
should naturally regulate the amount of wax in the ear canal without any
issues.

Inserting cotton buds into the ear should be avoided, as this can press
the wax in further and cause impaction.
There are three main methods for removing ear wax:
• Ear drops - usually olive oil or sodium bicarbonate 5%
• Ear irrigation - squirting water in the ears to clean away the wax
• Microsuction - using a tiny suction device to suck out the wax
 Ear drops may be enough to clear the ears. If not, ear irrigation can
often be performed in primary care. Where there
are contraindications to ear irrigation (e.g., perforated tympanic
membrane or infection), microsuction can be performed by specialist
ear, nose and throat services.
 Tinnitus
Tinnitus refers to a persistent addition sound that is heard but not
present in the surrounding environment. It may be described as a “ringing
in the ears”, but can also be a buzzing, hissing or humming noise.

The additional noise experienced with tinnitus is thought to be the

result of a background sensory signal produced by the cochlea that is
not effectively filtered out by the central auditory system. In a quiet
enough environment, almost everyone will experience some background
noise (tinnitus). This becomes more prominent the more attention it is
given.

Causes

Primary tinnitus has no identifiable cause and often occurs with

sensorineural hearing loss.

Secondary tinnitus refers to tinnitus with an identifiable cause.

Causes include:
• Impacted ear wax
• Ear infection
• Ménière's disease
• Noise exposure
• Medications (e.g., loop diuretics, gentamicin and chemotherapy
drugs such as cisplatin)
• Acoustic neuroma
• Multiple sclerosis
• Trauma
• Depression

Tinnitus may also be associated with systemic conditions:

• Anaemia
• Diabetes
• Hypothyroidism or hyperthyroidism
 • Hyperlipidaemia

Objective tinnitus refers to when the patient can objectively hear an

extra sound within their head. This sound can also be observable on
examination by auscultating with a stethoscope around the ear. Actual
additional sounds may be caused by:
• Carotid artery stenosis (pulsatile carotid bruit)
• Aortic stenosis (radiating pulsatile murmur sounds)
• Arteriovenous malformations (pulsatile)
• Eustachian tube dysfunction (popping or clicking noises)

TOM TIP: I think of primary tinnitus as the ears trying to “turn up

the volume” when they cannot hear the surrounding noises as well.
This is a helpful way of explaining it to patients who have tinnitus
associated with hearing loss. Using hearing aids allows the ears to
pick up noises better and “turn the volume down”, reducing the
tinnitus. The actual cause of tinnitus is not entirely understood, so
this is not entirely accurate, but it is a helpful analogy.

Assessment

Ask about the pattern of symptoms:

• Unilateral or bilateral
• Frequency and duration
• Severity
• Pulsatile or non-pulsatile (pulsatile may indicate a cardiovascular
cause, such as carotid artery stenosis with a bruit)

A focused history and examination can be used to identify any

underlying causes, including:
• Contributing factors, such as hearing loss or noise exposure
• Associated symptoms (e.g., hearing loss, vertigo, pain or
discharge)
• Stress and anxiety
• Otoscopy to look for causes such as ear wax or infection
• Weber’s and Rinne’s tests for hearing loss

Investigations
 The NICE clinical knowledge summaries (updated March 2020)
suggest considering blood tests for possible underlying causes:
• Full blood count (anaemia)
• Glucose (diabetes)
• TSH (thyroid disorders)
• Lipids (hyperlipidaemia)

Audiology can be used to assess the hearing in detail and help

establish the underlying cause.

Imaging (e.g., CT or MRI) may be rarely required to investigate for

underlying causes such as vascular malformations or acoustic neuromas.

Red Flags

Red flags that could indicate a serious underlying cause and the need
for specialist assessment include:
• Unilateral tinnitus
• Pulsatile tinnitus
• Hyperacusis (hypersensitivity, pain or distress with environmental
sounds)
• Associated unilateral hearing loss
• Associated sudden onset hearing loss
• Associated vertigo or dizziness
• Headaches or visual symptoms
• Associated neurological symptoms or signs (e.g., facial nerve palsy
or signs of stroke)
• Suicidal ideation related to the tinnitus

Management

Tinnitus tends to improve or resolve over time without any

interventions.

Underlying causes of tinnitus can be treated, such as impacted ear

wax or infection.

Several measures can be used to help improve and manage

symptoms:
• Hearing aids
• Sound therapy (adding background noise to mask the tinnitus)
• Cognitive behavioural therapy
 Vertigo
Vertigo is a descriptive term for a sensation that there is movement
between the patient and their environment. They may feel they are
moving, or that the room is moving. Often this is a horizontal spinning
sensation, similar to how you feel after turning in circles then stopping
abruptly.

Vertigo is often associated with nausea, vomiting, sweating and

feeling generally unwell.

Pathophysiology

The sensory inputs that are responsible for maintaining balance and
posture are:
• Vision
• Proprioception
• Signals from the vestibular system

Vertigo is caused by a mismatch between these sensory inputs.

The vestibular system is the most important sensory system to

understand when learning about vertigo. The vestibular apparatus is
located in the inner ear. It consists of three loops called the semicircular
canals that are filled with a fluid called endolymph. These semicircular
canals are oriented in different directions to detect various movements of
the head. As the head turns, the fluid shifts inside the canals. This fluid
shift is detected by tiny hairs called stereocilia found in a section of the
canal called the ampulla. This sensory input of shifting fluid is transmitted
to the brain by the vestibular nerve and lets the brain know that the head
is moving in a particular direction.
 The vestibular nerve carries signals from the vestibular
apparatus to the vestibular nucleus in the brainstem and
the cerebellum. The vestibular nucleus then sends signals to
the oculomotor, trochlear and abducens nuclei that control eye
movements and the thalamus, spinal cord and cerebellum. The
cerebellum is responsible for coordinating movement throughout the
body. Therefore, the vestibular signals help the central nervous system
coordinate eye movements and other movements throughout the body.

Vertigo can be caused by either a:

• Peripheral problem, usually affecting the vestibular system
• Central problem, usually involving the brainstem or the
cerebellum

Peripheral Vertigo

There are several peripheral (vestibular) causes of vertigo. The four

most common causes to be familiar with are:
• Benign paroxysmal positional vertigo
• Ménière's disease
 • Vestibular neuronitis
• Labyrinthitis

Benign paroxysmal positional vertigo (BPPV) is caused by crystals

of calcium carbonate called otoconia that become displaced into the
semicircular canals. They may be displaced by a viral infection, head
trauma, ageing or without a clear cause. The crystals disrupt the normal
flow through the canals and therefore disrupt the function of the system.
The symptoms are usually positional, because movement is required to
confuse the system. Therefore, attacks of vertigo are triggered by
movement and can last around a minute before the symptoms settle.
Often symptoms occur over several weeks and then resolve, then can
reoccur weeks or months later. A special test called the Dix-Hallpike
manoeuvre can be used to diagnose BPPV.

Ménière's disease is caused by an excessive buildup of endolymph

in the semicircular canals, causing a higher pressure than normal,
disrupting the sensory signals. It causes attacks of hearing loss, tinnitus,
vertigo and a sensation of fullness in the ear. These attacks typically last
several hours before settling. It most often occurs in middle-aged adults
and is not associated with movement. The symptoms are not positional.
Patients will have spontaneous nystagmus during attacks (nystagmus is
discussed in more detail later). Over time, the patient’s hearing will
gradually deteriorate.

Acute vestibular neuronitis describes inflammation of the vestibular

nerve. This is usually attributed to a viral infection. Typically, the history is
of acute onset of vertigo that improves within a few weeks.

Labyrinthitis describes inflammation of the structures of the inner

ear. This is usually attributed to a viral infection. Usually the history is of
acute onset of vertigo that improves within a few weeks. Labyrinthitis can
cause hearing loss, which distinguishes it from vestibular neuronitis.

There are several other peripheral causes of vertigo. These are:

• Trauma to the vestibular nerve
• Vestibular nerve tumours (acoustic neuromas)
• Otosclerosis
 • Hyperviscosity syndromes
• Herpes zoster infection (often with facial nerve weakness and
vesicles around the ear - Ramsay Hunt syndrome)

Central Causes of Vertigo

Pathology that affects the cerebellum or the brainstem can disrupt

the signals from the vestibular system and cause vertigo. The most
common central causes of vertigo are:
• Posterior circulation infarction (stroke)
• Tumour
• Multiple sclerosis
• Vestibular migraine

All the central causes of vertigo will cause sustained, non-positional

vertigo.

Posterior circulation infarction will have a sudden onset and may

be associated with other symptoms, such as ataxia, diplopia, cranial
nerve defects or limb symptoms.

Tumours in the cerebellum or brainstem will have a gradual onset

with associated symptoms of cerebellar or brainstem dysfunction.

Multiple sclerosis may cause relapsing and remitting symptoms, with

other associated features of multiple sclerosis, such as optic neuritis or
transverse myelitis.

Vestibular migraine will cause symptoms lasting minutes to hours,

often associated with visual aura and headache. Attacks may be triggered
by:
• Stress
• Bright lights
• Strong smells
• Certain foods (e.g. chocolate, cheese and caffeine)
• Dehydration
• Menstruation
• Abnormal sleep patterns
 History

When a patient presents with “dizziness”, it is important to first

distinguish between vertigo and lightheadedness. Ask whether the
“room is moving” (vertigo) or whether they feel more of a
lightheadedness.

Ask about symptoms that will help you differentiate between central
and peripheral vertigo. The table below gives a general idea of the
distinguishing features:

Peripheral
Central Vertigo
Vertigo
Gradual onset
Onset Sudden onset
(except stroke)
Short (seconds or
Duration Persistent
minutes)
Hearing loss or Often present
Usually not
tinnitus (except BPPV)
Coordination Intact Impaired
Nausea More severe Mild

Key features that may point to a specific cause are:

• Recent viral illness (labyrinthitis or vestibular neuronitis)
• Headache (vestibular migraine, cerebrovascular accident or brain
tumour)
• Typical triggers (vestibular migraine)
• Ear symptoms, such as pain or discharge (infection)
• Acute onset neurological symptoms (stroke)

Examination

There are four things to examine when assessing a patient presenting

with vertigo:
• Ear examination to look for signs of infection or other pathology
• Neurological examination to assess for central causes of vertigo
(e.g., stroke or multiple sclerosis)
 • Cardiovascular examination to assess for cardiovascular causes
of dizziness (e.g., arrhythmias or valve disease)
• Special tests (see below)

Cerebellar examination is an important part of a full neurological

examination. The components can be remembered with the DANISH
mnemonic:
• D - Dysdiadochokinesia
• A - Ataxic gait (ask the patient to walk heel-to-toe)
• N - Nystagmus (see below for more detail)
• I - Intention tremor
• S - Speech (slurred)
• H - Heel-shin test

Special tests that may be helpful in patients with dizziness or vertigo

include:
• Romberg’s test (screens for problems with proprioception or
vestibular function)
• Dix-Hallpike manoeuvre (to diagnose BPPV)
• HINTS examination (to distinguish between central and peripheral
vertigo)

HINTS Examination

The HINTS examination can be used to distinguish between central

and peripheral vertigo. It stands for:

• HI - Head Impulse
• N - Nystagmus
• TS - Test of Skew

Head Impulse Test

The head impulse test involves the patient sitting upright and fixing
their gaze on the examiner's nose. The examiner holds the patient's head
and rapidly jerks it 10-20 degrees in one direction while the patient
continues looking at the examiner's nose. The head is moved slowly back
to the centre before repeating in the opposite direction. Ensure they have
no neck pain or pathology before performing the test.
 A patient with a normally functioning vestibular system will keep their
eyes fixed on the examiner's nose.

In a patient with an abnormally functioning vestibular system (e.g.,

vestibular neuronitis or labyrinthitis), the eyes will saccade (rapidly move
back and forth) as they eventually fix back on the examiner.

The head impulse test helps diagnose a peripheral cause of vertigo.

It will be normal if the patient has no current symptoms or a central
cause of vertigo.

Nystagmus

Nystagmus can be demonstrated by having the patient look left and

right. The eyes rapidly saccade or oscillate, meaning they shake side to
side as they try to settle into place. A few beats can be normal. Unilateral
horizontal nystagmus is more likely to be a peripheral cause. Bilateral
or vertical nystagmus suggests a central cause.

Test of Skew

The test of skew (also called the alternate cover test) involves the
patient sitting upright and fixing their gaze on the examiner’s nose. The
examiner covers one eye at a time, alternating between covering either
eye. The eyes should remain fixed on the examiner’s nose with no
deviation. If there is a vertical correction when an eye is uncovered (the
eye has drifted up or down and needs to move vertically to fix on the nose
when uncovered), this indicates a central cause of vertigo.

Management

Patients with suspected central vertigo need referral for further

investigation (e.g., CT or MRI head) to establish the cause.

For peripheral vertigo, short-term options for managing symptoms

include:
• Prochlorperazine
• Antihistamines (e.g., cyclizine, cinnarizine and promethazine)
 Betahistine may be used to help reduce the attacks in patients
diagnosed with Ménière's disease.

Epley manoeuvre can be effective in treating BPPV.

Vestibular migraine is usually managed by avoiding triggers and

lifestyle changes (e.g., getting enough sleep and staying hydrated).
Medical management is similar to migraines, with:
• Triptans for the acute symptoms (e.g., sumatriptan)
• Propranolol, topiramate or amitriptyline to prevent attacks

The DVLA guide for medical professionals (updated March 2021)

states that patients must not drive and must inform the DVLA if they are
liable to “sudden and unprovoked or unprecipitated episodes of disabling
dizziness”.
 Benign Paroxysmal Positional Vertigo
Benign paroxysmal positional vertigo (BPPV) is a common cause of
recurrent episodes of vertigo triggered by head movement. It is a
peripheral cause of vertigo, meaning the problem is located in the inner
ear rather than the brain. It is more common in older adults.

Presentation

A variety of head movements can trigger attacks of vertigo. A common

trigger is turning over in bed. Symptoms settle after around 20 - 60
seconds, and patients are asymptomatic between attacks. Often
episodes occur over several weeks and then resolve, but can reoccur
weeks or months later.
BPPV does not cause hearing loss or tinnitus.

Pathophysiology

BPPV is caused by crystals of calcium

carbonate called otoconia that become displaced into the semicircular
canals. This occurs most often in the posterior semicircular canal.
They may be displaced by a viral infection, head trauma, ageing or
without a clear cause.
 The crystals disrupt the normal flow of endolymph through the
canals, confusing the vestibular system. Head movement creates the flow
of endolymph in the canals, triggering episodes of vertigo.

Dix-Hallpike Manoeuvre

The Dix-Hallpike manoeuvre can be used to diagnose BPPV (Dix for

Dx - diagnosis). It involves moving the patient’s head in a way that
causes endolymph to flow through the semicircular canals, triggering
vertigo in patients with BPPV. Check the patient can do the manoeuvre
safely before performing it, for example, ensuring they have no neck pain
or pathology.

To perform the manoeuvre:

• The patient sits upright on a flat examination couch with their head
turned 45 degrees to one side (turned to the right to test the right ear
and left to test the left ear)
 • Support the patient’s head to stay in the 45 degree position while
rapidly lowering the patient backwards until their head is hanging off
the end of the couch, extended 20-30 degrees
• Hold the patient’s head still, turned 45 degrees to one side and
extended 20-30 degrees below the level of the couch
• Watch the eyes closely for 30-60 seconds, looking for nystagmus
• Repeat the test with the head turned in the other direction

In patients with BPPV, the Dix-Hallpike manoeuvre will trigger

rotational nystagmus and symptoms of vertigo. The eye will have
rotational beats of nystagmus towards the affected ear (clockwise with left
ear and anti-clockwise for right ear BPPV).

Epley Manoeuvre

The Epley manoeuvre can be used to treat BPPV. The idea is to

move the crystals in the semicircular canal into a position that does not
disrupt endolymph flow.

To perform the manoeuvre:

• Follow the steps of the Dix-Hallpike manoeuvre, having the patient
go from an upright position with their head rotated 45 degrees (to the
affected side) down to a lying position with their head extended off
the end of the bed, still rotated 45 degrees
• Rotate the patient’s head 90 degrees in the opposite direction, past
the central position
• Have the patient roll onto their side so their head rotates a further
90 degrees in the same direction
• Have the patient sit up sideways with the legs off the side of the
couch
• Position the head in the central position with the neck flexed 45
degrees, with the chin towards the chest
• At each stage, support the patient’s head in place for 30 seconds
and wait for any nystagmus or dizziness to settle

TOM TIP: Watch videos of the Dix-Hallpike and Epley

manoeuvres and practice performing them on your friends. It is
worth remembering the names, indications and interpretation, which
may be tested in your MCQ exams. I would be surprised if you are
asked to perform the manoeuvres in your OSCEs. However, it is
worth learning how to perform them as they are not too difficult, and
you can impress patients, friends, relatives or seniors if you can
perform them at will.

Brandt-Daroff Exercises

Brandt-Daroff exercises can be performed by the patient at home to

improve the symptoms of BPPV. These involve sitting on the end of a bed
and lying sideways, from one side to the other, while rotating the head
slightly to face the ceiling. The exercises are repeated several times a day
until symptoms improve.
 Vestibular Neuronitis
Vestibular neuronitis describes inflammation of the vestibular nerve.
This is usually attributed to a viral infection.

Pathophysiology

The inner ear contains the bony labyrinth, a complex bony structure
containing fluids (perilymph and endolymph). The inner ear is
comprised of three parts:
• Semicircular canals
• Vestibule (middle section)
• Cochlea

The semicircular canals and otolith organs (utricle and saccule)

within the vestibule are responsible for detecting movement of the head.
Together they form the vestibular system:
• The semicircular canals detect rotation of the head
• The otolith organs detect gravity and linear acceleration

The cochlea is responsible for hearing.

The vestibular nerve transmits signals from the vestibular system

(the semicircular canals and vestibule) to the brain to help with
balance. The cochlear nerve transmits signals from the cochlea to
provide hearing. Together they form the vestibulocochlear nerve (the
8th cranial nerve).

Vestibular neuronitis refers to inflammation of the vestibular

nerve. A viral infection may trigger this inflammation. It distorts the signals
travelling from the vestibular system to the brain, confusing the signal
required to sense movements of the head. This results in episodes of
vertigo, where the brain thinks the head is moving when it is not.

Presentation
 Typically, the history involves the acute onset of vertigo. In addition,
there may be a history of a recent viral upper respiratory tract
infection.

Symptoms are most severe for the first few days. Initially, vertigo may
be constant, after which it is triggered or worsened by head movement. It
is often associated with:
• Nausea and vomiting (may be severe)
• Balance problems

It is essential to differentiate between peripheral (inner ear) and

central (brain) causes when a patient presents with vertigo. Any
neurological signs or symptoms should make you consider a central
cause of vertigo rather than vestibular neuronitis. This may require urgent
management, particularly if posterior circulation infarction (stroke) is
suspected.

TOM TIP: Tinnitus and hearing loss are not features of vestibular
neuronitis, as the cochlea and cochlear nerve are not affected. If
tinnitus and hearing loss are also present, consider labyrinthitis or
Ménière's disease as differential diagnoses. You can remember this
with:
• Labyrinthitis – Loss of hearing
• Neuronitis – No loss of hearing

The Head Impulse Test

The head impulse test can be used to diagnose peripheral causes of

vertigo, resulting from problems with the vestibular system (e.g.,
vestibular neuronitis or labyrinthitis).

The head impulse test involves the patient sitting upright and fixing
their gaze on the examiner's nose. The examiner holds the patient's head
and rapidly jerks it 10-20 degrees in one direction while the patient
continues looking at the examiner's nose. The head is slowly moved back
to the centre before repeating in the opposite direction. Ensure they have
no neck pain or pathology before performing the test.
 A patient with a normally functioning vestibular system will keep their
eyes fixed on the examiner's nose.

In a patient with an abnormally functioning vestibular system (e.g.,

vestibular neuronitis or labyrinthitis), the eyes will saccade (rapidly move
back and forth) as they eventually fix back on the examiner.

The head impulse test helps diagnose a peripheral cause of vertigo.

It will be normal if the patient has no current symptoms or a central
cause of vertigo.

Management

The management here is adapted from the NICE clinical knowledge

summaries (updated 2017). Always check local and national guidelines
when treating patients.

Patients may need admission if they are becoming dehydrated due to

severe nausea and vomiting.

For peripheral vertigo, short-term options for managing symptoms

include:
• Prochlorperazine
• Antihistamines (e.g., cyclizine, cinnarizine and promethazine)

NICE advise that symptomatic treatment can be used for up to 3 days.

Extended use may slow down the recovery.

NICE also recommend referral if the symptoms do not improve after 1

week or completely resolve after 6 weeks, as they may require further
investigation or vestibular rehabilitation therapy (VRT).

Prognosis

Symptoms are most severe for the first few days, after which they
gradually resolve over the following 2-6 weeks. Benign paroxysmal
positional vertigo (BPPV) may develop after vestibular neuronitis.
 Labyrinthitis
Labyrinthitis refers to inflammation of the bony labyrinth of the inner
ear, including the semicircular canals, vestibule (middle section) and
cochlea. The inflammation is usually attributed to a viral upper
respiratory tract infection.

Rarely labyrinthitis can be caused by a bacterial infection. This may be

an inflammatory response to a nearby infection or the result of bacteria or
bacterial toxins entering the labyrinth. It is usually secondary to otitis
media or meningitis.

Presentation

Labyrinthitis presents with acute onset vertigo, similarly to vestibular

neuronitis.

Unlike vestibular neuronitis, labyrinthitis can also be associated with:

• Hearing loss
• Tinnitus

Patients may have symptoms associated with the causative virus,

such as a cough, sore throat and blocked nose.

Diagnosis

A clinical diagnosis is based on history and examination findings. It

is important to exclude a central cause of the vertigo.

The head impulse test can be used to diagnose peripheral causes of

vertigo, resulting from problems with the vestibular system (e.g.,
vestibular neuronitis or labyrinthitis).

Management

Management is the same as with vestibular neuronitis, with supportive

care and short-term use (up to 3 days) of medication to suppress the
symptoms. Options for managing symptoms are:
• Prochlorperazine
• Antihistamines (e.g., cyclizine, cinnarizine and promethazine)

Antibiotics are used to treat bacterial labyrinthitis. The underlying

infection (e.g., otitis media or meningitis) needs appropriate treatment.

Patients rarely have lasting symptoms, including permanent hearing

impairment. This is more common after bacterial labyrinthitis, particularly
associated with meningitis.

TOM TIP: Remember hearing loss as a key complication of

meningitis. All patients with meningitis are offered audiology
assessment as soon as they have recovered to assess for hearing
impairment. This complication comes up often in exams and is
worth remembering.
 Ménière's Disease
Ménière's disease is a long-term inner ear disorder that causes
recurrent attacks of vertigo, and symptoms of hearing loss, tinnitus and
a feeling of fullness in the ear.

TOM TIP: Remember the typical triad of symptoms in Ménière's

disease, as this is commonly tested in exams:
• Hearing loss
• Vertigo
• Tinnitus

Pathophysiology

Ménière's disease is associated with the excessive buildup of

endolymph in the labyrinth of the inner ear, causing a higher pressure
than normal and disrupting the sensory signals. This increased pressure
of the endolymph is called endolymphatic hydrops.

Presentation

The typical patient is a 40-50 year old, presenting with unilateral

episodes of vertigo, hearing loss, and tinnitus.

Vertigo in Ménière's disease comes in episodes. These last for 20

minutes to several hours before settling. These episodes can come in
clusters over several weeks, followed by prolonged periods (often
months) without vertigo symptoms. Vertigo is not triggered by movement
or posture.

Hearing loss in Ménière's disease typically fluctuates at first,

associated with vertigo attacks, then gradually becomes more permanent.
It is sensorineural hearing loss, generally unilateral and affects low
frequencies first.

Tinnitus initially occurs with episodes of vertigo before eventually

becoming more permanent. It is usually unilateral.
 Other symptoms can include:
• A sensation of fullness in the ear
• Unexplained falls (“drop attacks”) without loss of consciousness
• Imbalance, which can persist after episodes of vertigo resolve

Spontaneous nystagmus may be seen during an acute attack. This

is usually in one direction (unidirectional).

Diagnosis

Diagnosis of Ménière's disease is clinical, based on the signs and

symptoms. It will be made by an ear, nose and throat (ENT) specialist.

Patients will need an audiology assessment to evaluate their hearing

loss.

Management

Management involves:
• Managing symptoms during an acute attack
• Prophylactic medication to reduce the frequency of attacks

For acute attacks, short-term options for managing symptoms include:

• Prochlorperazine
• Antihistamines (e.g., cyclizine, cinnarizine and promethazine)

Prophylaxis is with:
• Betahistine
 Acoustic Neuroma
Acoustic neuromas are benign tumours of the Schwann cells that
surround the auditory nerve (vestibulocochlear nerve) that innervates
the inner ear.

They are also called vestibular schwannomas, as they originate

from the Schwann cells. Schwann cells are found in the peripheral
nervous system and provide the myelin sheath around neurones.

They occur at the cerebellopontine angle and are sometimes

referred to as cerebellopontine angle tumours.

Acoustic neuromas are usually unilateral. Bilateral acoustic

neuromas are associated with neurofibromatosis type II.
 TOM TIP: Bilateral acoustic neuromas almost certainly indicate
neurofibromatosis type II. This is a popular association in exams, so
worth remembering.

Presentation

The typical patient is a 40-60 year old presenting with a gradual onset
of:
• Unilateral sensorineural hearing loss (often the first symptom)
• Unilateral tinnitus
• Dizziness or imbalance
• A sensation of fullness in the ear

They can also be associated with a facial nerve palsy if the tumour
grows large enough to compress the facial nerve.

Investigations

Audiometry is used to assess hearing loss.

Brain imaging (MRI or CT) is used to establish the diagnosis and

features of the tumour. MRI provides more detail than CT.

Management

ENT specialist management options include:

• Conservative management with monitoring may be used if there
are no symptoms, or treatment is inappropriate
• Surgery to remove the tumour (partial or total removal)
• Radiotherapy to reduce the growth

Notable risks associated with treatment are:

• Vestibulocochlear nerve injury, with permanent hearing loss or
dizziness
• Facial nerve injury, with facial weakness
 Cholesteatoma
A cholesteatoma is an abnormal collection of squamous epithelial
cells in the middle ear. It is non-cancerous but can invade local tissues
and nerves and erode the bones of the middle ear. It can predispose to
significant infections.

Confusingly, cholesteatoma has nothing to do with cholesterol or a

tumour.

Pathophysiology

The pathophysiology is not fully understood. Squamous epithelial

cells originate from the outer surface of the tympanic membrane. The
main theory is that negative pressure in the middle ear, caused by
Eustachian tube dysfunction, causes a pocket of the tympanic
membrane to retract into the middle ear. Essentially, a small area of the
tympanic membrane gets sucked inwards. The squamous epithelial cells
of this pocket continue to proliferate and grow into the surrounding space,
bones and tissues. It can damage the ossicles (the tiny bones of the
middle ear involved in hearing), resulting in permanent hearing loss.

Presentation

The typical presenting symptoms are:

• Foul discharge from the ear
• Unilateral conductive hearing loss

As the cholesteatoma continues to expand into the surrounding

spaces and tissues, further symptoms may develop, including:
• Infection
• Pain
• Vertigo
• Facial nerve palsy
 Otoscopy can show an abnormal build-up of whitish debris or crust in
the upper tympanic membrane. However, it may not be possible to
visualise the eardrum if discharge or wax are blocking the canal.

Management

A CT head can be used to confirm the diagnosis and plan for surgery.
MRI may help assess invasion and damage to local soft tissues.

Treatment involves surgical removal of the cholesteatoma.

 Facial Nerve Palsy
Facial nerve palsy refers to isolated dysfunction of the facial nerve.
This typically presents with a unilateral facial weakness. It is important
to understand some basics about the pathway and function of the facial
nerve.

Facial Nerve Pathway

The facial nerve exits the brainstem at the cerebellopontine angle.

On its journey to the face, it passes through the temporal
bone and parotid gland.

It then divides into five branches that supply different areas of the
face:
• Temporal
• Zygomatic
• Buccal
• Marginal mandibular
• Cervical
 Facial Nerve Function

There are three functions of the facial nerve: motor, sensory and
parasympathetic.

Motor

It supplies the muscles of facial expression, the stapedius in the

inner ear and the posterior digastric, stylohyoid and platysma
muscles in the neck.

Sensory

It carries taste from the anterior 2/3 of the tongue.

 Parasympathetic

It provides the parasympathetic supply to the:

• Submandibular and sublingual salivary glands
• Lacrimal gland (stimulating tear production)

Upper Versus Lower Motor Neurone Lesion

A common exam task is to distinguish between an upper motor

neurone and lower motor neurone facial nerve palsy. It is essential to
make this distinction because, in a patient with a new-onset upper motor
neurone facial nerve palsy, you should be referring immediately for a
suspected stroke. In contrast, patients with a lower motor neurone facial
nerve palsy can be managed with less urgency.

Each side of the forehead has upper motor neurone

innervation by both sides of the brain. However, each side of the
forehead only has lower motor neurone innervation from one side of
the brain.

In an upper motor neurone lesion, the forehead will be spared,

and the patient can move their forehead on the affected side.

In a lower motor neurone lesion, the forehead will NOT be spared,

and the patient cannot move their forehead on the affected side.

You can differentiate between an upper and lower motor neurone

lesion by asking the patient to raise their eyebrows. If they can raise both
eyebrows and wrinkle both sides of the forehead, the patient has an
upper motor neurone lesion. If the eyebrow on the affected side cannot
be raised and the forehead remains smooth, the patient has a lower
motor neurone lesion.
 Upper Motor Neurone Lesions

Unilateral upper motor neurone lesions occur in:

• Cerebrovascular accidents (strokes)
• Tumours

Bilateral upper motor neurone lesions are rare. They may occur in:
• Pseudobulbar palsies
• Motor neurone disease

Bell’s Palsy

Bell’s palsy is a relatively common condition. It is idiopathic, meaning

there is no apparent cause. It presents as a unilateral lower motor
neurone facial nerve palsy. The majority of patients fully recover over
several weeks, but recovery may take up to 12 months. A third are left
with some residual weakness.

If patients present within 72 hours of developing symptoms, NICE

clinical knowledge summaries (updated 2019) recommend considering
prednisolone as treatment, either:
• 50mg for 10 days
• 60mg for 5 days followed by a 5-day reducing regime, dropping the
dose by 10mg per day
 Patients also require lubricating eye drops to prevent the eye on the
affected side from drying out and being damaged. If they develop pain in
the eye, they need an ophthalmology review for exposure keratopathy.
The eye can be taped closed at night.

Ramsay-Hunt Syndrome

Ramsay-Hunt syndrome is caused by the herpes zoster virus. It

presents as a unilateral lower motor neurone facial nerve palsy. Patients
stereotypically have a painful and tender vesicular rash in the ear canal,
pinna and around the ear on the affected side. This rash can extend to the
anterior two-thirds of the tongue and hard palate.

Treatment should ideally be initiated within 72 hours. Treatment is

with:
• Prednisolone
• Aciclovir

Patients also require lubricating eye drops.

TOM TIP: Ramsay-Hunt syndrome is a very popular presentation

in MCQ exams. Look out for that patient with a facial nerve palsy and
vesicular rash around their ear.

Other Causes of Lower Motor Neurone Facial Nerve Palsy

Infection:
• Otitis media
• Malignant otitis externa
• HIV
• Lyme disease

Systemic disease:
• Diabetes
• Sarcoidosis
• Leukaemia
• Multiple sclerosis
• Guillain–Barré syndrome
Tumours:
• Acoustic neuroma
• Parotid tumour
• Cholesteatoma

Trauma:
• Direct nerve trauma
• Damage during surgery
• Base of skull fractures
 Nosebleeds
Nosebleeds are also known as epistaxis. Bleeding usually originates
from Kiesselbach’s plexus, which is located in Little’s area. This is an
area of the nasal mucosa at the front of the nasal cavity that contains a
lot of blood vessels. When the mucosa is disrupted and the blood vessels
are exposed, they become prone to bleeding.

TOM TIP: Little’s area (the area most affected by Little fingers
picking noses) is a popular topic in exams. Remember the name of
this area as examiners like to ask, “what is the most likely location
of the bleeding?”

Presentation

Nosebleeds are common in young children and older adults. They can
be triggered by:
• Nose picking
• Colds
 • Sinusitis
• Vigorous nose-blowing
• Trauma
• Changes in the weather
• Coagulation disorders (e.g., thrombocytopenia or Von Willebrand
disease)
• Anticoagulant medication (e.g., aspirin, DOACs or warfarin)
• Snorting cocaine
• Tumours (e.g., squamous cell carcinoma)

When a patient swallows blood during a nosebleed, they may present

with vomiting blood.

Bleeding is usually unilateral. Bleeding from both nostrils may

indicate bleeding posteriorly in the nose. Posterior bleeding presents a
higher risk of aspiration of blood.

Management

Nosebleeds will usually resolve without needing any medical

assistance. Recurrent and significant nosebleeds might require further
investigation to look for an underlying cause, such as thrombocytopenia
or clotting disorders.

You may have to advise patients on how to manage a nosebleed in an

exam:
• Sit up and tilt the head forwards (tilting the head backwards is not
advised as blood will flow towards the airway)
• Squeeze the soft part of the nostrils together for 10 - 15 minutes
• Spit out any blood in the mouth, rather than swallowing

When bleeding does not stop after 10 - 15 minutes, the nosebleed is

severe, bleeding is from both nostrils, or the patient is haemodynamically
unstable, hospital admission may be required. Treatment options are:
• Nasal packing using nasal tampons or inflatable packs
• Nasal cautery using silver nitrate sticks

After treating an acute nosebleed, consider prescribing

Naseptin nasal cream (chlorhexidine and neomycin) four times daily
for 10 days to reduce any crusting, inflammation and infection. This is
contraindicated in peanut or soya allergy.
 Sinusitis
Sinusitis refers to inflammation of the paranasal sinuses in the face.
This is usually accompanied by inflammation of the nasal cavity and can
be referred to as rhinosinusitis. It is very common.

Sinusitis can be:

• Acute (less than 12 weeks)
• Chronic (more than 12 weeks)

Basic Anatomy

The paranasal sinuses are hollow spaces within the bones of the
face, arranged symmetrically around the nasal cavity. They produce
mucous and drain into the nasal cavities via holes called ostia. Blockage
of the ostia prevents drainage of the sinuses, resulting in sinusitis.

There are four sets of paranasal sinuses:

• Frontal sinuses (above the eyebrows)
• Maxillary sinuses (either side of the nose below the eyes)
• Ethmoid sinuses (in the ethmoid bone in the middle of the nasal
cavity)
• Sphenoid sinuses (in the sphenoid bone at the back of the nasal
cavity)
 Causes

Inflammation of the sinuses can be caused by:

• Infection, particularly following viral upper respiratory tract
infections
• Allergies, such as hayfever (with allergic rhinitis)
• Obstruction of drainage, for example, due to a foreign body, trauma
or polyps
• Smoking

Patients with asthma are more likely to suffer from sinusitis.

Presentation

The typical presentation of acute sinusitis is following a recent viral

upper respiratory tract infection, presenting with:
• Nasal congestion
• Nasal discharge
• Facial pain or headache
• Facial pressure
• Facial swelling over the affected areas
• Loss of smell
 Examination may reveal:
• Tenderness to palpation of the affected areas
• Inflammation and oedema of the nasal mucosa
• Discharge
• Fever
• Other signs of systemic infection (e.g., tachycardia)

Chronic sinusitis involves a similar presentation but with a duration

of more than 12 weeks. Chronic sinusitis may be associated with nasal
polyps, which are growths of the nasal mucosa.

Investigations

In most cases, investigations are not necessary. In patients with

persistent symptoms despite treatment, investigations include:
• Nasal endoscopy
• CT scan

Management

This section is a brief outline based on the NICE clinical knowledge

summaries (updated March 2021). Always check the full local and national
guidelines when treating patients.

Patients with systemic infection or sepsis require admission to hospital

for emergency management.

NICE recommend not offering antibiotics to patients with symptoms

for up to 10 days. Most cases are caused by a viral infection and resolve
within 2-3 weeks.

NICE recommend for patients with symptoms that are not improving
after 10 days, the options of:
• High dose steroid nasal spray for 14 days (e.g., mometasone 200
mcg twice daily)
• A delayed antibiotic prescription, used if worsening or not
improving within 7 days (phenoxymethylpenicillin first-line)

Options for chronic sinusitis are:

 • Saline nasal irrigation
• Steroid nasal sprays or drops (e.g., mometasone or fluticasone)
• Functional endoscopic sinus surgery (FESS)

Nasal Spray Technique

Steroid nasal sprays are often misused, which means they will not be
as effective. A good question to ask is, “do you taste the spray at the back
of your throat after using it?” Tasting the spray means it has gone past the
nasal mucosa and will not be as effective.

The technique involves:

• Tilting the head slightly forward
• Using the left hand to spray into the right nostril, and vice versa
(this directs the spray slightly away from the septum)
• NOT sniffing hard during the spray
• Very gently inhaling through the nose after the spray

TOM TIP: It is worth learning and practising how to explain the

use of a steroid nasal spray. You may be asked to explain how to
use a steroid nasal spray in your OSCEs. I probably explain the
technique several times a month in general practice.

Functional Endoscopic Sinus Surgery

Functional endoscopic sinus surgery (FESS) involves using a small

endoscope inserted through the nostrils and sinuses. Instruments are
used to remove or correct any obstructions to the sinuses. Obstruction
may be caused by swollen mucosa, bone, polyps or a deviated septum
(surgery to correct a deviated septum is call septoplasty). Balloons may
be inflated to dilate the opening of the sinuses.

Patients need a CT scan before the procedure to confirm the

diagnosis and assess the structures.
 Nasal Polyps
Nasal polyps are growths of the nasal mucosa that can occur in the
nasal cavity or sinuses. They are often associated with inflammation,
particularly with chronic rhinitis. They grow slowly and gradually obstruct
the nasal passage.

Polyps are usually bilateral. Unilateral nasal polyps are a red flag and
should raise suspicions of tumours.

TOM TIP: If you remember one thing about nasal polyps,

remember that unilateral polyps are concerning for malignancy and
require a specialist referral for assessment.

Associations

Nasal polyps are associated with several conditions:

• Chronic rhinitis or sinusitis
• Asthma
• Samter’s triad (nasal polyps, asthma and aspirin
intolerance/allergy)
• Cystic fibrosis
• Eosinophilic granulomatosis with polyangiitis (Churg-Strauss
syndrome)

Presentation

Nasal polyps may be found on examination in patients presenting

with:
• Chronic rhinosinusitis
• Difficulty breathing through the nose
• Snoring
• Nasal discharge
• Loss of sense of smell (anosmia)
 You can examine the nose with a nasal speculum, which holds the
nostrils open. Alternatively, you can use an otoscope with a large
speculum attached. A specialist can perform nasal endoscopy to
visualise the nasal cavity in detail to assess any polyps.

Nasal polyps appear as round pale grey/yellow growths on the

mucosal wall.

Management

Unilateral polyps should be referred for specialist assessment to

exclude malignancy.

Medical management involves intranasal topical steroid drops or

spray.

Surgical management is used where medical treatment fails. This

involves removing the polyps:
• Intranasal polypectomy is used where the polyps are visible close
to the nostrils
• Endoscopic nasal polypectomy is used where the polyps are
further inside the nose or in the sinuses
 Obstructive Sleep Apnoea
Obstructive sleep apnoea is caused by collapse of the pharyngeal
airway. It is characterised by episodes of apnoea during sleep, where the
person stops breathing periodically for up to a few minutes. The partner
usually reports this happening, and the patient is unaware of the
episodes.

Risk Factors

• Middle age
• Male
• Obesity
• Alcohol
• Smoking

Features
 • Episodes of apnoea during sleep (often reported by their partner)
• Snoring
• Morning headache
• Waking up unrefreshed from sleep
• Daytime sleepiness
• Concentration problems
• Reduced oxygen saturation during sleep

Severe cases can cause hypertension, heart failure and can

increase the risk of myocardial infarction and stroke.

Epworth Sleepiness Scale

The Epworth Sleepiness Scale is used to assess symptoms of

sleepiness associated with obstructive sleep apnoea.

TOM TIP: If interviewing someone you suspect has obstructive

sleep apnoea, ask about daytime sleepiness and occupation.
Daytime sleepiness is a crucial feature that should make you
suspect obstructive sleep apnoea. Patients that need to be fully alert
for work, for example, heavy goods vehicle operators, require an
urgent referral and may need amended work duties whilst awaiting
assessment and treatment.

Management

Patients with obstructive sleep apnoea require referral to an ENT

specialist or a specialist sleep clinic to perform sleep studies. This
involves the patient sleeping in a laboratory whilst staff monitor their
oxygen saturation, heart rate, respiratory rate and breathing to establish
any episodes of apnoea and the extent of their snoring.

The first step in management is to correct reversible risk factors by

advising them to stop drinking alcohol, stop smoking and lose weight.

The next step is to use a continuous positive airway pressure

(CPAP) machine that provides continuous pressure to maintain the
patency of the airway.
 Surgery is another option. This involves quite significant surgical
reconstruction of the soft palate and jaw. The most common procedure is
called a uvulopalatopharyngoplasty (UPPP).
 Tonsillitis
Tonsillitis refers to inflammation of the tonsils.

The most common cause of tonsillitis is a viral infection. Viral

infections do not require or respond to antibiotics.

The most common cause of bacterial tonsillitis is group A

streptococcus (Streptococcus pyogenes). This can be effectively
treated with penicillin V (phenoxymethylpenicillin). The second most
common bacterial cause of tonsillitis is Streptococcus pneumoniae.

Other causes:
• Haemophilus influenzae
• Moraxella catarrhalis
• Staphylococcus aureus

Waldeyer’s Tonsillar Ring

In the pharynx, at the back of the throat, there is a ring of lymphoid

tissue. There are six areas of lymphoid tissue in Waldeyer's ring,
comprising of the adenoids, tubal tonsils, palatine tonsils and
the lingual tonsil. The palatine tonsils are the ones typically infected and
enlarged in tonsillitis. These are the tonsils on either side at the back of
the throat.

Presentation

A typical presentation of acute tonsillitis is with:

• Sore throat
• Fever (above 38°C)
• Pain on swallowing

Examination of the throat will reveal red, inflamed and enlarged

tonsils, with or without exudates. Exudates are small white patches of
pus on the tonsils.
 There may be anterior cervical lymphadenopathy, which refers to
swollen, tender lymph nodes in the anterior triangle of the neck (anterior
to the sternocleidomastoid muscle and below the mandible). The
tonsillar lymph nodes are just behind the angle of the mandible
(jawbone).

Centor Criteria

The Centor criteria can be used to estimate the probability that

tonsillitis is due to bacterial infection and will benefit from antibiotics.

A score of 3 or more gives a 40 – 60 % probability of bacterial

tonsillitis, and it is appropriate to offer antibiotics. A point is given if each
of the following features are present:
• Fever over 38ºC
• Tonsillar exudates
• Absence of cough
• Tender anterior cervical lymph nodes (lymphadenopathy)

FeverPAIN Score

The FeverPAIN score is an alternative to the Centor criteria. A score of

2 - 3 gives a 34 - 40% probability, and 4 - 5 gives a 62 - 65% probability of
bacterial tonsillitis:
• Fever during previous 24 hours
• P - Purulence (pus on tonsils)
• A - Attended within 3 days of the onset of symptoms
• I - Inflamed tonsils (severely inflamed)
• N - No cough or coryza

Management

Consider admission if:

• Immunocompromised
• Systemically unwell
• Dehydrated
• Stridor
• Respiratory distress
 • Peritonsillar abscess
• Cellulitis

When tonsillitis is the most likely diagnosis, calculate the Centor

criteria or FeverPAIN score.

Educate patients with likely viral tonsillitis and give safety net advice
about when to seek medical advice. Advise simple analgesia with
paracetamol and ibuprofen to control pain and fever. NICE clinical
knowledge summaries suggest advising patients to return if the pain has
not settled after 3 days or the fever rises above 38.3ºC. Starting
antibiotics or an alternative diagnosis should be considered.

Consider prescribing antibiotics if the Centor score is ≥ 3, or

the FeverPAIN score is ≥ 4. Also, consider antibiotics if they are at risk of
more severe infections, such as young infants, immunocompromised
patients, those with significant co-morbidities, or a history of rheumatic
fever.

Delayed prescriptions can be considered. This involves educating

patients or parents about the likely viral nature of the sore throat and
providing a prescription to be collected only if the symptoms worsen or do
not improve in the next 2 – 3 days.

Choice of Antibiotic

Penicillin V (also called phenoxymethylpenicillin) for a 10-day

course is typically first-line. It has a relatively narrow spectrum of activity
and is effective against Streptococcus pyogenes.

Clarithromycin is the usual first-line choice in true penicillin allergy.

Complications

• Peritonsillar abscess, also known as quinsy

• Otitis media, if the infection spreads to the inner ear
• Scarlet fever
• Rheumatic fever
• Post-streptococcal glomerulonephritis
• Post-streptococcal reactive arthritis
 Quinsy
Quinsy is the common name for a peritonsillar abscess. Peritonsillar
abscess arises when there is a bacterial infection with trapped pus,
forming an abscess in the region of the tonsils.

Peritonsillar abscess is a complication of untreated or partially

treated tonsillitis, although it can arise without tonsillitis.

Quinsy can occur just as frequently in teenagers and adults as it does

in children, unlike tonsillitis which is much more common in children.

Presentation

Patients present with similar symptoms to tonsillitis:

• Sore throat
• Painful swallowing
• Fever
• Neck pain
• Referred ear pain
• Swollen tender lymph nodes

Additional symptoms that can indicate a peritonsillar abscess include:

• Trismus, which refers to when the patient is unable to open their
mouth
• Change in voice due to the pharyngeal swelling, described in
textbooks as a “hot potato voice”
• Swelling and erythema in the area beside the tonsils

Bacteria

Quinsy is usually due to a bacterial infection. The most common

organism is streptococcus pyogenes (group A strep), but it is also
commonly caused by staphylococcus aureus and haemophilus
influenzae.
 Management

Patients should be referred into hospital under the care of the ENT
team for incision and drainage of the abscess under general
anaesthetic.

Quinsy typically has an underlying bacterial cause. Therefore,

antibiotics are appropriate before and after surgery. A broad-spectrum
antibiotic such as co-amoxiclav would be an appropriate choice to cover
the common causes, but local guidelines will guide antibiotic selection
according to local bacterial resistance.

Some ENT surgeons give steroids (i.e. dexamethasone) to settle

inflammation and help recovery, although this is not universal.
 Tonsillectomy
Tonsillectomy is the name for the surgical removal of the tonsils.
Removing the tonsils prevents further episodes of tonsillitis, although
patients can still get a sore throat from other causes (e.g., pharyngitis).
The procedure is performed under a general anaesthetic as a day case.
Patients can usually go home the same day after a period of observation.

Indications

The SIGN guidelines (2010) give the indications for tonsillectomy. The
number of episodes of acute sore throat they specify for a tonsillectomy
are:
• 7 or more in 1 year
• 5 per year for 2 years
• 3 per year for 3 years

Other indications are:

• Recurrent tonsillar abscesses (2 episodes)
• Enlarged tonsils causing difficulty breathing, swallowing or snoring

Complications

• Sore throat where the tonsillar tissue has been removed (this can
last 2 weeks)
• Damage to teeth
• Infection
• Post-tonsillectomy bleeding
• Risks associated with a general anaesthetic

Post Tonsillectomy Bleeding

Post tonsillectomy bleeding is the main significant complication after a

tonsillectomy. Significant bleeding can occur in up to 5% of patients who
have had a tonsillectomy. It can happen up to 2 weeks after the operation.
Bleeding can be severe and, in rare cases, life-threatening, due to
aspiration of blood.

Management:
• Call the ENT registrar and get them involved early
• Get IV access and send bloods including an FBC, clotting screen,
group and save and crossmatch
• Keep the patient calm and give adequate analgesia
• Sit them up and encourage them to spit out the blood rather than
swallowing
• Make the patient nil by mouth in case an anaesthetic and
operation is required
• IV fluids for maintenance and resuscitation, if required

If there is severe bleeding or airway compromise, call an anaesthetist.

Intubation may be required.

Before going back to theatre there are two options for stopping less
severe bleeds:
• Hydrogen peroxide gargle
• Adrenalin soaked swab applied topically
 Neck Lumps
Neck lumps are a relatively common presentation, particularly in
primary care and exams. Being able to identify and manage the different
causes is helpful.

Basic Anatomy

There are three areas when describing the location of a neck lump:
• Anterior triangle
• Posterior triangle
• Midline (vertically along the centre of the neck)

The two triangles are on either side of the sternocleidomastoid

muscle.

The borders of the anterior triangle are:

• Mandible forms the superior border
• Midline of the neck forms the medial border
• Sternocleidomastoid forms the lateral border

The borders of the posterior triangle are:

• Clavicle forms the inferior border
• Trapezius forms the posterior border
• Sternocleidomastoid forms the lateral border

Differential Diagnosis

In adults:
• Normal structures (e.g., a bony prominence)
• Skin abscess
• Lymphadenopathy (enlarged lymph nodes)
• Tumour (e.g., squamous cell carcinoma or sarcoma)
• Lipoma
• Goitre (swollen thyroid gland) or thyroid nodules
• Salivary gland stones or infection
 • Carotid body tumour
• Haematoma (a collection of blood after trauma)
• Thyroglossal cysts
• Branchial cysts

Neck lumps in young children may also be caused by:

• Cystic hygromas
• Dermoid cysts
• Haemangiomas
• Venous malformation

TOM TIP: It is not uncommon for patients to present worried

about a normal bony prominence in the neck. Common areas of
concern are the hyoid bone, mastoid process and transverse
processes of C1.

History

The purpose of taking a history is to gain:

• General information about the symptoms (e.g., when the lump first
appeared and how quickly it has grown)
• Features that suggest or exclude a particular diagnosis (e.g., night
sweats indicating lymphoma)
• Risk factors for that condition (e.g., family history, age and smoking
status)
• General fitness for further investigations and treatment (e.g., co-
morbidities and medications such as anticoagulants)

Examination

When examining a neck lump, the things to establish are:

• Location (anterior triangle, posterior triangle or midline)
• Size
• Shape (oval, round or irregular)
• Consistency (hard, soft or rubbery)
• Mobile or tethered to the skin or underlying tissues
• Skin changes (erythema, tethering or ulceration)
• Warmth (e.g., infection)
 • Tenderness (e.g., infection)
• Pulsatile (e.g., carotid body tumours)
• Movement with swallowing (e.g., thyroid lumps) or sticking their
tongue out (e.g., thyroglossal cysts)
• Transilluminates with light (e.g., branchial cyst)

A general examination can be used to look for signs of the underlying

cause, such as:
• Ear, nose and throat infections (e.g., reactive lymph nodes)
• Weight loss (e.g., malignancy or hyperthyroidism)
• Skin pallor and bruising (e.g., leukaemia)
• Focal chest sounds (e.g., lung cancer)
• Clubbing (e.g., lung cancer)
• Hepatosplenomegaly (e.g., leukaemia)

Neck Lump Red-Flag Referral Criteria

The NICE guidelines on suspected cancer (updated January 2021)

suggest a two week wait referral for:
• An unexplained neck lump in someone aged 45 or above
• A persistent unexplained neck lump at any age

They recommend considering an urgent ultrasound scan in patients

with a lump that is growing in size. This should be within 2 weeks in
patients 25 and older and within 48 hours in patients under 25. They
require a two week wait referral if the ultrasound is suggestive of soft
tissue sarcoma.

TOM TIP: Patients presenting to primary care with symptoms and

signs that are suspicious of cancer require either urgent direct-
access investigations or a two week wait referral. The NICE
guidelines on “suspected cancer: recognition and referral” set out
their recommendations by either the site or the symptom, making it
really easy to quickly look up the referral criteria. There is also a
section for non-specific symptoms, such as unexplained weight
loss, appetite loss and deep vein thrombosis.

Investigations
 Blood tests may be helpful depending on the suspected cause of the
neck lump. Not everyone with a neck lump will require blood tests. The
choice of test will depend on the suspected cause:
• FBC and blood film for leukaemia and infection
• HIV test
• Monospot test or EBV antibodies for infectious mononucleosis
• Thyroid function tests for goitre or thyroid nodules
• Antinuclear antibodies for systemic lupus erythematosus
• Lactate dehydrogenase (LDH) is a very non-specific tumour
marker for Hodgkin’s lymphoma

Imaging may involve:

• Ultrasound (often the first-line investigation for neck lumps)
• CT or MRI scans
• Nuclear medicine scan (e.g., for toxic thyroid nodules or PET
scans for metastatic cancer)

Biopsy may be required to gain a tissue sample (histology) to

establish the exact cause. This may be with:
• Fine needle aspiration cytology - aspirating cells from the lump
using a needle
• Core biopsy - taking a sample of tissue with a thicker needle
• Incision biopsy - cutting out a tissue sample with a scalpel
• Removal of the lump - the entire lump can be removed and
examined

Lymphadenopathy

Lymphadenopathy refers to enlarged lymph nodes. There are a long

list of causes of enlarged lymph nodes, which can be generally grouped
into:
• Reactive lymph nodes (e.g., swelling caused by viral upper
respiratory tract infections, dental infection or tonsillitis)
• Infected lymph nodes (e.g., tuberculosis, HIV or infectious
mononucleosis)
• Inflammatory conditions (e.g., systemic lupus erythematosus or
sarcoidosis)
• Malignancy (e.g., lymphoma, leukaemia or metastasis)
 Enlarged supraclavicular nodes are the most concerning for
malignancy of the cervical lymph nodes. They may be caused by
malignancy in the chest or abdomen and require further investigation.

Features that suggest malignancy are:

• Unexplained (e.g., not associated with an infection)
• Persistently enlarged (particularly over 3cm in diameter)
• Abnormal shape (normally oval shaped where the length is more
than double the width)
• Hard or “rubbery”
• Non-tender
• Tethered or fixed to the skin or underlying tissues
• Associated symptoms, such as night sweats, weight loss, fatigue or
fevers

Infectious Mononucleosis

Infectious mononucleosis is a cause of lymphadenopathy. It is caused

by infection with the Epstein Barr virus (EBV) and most often affects
teenagers and young adults. EBV is found in the saliva of infected
individuals and may be spread by kissing or sharing cups, toothbrushes
and other equipment that transmit saliva.

Infectious mononucleosis presents with:

• Fever
• Sore throat
• Fatigue
• Lymphadenopathy

Mononucleosis can present with an intensely itchy maculopapular

rash in response to amoxicillin or cefalosporins.

The first-line investigation is the Monospot test. It is also possible to

test for IgM (acute infection) and IgG (immunity) to the Epstein Barr
virus.

Management is supportive. Patients should avoid alcohol (risk of liver

impairment) and contact sports (risk of splenic rupture).
 Lymphoma

Lymphomas are a group of cancers that affect the lymphocytes inside

the lymphatic system. These cancerous cells proliferate within the
lymph nodes and cause the lymph nodes to become abnormally large
(lymphadenopathy).

There are two categories of lymphoma: Hodgkin’s lymphoma and

non-Hodgkin’s lymphoma. Hodgkin’s lymphoma is a specific disease
and non-Hodgkins lymphoma encompasses all the other lymphomas.
Hodgkin’s lymphoma is the most likely specific type of lymphoma to
appear in your exams.

Overall, 1 in 5 lymphomas are Hodgkin’s lymphoma. It is caused by

proliferation of lymphocytes. There is a bimodal age distribution with
peaks around aged 20 and 75 years.

Lymphadenopathy is the key presenting symptom. The enlarged

lymph node or nodes might be in the neck, axilla (armpit) or inguinal
(groin) region. They are characteristically non-tender and feel “rubbery”.
Some patients will experience pain in the lymph nodes when they
drink alcohol.

B symptoms are the systemic symptoms of lymphoma:

• Fever
• Weight loss
• Night sweats

The Reed-Sternberg cell is the key finding from a lymph node biopsy
in patients with Hodgkin’s lymphoma.

The Ann Arbor staging system is used for both Hodgkins and non-
Hodgkins lymphoma.

Leukaemia

Leukaemia is the name for cancer of a particular line of the stem cells
in the bone marrow. This causes the unregulated production of certain
types of blood cells. They can be classified depending on how rapidly
they progress (chronic is slow and acute is fast) and the cell line that is
affected (myeloid or lymphoid) to make four main types:
• Acute myeloid leukaemia
• Acute lymphoblastic leukaemia
• Chronic myeloid leukaemia
• Chronic lymphocytic leukaemia

The presentation of leukaemia is quite non-specific. If leukaemia

appears on your list of differentials then the initial investigation is an
urgent full blood count. Some typical features are:
• Fatigue
• Fever
• Pallor due to anaemia
• Petechiae and abnormal bruising due to thrombocytopenia
• Abnormal bleeding
• Lymphadenopathy
• Hepatosplenomegaly

Thyroid Pathology

A goitre refers to generalised swelling of the thyroid gland. A goitre

can be caused by:

• Graves disease (hyperthyroidism)

• Toxic multinodular goitre (hyperthyroidism)
• Hashimoto’s thyroiditis (hypothyroidism)
• Iodine deficiency
• Lithium

Individual lumps can occur in the thyroid due to:

• Benign hyperplastic nodules
• Thyroid cysts
• Thyroid adenomas (benign tumours that can release excessive
thyroid hormone)
• Thyroid cancer (papillary or follicular)
• Parathyroid tumours

Salivary Gland Pathology

 The three salivary gland locations are the:
• Parotid glands
• Submandibular glands
• Sublingual glands

These can enlarge for three main reasons:

• Stones blocking the drainage of the glands through the ducts
(sialolithiasis)
• Infection
• Tumours (benign or malignant)

Carotid Body Tumours

The carotid body is a structure located just above the carotid

bifurcation (where the common carotid splits into the internal and
external carotids). It contains glomus cells, which
are chemoreceptors that detect the oxygen, carbon dioxide and pH of
the blood. Groups of these glomus cells are called paraganglia.

Carotid body tumours are formed by excessive growth of the glomus

cells. They are also called paragangliomas. Most are benign. They
present with a slow-growing lump that is:
• In the upper anterior triangle of the neck (near the angle of the
mandible)
• Painless
• Pulsatile
• Associated with a bruit on auscultation
• Mobile side-to-side but not up and down
 Carotid body tumours may compress nearby cranial nerves:
• Glossopharyngeal (IX)
• Vagus (X)
• Accessory (XI)
• Hypoglossal (XII)

Pressure on the vagus nerve may result in Horner syndrome, with a

triad of:
• Ptosis
• Miosis
• Anhidrosis (loss of sweating)
 A characteristic finding on imaging investigations is splaying
(separating) of the internal and external carotid arteries (lyre sign).

They are mostly treated with surgical removal.

Lipoma

Lipomas are benign tumours of fat (adipose) tissue. They can occur
almost anywhere on the body where there is adipose tissue.

On examination, lipomas are typically:

• Soft
• Painless
• Mobile
• Do not cause skin changes

They are typically treated conservatively with reassurance (after

excluding other pathology). Alternatively, they can be surgically removed.

Thyroglossal Cyst
 During fetal development, the thyroid gland starts at the base of the
tongue. From here, it gradually travels down the neck to the final position
in front of the trachea, beneath the larynx. It leaves a track behind called
the thyroglossal duct, which then disappears. When part of the
thyroglossal duct persists, it can give rise to a fluid-filled cyst. This is
called a thyroglossal cyst.

Ectopic thyroid tissue is a key differential diagnosis, as this

commonly occurs at a similar location.

Thyroglossal cysts occur in the midline of the neck. They are:

 • Mobile
• Non-tender
• Soft
• Fluctuant

Thyroglossal cysts move up and down with movement of the tongue.

This is a key feature that demonstrates a midline neck lump is a
thyroglossal cyst. This occurs due to the connection between the
thyroglossal duct and the base of the tongue.

Ultrasound or CT scan can confirm the diagnosis.

Thyroglossal cysts are usually surgically removed to provide

confirmation of the diagnosis on histology and prevent infections. The
cyst can reoccur after surgery unless the entire thyroglossal duct is
removed.

The main complication is infection of the cyst, causing a hot, tender

and painful lump.

TOM TIP: Remember the key feature of thyroglossal cysts

moving with movement of the tongue. This is a unique fact that
examiners like to use to test your knowledge. Look out for a
thyroglossal cyst as a differential of a neck lump in your MCQ exam.
If you come across a midline neck lump in a child in your OSCEs,
ask them to stick their tongue out and look for the lump moving
upwards.

Branchial Cyst

A branchial cyst is a congenital abnormality that arises when

the second branchial cleft fails to form properly during fetal
development. This leaves a space surrounded by epithelial tissue in the
lateral aspect of the neck. This space can fill with fluid. This fluid-filled
lump is called a branchial cyst. Branchial cysts arising from the first, third
and fourth branchial clefts are possible, although they are much rarer.
 Branchial cysts present as a round, soft, cystic swelling between the
angle of the jaw and the sternocleidomastoid muscle in the anterior
triangle of the neck. This swelling will transilluminate with light, as the
fluid in the cyst transmits the light throughout the cyst. To transilluminate
the cyst, hold a pen torch flat against the skin and watch as the whole
lump lights up.

Branchial cysts tend to present after the age of 10 years, most

commonly in young adulthood when the cyst becomes noticeable or
infected.

Management of a branchial cyst is either:

• Conservative, without any active intervention, where it is not
causing problems
• Surgical excision where recurrent infections are occurring, there
is diagnostic doubt, or it is causing other problems

TOM TIP: Branchial cysts may appear in exams as a differential

of neck lumps in teenagers or as part of a neck examination in an
OSCE. Remembering the key features will help you differentiate
them in your exams. They are just anterior to the
sternocleidomastoid muscle, round and soft and transilluminate
with light.
 Head and Neck Cancer
Head and neck cancer can affect a variety of locations. They are
usually squamous cell carcinomas arising from the squamous cells of
the mucosa.

Locations

The potential areas affected by head and neck cancer are:

• Nasal cavity
• Paranasal sinuses
• Mouth
• Salivary glands
• Pharynx (throat)
• Larynx (epiglottis, supraglottis, vocal cords, glottis and subglottis)

Head and neck cancers usually spread to the lymph nodes first.
Squamous cell carcinoma cells may be found in an enlarged, abnormal
lymph node (lymphadenopathy), while the original tumour cannot be
found. This is called cancer of unknown primary.

Risk Factors

• Smoking
• Chewing tobacco
• Chewing betel quid (a habit in south-east Asia)
• Alcohol
• Human papillomavirus (HPV), particularly strain 16
• Epstein–Barr virus (EBV) infection

HPV also causes cervical cancer. The HPV vaccine (Gardasil)

protects against strains 6, 11, 16 and 18.

Red Flags
 Presenting symptoms and signs that may indicate head and neck
cancer are:
• Lump in the mouth or on the lip
• Unexplained ulceration in the mouth lasting more than 3 weeks
• Erythroplakia or erythroleukoplakia
• Persistent neck lump
• Unexplained hoarseness of voice
• Unexplained thyroid lump

Management

Management will be guided by the multidisciplinary team (MDT). It

will be dependent on the location, stage and individual patient factors.

Staging usually involves the TNM staging system, grading the

tumour, node involvement and metastases.

Treatment may involve any combination of:

• Chemotherapy
• Radiotherapy
• Surgery
• Targeted cancer drugs (i.e., monoclonal antibodies)
• Palliative care

Cetuximab is an example of a monoclonal antibody used in treating

squamous cell carcinomas of the head and neck. It may also be used to
treat bowel cancer. It targets epidermal growth factor receptors,
blocking the activation of these receptors and inhibiting the growth and
metastasis of the tumour.
 Tongue Conditions
Glossitis

Glossitis refers to an inflamed tongue. The tongue becomes red,

sore and swollen. The papillae of the tongue atrophy (shrink), giving the
tongue a smooth appearance. It is sometimes described as “beefy”.

Causes:
• Iron deficiency anaemia
• B12 deficiency
• Folate deficiency
• Coeliac disease
• Injury or irritant exposure

Management involves correcting the underlying cause.

Angioedema

Angioedema refers to fluid accumulating in the tissues, resulting in

swelling. It can affect a number of areas, such as the limbs, face and lips.
It can affect the tongue, causing the tongue to swell.

The three top causes of angioedema to remember for exams are:

• Allergic reactions
• ACE inhibitors
• C1 esterase inhibitor deficiency (hereditary angioedema)

Oral Candidiasis

Oral candidiasis is also called oral thrush. It refers to an overgrowth of

candida, a type of fungus, in the mouth. This results in white spots or
patches that coat the surface of the tongue and palate.

Several common factors can predispose someone to develop oral

candidiasis:
 • Inhaled corticosteroids (particularly with poor technique, not
using a spacer and not rinsing with water afterwards)
• Antibiotics (disrupt the normal bacterial flora giving candida a
chance to thrive)
• Diabetes
• Immunodeficiency (consider HIV)
• Smoking

Treatment options are:

• Miconazole gel
• Nystatin suspension
• Fluconazole tablets (in severe or recurrent cases)

Geographic Tongue

Geographic tongue is an inflammatory condition where patches of the

tongue's surface lose the epithelium and papillae. The patches form
irregular shapes on the tongue, resembling a map, with countries and
oceans bordering each other. The condition tends to relapse and remit,
with episodes of the abnormal tongue appearance that can last days to
weeks before resolving or changing. The cause of these changes is not
known.

Geographic tongue often occurs without any associations. However, it

can be related to:
• Stress and mental illness
• Psoriasis
• Atopy (asthma, hayfever and eczema)
• Diabetes

Geographic tongue is a benign condition and does not cause any

harmful effects. It does not usually require any treatment. Symptoms such
as discomfort or burning are sometimes treated with topical steroids or
antihistamines.

Strawberry Tongue

A strawberry tongue occurs when the tongue becomes swollen and

red, and the papillae become enlarged, white and prominent.
 The two key causes of a strawberry tongue to remember are:
• Scarlet fever
• Kawasaki disease

Black Hairy Tongue

Black hairy tongue results from decreased shedding (exfoliation)

of keratin from the tongue's surface. The papillae elongate and take on
the appearance of hairs. Bacteria and food cause the dark pigmentation.
This gives the appearance of black hair on the tongue. Patients may also
report sticky saliva and a metallic taste.

Black hairy tongue may be due to dehydration, a dry mouth, poor oral
hygiene and smoking.

Management involves ensuring adequate hydration, gentle brushing

of the tongue and stopping smoking.
 Mouth and Gum Conditions
Leukoplakia

Leukoplakia is characterised by white patches in the mouth, often on

the tongue or inside the cheeks (on the buccal mucosa). It is a
precancerous condition, meaning it increases the risk of squamous cell
carcinoma of the mouth.

The patches are asymptomatic, irregular and slightly raised. They are
fixed in place, meaning they cannot be scraped off.

They may require a biopsy to exclude abnormal cells (dysplasia) or

cancer. Management involves stopping smoking, reducing alcohol intake,
close monitoring and potentially laser removal or surgical excision.

Erythroplakia

Erythroplakia is similar to leukoplakia, except the lesions are red.

Erythroleukoplakia refers to lesions that are a mixture of red and white.
Both erythroplakia and erythroleukoplakia are associated with a high risk
of squamous cell carcinoma and should be referred urgently to exclude
cancer.

Lichen Planus

Lichen planus is an autoimmune condition that causes localised

chronic inflammation of the skin. The skin has shiny, purplish, flat-
topped, raised areas with white lines across the surface
called Wickham’s striae. It usually occurs in patients over 45 and is more
common in women.

Lichen planus can also affect the mucosal membranes, including the
mouth. Often it only affects the mouth.

In the mouth, it can form three patterns:

• Reticular
 • Erosive
• Plaque

A reticular pattern involves a net-like web of white lines called

Wickham’s striae.

Erosive lesions are where the surface layer of the mucosa is eroded,
leaving bright red and sore areas of mucosa.

Plaques are larger continuous areas of white mucosa.

Management involves good oral hygiene, stopping smoking and

topical steroids.

Gingivitis

Gingivitis refers to inflammation of the gums. This can present with

swollen gums, bleeding after brushing, painful gums and bad breath
(halitosis). Gingivitis can lead to periodontitis if not adequately managed.

Periodontitis refers to severe and chronic inflammation of the gums

and the tissues that support the teeth. This often leads to loss of teeth.

Acute necrotising ulcerative gingivitis is a rapid onset of more

severe inflammation of the gums. It presents similarly to gingivitis,
however, it is painful. Anaerobic bacteria usually cause this.

The risk factors for gingivitis are:

• Plaque build-up on the teeth (inadequate brushing)
• Smoking
• Diabetes
• Malnutrition
• Stress

Bacteria live in plaque, damaging the teeth and gums. Hardened

plaque is called tartar.

Patients with gingivitis will be managed by a dentist. Treatment

involves:
 • Good oral hygiene
• Stopping smoking
• Dental hygienist treatment to remove plaque and tartar
• Chlorhexidine mouth wash
• Antibiotics for acute necrotising ulcerative gingivitis (e.g.,
metronidazole)
• Dental surgery if required

Gingival Hyperplasia

Gingival hyperplasia refers to abnormal growth of the gums. The gums

are notably enlarged around the teeth.

Possible causes of gingival hyperplasia include:

• Gingivitis
• Pregnancy
• Vitamin C deficiency (scurvy)
• Acute myeloid leukaemia
• Medications, particularly calcium channel blockers, phenytoin and
ciclosporin

Aphthous Ulcers

Aphthous ulcers are very common, small, painful ulcers of the mucosa
in the mouth. They have a well-circumscribed, punched-out, white
appearance.

Aphthous ulcers commonly occur in otherwise healthy people, with no

underlying cause. They may be triggered by emotional or physical stress,
trauma to the mucosa or particular foods.

They may also be an indication of underlying conditions, notably:

• Inflammatory bowel disease (Crohn’s disease and ulcerative
colitis)
• Coeliac disease
• Behçet disease
• Vitamin deficiency (e.g., iron, B12, folate and vitamin D)
• HIV
 Aphthous ulcers usually heal within 2 weeks. Manageable ulcers do
not require any intervention.

Topical treatments can be used to treat symptoms of aphthous ulcers,

including:
• Choline salicylate (e.g., Bonjela)
• Benzydamine (e.g., Difflam spray)
• Lidocaine

Topical corticosteroids can be used in more severe ulcers. These may

reduce the duration and severity of symptoms. Options include:
• Hydrocortisone buccal tablets applied to the lesion
• Betamethasone soluble tablets applied to the lesion
• Beclomethasone inhaler sprayed directly onto the lesion

The NICE guidelines on suspected cancer (updated January 2021)

recommend a two week wait referral in patients with “unexplained
ulceration” lasting over 3 weeks.
 Orthopaedics
Osteoarthritis
Elective Joint Replacement
Fractures
Hip Fractures
Compartment Syndrome
Osteomyelitis
Sarcoma
Back Pain and Sciatica
Cauda Equina Syndrome
Spinal Stenosis
Meralgia Paresthetica
Trochanteric Bursitis
Meniscal Tears
Anterior Cruciate Ligament Injury
Osgood-Schlatter Disease
Bakers Cyst
Achilles Tendinopathy
Achilles Tendon Rupture
Common Foot Problems
Frozen Shoulder
Rotator Cuff Tears
Shoulder Dislocation
Olecranon Bursitis
Repetitive Strain Injury
Epicondylitis
De Quervain’s Tenosynovitis
Trigger Finger
Dupuytren’s Contracture
Carpal Tunnel Syndrome
Ganglion Cysts
 Osteoarthritis
Osteoarthritis is often described as “wear and tear” in the joints. It is
not an inflammatory condition like rheumatoid arthritis. It occurs in the
synovial joints and results from a combination of genetic factors,
overuse and injury.

Osteoarthritis is thought to result from an imbalance between the

cartilage wearing down and the chondrocytes repairing it, leading to
structural issues in the joint.

Risk factors include obesity, age, occupation, trauma, being female

and family history.

Commonly Affected Joints

• Hips
• Knees
• Sacro-iliac joints
• Distal-interphalangeal (DIP) joints in the hands
• The carpometacarpal (CMC) joint at the base of the thumb
• Wrist
• Cervical spine (cervical spondylosis)

Four Key X-ray Changes (LOSS)

• L - Loss of joint space

• O - Osteophytes (bone spurs)
• S - Subarticular sclerosis (increased density of the bone along the
joint line)
• S - Subchondral cysts (fluid-filled holes in the bone)

X-ray changes do not necessarily correlate with symptoms. Significant

x-ray changes might be found incidentally in someone without symptoms.
Equally, someone with severe symptoms of osteoarthritis may have only
mild changes on an x-ray.
 Presentation

Osteoarthritis presents with joint pain and stiffness. The pain and
stiffness tends to be worse with activity and at the end of the day, in
contrast to inflammatory arthritis, where activity improves symptoms and
the symptoms tend to be worse first thing in the morning. Osteoarthritis
leads to deformity, instability and reduced function of the joint.

General signs of osteoarthritis are:

• Bulky, bony enlargement of the joint
• Restricted range of motion
• Crepitus on movement
• Effusions (fluid) around the joint

TOM TIP: Patients may present with referred pain caused by

arthritis, particularly in the adjacent joints. For example, in patients
presenting with lower back pain or knee pain, consider a problem
with the hip.

Signs in the Hands

• Heberden’s nodes (in the DIP joints)

• Bouchard’s nodes (in the PIP joints)
• Squaring at the base of the thumb (CMC joint)
• Weak grip
• Reduced range of motion

The carpometacarpal joint at the base of the thumb is a saddle joint,

with the thumb's metacarpal bone sat on the trapezius bone, using it like a
saddle. It gets a lot of use from everyday activities, making it very prone to
wear.
 Diagnosis

The NICE guidelines (updated 2020) suggest that a diagnosis can be

made without any investigations if the patient is over 45, has typical pain
associated with activity and has no morning stiffness (or stiffness
lasting under 30 minutes).

Management

The NICE guidelines recommend a holistic approach to managing

patients with osteoarthritis. It is a long-term condition that can be difficult
to manage. Start with patient education about the condition and advise
on lifestyle changes, such as:
• Weight loss if overweight, to reduce the load on the joint
 • Physiotherapy to improve strength and function
• Occupational therapy to support activities and function (e.g.,
special devices and adaptations to the home)
• Orthotics to support activities and function (e.g., knee braces)

The use of analgesia involves a stepwise approach to control

symptoms:

1. Oral paracetamol and topical NSAIDs

2. Add oral NSAIDs (consider co-prescribing a proton pump

inhibitor, such as omeprazole, to protect the stomach)
3. Consider opiates such as codeine

Topical capsaicin (chilli pepper) cream may be helpful, where

available.

Intra-articular steroid injections provide a temporary reduction in

inflammation and improve symptoms.

Joint replacement can be used in severe cases. The hips and knees
are the most commonly replaced joints.

Medication Notes

NSAIDs (e.g., ibuprofen or naproxen) are very effective for

musculoskeletal pain. However, they need to be used with caution,
particularly in older patients and those on anticoagulants, such as aspirin
or DOACs. They are better used intermittently, for a short time to get the
pain under control, rather than continuously. They have several potential
adverse effects, including:
• Gastrointestinal side-effects, such as gastritis and peptic ulcers
(leading to upper GI bleeding)
• Renal side-effects, such as acute kidney injury (e.g., acute tubular
necrosis) or progressive kidney disease
• Cardiovascular side-effects, such as hypertension, heart failure,
myocardial infarction and stroke
• Exacerbating asthma
 Opiates should be used cautiously, as they can have significant side
effects, and patients can develop tolerance, dependence and withdrawal
symptoms. There is minimal evidence that they work for chronic pain.
They often result in patients becoming dependent without benefitting from
pain relief.
 Elective Joint Replacement
The most common joints replaced electively are the hip, knee and
shoulder. The most common indication is osteoarthritis. Most patients
that have elective joint replacements are over 60.

Artificial joints are built to last more than 10-15 years. However, they
may be affected by loosening, wear and dislocation. Some patients
may require further surgery and replacement of the artificial joint at some
point.

Joint replacement is major surgery. Patients need to have the

alternatives discussed before deciding to undergo surgery. The other
options include analgesia, steroid injections and physiotherapy.

Indications

Osteoarthritis is the most common indication for an elective joint

replacement. It is not usually performed until symptoms are severe and
not manageable with conservative treatments.

Joints may also require replacement for:

• Fractures
• Septic arthritis
• Osteonecrosis
• Bone tumours
• Rheumatoid arthritis

Options

There are several options for elective joint replacement surgery:

• Total joint replacement - replacing both articular surfaces of the
joint
• Hemiarthroplasty - replacing half of the joint (e.g., the head of the
femur in the hip joint)
 • Partial joint resurfacing - replacing part of the joint surfaces (e.g.,
only the medial joint surfaces of the knee)

Total Hip Replacement

Usually, a lateral incision over the outer aspect of the hip is used.
The hip joint is dislocated (separated) to give access to both articular
surfaces.

The head of the femur is removed. A metal or ceramic replacement

head of femur, on a metal stem, is used to replace it. The stem can either
be cemented into the shaft of the femur or carefully pushed into the shaft
to make a tight enough fit to hold it securely in place. Uncemented stems
have a rough surface that holds them tightly in place.

The acetabulum (socket) of the pelvis is hollowed out and replaced

by a metal socket, which is cemented or screwed into place. A spacer is
used between the new head and socket to complete the new artificial
joint.
 Total Knee Replacement

Usually, a vertical, anterior incision is made down the front of the

knee. The patella is rotated out of the way to allow access to the knee
joint.

The articular surfaces (the cartilage and some of the bone) of the
femur and tibia are removed. A new metal surface replaces these. They
can be either cemented or pushed tightly into place.

A spacer is added between the new articular surfaces of the femur

and tibia to complete the new artificial joint.
 Total Shoulder Replacement

Usually, an anterior incision is made down the front of the shoulder,

along the deltoid. The shoulder joint is dislocated (separated) to give
access to both articular surfaces.

The head of the humerus is removed and replaced with a metal or

ceramic ball. This replacement head is attached to the humerus either by
a metal stem or screws (stemless).

The glenoid (socket) is hollowed out and replaced by a metal socket.

This completes the artificial shoulder joint.

Reverse Total Shoulder Replacement

A reverse total shoulder replacement involves adding a sphere in

place of the glenoid (socket) and a spacer with a cup to replace the
head of the humerus. This reverses the normal ball-in-cup structure of the
shoulder joint, but the joint function remains the same.

Before Surgery

Planning for joint replacement surgery will involve:

• X-rays
• CT or MRI scans may be required for a more detailed assessment
• Pre-operative assessment (pre-op)
• Consent for surgery
• Bloods (including group and save and crossmatching of blood)
• Medication changes if needed (e.g., temporarily stopping
anticoagulation)
• Venous thromboembolism assessment
• Fasting immediately before surgery
• The limb will be marked with the patient awake to ensure the
operation is performed on the correct joint

During Surgery

Joint replacement surgery requires a general anaesthetic.

Alternatively, a spinal anaesthetic may be used for lower limb surgery.
 Prophylactic antibiotics are given before the procedure to reduce
the risk of infection.

Tranexamic acid may be used to minimise blood loss during the

procedure.

After Surgery

Post-operative management after joint replacement surgery involves:

• Analgesia
• Physiotherapy to guide when and how to mobilise
• VTE prophylaxis
• Post-operative x-rays
• Post-operative full blood count (to check for anaemia)
• Monitoring for complications (e.g., deep vein thrombosis or
infection)

VTE prophylaxis usually involves low molecular weight heparin

(LMWH). The 2018 NICE guidelines on VTE prophylaxis have specific
recommendations on potential regimes that can be used after joint
replacement surgery (see full national and local guidelines when treating
patients). This involves the option of LMWH for:
• 28 days post elective hip replacement
• 14 days post elective knee replacement

Other measures that may be used for VTE prophylaxis after joint
replacement surgery are:
• Aspirin
• DOACs (e.g., rivaroxaban)
• Anti-embolism stockings

Risks

The generic risks of joint replacement surgery are:

• Risks of the anaesthetic
• Pain
• Bleeding
• Infection (infection of the prosthesis can be highly problematic - see
below)
 • Damage to nearby structures (e.g., nerves or arteries)
• Stiffness or restricted range of motion in the joint
• Joint dislocation
• Loosening
• Fracture during the procedure
• Venous thromboembolism (DVT or PE)

Prosthetic Joint Infections

Infection in a prosthetic joint is a big problem. This occurs in around

1% of joint replacements and extensive measures are taken to prevent it,
such as perioperative prophylactic antibiotics. It is more likely to occur in
revision surgery rather than during the initial joint replacement. The most
common organism is Staphylococcus aureus (a common skin
organism).

Risk factors for prosthetic joint infection are:

• Prolonged operative time
• Obesity
• Diabetes

Symptoms include:
• Fever
• Pain
• Swelling
• Erythema
• Increased warmth

Diagnosis involves a combination of clinical findings, x-rays, blood

tests (raised inflammatory markers), cultures (e.g., blood or synovial fluid)
and findings during further operations.

Management involves repeat surgery and prolonged antibiotics (over

months). Surgery may involve joint irrigation, debridement or complete
replacement.
 Fractures
Types of Fracture

A compound fracture is when the skin is broken and the broken

bone is exposed to the air. The broken bone can puncture through the
skin.

A stable fracture refers to when the sections of bone remain in

alignment at the fracture.

A pathological fracture refers to when a bone breaks due to an

abnormality within the bone (see below).

There are terms used to describe the way a bone has fractured:
• Transverse
• Oblique
• Spiral
• Segmental
• Comminuted (breaking into multiple fragments)
• Compression fractures (affecting the vertebrae in the spine)
• Greenstick
• Buckle (torus)
• Salter-Harris (growth plate fracture)

Greenstick and buckle fractures typically occur in children rather

than adults. Salter-Harris fractures only occur in children (adults do not
have growth plates).
 Wrist Fractures

A Colle’s fracture refers to a transverse fracture of the distal radius

near the wrist, causing the distal portion to displace posteriorly
(upwards), causing a “dinner fork deformity”. This is usually the result of
a fall onto an outstretched hand (FOOSH).

A scaphoid fracture is often caused by a FOOSH. The scaphoid is

one of the carpal bones and is located below the base of the thumb. A
key sign of a scaphoid fracture is tenderness in the anatomical
snuffbox (the groove between the tendons when extending the thumb). It
is worth noting that the scaphoid has a retrograde blood supply, with
blood vessels supplying the bone from only one direction. This means a
fracture can cut off the blood supply, resulting in avascular necrosis and
non-union.

TOM TIP: Some key bones have vulnerable blood supplies, where
a fracture can lead to avascular necrosis, impaired healing, and non-
union. These are the scaphoid bone, the femoral head, the humeral
head and the talus, navicular and fifth metatarsal in the foot. These
are worth remembering for your exams.

Ankle Fractures

Ankle fractures involve the lateral malleolus (distal fibula) or the

medial malleolus (distal tibia).

The Weber classification can be used to describe fractures of the

lateral malleolus (distal fibula). The fracture is described in relation to
the distal syndesmosis (fibrous join) between the tibia and fibula. This
tibiofibular syndesmosis is very important for the stability and function
of the ankle joint. If the fracture disrupts the syndesmosis, surgery is more
likely to be required in order to regain good stability and function of the
joint.

The Weber classification defines fractures of the lateral malleolus as:

• Type A - below the ankle joint - will leave the syndesmosis intact
• Type B - at the level of the ankle joint - the syndesmosis will be
intact or partially torn
• Type C - above the ankle joint - the syndesmosis will be disrupted
 Pelvic Ring Fractures

The pelvis forms a ring. When one part of the pelvic ring fractures,
another part will also fracture (similar to breaking a polo mint).

Pelvic fractures often lead to significant intra-abdominal bleeding,

either due to vascular injury or from the cancellous bone of the pelvis.
This can lead to shock and death, so needs emergency resuscitation and
trauma management.

Pathological Fractures

Pathological fractures occur due to an underlying disease of the

bone, such as a tumour, osteoporosis or Paget’s disease of the bone.
They may occur with minor trauma or even spontaneously without any
history of trauma. Common sites are the femur and the vertebral bodies.

The main cancers that metastasise to the bones are (mnemonic:

PoRTaBLe):
 • Po - Prostate
• R - Renal
• Ta - Thyroid
• B - Breast
• Le - Lung

Fragility Fractures

Fragility fractures occur due to weakness in the bone, usually due to

osteoporosis. They often occur without the appropriate trauma that is
typically required to break a bone. For example, a patient may present
with a fractured femur after a minor fall.

A patient’s risk of a fragility fracture over the next 10 years can be

predicted using the FRAX tool.

Bone mineral density can be measured using a DEXA scan.

The WHO criteria for osteopenia and osteoporosis are:

T Score at the Hip Bone Mineral Density

More than -1 Normal
-1 to -2.5 Osteopenia
Less than -2.5 Osteoporosis
Less than -2.5 plus a fracture Severe Osteoporosis

The NOGG guidelines can be used to guide the medical treatments

appropriate for an individual based on their FRAX score. The first-line
medical treatments for reducing the risk of fragility fractures are:
• Calcium and vitamin D
• Bisphosphonates (e.g., alendronic acid)

Bisphosphonates work by interfering with osteoclasts and reducing

their activity, preventing the reabsorption of bone. There are a few key
side effects to remember:
• Reflux and oesophageal erosions (oral bisphosphonates are
taken on an empty stomach while sitting upright for 30 minutes
 before moving or eating to prevent this)
• Atypical fractures (e.g. atypical femoral fractures)
• Osteonecrosis of the jaw
• Osteonecrosis of the external auditory canal

Denosumab is a monoclonal antibody that works by blocking the

activity of osteoclasts. It is an alternative to bisphosphonates where they
are contraindicated, not tolerated or not effective.

Imaging

X-rays are the initial imaging investigation when a bone fracture is

suspected. Two views (two x-rays taken from different angles) are
always required, as a single view may miss a fraction.

CT scans give a more detailed view of the bones when the x-rays are
inconclusive or further information is needed.

Principles of Fracture Management

The first principle is to achieve mechanical alignment of the fracture

by:
• Closed reduction via manipulation of the limb
• Open reduction via surgery

The second principle is to provide relative stability for some time to

allow healing to occur. This can be done by fixing the bone in the correct
position while it heals. There are various ways the bone can be fixed in
position:

• External casts (e.g., plaster cast)

• K wires
• Intramedullary wires
• Intramedullary nails
• Screws
• Plate and screws

Management
 Patients presenting to A&E will be investigated with x-rays to establish
the diagnosis.

Patients with fractures require appropriate pain management.

Straightforward fractures may be managed in A&E (e.g., a Colle’s

fracture in a young adult). They may require closed reduction if the
bones are out of alignment. A plaster cast may be applied, and the
patient can be discharged with a follow-up appointment in the fracture
clinic.

Complex fractures and those requiring surgery (e.g., hip fractures) are
referred to the on-call trauma and orthopaedics team. They are
admitted and made nil by mouth if they may need an operation. They are
discussed at the trauma meeting the following day (typically, this starts
at 7.45 am), then seen on the morning ward round. A plan will be made for
further management at this stage.

Complications

The complications will depend on the location and nature of the

fracture.

Possible early complications include:

• Damage to local structures (e.g., tendons, muscles, arteries,
nerves, skin and lung)
• Haemorrhage leading to shock and potentially death
• Compartment syndrome
• Fat embolism (see below)
• Venous thromboembolism (DVTs and PEs) due to immobility

Possible longer-term complications include:

• Delayed union (slow healing)
• Malunion (misaligned healing)
• Non-union (failure to heal)
• Avascular necrosis (death of the bone)
• Infection (osteomyelitis)
• Joint instability
• Joint stiffness
 • Contractures (tightening of the soft tissues)
• Arthritis
• Chronic pain
• Complex regional pain syndrome

Fat Embolism

Fat embolism can occur following the fracture of long bones (e.g.,
femur). Fat globules are released into the circulation following a fracture
(possibly from the bone marrow). These globules may become lodged in
blood vessels (e.g., pulmonary arteries) and cause blood flow obstruction.

Fat embolisation can cause a systemic inflammatory response,

resulting in fat embolism syndrome.

Fat embolism typically presents around 24-72 hours after the fracture.
Gurd’s criteria can be used for the diagnosis.

Gurd’s major criteria:

• Respiratory distress
• Petechial rash
• Cerebral involvement

There is a long list of Gurd’s minor criteria, including:

• Jaundice
• Thrombocytopenia
• Fever
• Tachycardia

Operating early to fix the fracture reduces the risk of fat embolism
syndrome.

It can lead to multiple organ failure. Management is supportive while

the condition improves. The mortality rate is around 10%.
 Hip Fractures
Hip fractures are common and lead to significant morbidity and
mortality. The 30-day mortality is 5-10%. Half of patients become less
independent after a hip fracture.

Increasing age and osteoporosis are major risk factors for hip
fractures. Females are affected more often than males.
Due to the morbidity and mortality with hip fractures, they are
generally prioritised on the trauma list with the aim to perform surgery
within 48 hours. There is a medical specialty called orthogeriatrics, that
focuses on identifying and optimising the medical co-morbidities and
complications of inpatients on the orthopaedic ward, particularly elderly
patients with hip fractures.

Hip fractures can be categorised into:

• Intra-capsular fractures
• Extra-capsular fractures

Basic Anatomy

There are some basic structures of the top of the femur:

• Head
• Neck
• Greater trochanter (lateral)
• Lesser trochanter (medial)
• Intertrochanteric line
• Shaft (body)

The capsule of the hip joint is a strong fibrous structure. It attaches to

the rim of the acetabulum on the pelvis and the intertrochanteric
line on the femur. It surrounds the neck and head of the femur.

The head of the femur has a retrograde blood supply. The medial
and lateral circumflex femoral arteries join the femoral neck just
proximal to the intertrochanteric line. Branches of this artery run along
the surface of the femoral neck, within the capsule, towards the femoral
head. They provide the only blood supply to the femoral head. A fracture
of the intra-capsular neck of the femur can damage these blood vessels,
removing the blood supply to the femoral head, leading to avascular
necrosis. Therefore, patients with a displaced intra-capsular fracture
need to have the femoral head replaced with a hemiarthroplasty or total
hip replacement.

TOM TIP: It is worth understanding and remembering the concept

of the retrograde blood supply to the head of the femur and how this
determines the choice of operation (explained below). When I did an
FY1 job in trauma and orthopaedics, the juniors were questioned on
this concept almost every time a patient with a hip fracture was
admitted. Being able to identify the type of hip fracture on an x-ray
(intra-capsular or extra-capsular) and justify the choice of operation
made trauma meetings much less stressful.

Intra-Capsular Fractures

Intra-capsular fractures involve a break in the femoral neck, within the

capsule of the hip joint. This affects the area proximal to the
intertrochanteric line.
 The Garden classification is used for intra-capsular neck of femur
fractures:
• Grade I - incomplete fracture and non-displaced
• Grade II - complete fracture and non-displaced
• Grade III - partial displacement (trabeculae are at an angle)
• Grade IV - full displacement (trabeculae are parallel)

Non-displaced intra-capsular fractures may have an intact blood

supply to the femoral head, meaning it may be possible to preserve the
femoral head without avascular necrosis occurring. They can be treated
with internal fixation (e.g., with screws) to hold the femoral head in place
while the fracture heals.

Displaced intra-capsular fractures (grade III and IV) disrupt the blood
supply to the head of the femur. Therefore, the femoral head needs to be
removed and replaced.
 Hemiarthroplasty involves replacing the head of the femur but
leaving the acetabulum (socket) in place. Cement is used to hold the
stem of the prosthesis in the shaft of the femur. This is generally offered
to patients who have limited mobility or significant co-morbidities.

Total hip replacement involves replacing both the head of the femur
and the socket. This is generally offered to patients who can walk
independently and are fit for surgery.

Extra-Capsular Fractures

Extra-capsular fractures leave the blood supply to the head of the

femur intact. Therefore, the femoral head does not need to be replaced.

Intertrochanteric fractures occur between the greater and lesser

trochanter. These are treated with a dynamic hip screw (AKA sliding
hip screw). A screw goes through the neck and into the head of the
femur. A plate with a barrel that holds the screw is screwed to the outside
of the femoral shaft. The screw that goes through the femur to the head
allows some controlled compression at the fracture site, whilst still holding
it in the correct alignment. Adding some controlled compression across
the fracture improves healing.

Subtrochanteric fractures occur distal to the lesser trochanter

(although within 5cm). The fracture occurs to the proximal shaft of the
femur. These may be treated with an intramedullary nail (a metal pole
inserted through the greater trochanter into the central cavity of the shaft
of the femur).

Hip Fracture Presentation

The typical scenario is an older patient (over 60) who has fallen,
presenting with:
• Pain in the groin or hip, which may radiate to the knee
• Not able to weight bear
• Shortened, abducted and externally rotated leg

An essential part of assessing patients with a new hip fracture is to

determine any other acute illnesses. There is often a good reason for
them to fall and break a hip. They may also be suffering with:
• Anaemia
• Electrolyte imbalances
• Arrhythmias
• Heart failure
• Myocardial infarction
• Stroke
 • Urinary or chest infection

These conditions need to be identified as early as possible so that the

patient can be optimised and surgery can proceed with minimal delays.

TOM TIP: The term “mechanical fall” is often used to imply a

simple explanation for why the patient fell, such as tripping over an
object or being knocked over. It is worth exploring the fall in more
detail. In many cases, there may be a correctable underlying medical
cause for the fall, such as anaemia, arrhythmia or even underlying
Parkinson’s disease. There may also be social contributors to the
fall, such as dehydration, incorrect eyewear, poor footwear or
obstacles in the home. If you identify an underlying reversible
cause, you could make a big difference to that patient and impress
your orthogeriatric colleagues.

Imaging

X-rays are the initial investigation of choice. Two views are essential,
as a single view can miss the fracture. Anterior-to-posterior (AP) and
lateral views are standard.

Shenton’s line can be seen on an AP x-ray of the hip. It is one

continuous curving line formed by the medial border of the femoral neck
and continues to the inferior border of the superior pubic ramus.
Disruption of Shenton’s line is a key sign of a fractured neck of femur
(NOF).

MRI or CT scanning may be used where the x-ray is negative, but a

fracture is still suspected.

Management

On admission, patients require:

• Appropriate analgesia
• Investigations to establish the diagnosis (e.g., x-rays)
• Venous thromboembolism risk assessment and prophylaxis (e.g.,
low molecular weight heparin)
 • Pre-operative assessment (including bloods and an ECG) to
ensure they are fit and optimised for surgery
• Orthogeriatric input

The NICE guidelines (updated 2017) say that surgery should be

carried out either the same day or the day after the patient is admitted
(within 48 hours).

The operation should allow the patient to weight bear straight away.
This allows the physiotherapists to start mobilisation and rehabilitation as
soon as possible after the operation. Post-operative analgesia is
important to encourage the patient to mobilise as quickly as possible.
 Compartment Syndrome
Compartment syndrome is where the pressure within a fascial
compartment is abnormally elevated, cutting off the blood flow to the
contents of that compartment.

Fascial compartments involve muscles, nerves and blood vessels

surrounded by fascia. Fascia is a sheet of strong, fibrous connective
tissue that encases the contents of the compartment. It is not able to
stretch or expand.

Acute compartment syndrome is an orthopaedic emergency

requiring surgery (fasciotomy) to relieve the pressure within the
compartment and restore blood flow. Without prompt treatment, tissue
necrosis (death) and permanent damage can occur.

Compartment syndrome can be classified as acute or chronic. Most

of this section relates to acute compartment syndrome.

Acute compartment syndrome is usually associated with an acute

injury, where bleeding or tissue swelling (oedema) associated with the
injury increases the pressure within the compartment.

Presentation

Acute compartment syndrome most often affects one of the fascial

compartments in the legs, but it can also affect the forearm, feet, thigh
and buttocks.

It usually presents after an acute injury, particularly:

• Bone fractures
• Crush injuries

Acute compartment syndrome presents with the 5 P’s:

• P - Pain “disproportionate” to the underlying injury, worsened by
passive stretching of the muscles
• P - Paresthesia
 • P - Pale
• P - Pressure (high)
• P - Paralysis (a late and worrying feature)

Note that pulseless is not a feature, differentiating it from acute limb

ischaemia. The pulses may remain intact depending on which
compartment is affected.

TOM TIP: Disproportionate pain is a key characteristic of

compartment syndrome. The pain is so severe that pain medications
are not effective. If you see a patient with disproportionate pain after
an injury in your exams, the diagnosis is probably compartment
syndrome.

Management

Acute compartment syndrome is primarily a clinical diagnosis based

on the signs and symptoms.

Needle manometry can be used to measure the compartment

pressure. A device (manometer) measures the resistance to injecting
saline through a needle into the compartment.
Initial management involves:
• Escalating to the orthopaedic registrar or consultant
• Removing any external dressings or bandages
• Elevating the leg to heart level
• Maintaining good blood pressure (avoiding hypotension)

Emergency fasciotomy is the definitive management. Ideally, this

should be as soon as possible after injury (e.g., within 6 hours). If it is
delayed, irreversible damage may occur, and fasciotomy may not be
beneficial.

Fasciotomy involves a surgical operation to cut through the fascia,

down the entire length of the compartment, and release the pressure. The
compartment is explored to identify and debride any necrotic muscle
tissue. The wound is left open and covered with a dressing.
 Patients require repeated trips to theatre (every few days) to explore
the compartment for necrotic tissue, which needs to be debrided. As the
swelling improves, the wound can be gradually closed, which can take
several weeks. A skin graft may be required if the wound cannot be
closed around the compartment.

Chronic Compartment Syndrome

Chronic compartment syndrome (also called chronic exertional

compartment syndrome) is usually associated with exertion. During
exertion, the pressure within the compartment rises, blood flow to the
compartment is restricted, and symptoms start. During rest, the pressure
falls, and symptoms begin to resolve.

Unlikely acute compartment syndrome, chronic compartment

syndrome is not an emergency.

Symptoms are usually isolated to a specific location at the affected

compartment. Symptoms include pain, numbness or paresthesia (pins
and needles). They are made worse by increasing activity and resolve
quickly with rest.

Needle manometry can be used to measure the pressure in the

compartment before, during and after exertion to confirm the diagnosis. It
may be treated with a fasciotomy.
 Osteomyelitis
Osteomyelitis refers to inflammation of the bone and bone marrow,
usually caused by bacterial infection.

Haematogenous osteomyelitis refers to when a pathogen is carried

through the blood and seeded in the bone. This is the most common
mode of infection. Alternatively, osteomyelitis can occur due to direct
contamination of the bone, for example, at a fracture site or during an
orthopaedic operation.

Staphylococcus aureus causes most cases of osteomyelitis.

Osteomyelitis can be acute or chronic. Patients may develop

recurring or chronic infections after treatment for acute osteomyelitis.

Risk Factors

The key risk factors for developing osteomyelitis are:

• Open fractures
• Orthopaedic operations, particularly with prosthetic joints
• Diabetes, particularly with diabetic foot ulcers
• Peripheral arterial disease
• IV drug use
• Immunosuppression

Infection in a prosthetic joint is a big problem. This occurs in around

1% of joint replacements, and extensive measures are taken to prevent it,
such as perioperative prophylactic antibiotics. It is more likely to occur in
revision surgery compared with an initial joint replacement.

Presentation

The typical presentation of osteomyelitis is with:

• Fever
• Pain and tenderness
 • Erythema
• Swelling

The presentation of osteomyelitis can be quite non-specific, with

generalised symptoms of infection such as fever, lethargy, nausea and
muscle aches.

Investigations

X-rays often do not show any changes, particularly in early disease.

They cannot be used to exclude osteomyelitis. The potential signs of
osteomyelitis on an x-ray are:
• Periosteal reaction (changes to the surface of the bone)
• Localised osteopenia (thinning of the bone)
• Destruction of areas of the bone

MRI scans are the best imaging investigation for establishing a

diagnosis.

Blood tests will show raised inflammatory markers (e.g., WBC,

CRP and ESR).

Blood cultures may be positive for the causative organism.

Bone cultures can be performed to establish the causative organism

and the antibiotic sensitivities.

Management

Management involves a combination of:

• Surgical debridement of the infected bone and tissues
• Antibiotic therapy

Prolonged courses of antibiotics are required to treat osteomyelitis.

The BNF page on osteomyelitis recommends for acute osteomyelitis:
• 6 weeks of flucloxacillin, possibly with rifampicin or fusidic acid
added for the first 2 weeks

Alternatives to flucloxacillin are:

 • Clindamycin in penicillin allergy
• Vancomycin or teicoplanin when treating MRSA

Chronic osteomyelitis usually requires 3 months or more of

antibiotics.

Osteomyelitis associated with prosthetic joints (e.g., a hip

replacement) may require complete revision surgery to replace the
prosthesis.
 Sarcoma
Sarcomas are cancers originating in the muscles, bones or other
types of connective tissue. There are many subtypes of sarcoma, which
vary in their histology, location and degree of malignancy.

Types of bone sarcoma include:

• Osteosarcoma - the most common form of bone cancer
• Chondrosarcoma - cancer originating from the cartilage
• Ewing sarcoma - a form of bone and soft tissue cancer most often
affecting children and young adults

Types of soft tissue sarcoma include:

• Rhabdomyosarcoma - originating from skeletal muscle
• Leiomyosarcoma - originating from smooth muscle
• Liposarcoma - originating from adipose (fat) tissue
• Synovial sarcoma - originating from soft tissues around the joints
• Angiosarcoma - originating from the blood and lymph vessels
• Kaposi’s sarcoma - cancer caused by human herpesvirus 8, most
often seen in patients with end-stage HIV, causing typical red/purple
raised skin lesions but also affecting other parts of the body

The prognosis depends greatly on the type, location, size and stage of
the sarcoma. It can range from a greater than 90% 5-year survival for well-
differentiated and resectable liposarcoma, to less than 10% for
angiosarcoma affecting the liver.

Presentation

The presenting symptoms of sarcoma will vary dependent on the

location and size of the lesion. The key features that should raise
suspicions are:
• A soft tissue lump, particularly if growing, painful or large
• Bone swelling
• Persistent bone pain
 Investigations

X-ray is the initial investigation for bony lumps or persistent pain.

Ultrasound is the initial investigation for soft tissue lumps.

CT or MRI scans may be used to visualise the lesion in more detail

and look for metastatic spread (particularly a CT thorax, as sarcoma most
often spreads to the lungs).

Biopsy is required to look at the histology of the cancer.

Staging

Staging is either with the TNM staging system or a number system

that grades the cancer from stage 1 (earliest) to stage 4 (most advanced).

The most common location for sarcoma to metastasise to is the lungs.

Management

Management will be guided by the sarcoma multidisciplinary team

(MDT). There are specialist sarcoma centres in various locations in the
UK that specialise in managing sarcoma. This concentrates the expertise
about these relatively rare and often challenging cancers to ensure
patients get the best care.

Sarcoma treatment will depend on the type, location, size and stage of
the sarcoma. This may involve:
• Surgery (surgical resection is the preferred treatment)
• Radiotherapy
• Chemotherapy
• Palliative care
 Back Pain and Sciatica
Low back pain is very common and has many causes. Lumbago is
another term for low back pain. Non-specific or mechanical lower back
pain refers to the majority of patients who do not have a specific disease
causing their lower back pain.

Sciatica refers to the symptoms associated with irritation of the

sciatic nerve.

Acute low back pain should improve within 1-2 weeks. Recovery can
take longer (4-6 weeks) for sciatica.

Chronic lower back pain can have a massive impact on the patient’s
quality of life and be difficult to manage.

There are several challenges with managing patients with lower back
pain:
• Identifying serious underlying pathology
• Speeding up recovery
• Reducing the risk of chronic lower back pain
• Managing symptoms in chronic lower back pain

Causes of Mechanical Back Pain

The causes of mechanical back pain include:

• Muscle or ligament sprain
• Facet joint dysfunction
• Sacroiliac joint dysfunction
• Herniated disc
• Spondylolisthesis (anterior displacement of a vertebra out of line
with the one below)
• Scoliosis (curved spine)
• Degenerative changes (arthritis) affecting the discs and facet
joints
 Causes of Neck Pain

The causes of neck pain include:

• Muscle or ligament strain (e.g., poor posture or repetitive
activities)
• Torticollis (waking up with a unilaterally stiff and painful neck due
to muscle spasm)
• Whiplash (typically after a road traffic accident)
• Cervical spondylosis (degenerative changes to the vertebrae)

Red-Flag Causes of Back Pain

It is essential to look out for features that may indicate underlying:

• Spinal fracture (e.g., major trauma)
• Cauda equina (e.g., saddle anaesthesia, urinary retention,
incontinence or bilateral neurological signs)
• Spinal stenosis (e.g., intermittent neurogenic claudication)
• Ankylosing spondylitis (e.g., age under 40, gradual onset,
morning stiffness or night-time pain)
• Spinal infection (e.g., fever or a history of IV drug use)

Other Causes of Back Pain

Keep in mind that back pain may not always be related to the spine.
There is a long list of abdominal and thoracic conditions that can cause
back pain, including:

• Pneumonia
• Ruptured aortic aneurysms
• Kidney stones
• Pyelonephritis
• Pancreatitis
• Prostatitis
• Pelvic inflammatory disease
• Endometriosis

Sciatica
 The spinal nerves L4 - S3 come together to form the sciatic nerve.
The sciatic nerve exits the posterior part of the pelvis through the greater
sciatic foramen, in the buttock area on either side. It travels down the
back of the leg. At the knee, it divides into the tibial nerve and the
common peroneal nerve.

The sciatic nerve supplies sensation to the lateral lower leg and the
foot. It supplies motor function to the posterior thigh, lower leg and foot.

Sciatica causes unilateral pain from the buttock radiating down the
back of the thigh to below the knee or feet. It might be described as an
“electric” or “shooting” pain. Other symptoms are paraesthesia (pins and
needles), numbness and motor weakness. Reflexes may be affected
depending on the affected nerve root.
The main causes of sciatica are lumbosacral nerve root
compression by:
• Herniated disc
• Spondylolisthesis (anterior displacement of a vertebra out of line
with the one below)
• Spinal stenosis

Bilateral sciatica is a red flag for cauda equina syndrome.

History and Examination

When assessing any pain, you can use the SOCRATES mnemonic:

• S - Site
• O - Onset
• C - Character
• R - Radiation
• A - Associations
• T - Timing
• E - Exacerbating and relieving factors
• S - Severity

Key symptoms in the history are:

• Major trauma (spinal fracture)
• Stiffness in the morning or with rest (ankylosing spondylitis)
• Age under 40 (ankylosing spondylitis)
• Gradual onset of progressive pain (ankylosing spondylitis or
cancer)
• Night pain (ankylosing spondylitis or cancer)
• Age over 50 (cancer)
• Weight loss (cancer)
• Bilateral neurological motor or sensory symptoms (cauda equina)
• Saddle anaesthesia (cauda equina)
• Urinary retention or incontinence (cauda equina)
• Faecal incontinence (cauda equina)
 • History of cancer with potential metastasis (cauda equina or
spinal metastases)
• Fever (spinal infection)
• IV drug use (spinal infection)

Key findings on examination are:

• Localised tenderness to the spine (spinal fracture or cancer)
• Bilateral neurological motor or sensory signs (cauda equina)
• Bladder distention implying urinary retention (cauda equina)
• Reduced anal tone on PR examination (cauda equina)

The sciatic stretch test can be used to help diagnose sciatica. The
patient lies on their back with their leg straight. The examiner lifts one leg
from the ankle with the knee extended until the limit of hip flexion is
reached (usually around 80-90 degrees). Then the examiner dorsiflexes
the patient’s ankle. Sciatica-type pain in the buttock/posterior thigh
indicates sciatic nerve root irritation. Symptoms improve with flexing the
knee.

TOM TIP: It is worth remembering the main cancers that

metastasise to the bones. A history of these in an exam patient
presenting with back pain should make you think of possible cauda
equina or spinal metastases. You can remember them with the
PoRTaBLe mnemonic:

• Po - Prostate
• R - Renal
• Ta - Thyroid
• B - Breast
• Le - Lung

Investigations

Generally, patients with mechanical/non-specific lower back pain can

be diagnosed clinically and do not require further investigations.

X-rays or CT scans can be used to diagnose spinal fractures.

 Bladder scans can be used to assess for urinary retention in
suspected cauda equina (pre and post void volumes).

An emergency MRI scan is required in patients with suspected cauda

equina (within hours of the presentation).

Investigations for suspected ankylosing spondylitis are:

• Inflammatory markers (CRP and ESR)
• X-ray of the spine and sacrum (may show a fused “bamboo spine”
in later-stage disease)
• MRI of the spine (may show bone marrow oedema early in the
disease)

STarT Back Screening Tool

The STarT Back tool was developed by Keele University to stratify the
risk of a patient presenting with acute back pain developing chronic back
pain. This helps guide the intensity of the initial interventions (e.g., referral
for group exercises, physiotherapy and cognitive behavioural therapy).

It involves 9 questions that assess the patient’s function and

psychological response to the back pain. It gives a:
• Total score (out of 9)
• Subscore on the 4 psychosocial questions (out of 4)

The interpretation gives a risk of developing chronic back pain:

Low Risk Medium Risk High Risk

Total Score 3 or less More than 3 More than 3
Subscore 3 or less 3 or less More than 3

Managing Acute Lower Back Pain

First, exclude serious underlying causes. If concerned about

symptoms or signs of an underlying condition, arrange further
investigations and refer appropriately. For example:
• Same-day referral to the on-call orthopaedic team for an urgent
MRI scan if cauda equina is suspected
 • Inflammatory markers and an urgent rheumatology review if
ankylosing spondylitis is suspected
• Full in-line spinal immobilisation, admission to a trauma unit and x-
rays/CT scans for spinal injury after major trauma

Patients with neurological symptoms or signs on examination,

particularly if progressive or severe, may require referral to orthopaedics
or neurosurgery (potentially urgently).

The StarT Back tool can be used to stratify the risk of developing
chronic back pain.

The NICE clinical knowledge summaries (updated 2020) give the

options for managing non-specific low back pain based on the outcome of
risk stratification, as briefly summarised below (always check the latest
guidelines when treating patients).

Patients at low risk of chronic back pain can generally be managed

with:
• Self-management
• Education
• Reassurance
• Analgesia
• Staying active and continuing to mobilise as tolerated

Additional options for patients at medium or high risk of developing

chronic back pain include:
• Physiotherapy
• Group exercise
• Cognitive behavioural therapy

The NICE clinical knowledge summaries advise for analgesia:

• NSAIDs (e.g., ibuprofen or naproxen) first-line
• Codeine as an alternative
• Benzodiazepines (e.g., diazepam) for muscle spasm (short-term
only: up to 5 days)

They specifically state not to use opioids, antidepressants,

amitriptyline, gabapentin or pregabalin for low back pain.
 Patients need safety-net advice to report red flag symptoms, such as
saddle anaesthesia or incontinence.

Radiofrequency denervation may be an option in patients with

chronic low back pain originating in the facet joints. Radiofrequency is
used to target and damage the medial branch nerves that supply
sensation to the facet joints associated with the back pain. This is done
under a local anaesthetic.

Management of Sciatica

The initial management of sciatica is mostly the same as acute low

back pain.

The NICE clinical knowledge summaries (updated 2020) state not to

use medications such as gabapentin, pregabalin, diazepam or oral
corticosteroids for sciatica. They state not to use opioids for chronic
sciatica.

They suggest considering a neuropathic medication if symptoms are

persisting or worsening at follow up, but not gabapentin or pregabalin,
leaving at the main choices of:

• Amitriptyline
• Duloxetine

Specialist management options for chronic sciatica include:

• Epidural corticosteroid injections

• Local anaesthetic injections
• Radiofrequency denervation
• Spinal decompression
 Cauda Equina Syndrome
Cauda equina syndrome is a surgical emergency where the nerve
roots of the cauda equina at the bottom of the spine are compressed. It
requires emergency decompression surgery to prevent permanent
neurological dysfunction. However, even with immediate decompression,
patients may still not regain full function.

Pathophysiology

The cauda equina (translated as “horse’s tail”) is a collection of nerve

roots that travel through the spinal canal after the spinal cord terminates
around L2/L3. The spinal cord tapers down at the end in a section called
the conus medullaris. The nerve roots exit either side of the spinal
column at their vertebral level (L3, L4, L5, S1, S2, S3, S4, S5 and Co).

The nerves of the cauda equina supply:

• Sensation to the perineum, bladder and rectum
• Motor innervation to the lower limbs and the anal and urethral
sphincters
• Parasympathetic innervation of the bladder and rectum

In cauda equina syndrome, the nerves of the cauda equina are

compressed. There are several possible causes of compression,
including:
• Herniated disc (the most common cause)
• Tumours, particularly metastasis
• Spondylolisthesis (anterior displacement of a vertebra out of line
with the one below)
• Abscess (infection)
• Trauma
 Red Flags

The key red flags to look out for are:

• Saddle anaesthesia (loss of sensation in the perineum - around
the genitals and anus)
• Loss of sensation in the bladder and rectum (not knowing when
they are full)
• Urinary retention or incontinence
• Faecal incontinence
• Bilateral sciatica
• Bilateral or severe motor weakness in the legs
• Reduced anal tone on PR examination

TOM TIP: A common way people ask about saddle anaesthesia

when taking a history is to ask, “does it feel normal when you wipe
after opening your bowels?”

Management

Cauda equina is a neurosurgical emergency. It requires:

• Immediate hospital admission
• Bladder scans can be used to assess for urinary retention in
suspected cauda equina
• Emergency MRI scan to confirm or exclude cauda equina
syndrome
 • Neurosurgical input to consider lumbar decompression
surgery

Surgery should be performed as soon as possible to increase the

chances of regaining function. Even with early surgery, patients can be
left with bladder, bowel or sexual dysfunction. Leg weakness and sensory
impairment can also persist.

Metastatic Spinal Cord Compression

When a metastatic lesion compresses the spinal cord (before the

end of the spinal cord and the start of the cauda equina), this is called
metastatic spinal cord compression (MSCC). This is different to cauda
equina, which specifically refers to compression of the cauda equina.

MSCC presents similarly to cauda equina, with back pain and motor
and sensory signs and symptoms. A key feature is back pain that is
worse on coughing or straining.

MSCC is an oncological emergency and requires rapid imaging and

management. There are specialist MSCC coordinators who should be
involved early to coordinate the imaging and treatment of patients with
MSCC.

Treatments will depend on individual factors. They may include:

• High dose dexamethasone (to reduce swelling in the tumour and
relieve compression)
• Analgesia
• Surgery
• Radiotherapy
• Chemotherapy

TOM TIP: Cauda equina presents with lower motor neurone signs
(reduced tone and reduced reflexes). The nerves being compressed
are lower motor neurones that have already exited the spinal cord.
When the spinal cord is being compressed higher up by metastatic
spinal cord compression, upper motor neurone signs (increased
tone, brisk reflexes and upgoing plantar reflexes) will be seen.
 Spinal Stenosis
Spinal stenosis refers to the narrowing of part of the spinal canal,
resulting in compression of the spinal cord or nerve roots. This usually
affects the cervical or lumbar spine. This section focuses on lumbar
spinal stenosis, which is the most common type.

Spinal stenosis is more likely to occur in patients older than 60 years,

relating to degenerative changes in the spine.

Types

There are three types:

• Central stenosis - narrowing of the central spinal canal
• Lateral stenosis - narrowing of the nerve root canals
• Foramina stenosis - narrowing of the intervertebral foramina

Causes

Several conditions can cause the spinal canal to narrow, including:

• Congenital spinal stenosis
• Degenerative changes, including facet joint changes, disc disease
and bone spurs
• Herniated discs
• Thickening of the ligamenta flava or posterior longitudinal
ligament
 • Spinal fractures
• Spondylolisthesis (anterior displacement of a vertebra out of line
with the one below)
• Tumours

Presentation

Symptoms of spinal stenosis tend to have a gradual onset (as

opposed to cauda equina syndrome or sudden disc herniation with cord
compression).

The severity of symptoms will depend on the degree of narrowing and

spinal cord compression. Symptoms may be subtle with mild
compression. Severe compression can present with features of cauda
equina syndrome (saddle anaesthesia, sexual dysfunction and
incontinence of the bladder and bowel), requiring emergency
management.
Intermittent neurogenic claudication is a key presenting feature of
lumbar spinal stenosis with central stenosis. It is sometimes referred to
as pseudoclaudication. Typical symptoms are:
• Lower back pain
• Buttock and leg pain
• Leg weakness

The symptoms are absent at rest and when seated but occur with
standing and walking. Bending forward (flexing the spine) expands the
spinal canal and improves symptoms. Standing straight (extending the
spine) narrows the canal and worsens the symptoms.

Lateral stenosis and foramina stenosis in the lumbar spine tends to

cause symptoms of sciatica.

The term radiculopathy refers to compression of the nerve roots as

they exit the spinal cord and spinal column, leading to motor and sensory
symptoms.

TOM TIP: The important thing for your exams is to spot the
typical symptoms of intermittent neurogenic claudication. At first
glance, they are similar to peripheral arterial disease. The exam
question might specify that the peripheral pulses or the ankle-
brachial pressure index (ABPI) are normal, in which case the
diagnosis is more likely to be spinal stenosis. Additionally, patients
with spinal stenosis are more likely to struggle with back pain,
whereas back pain is not a feature of peripheral arterial disease.

Investigations

MRI is the primary imaging investigation for diagnosing spinal

stenosis.

Investigations to exclude peripheral arterial disease (e.g., ankle-

brachial pressure index and CT angiogram) may be appropriate where
symptoms of intermittent claudication are present.

Management

Management will be guided by a spinal specialist based on individual

factors. Options include:
• Exercise and weight loss (if appropriate)
• Analgesia
• Physiotherapy
• Decompression surgery where conservative treatment fails (with
variable results)

Laminectomy refers to the removal of part or all of the lamina from

the affected vertebra. The laminae are the bony parts that form the
posterior part of the vertebral foramen (forming the spinal canal) and
attaches to the spinous process.

The benefits of epidural injections with local anaesthetic and

corticosteroids are unclear, and they are not generally used.
 Meralgia Paraesthetica
Meralgia paraesthetica refers to localised sensory symptoms of the
outer thigh caused by compression of the lateral femoral cutaneous
nerve. It is a mononeuropathy, meaning it only affects a single nerve.

Basic Anatomy

The lateral femoral cutaneous nerve originates from varying

combinations of L1, L2 and L3 nerve roots. It comes from behind the
psoas muscle, around the surface of the iliacus muscle and under the
inguinal ligament onto the thigh, just medial and inferior to the anterior
superior iliac spine (ASIS).

It supplies sensory innervation to the upper-outer thigh. Pressure,

deformity or trauma to the nerve can occur at several places. Notably, this
can occur where it passes below the inguinal ligament.

The lateral femoral cutaneous nerve only carries sensory signals.

Therefore, there are no motor symptoms with meralgia paraesthetica.
 Presentation

Patients present with abnormal sensations (dysaesthesia) and loss

of sensation (anaesthesia) in the lateral femoral cutaneous
nerve distribution. The skin of the upper-outer thigh is affected. Patients
may describe symptoms of:
 • Burning
• Numbness
• Pins and needles
• Cold sensation

There may also be localised hair loss.

Symptoms are aggravated by walking or standing for a long duration,

and improve when sitting down.

Symptoms are often worse with extension of the hip on the affected
side. This can be used to reproduce symptoms on examination.

Diagnosis

The diagnosis is mainly clinical, based on history and examination

findings. Investigations may be used to rule out other causes (e.g., nerve
root compression in the spine or pelvic tumours compressing the nerve).

Management

Symptoms vary from mild and self-limiting to severe and persistent.

Management can be conservative, medical or surgical.

Conservative management involves:

• Rest
• Looser clothing (tight clothes such as belts may add pressure to the
nerve)
• Weight loss (if appropriate)
• Physiotherapy

Medical management is based around analgesia if pain is a feature,

such as:
• Paracetamol
• NSAIDs
• Neuropathic analgesia (e.g., amitriptyline, gabapentin, pregabalin
or duloxetine)
• Local injections of steroids or local anaesthetics
Surgical management may involve:
• Decompression - removing pressure on the nerve
• Transection - cutting the nerve
• Resection - removing the nerve
 Trochanteric Bursitis
Trochanteric bursitis refers to inflammation of a bursa over the
greater trochanter on the outer hip. It produces pain localised at the
outer hip, referred to as greater trochanteric pain syndrome.

Bursae are sacs created by synovial membrane filled with a small

amount of synovial fluid. They are found at bony prominences (e.g., at
the greater trochanter, knee, shoulder and elbow). They act to reduce
friction between the bones and soft tissues during movement.

Bursitis refers to inflammation of a bursa. This causes thickening of

the synovial membrane and increased fluid production, causing swelling.
The inflammation can have several causes:
• Friction from repetitive movements
 • Trauma
• Inflammatory conditions (e.g., rheumatoid arthritis)
• Infection - referred to as septic bursitis

Presentation

The typical presentation is a middle-aged patient with gradual-onset

lateral hip pain (over the greater trochanter) that may radiate down the
outer thigh. The pain is described as aching or burning. It is worse with
activity, standing after sitting for a prolonged period and trying to sit cross-
legged. It may disrupt sleep and be difficult to find a comfortable lying
position.

On examination, there is tenderness over the greater trochanter.

There is not usually any swelling (unlikely bursitis in other areas).

The NICE clinical knowledge summaries (updated 2016) suggest

special tests to establish the diagnosis:
• Trendelenburg test
• Resisted abduction of the hip
• Resisted internal rotation of the hip
• Resisted external rotation of the hip

The Trendelenburg test involves asking the patient to stand one-

legged on the affected leg. Normally, the other side of the pelvis should
remain level or tilt upwards slightly. A positive Trendelenburg test is when
the other side of the pelvis drops down, suggesting weakness in the
affected hip.

To perform the resisted movements, ask the patient to perform a

movement while you resist that movement. For example, with the patient
lying supine, ask them to abduct their leg at the hip while you resist the
movement. This causes the soft tissues associated with the bursa to
tighten, causing pain. Pain on resisted movement supports a diagnosis of
bursitis.

Management

The diagnosis is based on the history and examination findings.

 Management options are:

• Rest
• Ice
• Analgesia (e.g., ibuprofen or naproxen)
• Physiotherapy
• Steroid injections

Rarely, trochanteric bursitis can be caused by infection. This may

present with warmth, erythema, swelling and pain over the bursa. The
patient may have a fever. Treatment involves antibiotics.

It can take 6-9 months to recover fully, sometimes longer.

 Meniscal Tears
Meniscal tears are a common form of knee injury. They involve
damage to the meniscus, which is the cartilage in the knee joint. It is
sometimes described to patients as damage to the cartilage.

Basic Knee Anatomy

The knee is a hinge joint. Between the femur and the tibia are the
menisci. There is a medial and lateral meniscus. The rounded bones at
the end of the femur (condyles) do not match the slightly convex areas
(also called condyles) at the top of the tibia. Therefore, the menisci help
the femur and tibia fit together and move smoothly across each other.
They act as a shock absorber, distribute weight throughout the joint and
help stabilise the joint.

Also in the knee is a joint between the anterior femur and the patella
(patellofemoral joint). The patella sits in a groove on the femur called
the trochlea (or patellofemoral groove). The quadriceps tendon
attaches to the patella, which is attached to the tibia by the patellar
tendon. Contraction of the quadriceps muscles causes knee extension
by pulling through the patella.

There are four ligaments in the knee:

• Anterior cruciate ligament
• Posterior cruciate ligament
• Lateral collateral ligament
• Medial collateral ligament
 Presentation

Meniscal tears often occur during twisting movements in the knee. In

young patients, this often happens when playing sports.

With increasing age, the meniscus becomes more prone to injury.

Tears can occur with minor twisting movements in older patients (e.g.,
standing from seated with an awkward twist in the knee).

The initial injury can be accompanied by a “pop” sound or sensation.

Symptoms include:

• Pain
• Swelling
• Stiffness
• Restricted range of motion
• Locking of the knee
• Instability or the knee “giving way”

Pain may be referred to the hip or lower back.

Examination findings are:

• Localised tenderness to the joint line
 • Swelling
• Restricted range of motion

Traditionally, the two key special tests for meniscal tears are
McMurray’s test and the Apley grind test. These are generally not used
or recommended in clinical practice as they can cause pain and may
worsen the meniscal injury.

McMurray’s Test

McMurray’s test involves the patient lying supine. The examiner

takes the leg and flexes the knee.

While internally rotating the tibia (by turning the foot inwards) and
applying varus pressure to the knee (applying outward pressure to the
inside of the knee), carefully extend the knee. Pain or restriction indicates
lateral meniscal damage.

Repeating the flexed-to-extended movement with external rotation of

the tibia and valgus (inward) pressure on the knee tests for medial
meniscal damage.

Apley Grind Test

The Apley grind test involves the patient lying prone and flexing the
knee to 90 degrees with the thigh flat on the couch. Downward pressure is
applied through the leg into the knee, and the tibia is internally and
externally rotated at the same time. Pain indicates a positive result,
suggesting meniscal damage. The pain is localised to the area of damage
(e.g., medial or lateral meniscus).

Ottawa Knee Rules

Bone fractures are worth considering as a differential diagnosis in

patients presenting with acute knee injuries. The Ottawa knee rules can
be used to determine whether a patient requires an x-ray of the knee
after an acute knee injury to look for a fracture.
 The Ottawa knee rules state that a patient requires a knee x-ray if any
of the following are present:
• Age 55 or above
• Patella tenderness (with no tenderness elsewhere)
• Fibular head tenderness
• Cannot flex the knee to 90 degrees
• Cannot weight bear (cannot take 4 steps - limping steps still count)

Investigations

MRI scan is usually the first-line imaging investigation for establishing

the diagnosis.

Arthroscopy can be used to visualise the meniscus within the joint

and is the gold-standard investigation for diagnosing a meniscal tear.
Arthroscopy can also be used to repair or remove damaged sections of
the meniscus.

Management

The NICE clinical knowledge summaries on knee pain (updated 2017)

recommend urgent referral in patients with an acute onset of knee pain
associated with symptoms suggestive of an acute meniscal tear. Local
pathways vary, and this may involve sending the patient to A&E or the
fracture clinic. Key symptoms include:
• A “pop”
• Rapid onset swelling
• Instability or giving way
• Locking

Conservative management of most acute soft tissue injuries,

including meniscal tears, is with the RICE mnemonic:
• R - Rest
• I - Ice
• C - Compression
• E - Elevation

NSAIDs are usually used first-line for analgesia in musculoskeletal

injuries.
 Physiotherapy can be used for rehabilitation after the initial pain and
swelling have settled.

Surgery may be required. This involves arthroscopy (keyhole

surgery) of the knee joint. The main options are:
• Repair of the meniscus, if possible
• Resection of the affected portion of the meniscus (this often results
in osteoarthritis)
 Anterior Cruciate Ligament Injury
Injury to either the anterior cruciate ligament (ACL) or posterior
cruciate ligament (PCL) can cause instability in the knee.

Damage to the ACL is common, particularly among athletes. PCL

injuries are less common.

Basic Anatomy

At the top of the tibia, there are the medial and lateral condyles,
which are slightly convex surfaces that correspond to the condyles of the
femur. Between the condyles, there is an intercondylar area. The
cruciate ligaments are named after where they attach to the tibia:
• The ACL attaches at the anterior intercondylar area on the tibia
• The PCL attaches at the posterior intercondylar area on the tibia
 There are rounded areas of bone at the end of the femur, which are
also called condyles. At the back of the distal end of the femur is an
intercondylar notch, which is a groove between the two condyles. Both
cruciate ligaments originate from the intercondylar notch, the ACL on
the lateral aspect and the PCL on the medial aspect.

The ACL stops the tibia from sliding forward in relation to the femur.
The PCL stops the tibia sliding backwards in relation to the femur.

Presentation

The ACL is typically damaged during a twisting injury to the knee.

The injury causes:

• Pain
 • Swelling
• “Pop” sound or sensation

Patients with ACL injuries will have instability of the knee joint. The
tibia can move anteriorly below the femur. The knee can buckle, and
patients often feel a lack of confidence that the knee is stable. Over time,
muscle weakness develops, and there is an increased risk of other knee
injuries (e.g., meniscal tears).

The anterior drawer test can be used to assess for anterior cruciate
ligament damage. The patient is supine with the hip flexed to 45 degrees
and the knee flexed to 90 degrees, with the foot flat on the couch. The
examiner sits on the patient’s toes to stabilise the foot. The examiner
holds the leg just below the knee and pulls the proximal tibia anteriorly,
sliding it forward from the femur at the knee. In a normal knee, there will
be slight anterior movement of the proximal tibia but a definite end-point
to movement, as the ACL holds the joint securely. With ACL damage, the
tibia can move an excessive distance anteriorly, and the examiner will not
be able to feel a clear end-point to the movement.

The Lachman test is similar to the anterior drawer test, but the knee
is tested while flexed at around 20-30 degrees.

Examination can be difficult to interpret shortly after the injury due to

pain and swelling. Examination after the acute pain and swelling has
settled is more likely to be accurate.

Investigations

MRI scan is usually the first-line imaging investigation for establishing

the diagnosis.

Arthroscopy can be used to visualise the cruciate ligaments and is

the gold-standard investigation for diagnosing a cruciate ligament tear.

Management

The NICE clinical knowledge summaries on knee pain (updated 2017)

recommend urgent referral in patients with an acute onset of knee pain
associated with symptoms suggestive of an acute anterior cruciate
ligament tear. Local pathways vary, and this may involve sending the
patient to A&E or the fracture clinic. Symptoms suggestive of an acute
anterior cruciate ligament tear include:
• A “pop”
• Rapid onset swelling
• Instability or giving way

Conservative management involves RICE:

• R - Rest
• I - Ice
• C - Compression
• E - Elevation

NSAIDs are usually used first-line for analgesia in musculoskeletal

injuries.

Crutches and knee braces may be required to help protect the knee
while mobilising.

Physiotherapy can be used before and after surgery for

rehabilitation.

Arthroscopic surgery to reconstruct the ligament is often required,

particularly in active and young patients. The type and timing of surgery
will be based on individual factors, such as the extent of the ACL injury
and the patient’s activities (e.g., are they a young competitive athlete or a
sedentary older patient). A new ligament is formed using a graft of tendon
from another location. Options for graft tendons used to reconstruct the
ACL include:
• Hamstring tendon
• Quadriceps tendon
• Bone-patellar tendon-bone (taking part of the patella tendon as
well as the bone it inserts into)
 Osgood-Schlatter Disease
Osgood-Schlatter disease is caused by inflammation at the tibial
tuberosity where the patella ligament/tendon inserts. It is a common
cause of anterior knee pain in adolescents.

It typically occurs in patients aged 10 – 15 years and is more common

in males. Osgood-Schlatter disease is usually unilateral, but it can be
bilateral.

Pathophysiology

The patella ligament/tendon inserts into the tibial tuberosity. In

patients with Osgood-Schlatter disease, multiple minor avulsion
fractures occur where the patella ligament pulls away tiny pieces of the
bone. This leads to growth of the tibial tuberosity, causing a visible lump
below the knee. Initially, this lump is tender due to inflammation. As the
bone heals and the inflammation settles, the lump becomes hard and
non-tender.

A hard, non-tender lump is then permanently present at the tibial

tuberosity.
Presentation

Osgood-Schlatter disease presents with a gradual onset of symptoms:

• Visible or palpable hard and tender lump at the tibial tuberosity
• Pain in the anterior aspect of the knee
• The pain is exacerbated by physical activity, kneeling and on
extension of the knee

Management
 Initial management focuses on reducing pain and inflammation,
including:

• Reduction in physical activity

• Ice
• NSAIDS (e.g., ibuprofen) for symptomatic relief

Once symptoms settle, stretching and physiotherapy can be used to

strengthen the joint and improve function.

Prognosis

Symptoms will fully resolve over time. The patient is usually left with a
hard bony lump on their knee.

A rare complication is a complete avulsion fracture, where the tibial

tuberosity is separated from the rest of the tibia. This requires surgical
intervention.
 Baker’s Cyst
Baker’s cysts are also called popliteal cysts. A Baker’s cyst is a fluid-
filled sac in the popliteal fossa, causing a lump or swelling at the back of
the knee.

The popliteal fossa is the diamond-shaped hollow area formed by

the:
• Semimembranosus and semitendinosus tendons (superior and
medial)
• Biceps femoris tendon (superior and lateral)
• Medial head of the gastrocnemius (inferior and medial)
• Lateral head of the gastrocnemius (inferior and lateral)

Pathophysiology

In adults, Baker’s cysts are usually secondary to degenerative

changes in the knee joint. They can be associated with:
• Meniscal tears (an important underlying cause)
• Osteoarthritis
• Knee injuries
• Inflammatory arthritis (e.g., rheumatoid arthritis)

Synovial fluid is squeezed out of the knee joint and collects in the
popliteal fossa. A connection between the synovial fluid in the joint and
the Baker’s cyst can remain, allowing the cyst to continue enlarging as
more fluid collects there.

Baker’s cysts are contained within the soft tissues. They do not have
their own epithelial lining.

Presentation

Patients may present with symptoms localised to the popliteal fossa:

• Pain or discomfort
• Fullness
 • Pressure
• A palpable lump or swelling
• Restricted range of motion in the knee (with larger cysts)

On examination, the lump will be most apparent when the patient

stands with their knees fully extended. The lump will get smaller or
disappear when the knee is flexed to 45 degrees (Foucher’s sign).

Oedema may occur if the cyst compresses the venous drainage of the
leg.

Ruptured Baker’s Cyst

Baker’s cysts can rupture if the pressure is large enough.

A ruptured Baker’s cyst will cause inflammation in the surrounding

tissues and calf muscle, presenting with:

• Pain
• Swelling
• Erythema

A critical differential diagnosis of a ruptured Baker’s cyst is a deep

vein thrombosis (DVT).

A ruptured Baker’s cyst can rarely cause compartment syndrome.

Differential Diagnoses

The key differential diagnoses of a lump in the popliteal fossa are:

• Deep vein thrombosis
• Abscess
• Popliteal artery aneurysm
• Ganglion cyst
• Lipoma
• Varicose veins
• Tumour

Investigations
 Ultrasound is usually the first-line investigation to confirm the
diagnosis. It is also used to rule out a DVT.

MRI can evaluate the cyst further if required, for example, before
surgery. They can also demonstrate underlying knee pathology, such as
meniscal tears.

Management

No treatment is required for asymptomatic Baker’s cysts.

Non-surgical management for symptomatic Baker’s cysts include:

• Modified activity to avoid exacerbating symptoms
• Analgesia (e.g., NSAIDs)
• Physiotherapy
• Ultrasound-guided aspiration
• Steroid injections

Surgical management typically involves arthroscopic procedures to

treat underlying knee pathology contributing to the cyst, such as
degenerative changes or meniscal tears. Resection of the cyst is difficult,
and the cyst is likely to recur, particularly when another knee pathology is
present.
 Achilles Tendinopathy
The Achilles tendon connects the calf muscles (gastrocnemius and
soleus) to the heel (the calcaneus bone). Flexion of the calf muscles
pulls on the Achilles and causes plantar flexion of the ankle.

Achilles tendinopathy involves damage, swelling, inflammation and

reduced function in the Achilles tendon.

There are two types of Achilles tendinopathy:

• Insertion tendinopathy (within 2cm of the insertion point on the
calcaneus)
• Mid-portion tendinopathy (2-6 cm above the insertion point)

Risk Factors

• Sports that stress the Achilles (e.g., basketball, tennis and track
athletics)
• Inflammatory conditions (e.g., rheumatoid arthritis and ankylosing
spondylitis)
• Diabetes
• Raised cholesterol
• Fluoroquinolone antibiotics (e.g., ciprofloxacin and levofloxacin)

Presentation

The typical presentation is with a gradual onset of:

• Pain or aching in the Achilles tendon or heel, with activity

• Stiffness
• Tenderness
• Swelling
• Nodularity on palpation of the tendon

Management
 Achilles tendinopathy is a clinical diagnosis and does not usually
require any investigations to diagnose. It is essential to exclude Achilles
tendon rupture, for example, using Simmonds’ calf squeeze test.
Ultrasound is used to diagnose Achilles tendon rupture.

Management options are:

• Rest and altered activities
• Ice
• Analgesia
• Physiotherapy
• Orthotics (e.g., insoles)
• Extracorporeal shock-wave therapy (ESWT)
• Surgery to remove nodules and adhesions or alter the tendon may
be used where other treatments fail

Steroid injections into the Achilles tendon are avoided due to the
risk of tendon rupture.
 Achilles Tendon Rupture
Achilles tendon rupture is a sudden onset injury resulting in rupture of
the Achilles tendon and a loss of the connection between the calf muscles
(gastrocnemius and soleus) to the heel (the calcaneus bone).

Risk factors for Achilles tendon rupture are:

• Sports that stress the Achilles (e.g., basketball, tennis and track
athletics)
• Increasing age
• Existing Achilles tendinopathy
• Family history
• Fluoroquinolone antibiotics (e.g., ciprofloxacin and levofloxacin)
• Systemic steroids

TOM TIP: It is worth remembering the association between

fluoroquinolone antibiotics and Achilles tendinopathy and rupture.
Rupture can occur spontaneously within 48 hours of starting
treatment. This knowledge is commonly tested in exams. It is also
important to warn patients starting fluoroquinolone antibiotics to
look out for any signs of Achilles tendinitis and stop treatment if
they occur.

Presentation

The typical presentation is:

• Sudden onset of pain in the Achilles or calf
• A snapping sound and sensation
• Feeling as though something has hit them in the back of the leg

There are often no prior warning signs or symptoms.

Signs on examination are:

• When relaxed in a dangled position, the affected ankle will rest in a
more dorsiflexed position
• Tenderness to the area
 • A palpable gap in the Achilles tendon (although swelling might
hide this)
• Weakness of plantar flexion of the ankle (dorsiflexion is
unaffected)
• Unable to stand on tiptoes on the affected leg alone
• Positive Simmonds’ calf squeeze test

Simmonds’ calf squeeze test is the special test for Achilles tendon
rupture. The patient is positioned prone or kneeling with the feet hanging
freely off the end of the bench or couch. When squeezing the calf muscle
in a leg with an intact Achilles, there will be plantar flexion of the ankle.
Squeezing the calf pulls on the Achilles. When the Achilles is ruptured,
the connection between the calf and the ankle is lost. Squeezing the calf
will not cause plantar flexion of the ankle in a leg with a ruptured Achilles.
A lack of plantar flexion is a positive result.

Diagnosis

Ultrasound is the investigation of choice for confirming the diagnosis.

Management

Patients with suspected Achilles rupture should be reviewed by

orthopaedics on the same day.

Immediate management involves:

• Rest and immobilisation

• Ice
• Elevation
• Analgesia

Venous thromboembolism prophylaxis needs to be considered

while the ankle is immobilised.

There is a debate between non-surgical and surgical management.

Healing rates are similar between the two. Non-surgical management
avoids the risks associated with surgery (e.g., anaesthetic risks, poor
wound healing and infection) but has a higher risk of re-rupture.
 Non-surgical management involves applying a specialised boot to
immobilise the ankle. The first boot involves full plantar flexion of the
ankle. Over time, the boots are altered to gradually move the ankle from
full plantar flexion to a neutral position. This process takes 6-12 weeks,
during which the Achilles tendon heals. A long rehabilitation process is
required to get back to full pre-injury function.

Surgical management involves surgically reattaching the Achilles.

After surgery, a similar process is followed to non-surgical management,
with boots that immobilise the ankle initially in a plantar-flexed position,
gradually adjusted to a neutral position. This is followed by a long
rehabilitation process to get back to full pre-injury function.
 Common Foot Problems
Plantar Fasciitis

Plantar fasciitis is inflammation of the plantar fascia.

The plantar fascia is thick connective tissue. It attaches to the

calcaneus at the heel, travels along the sole of the foot and branches out
to connect to the flexor tendons of the toes.

Presentation is with a gradual onset of pain on the plantar aspect of

the heel. This is worse with pressure, particularly when walking or
standing for prolonged periods. There is tenderness to palpation of this
area.

Management involves:
• Rest
• Ice
• Analgesia (e.g., NSAIDs)
 • Physiotherapy
• Steroid injections (can be very painful and rarely cause rupture of
the plantar fascia or fat pad atrophy)

Rarely, specialist management may be required, with:

• Extracorporeal shockwave therapy
• Surgery

Fat Pad Atrophy

Fat pad atrophy affects the fat pad over the heel of the foot (under the
calcaneus). The fat pad protects the heel from impact.

Atrophy (wasting away) of the fat pad can occur with age or
inflammation from repetitive impacts, such as jumping activities, running,
walking, and obesity. Local steroid injections (used to treat plantar
fasciitis) can cause fat pad atrophy.
Symptoms are similar to plantar fasciitis, with pain and tenderness
over the plantar aspect of the heel. Symptoms are worse with activities,
particularly when barefoot on hard surfaces.

The thickness of the fat pad can be measured with an ultrasound

scan.

Management involves comfortable shoes, custom insoles, adapting

activities (e.g., avoiding high heels) and weight loss if appropriate.

Morton’s Neuroma

Morton’s neuroma refers to the dysfunction of a nerve in the

intermetatarsal space (between the toes) towards the top of the foot.
The abnormal nerve is usually located between the third and fourth
metatarsal. It is caused by irritation of the nerve relating to the
biomechanics of the foot. High-heels or narrow shoes may exacerbate it.
Typical symptoms are:
• Pain at the front of the foot at the location of the lesion
• The sensation of a lump in the shoe
• Burning, numbness or “pins and needles” felt in the distal toes

There are several ways to test for Morton’s neuroma:

 • Deep pressure applied to the affected intermetatarsal space on
the dorsal foot causes pain
• Metatarsal squeeze test - squeezing the forefoot with one hand to
create a concave shape to the plantar aspect while using the other
hand to press the affected area on the plantar side of the foot
causes pain
• Mulder’s sign - a painful click is felt when using two hands on
either side of the foot to manipulate the metatarsal heads to rub the
neuroma

Ultrasound or MRI can be used to confirm the diagnosis.

Management options include:

• Adapting activities (e.g., avoiding high heels)
• Analgesia (NSAIDs if suitable)
• Insoles
• Weight loss if appropriate
• Steroid injections
• Radiofrequency ablation
• Surgery (e.g., excision of the neuroma)

Bunions (Hallux Valgus)

The medical name for bunions is hallux valgus (hallux refers to the
big toe, and valgus refers to the angle of the deformity).

A bunion is a bony lump created by a deformity at the

metatarsophalangeal joint (MTP) at the base of the big toe. The first
metatarsal becomes angled medially, the big toe (hallux) become
angled laterally (towards the other toes), and the MTP joint becomes
inflamed and enlarged. Over time, additional stress on the joint can result
in osteoarthritis.
 Bunions develop slowly. The cause is not clear. They can be painful,
particularly when walking and wearing tight shoes.
 Weight-bearing x-rays can be used to assess the extent of the
deformity.

Conservative management is with wide, comfortable shoes and

analgesia. Patients can use bunion pads to protect the bunion from
friction inside their shoes.

Surgery is the definitive treatment. There are various options

depending on individual factors. The aim is to realign the bones and
correct the deformity.

Gout

Gout is a common cause of pain and swelling in the

metatarsophalangeal joint (MTP) at the base of the big toe. It can also
affect the ankle, wrists, base of the thumb or knee.

Gout is a type of crystal arthropathy associated with chronically high

blood uric acid levels. Urate crystals collect in the joint, causing it to
become acutely hot, swollen and painful.

Diagnosis is usually made clinically. It is essential to exclude septic

arthritis as a differential diagnosis. This may require joint fluid
aspiration.

Aspirated fluid will show:

• No bacterial growth
• Needle shaped crystals
• Negatively birefringent of polarised light
• Monosodium urate crystals

Management during the acute flare is with:

• NSAIDs (e.g. ibuprofen) are first-line
• Colchicine second-line
• Steroids can be considered third-line

Allopurinol is a xanthine oxidase inhibitor used for the

prophylaxis of gout. It reduces the uric acid level.
 Lifestyle changes can reduce the risk of developing gout. This
involves losing weight, staying hydrated and minimising the consumption
of alcohol and purine-based foods (such as meat and seafood).

TOM TIP: Do not initiate allopurinol prophylaxis until after the

acute attack has settled. Starting allopurinol can cause or worsen an
attack of gout. When a patient is already using allopurinol, they can
continue taking it during further acute episodes.
 Frozen Shoulder
Frozen shoulder is also called adhesive capsulitis. It is a relatively
common cause of shoulder pain and stiffness. The loss of range of
motion and function in the shoulder joint can significantly impair activities.

It most commonly affects people in middle age. Diabetes is a key risk

factor.

Adhesive capsulitis can be:

• Primary - occurring spontaneously without any trigger
• Secondary - occurring in response to trauma, surgery or
immobilisation

Pathophysiology

The glenohumeral joint is the ball and socket joint in the shoulder. It is
surrounded by connective tissue that forms the joint capsule.

In adhesive capsulitis, inflammation and fibrosis in the joint capsule

lead to adhesions (scar tissue). The adhesions bind the capsule and
cause it to tighten around the joint, restrict movement in the joint.

Presentation

There is a typical course of symptoms, with three phases:

• Painful phase - shoulder pain is often the first symptom and may
be worse at night
• Stiff phase - shoulder stiffness develops and affects both active
and passive movement (external rotation is the most affected) - the
pain settles during this phase
• Thawing phase - there is a gradual improvement in stiffness and a
return to normal

The entire illness lasts 1-3 years before resolving (e.g., 6 months in
each phase). However, a large number of patients (up to 50%) have
persistent symptoms.
 Differential Diagnosis

The main differentials in a patient presenting with shoulder pain not

preceded by trauma or an acute injury are:
• Supraspinatus tendinopathy
• Acromioclavicular joint arthritis
• Glenohumeral joint arthritis

Rare but important differentials to keep in mind are:

• Septic arthritis
• Inflammatory arthritis
• Malignancy (e.g., osteosarcoma or bony metastasis)

Shoulder pain preceded by trauma or an acute injury may be due to:

• Shoulder dislocation
• Fractures (e.g., proximal humerus, clavicle or rarely the scapula)
• Rotator cuff tear

Supraspinatus tendinopathy involves inflammation and irritation of

the supraspinatus tendon, particularly due to impingement at the point
where it passes between the humeral head and the acromion. The
empty can test (AKA Jobe test) can be used to assess for
supraspinatus tendinopathy. This involves the patient abducting the
shoulder to 90 degrees and fully internally rotating the arm as though they
are emptying a can of water. The examiner pushes down on the arm
while the patient resists. The test is positive if there is pain or the arm
gives way.

Acromioclavicular (AC) joint arthritis can be demonstrated on

examination by:
• Tenderness to palpation of the AC joint
• Pain is worse at the extremes of the shoulder abduction, from
around 170 degrees onwards when the arm is overhead
• Positive scarf test - pain caused by wrapping the arm across the
chest and opposite shoulder like a scarf

Diagnosis
 Adhesive capsulitis is a clinical diagnosis based on the history and
examination and excluding other causes of shoulder pain and stiffness.
Imaging investigations are not usually required.

X-rays are usually normal. However, they are helpful for diagnosing
osteoarthritis as a differential.

Ultrasound, CT or MRI scans can show a thickened joint capsule.

Management

Non-surgical options for improving symptoms and speeding up

recovery are:
• Continue using the arm but don’t exacerbate the pain
• Analgesia (e.g., NSAIDs)
• Physiotherapy
• Intra-articular steroid injections
• Hydrodilation (injecting fluid into the joint to stretch the capsule)

Surgery may be used in particularly resistant or severe cases. The

options are:
• Manipulation under anaesthesia - forcefully stretching the
capsule to improve the range of motion
• Arthroscopy - keyhole surgery on the shoulder to cut the
adhesions and release the shoulder
 Rotator Cuff Tears
Rotator cuff tears refer to injury to the tendons of the rotator cuff
muscles. The tendon may be partially or fully torn.

Tears of the rotator cuff can occur due to an acute injury (e.g., a fall
onto an outstretched hand) or degenerative changes with age. They may
be related to overhead activities, such as playing tennis or overhead
construction work.

Basic Anatomy

The rotator cuff is made of four muscles, each with a specific action at
the shoulder (mnemonic is SITS):
• S - Supraspinatus - abducts the arm
• I - Infraspinatus - externally rotates the arm
• T - Teres minor - externally rotates the arm
• S - Subscapularis - internally rotates the arm

Presentation

Rotator cuff tears may present either with an acute onset of symptoms
after an acute injury, or with a gradual onset of symptoms. Patients
typically present with:
• Shoulder pain
• Weakness and pain with specific movements relating to the site of
the tear (e.g., abduction with a supraspinatus tear)

Patients may find it difficult to get comfortable at night due to pain in

the shoulder, disrupting sleep.

Investigations

X-rays will not show soft tissue injuries such as rotator cuff tears.
They may be helpful for excluding bony pathology, such as osteoarthritis.

Ultrasound or MRI scans can diagnose a rotator cuff tear.

 Management

Patients with degenerative rotator cuff tears may be managed

conservatively, particularly where they are at increased risk of
complications from surgery. Active or young patients and those with acute
or full-thickness tears are more likely to be managed with surgery.
Surgery may be used where physiotherapy fails.

Non-surgical options are:

• Rest and adapted activities

• Analgesia (e.g., NSAIDs)
• Physiotherapy

There are many options for surgical management, depending on

individual factors. The main option is arthroscopic rotator cuff repair,
where the tendon is reattached to the bone during an arthroscopy
(keyhole surgery).
 Shoulder Dislocation
Shoulder dislocation is where the ball of the shoulder (head of the
humerus) comes entirely out of the socket (glenoid cavity of the
scapula).

Subluxation refers to a partial dislocation of the shoulder. The ball

does not come fully out of the socket and naturally returns back into place
shortly afterwards.

More than 90% of shoulder dislocations are anterior dislocations.

This is where the head of the humerus moves anteriorly (forward) in
relation to the glenoid cavity. This can occur when the arm is forced
backwards (posteriorly) whilst abducted and extended at the shoulder.
Picture someone reaching up and out to try and catch a heavy rock
travelling towards them.

Posterior dislocations are associated with electric shocks and

seizures.

TOM TIP: Exam questions might challenge you to distinguish

between anterior and posterior dislocations. The answer is almost
certainly an anterior dislocation unless the patient has had a seizure
or an electric shock.

Associated Damage

The glenoid labrum surrounds the glenoid cavity. The labrum is a

rim of cartilage that creates a deeper socket for the head of the humerus
to fit into. When the shoulder dislocates, the labrum can tear along one
edge.

Bankart lesions are tears to the anterior portion of the labrum. These
occur with repeated anterior subluxations or dislocations of the shoulder.

Hill-Sachs lesions are compression fractures of the posterolateral

part of the head of the humerus. As the shoulder dislocates anteriorly, the
posterolateral part of the humeral head impacts with the anterior rim of
the glenoid cavity. Part of the humeral head is damaged, making the
shoulder less stable and at risk of further dislocations.

Axillary nerve damage is a key complication. The axillary nerve

comes from the C5 and C6 nerve roots. Damage causes a loss of
sensation in the “regimental badge” area over the lateral deltoid. It
also leads to motor weakness in the deltoid and teres minor muscles.

Fractures can occur alongside shoulder dislocations, affecting the:

• Humeral head
• Greater tuberosity of the humerus
• Acromion of the scapula
• Clavicle

Rotator cuff tears may occur with shoulder dislocations, particularly

in older patients.

TOM TIP: Axillary nerve damage is a common association with

anterior dislocations to remember for your exams. This knowledge
may be tested in MCQs, where you are asked to identify the nerve,
location of sensory loss or muscles affected by weakness.

Presentation

Patients with a shoulder dislocation usually present after the acute

injury. They will almost certainly be aware that the shoulder is dislocated.
Shortly after the shoulder is dislocated, the muscles will go into spasm
and tighten around the joint.

They will hold their arm against the side of their body. The deltoid will
appear flattened, and the head of the humerus will cause a bulge and be
palpable at the front of the shoulder.

It is important to assess patients with a shoulder dislocation for:

• Fractures
• Vascular damage (e.g., absent pulses, prolonged capillary refill time
and pallor)
 • Nerve damage (e.g., loss of sensation in the “regimental patch”
area)

Apprehension Test

The apprehension test is a special test to assess for shoulder

instability, specifically in the anterior direction. It is likely to be positive
after previous anterior dislocation or subluxation of the shoulder. This
may be performed after recovery from any acute injuries.

The patient lies supine. The shoulder is abducted to 90 degrees, and

the elbow is flexed to 90 degrees. The shoulder is then slowly externally
rotated in this position while watching the patient. As the arm approaches
90 degrees of external rotation, patients with shoulder instability will
become anxious and apprehensive, worried that the shoulder will
dislocate. There is no pain associated with the movement, only
apprehension.

Investigations

X-rays may be used in an acute presentation to confirm a dislocation

and exclude fractures. They are not always required before reduction,
depending on the clinical findings and risk of a fracture (see local policies
and ask seniors). X-rays are performed after reduction to confirm the
shoulder is reduced and assess for fractures.

Magnetic resonance arthrography is an MRI scan of the shoulder

with a contrast injected into the shoulder joint. This can be used to assess
the shoulder for damage (e.g., Bankart and Hill-Sachs lesions) and plan
for surgery.

Arthroscopy involves inserting a camera into the shoulder joint to

visualise the structures.

Acute Management

Ideally, the shoulder should be relocated as soon as safely possible.

Muscle spasm occurs over time, making it harder to relocate the shoulder
and increasing the risk of neurovascular injury during relocation.
 Acute management of a shoulder dislocation involves:
• Analgesia, muscle relaxants and sedation as appropriate
• Gas and air (e.g., Entonox) may be used, which contains a mixture
of 50% nitrous oxide and 50% oxygen
• A broad arm sling can be applied to support the arm
• Closed reduction of the shoulder (after excluding fractures)
• Dislocations associated with a fracture may require surgery
• Post-reduction x-rays
• Immobilisation for a period after relocation of the shoulder

There are various options for closed reduction of shoulder

dislocations. See local guidelines and get experienced senior input when
managing shoulder dislocations and for guidance on relocation
techniques.

Ongoing Management

There is a high risk of recurrent dislocations, particularly in younger

patients.

Physiotherapy is recommended to improve the function of the

shoulder and reduce the risk of further dislocations.

Shoulder stabilisation surgery may be required to improve stability

and prevent further dislocations. This may be an arthroscopic or an open
procedure. Underlying structural problems are corrected, such as:
• Repairing Bankart lesions
• Tightening the shoulder capsule
• Bone graft using bone from the coracoid process to correct a
bony injury to the glenoid rim (Latarjet procedure)
• Correcting Hill-Sachs lesions (Remplissage procedure)

There is a prolonged period of recovery and rehabilitation after

shoulder stabilisation surgery (3 months or more).

Recurrent instability and dislocations can occur in up to 20% of

patients after surgery.
 Olecranon Bursitis
Olecranon bursitis refers to inflammation and swelling of the bursa
over the elbow. The olecranon is the bony lump at the elbow, which is
part of the ulna bone.

Bursae are sacs created by synovial membrane filled with a small

amount of synovial fluid. They are found at bony prominences (e.g., at
the greater trochanter, knee, shoulder and elbow). They act to reduce the
friction between the bones and soft tissues during movement.
 Bursitis is inflammation of a bursa. This causes thickening of the
synovial membrane and increased fluid production, causing swelling. This
inflammation can be caused by a number of things:
• Friction from repetitive movements or leaning on the elbow
• Trauma
• Inflammatory conditions (e.g., rheumatoid arthritis or gout)
• Infection - referred to as septic bursitis

Olecranon bursitis is sometimes called “student’s elbow”, as

students may lean on their elbow for prolonged periods while studying,
resulting in friction and mild trauma, leading to bursitis. It can also occur in
people with occupations that require leaning on the elbow, such as
plumbers or drivers.

Presentation

The typical presentation is a young/middle-aged man with an elbow

that is:
• Swollen
• Warm
• Tender
• Fluctuant (fluid-filled)

It is important to identify where bursitis is caused by infection.

Features of infection are:
• Hot to touch
• More tender
• Erythema spreading to the surrounding skin
• Fever
• Features of sepsis (e.g., tachycardia, hypotension and confusion)

An important differential diagnosis is septic arthritis. Consider septic

arthritis if there is:
• Swelling in the joint (rather than the bursa)
• Painful and reduced range of motion in the elbow

Aspiration
 The NICE clinical knowledge summaries (updated January 2021)
recommend aspiration of fluid from the bursa when an infection is
suspected.

They advise that the appearance can give an indication of the

underlying cause:
• Pus indicates infection
• Straw-coloured fluid indicates infection is less likely
• Blood-stained fluid may indicate trauma, infection or inflammatory
causes
• Milky fluid indicates gout or pseudogout

Aspiration should ideally be performed before starting antibiotics. The

fluid is sent to the lab for microscopy and culture. During microscopy,
they will examine for crystals (gout and pseudogout) and do gram-
staining for bacteria.

Management

Management options for olecranon bursitis include:

• Rest
• Ice
• Compression
• Analgesia (e.g., paracetamol or NSAIDs)
• Protecting the elbow from pressure or trauma
• Aspiration of fluid may be used to relieve pressure
• Steroid injections may be used in problematic cases where
infection has been excluded

When infection is suspected or cannot be excluded, management

involves:
• Aspiration of the fluid for microscopy and culture
• Antibiotics

The NICE CKS recommend flucloxacillin first-line, with clarithromycin

as an alternative.

Patients that are systemically unwell (e.g., immunocompromised or

have sepsis) need admission to hospital for further management,
including:

• Bloods (including lactate)

• Blood cultures
• IV antibiotics
• IV fluids
 Repetitive Strain Injury
Repetitive strain injury (RSI) is an umbrella term that refers to soft
tissue irritation, microtrauma and strain resulting from repetitive
activities. It can affect the muscles, tendons and nerves. Lateral
epicondylitis (tennis elbow) is a specific example of a repetitive strain
injury.

Causes

Almost any repetitive movement can result in repetitive strain injury if

done long enough. It often results from occupational activities, where the
same movement is performed for many hours at a time, day after day.
Some common examples of activities are:
• Working on an assembly line in a factory, doing the same
movements over and over
• Using a computer mouse or keyboard (affecting the wrist and
forearm)
• Having a poor posture for an extended period whilst reading or
using a computer (affecting the neck and shoulders)
• Texting or scrolling on a smartphone (affecting the base of the
thumb)

Certain characteristics of an activity increase the risk of repetitive

strain injury, such as:
• Small repetitive activities (e.g., scrolling on a smartphone)
• Vibration (e.g., using power tools)
• Awkward positions (e.g., painting a ceiling)

Presentation

Usually, there will be a history of repetitive activities, often related to

work.

Symptoms will be located in an area related to the activity. They can

include:
 • Pain, exacerbated by using the associated joints, muscles and
tendons
• Aching
• Weakness
• Cramping
• Numbness

On examination, the area may be tender to palpation. There may be

mild swelling in the area. It may be possible to recreate the pain by having
the patient perform specific movements that add resistance to the
affected soft tissues.

Diagnosis

The diagnosis is usually made clinically, based on the history and

examination findings, without investigations.

Investigations may be used to rule out other causes for the symptoms
(e.g., arthritis, inflammatory conditions or nerve compression), such as:
• X-rays (e.g., to look for osteoarthritis)
• Ultrasound (e.g., to look for synovitis in rheumatoid arthritis or
rotator cuff tears)
• Blood tests (e.g., inflammatory markers and rheumatoid factor for
rheumatoid arthritis)

Management

The RICE mnemonic can be applied to most soft tissue injuries. This
stands for:
• R - Rest
• I - Ice
• C - Compression
• E - Elevation

Rest and adapting activities are essential. If the repetitive movement

continues, the condition will get worse. This often involves the patient
discussing their duties with the occupational health department at their
place of work to amend their work tasks.
Other potentially helpful options include:
• Analgesia (e.g., NSAIDs)
• Physiotherapy
• Steroid injections (in specific scenarios)
 Epicondylitis
Epicondylitis refers to inflammation at the point where the tendons
of the forearm insert into the epicondyles at the elbow. It is a specific
type of repetitive strain injury.

There is a medial epicondyle and a lateral epicondyle on the distal

end of the humerus, either side of the elbow joint.

The tendons of the muscles that insert into the:

• Medial epicondyle act to flex the wrist
• Lateral epicondyle act to extend the wrist
 Epicondylitis is the result of repetitive use and injury to the tendons at
the point of insertion. Symptoms gradually worsen over weeks to months.
It most commonly affects patients in middle age.

Lateral Epicondylitis

Lateral epicondylitis is often called tennis elbow.

Lateral epicondylitis causes pain and tenderness at the lateral

epicondyle (outer elbow). The pain often radiates down the forearm. It
can lead to weakness in grip strength.

Mill’s test involves stretching the extensor muscles of the forearm

while palpating the lateral epicondyle. The elbow is extended, the forearm
supinated, and the wrist and fingers are extended. The examiner holds
the patient’s elbow with pressure on the lateral epicondyle. If this causes
pain, the test is positive, indicating lateral epicondylitis.

Cozen’s test starts with the elbow extended, forearm pronated, wrist
deviated in the direction of the radius and hand in a fist. The examiner
holds the patient’s elbow with pressure on the lateral epicondyle. The
examiner applies resistance to the back of the hand while the patient
extends the wrist. If this causes pain, the test is positive, indicating lateral
epicondylitis.

Medial Epicondylitis

Medial epicondylitis is often called golfer’s elbow.

Medial epicondylitis causes pain and tenderness at the medial

epicondyle (inner elbow). The pain often radiates down the forearm. It
can lead to weakness in grip strength.

A golfer’s elbow test involves stretching the flexor muscles of the

forearm while palpating the medial epicondyle. The elbow is extended,
forearm supinated and wrist and fingers are extended. The examiner
holds the patient’s elbow with pressure on the medial epicondyle. If this
causes pain, the test is positive, indicating medial epicondylitis.

Diagnosis

Epicondylitis is a clinical diagnosis based on the signs and

symptoms.

Management

In most patients, epicondylitis is self-limiting and resolves with time.

However, symptoms can take several years to resolve.
 Management options for epicondylitis include:
• Rest
• Adapting activities
• Analgesia (e.g., NSAIDs)
• Physiotherapy
• Orthotics, such as elbow braces or straps
• Steroid injections
• Platelet-rich plasma (PRP) injections
• Extracorporeal shockwave therapy

Rarely, surgery may be required to debride, release or repair

damaged tendons.
 De Quervain’s Tenosynovitis
De Quervain’s tenosynovitis is a condition where there is swelling and
inflammation of the tendon sheaths in the wrist. It primarily affects two
tendons:
• Abductor pollicis longus (APL) tendon
• Extensor pollicis brevis (EPB) tendon

It is a type of repetitive strain injury and results in pain on the radial

side of the wrist.

One notable cause of bilateral De Quervain’s tenosynovitis is in new

parents repetitively lifting newborn babies in a way that stresses the
tendons of the thumb. For this reason, it is sometimes referred to as
“mummy thumb”.

Basic Anatomy and Pathophysiology

The abductor pollicis longus acts to abduct the thumb and abduct
the wrist. The tendon inserts into the base of the first metacarpal bone
(at the base of the thumb).

The extensor pollicis brevis also acts to abduct the thumb and
abduct the wrist. The tendon inserts into the base of the proximal
phalanx of the thumb.

Tendon sheaths can surround tendons. A tendon sheath is formed by

connective tissue (synovial membrane) that covers the tendons and is
filled with synovial fluid. They help lubricate and protect the movement
of the tendons within them.

The extensor retinaculum is a fibrous band that wraps across the

back (dorsal side) of the wrist. The APL and EPB pass underneath the
extensor retinaculum. Repetitive movement of the APL and EPB under
the extensor retinaculum result in inflammation and swelling of the
tendon sheaths.
 Presentation

Patients present with symptoms at the radial aspect of the wrist near
the base of the thumb. Typical symptoms include:
• Pain, often radiating to the forearm
• Aching
• Burning
• Weakness
• Numbness
• Tenderness

There is a special test for De Quervain’s tenosynovitis called

Finkelstein’s test. There is some confusion about what this is,
depending on where you look. Most sources describe the first manoeuvre
below as Finkelstein’s test, but it may be Eichhoff’s test.

Finkelstein’s test (or maybe Eichhoff’s test) involves the patient

making a fist with their thumb inside their fingers. Then, the wrist is
adducted (ulnar deviation), causing strain on the APL and EPB tendons. If
this movement causes pain at the radial aspect of the wrist, the test is
positive, indicating De Quervain’s tenosynovitis.

The original Finkelstein’s test involves the patient resting their

forearm on a surface in a neutral position with the wrist hanging off and
unsupported. The examiner holds the patient’s thumb and passively
flexes the thumb into the palm, causing the wrist to adduct (ulnar
deviation), putting strain on the APL and EPB tendons. If this causes pain
at the radial aspect of the wrist, the test is positive, indicating De
Quervain’s tenosynovitis.

Management

Management can involve:

• Rest and adapting activities
• Using splints to restrict movements
• Analgesia (e.g., NSAIDs)
• Physiotherapy
• Steroid injections

Rarely, surgery may be required to release (cut) the extensor

retinaculum, releasing the pressure and creating more space for the
tendons.
 Trigger Finger
Trigger finger is a condition that causes pain and difficulty moving the
affected finger. It is also known as stenosing tenosynovitis.

Pathophysiology

The flexor tendons of the fingers pass through several tunnels

(sheaths) along the length of the fingers. In trigger finger, there is
thickening of the tendon or tightening of the sheath. This prevents the
tendon from smoothly moving through the sheath when the finger is
flexed and extended, causing pain, stiffness, or “catching” symptoms.

The most commonly affected part of the sheath is the first annular
pulley (A1) at the metacarpophalangeal (MCP) joint.

There may be a nodule on the tendon. When the finger is flexed, the
nodule is outside the A1 pulley. As the finger is extended from a flexed
position, the tendon nodule can get stuck at the entrance to the A1
pulley. This causes the finger to lock or get stuck in the bent position. It
may release suddenly with a painful pop or click.
 Risk Factors

Patients more likely to be affected by trigger finger are:

• In their 40s or 50s
• Women (more often than men)
• People with diabetes (more with type 1, but also type 2)

Presentation

The typical presentation is with a troublesome finger, that:

• Is painful and tender (usually around the MCP joint on the palm-
side of the hand)
• Does not move smoothly
• Makes a popping or clicking sound
• Gets stuck in a flexed position

Symptoms are typically worse in the morning and improve during the
day.

Diagnosis
 Trigger finger is a clinical diagnosis based on the history and
examination findings.

Management

Management options include:

• Rest and analgesia (a small number resolve spontaneously)
• Splinting
• Steroid injections
• Surgery to release the A1 pulley
 Dupuytren’s Contracture
Dupuytren’s contracture is a condition where the fascia of the hand
becomes thickened and tight, leading to finger contractures.

A contracture is a shortening of the soft tissues, leading to restricted

movement in a joint. In Dupuytren’s contracture, the finger is tightened
into a flexed position and cannot fully extend.

Pathophysiology

The palmar fascia of the hand forms a triangle of strong connective

tissue on the palm.

In Dupuytren’s contracture, the fascia of the hands becomes thicker

and tighter and develops nodules. Cords of dense connective tissue can
extend into the fingers, pulling the fingers into flexion and restricting their
ability to extend (contracture).

It is unclear why the fascia becomes thicker and tighter. It is thought to

be an inflammatory process in response to microtrauma.

Risk Factors

• Age
• Family history (autosomal dominant pattern)
• Male
• Manual labour, particularly with vibrating tools
• Diabetes (more with type 1, but also type 2)
• Epilepsy
• Smoking and alcohol

Presentation

The first sign of Dupuytren’s contracture is the development of hard

nodules on the palm. There may be skin thickening and pitting. Slowly,
the fascia becomes thicker, and the finger is pulled into flexion. It
becomes impossible to fully extend the affected finger.

A thick, nodular cord can be palpated from the palm into the affected
finger.

The ring finger is most often affected. The index finger is least likely
to be affected.

Dupuytren’s contracture can significantly affect the function of the

hand. However, patients do not usually experience pain with the
condition.

The table-top test is a straightforward test for Dupuytren’s

contracture. The patient tries to position their hands flat on a table. If the
hand cannot rest completely flat, the test is positive, suggesting
Dupuytren’s contracture.

Management

The options for Dupuytren’s contracture are essentially to do nothing

(conservative management) or to treat it surgically. There are three
options for surgical management.

Needle fasciotomy (also known as needle aponeurotomy) involves

inserting a needle through the skin to divide and loosen the cord that is
causing the contracture.

Limited fasciectomy involves removing the abnormal fascia and cord

to release the contracture.

Dermofasciectomy involves removing the abnormal fascia and cord,

as well as the associated skin. A skin graft is used to replace the removed
skin.
 Carpal Tunnel Syndrome
Carpal tunnel syndrome is caused by compression of the median
nerve as it travels through the carpal tunnel in the wrist, causing pain
and numbness in the median nerve distribution on the hand.

Basic Anatomy and Pathophysiology

The flexor retinaculum is a fibrous band that wraps across the front
(palmar side) of the wrist. It is also known as the transverse carpal
ligament. Between the carpal bones and the flexor retinaculum is a
passageway from the forearm to the hand called the carpal tunnel. The
median nerve and the flexor tendons of the forearm travel through the
carpal tunnel.
 Compression of the contents of the carpal tunnel (causing carpal
tunnel syndrome) is the result of either:
• Swelling of the contents (e.g., swelling of the tendon sheaths due
to repetitive strain)
• Narrowing of the tunnel

The palmar digital cutaneous branch of the median nerve (which

passes through the carpal tunnel) is responsible for sensory innervation
of the palmar aspects and full fingertips of the:
 • Thumb
• Index and middle finger
• The lateral half of ring finger

Note that the palmar cutaneous branch of the median nerve

provides sensation to the palm. However, this branch originates before
the carpal tunnel and does not travel through the carpal tunnel. Therefore,
it is not affected by carpal tunnel syndrome.

The median nerve also supplies the motor function to the three
thenar muscles. These muscles make up the muscular bulge at the base
of the thumb that is responsible for thumb movements:
• Abductor pollicis brevis (thumb abduction)
• Opponens pollicis (thumb opposition - reaching across the palm
to touch the tips of the fingers)
• Flexor pollicis brevis (thumb flexion)

The other muscle that controls thumb movement is the adductor

pollicis (thumb adduction). However, this is innervated by the ulnar
nerve. Whether this is classed as one of the thenar muscles depends on
where you look.

Risk Factors

In most cases, carpal tunnel syndrome is idiopathic, meaning no

clear cause is found.

There are a number of key risk factors:

• Repetitive strain
• Obesity
• Perimenopause
• Rheumatoid arthritis
• Diabetes
• Acromegaly
• Hypothyroidism

TOM TIP: When I was preparing for the PACES exam, the link
between bilateral carpal tunnel syndrome and acromegaly came up
several times. Cases would present a patient with symptoms of
bilateral carpal tunnel syndrome. The challenge was not only to
diagnose carpal tunnel syndrome but also to identify the features of
the underlying cause. Whenever you see a patient in an OSCE
station that has a diagnosis, ask yourself whether that diagnosis
might have an underlying cause and look for features of that cause.
For example, if you see a patient with bilateral carpal tunnel
syndrome, look for features that might suggest underlying
rheumatoid arthritis, diabetes, acromegaly or hypothyroidism. This
will take you from average exams scores to the very top scores.

Presentation

Carpal tunnel syndrome usually has a gradual onset of symptoms.

Initially, the symptoms are intermittent. Often, they are worse at night
time.

Carpal tunnel syndrome causes sensory symptoms in the

distribution of the palmar digital cutaneous branch of the median
nerve, affecting the palmar aspects and full fingertips of the:
• Thumb
• Index and middle finger
• The lateral half of ring finger

Sensory symptoms include:

• Numbness
• Paraesthesia (pins and needles or tingling)
• Burning sensation
• Pain

Patients often find the sensory symptoms worse at night. The

symptoms may cause them to wake up from sleep. They may describe
shaking their hand to try and relieve symptoms.

Motor symptoms of carpal tunnel syndrome affect the thenar

muscles, with:
• Weakness of thumb movements
• Weakness of grip strength
• Difficulty with fine movements involving the thumb
 • Wasting of the thenar muscles (muscle atrophy)

Special Tests

There are two special tests for carpal tunnel syndrome:

• Phalen’s test
• Tinnel’s test

Phalen’s test involves fully flexing the wrist and holding it in this
position. Often this is done by asking the patient to put the backs of their
hands together in front of them with the wrists bent inwards at 90 degrees.
The test is positive when this position triggers the sensory symptoms of
carpal tunnel, with numbness and paraesthesia in the median nerve
distribution.

Tinnel’s test involves tapping the wrist at the location where the
median nerve travels through the carpal tunnel. This is in the middle, at
the point where the wrist meets the hand. The test is positive when this
position triggers the sensory symptoms of carpal tunnel, with numbness
and paraesthesia in the median nerve distribution.

TOM TIP: I think of tapping a tin can (Tinnel’s) to remember the

difference between Phalen’s and Tinnel’s test.

Carpal Tunnel Questionnaire

The Kamath and Stothard carpal tunnel questionnaire (CTQ)

gives a score based on the symptoms. It can be used to predict the
likelihood of a diagnosis of carpal tunnel syndrome. A high score on the
questionnaire may replace the need for nerve conduction studies to
confirm the diagnosis.

It scores based on questions such as:

• Do symptoms wake you at night?
• Do you have special movements (e.g., shaking the hand) to
improve symptoms?
• Is your little finger affected? (Answering yes scores negatively,
making carpal tunnel syndrome less likely)
 Nerve Conduction Studies

Nerve conduction studies are the primary investigation for

establishing the diagnosis.

A small electrical current is applied by an electrode (nerve

stimulator) to the median nerve on one side of the carpal tunnel.
Recording electrodes over the median nerve on the other side of the
carpal tunnel record the electrical current that reaches them. This
demonstrates how well signals are passing through the carpal tunnel
along the median nerve.

Management

Management options for carpal tunnel syndrome are:

• Rest and altered activities
• Wrist splints that maintain a neutral position of the wrist, worn at
night (for a minimum of 4 weeks)
• Steroid injections
• Surgery

Carpal tunnel syndrome surgery is usually performed as a day case

procedure under local anaesthetic. It can be performed by open (with a
vertical incision at the wrist) or endoscopic (keyhole) surgery. The flexor
retinaculum (AKA transverse carpal ligament) is cut to release the
pressure on the median nerve.
 Ganglion Cysts
Ganglion cysts are sacs of synovial fluid that originate from the
tendon sheaths or joints. They commonly occur in the wrist and fingers
but can occur anywhere there is a joint or tendon sheath.

Ganglion cysts are thought to occur when the synovial membrane of

the tendon sheath or joint herniates, forming a pouch. Synovial fluid flows
from the tendon sheath or joint into the pouch, forming a cyst (a fluid-filled
sac).

Presentation

Ganglion cysts can appear rapidly (over days) or gradually. Patients

present with a visible and palpable lump. It is not usually painful. Rarely,
they may compress nerves, leading to sensory or motor symptoms.

On examination, ganglion cysts:

• Range in size from 0.5 to 5cm or more (most are 2cm or less)
• Firm and non-tender on palpation
• Well-circumscribed
 • Transilluminate (shining a torch into the cyst causes the whole
lump to light up)

Diagnosis

Ganglion cysts are mostly diagnosed clinically, based on the history

and examination findings.

X-rays will show normal bones and joints (unless there are co-existing
conditions).

Ultrasound can help confirm the diagnosis and exclude other causes
of lumps.

Management

Ganglion cysts may be managed conservatively, without any

intervention. 40-50% of cysts will resolve without any intervention, but this
can take several years.

Active management options for ganglion cysts are:

• Needle aspiration (draining the cyst by aspirating the fluid with a
needle)
• Surgical excision (open or endoscopic removing the cyst, usually
under local anaesthetic)

Needle aspiration has a high rate of recurrence (50% or more).

Surgical excision involves removing the entire cyst and the affected
part of the joint capsule or tendon sheath. Therefore, the recurrence rate
is low. However, there is a risk of complications, such as infection and
scarring.
 Anaesthetics and ICU
General Anaesthesia
Other Types of Anaesthesia
Common Procedures in Anaesthetics
Pain Management
Intensive Care Unit
Arterial Blood Gases
Respiratory Support
Cardiovascular Support
Renal Support
 General Anaesthesia
There are two main categories of anaesthesia:
• General anaesthesia - making the patient unconscious
• Regional anaesthesia - blocking sensation to an isolated area of
the body (e.g., a limb)

A general anaesthetic involves putting the patient in a state of

controlled unconsciousness. It is most often used so that a major surgical
operation can be performed. During a general anaesthetic, the patient will
be intubated or have a supraglottic airway device, and their breathing will
be supported and controlled by a ventilator. The patient will be
continuously monitored at all times immediately before, during and after a
general anaesthetic.

Fasting

Before a planned general anaesthetic, the patient will have a period of

fasting. The purpose of fasting is to make sure they have an empty
stomach, to reduce the risk of the stomach contents refluxing into the
oropharynx (throat), then being aspirated into the trachea (airway).
Gastric contents in the lungs creates an aggressive inflammatory
response, causing pneumonitis (inflammation of the lung tissue). The
risk of aspiration is highest before and during intubation, and when they
are being extubated. Once the endotracheal tube is correctly fitted, the
airway is blocked and protected from aspiration. Aspiration pneumonitis
and pneumonia are major causes of morbidity and mortality in
anaesthetics, although with planned procedures they are very rare.

Fasting for an operation typically involves:

• 6 hours of no food or feeds before the operation
• 2 hours of no clear fluids (fully “nil by mouth”)

In emergency situations the patient might not be fasted (rapid

sequence induction is discussed below).
 Preoxygenation

Before being put under a general anaesthetic, the patient will have a
period of several minutes where they breathe 100% oxygen. This creates
a reserve of oxygen for the period between when they lose
consciousness and are successfully intubated and ventilated (in case the
anaesthetist has difficulty establishing the airway). This step may need to
be skipped when an emergency general anaesthetic is required.

Premedication

Medications are given before the patient is put under a general

anaesthetic to relax them, reduce anxiety, reduce pain and make
intubation easier. These may include:
• Benzodiazepines (e.g., midazolam) to relax the muscles and
reduce anxiety (also causes amnesia)
• Opiates (e.g., fentanyl or alfentanyl) to reduce pain and reduce the
hypertensive response to the laryngoscope
• Alpha-2-adrenergic agonists (e.g., clonidine), which can help with
sedation and pain

Rapid Sequence Induction/Intubation

Rapid sequence induction/intubation (RSI) is used to gain control over

the airway as quickly and safely as possible where a patient is intubated
in an emergency scenario and detailed pre-planning is not possible. This
is considerably more risky, as the patient has often not been fasted (risk
of aspiration), and the anaesthetist has not had the chance to plan for
individual factors and potential problems (e.g., a difficult airway). It is also
used in non-emergency situations where the airway needs to be secured
quickly to avoid aspiration, such as in patients with gastro-oesophageal
reflux or pregnancy.

The procedure is designed to ensure successful intubation with an

endotracheal tube as soon as possible after induction (when the patient
is unconscious), to protect the airway. The biggest concern during RSI is
the aspiration of stomach contents into the lungs. The bed can be
positioned so the patient is more upright to reduce the reflux of contents
up the oesophagus. Cricoid pressure (pressing down on the cricoid
cartilage in the neck) may be used to compress the oesophagus and
prevent the stomach contents from refluxing into the pharynx (this is
somewhat controversial and should only be done by someone trained
and experienced).

Triad of General Anaesthesia

There is a triad of general anaesthesia:

• Hypnosis
• Muscle relaxation
• Analgesia

Hypnosis

Hypnotic agents are used to make the patient unconscious. They

can be given either intravenously or by inhalation.

Intravenous options for a general anaesthetic include:

• Propofol (the most commonly used)
• Ketamine
• Thiopental sodium (less common)
• Etomidate (rarely used)

Inhaled options for a general anaesthetic include:

• Sevoflurane (the most commonly used)
• Desflurane (less favourable as it is very bad for the environment)
• Isoflurane (very rarely used)
• Nitrous oxide (combined with other anaesthetic medications - may
be used for gas induction in children)

Sevoflurane, desflurane and isoflurane are volatile anaesthetic

agents. Volatile agents are liquid at room temperature and need to be
vaporised into a gas to be inhaled.

Vaporiser devices are used for inhaled volatile agents. The liquid
medication is poured into the machine. The machine then turns it into
vapour and mixes it with air in a controlled way. During the anaesthesia,
the concentration of the vaporised anaesthetic medication can be altered
to control the depth of anaesthesia.

Commonly, an intravenous medication will be used as an induction

agent (to induce unconsciousness), and inhaled medications will be
used to maintain the general anaesthetic during the operation. Inhaled
medications need to diffuse across the lung tissue and into the blood,
where it takes a while for them to reach an effective concentration. IV
agents have a head start, as they are infused directly into the blood and
can quickly reach an effective concentration.

Total intravenous anaesthesia (TIVA) involves using an intravenous

medication for induction and maintenance of the general anaesthetic.
Propofol is the most commonly used. This can give a nicer recovery (as
they wake up) compared with inhaled options.

Muscle Relaxation

Muscle relaxants block the neuromuscular junction from working.

Acetylcholine (a neurotransmitter) is released by the axon, but is
blocked from stimulating a response from the muscle. Muscle relaxants
are given to relax and paralyse the muscles. This makes intubation and
surgery easier. There are two categories:
• Depolarising (e.g., suxamethonium)
• Non-depolarising (e.g., rocuronium and atracurium)

Cholinesterase inhibitors (e.g., neostigmine) can reverse the

effects of neuromuscular blocking medications.

Sugammadex is used specifically to reverse the effects of certain

non-depolarising muscle relaxants (rocuronium and vecuronium).

Analgesia

Opiates are the most frequently used medication for analgesia (pain
relief). Common agents used in anaesthetics are:
• Fentanyl
• Alfentanil
• Remifentanil
 • Morphine

Antiemetics are often given at the end of the procedure by the

anaesthetist to prevent post-operative nausea and vomiting. Common
options for prophylaxis given at the end of the operation are:
• Ondansetron (5HT3 receptor antagonist) - avoided in patients at
risk of prolonged QT interval
• Dexamethasone (corticosteroid) - used with caution in diabetic or
immunocompromised patients
• Cyclizine (histamine (H1) receptor antagonist) – caution with heart
failure and elderly patients

Emergence

Before waking the patient, the muscle relaxant needs to have worn
off. It is not good for the patient to regain consciousness whilst still
paralysed (“awareness under anaesthesia”). A nerve stimulator may
be used to test the muscle responses to stimulation, to ensure the muscle
relaxant effects have ended. This is often tested on the ulnar nerve at the
wrist, watching for thumb movement (twitches). Alternatively, the facial
nerve can be stimulated at the temple while watching for movement in
the orbiculares oculi muscle at the eye. This involves a train-of-four
(TOF) stimulation, where the nerve is stimulated four times to see if the
muscle responses remain strong (indicating it has worn off) or whether
they get weaker with additional stimulation (indicating it has not fully worn
off). Medication can be used to reverse the effects of the muscle relaxants
as discussed above (e.g., sugammadex).

Once the muscle relaxant has worn off, the inhaled anaesthetic is
stopped. The concentration of the anaesthetic in the body will fall, and the
patient will regain consciousness. They are extubated at the point where
they are breathing for themselves.

Risks of General Anaesthesia

Sore throat and post-operative nausea and vomiting are common

adverse effects of general anaesthesia.
 Significant risks of general anaesthesia include:
• Accidental awareness (waking during the anaesthetic)
• Aspiration
• Dental injury, mainly when the laryngoscope is used for intubation
• Anaphylaxis
• Cardiovascular events (e.g., myocardial infarction, stroke and
arrhythmias)
• Malignant hyperthermia (rare)
• Death

Malignant Hyperthermia

Malignant hyperthermia is a rare but potentially fatal hypermetabolic

response to anaesthesia. The risk is mainly with:
• Volatile anaesthetics (isoflurane, sevoflurane and desflurane)
• Suxamethonium

There are genetic mutations that increase the risk of malignant

hyperthermia. These are inherited in an autosomal dominant pattern.

Malignant hyperthermia causes:

• Increased body temperature (hyperthermia)

• Increased carbon dioxide exhalation
• Tachycardia
• Muscle rigidity
• Acidosis
• Hyperkalaemia

It is treated with dantrolene. Dantrolene is a muscle relaxant that

works by interfering with the movement of calcium ions in skeletal muscle.
 Other Types of Anaesthesia
General anaesthesia has several side effects and risks. Where
possible, it is desirable to keep the patient awake and only anaesthetise
the area required for the operation. Generally, this leads to better pain
relief, fewer medication side effects and a smoother recovery.

Peripheral Nerve Blocks

Peripheral nerve blocks are a type of regional anaesthesia. The

patient remains awake during the procedure. A local anaesthetic is
injected around specific nerves, causing the area distal to the nerves to
be anaesthetised. This usually involves making a limb numb so that a
surgeon can operate without causing any pain. A screen is put up
between the patient and the operating site so that they cannot see the
operation taking place.

The injection is performed under ultrasound guidance, sometimes

with the help of a nerve stimulator, so that it can be accurately applied to
the area around the targeted nerve.

Regional anaesthesia will be performed where there are facilities

available to quickly induce a general anaesthetic if it is not effective or the
patient starts to experience pain. Patients are closely monitored. Sedation
may be given to help the patient relax.

Sometimes a patient may have a combination of regional and general

anaesthesia to reduce the physiological response during surgery and
improve pain management post-operatively.

Central Neuraxial Anaesthesia

Central neuraxial anaesthesia is also known as a spinal anaesthetic

or a spinal block. It is a type of regional anaesthesia. The most
common examples of when it is used are:
• Caesarean sections
 • Transurethral resection of the prostate (TURP)
• Hip fracture repairs

The patient remains awake during the procedure. A local anaesthetic

is injected into the cerebrospinal fluid, within the subarachnoid space.
It is only used in the lumbar spine, after the point where the spinal cord
ends, to avoid damaging the spinal cord. In practice, the needle is usually
inserted into the L3/4 or L4/5 spaces.

Neuraxial anaesthesia will cause numbness and paralysis of the areas

innervated by the spinal nerves below the level of the injection. Cold
spray applied to the skin is used to test whether the anaesthetic has
worked. It takes around 1-3 hours for the anaesthetic to wear off.

Epidural Anaesthesia

Epidural anaesthesia is most commonly used for analgesia in

pregnant women in labour and post-operatively after a laparotomy (open
abdominal surgery). Importantly, an epidural is different from a
neuraxial/spinal block.

An epidural involves inserting a small tube (catheter) into the epidural

space in the lower back. This is outside the dura mater, separate from
the spinal cord and CSF. Local anaesthetic medications are infused
through the catheter into the epidural space, where they diffuse to the
surrounding tissues and through to the spinal cord, where they have an
analgesic effect. This offers good pain relief during labour.
Levobupivacaine is often used, with or without fentanyl.
 Adverse effects:
• Headache if the dura is punctured, creating a hole for CSF to leak
from (“dural tap”)
• Hypotension
• Motor weakness in the legs
• Nerve damage (rare)
• Infection
• Haematoma (may cause spinal cord compression)

When used for analgesia in labour, the risks include:

• Prolonged second stage
• Increased probability of instrumental delivery

Patients need an urgent anaesthetic review if they develop significant

motor weakness (unable to straight leg raise). The catheter may be
incorrectly sited in the subarachnoid space (and cerebrospinal fluid)
rather than the epidural space.
 Local Anaesthesia

Local anaesthesia is used to numb a very specific area where a

procedure is being performed. The local anaesthetic (e.g., lidocaine) is
usually injected by the person performing the procedure (rather than
involving an anaesthetist). It is used for smaller operations and
procedures.

Common examples of procedures performed using a local anaesthetic

are:
• Skin sutures in A&E after a skin laceration
• Minor surgery to remove skin lesions
• Dental procedures
• Hand surgery (e.g., carpal tunnel syndrome surgery)
• Performing a lumbar puncture
• Inserting a central line
• Percutaneous procedures (e.g., percutaneous coronary
intervention)
 Common Procedures in Anaesthetics
Basic Upper Airway Anatomy

Endotracheal Intubation

An endotracheal tube (ETT) is a flexible plastic tube with an

inflatable cuff (balloon) at one end and a connector at the other. The tip of
the endotracheal tube is inserted through the mouth, throat (pharynx),
larynx and vocal cords into the trachea. Endotracheal tubes come in
different sizes, with the diameter written in mm (e.g., 7-7.5mm for women,
8-8.5mm for men).
 Once in the correct position, a syringe can be used to inflate the cuff
via the pilot line. There is a pilot balloon towards the end of the pilot
line, which inflates along with the cuff and allows the anaesthetist to
roughly assess how inflated the cuff is (while it is out of sight in the
trachea). The pressure in the cuff can be checked with a manometer
(pressure sensor) to avoid over or under-inflation. There is a valve on the
end of the pilot line that keeps the pilot balloon inflated.

The Murphy’s eye provides an extra hole on the side of the tip that
gas can flow through in the event that the main opening at the tip of the
ETT becomes occluded (blocked).

A laryngoscope is a metal blade attached to a handle, with a light

attached. It is inserted through the mouth and into the pharynx to visualise
the vocal cords. An endotracheal tube can be guided along the blade into
position in the trachea. A McGrath laryngoscope is a high-tech version
of a standard laryngoscope, which has a camera and screen attached so
that the vocal cords can be visualised via a live video feed.

A bougie is a device to help with intubation, notably when the vocal

cords cannot be visualised. The bougie is inserted into the trachea. The
endotracheal tube slides along the bougie into the correct position in the
airway. The bougie is then removed, and the endotracheal tube remains
in place.
 A stylet is another device to help with intubation. It is a stiff metal wire
(with a plastic coating) that is inserted into the endotracheal tube before
intubation is attempted. It can be bent to hold the endotracheal tube in a
specific shape. It is usually used to bend the tip of the endotracheal tube
anteriorly towards the trachea (to avoid going posteriorly into the
oesophagus).

Awake fibre-optic intubation is a special procedure where the

endotracheal tube is inserted with the patient awake, under the guidance
of an endoscope (camera). A long thin tube with a camera on the end
(endoscope) is inserted through the nose or mouth, down to a position
below the vocal cords. The endotracheal tube is then inserted over the
top of this tube into the correct position. Then the endoscope is removed,
leaving the endotracheal tube in position. This is used where there is
restricted mouth opening or difficult anatomy (e.g., after radiotherapy to
the neck). Putting the patient to sleep prior to inserting the endotracheal
tube is more risky, as a delay in intubation can lead to hypoxia.

Trismus refers to pain and restriction when opening the jaw. This can
make intubation more difficult and might need awake fibre-optic
intubation.

Supraglottic Airway Devices

A supraglottic airway device (SAD) is an alternative to endotracheal

intubation for ventilation. They are very commonly used in both elective
and emergency scenarios. They are the first option if intubation fails in a
difficult airway scenario.

The tip of the SAD will be located at the top of the oesophagus. The
cuff will fit around the opening of the larynx, forming a seal between the
device and the airway. The cuff can be inflatable or non-inflatable.
SADs with inflatable cuffs are called laryngeal mask airways (LMA). I-
gel is a type of non-inflatable SAD that uses a gel-like cuff that moulds to
the larynx.
 Other Airways

Oropharyngeal (Guedel) airways are inserted into the oropharynx.

They are rigid and create an air passage from in front of the teeth to the
base of the tongue, maintaining a patent upper airway. They are inserted
upside down, then rotated into position once the tip is past the tongue.
These are most often used when ventilating the patient via a face mask
and bag prior to inserting an SAD or ETT. The size is measured from the
centre of the mouth to the angle of the jaw.

Nasopharyngeal airways are slightly flexible tubes inserted through

the nose. They create an air passage from outside the nostril to the
pharynx (throat). The size is measured from the edge of the nostril to the
tragus of the ear. They are often used in emergency scenarios, for
example, in A&E or at cardiac arrests. They carry a risk of nosebleeds
(epistaxis). A base of skull fracture is a contraindication for inserting a
nasopharyngeal airway.

Tracheostomy

A tracheostomy refers to creating a new opening (-ostomy) in the

trachea (trache-). A hole is made in the front of the neck with direct
access to the trachea. A tracheostomy tube is inserted through the hole
into the trachea and held in place with stitches or a soft tie around the
neck (trach tie). Tracheostomies may be temporary or permanent,
depending on the indication.

They can be planned and inserted under a general anaesthetic or

performed in an emergency with general or local anaesthetic depending
on the circumstances. They are often inserted at the end of head and
neck operations, for example, after a laryngectomy procedure (where a
permanent tracheostomy will be required).

Indications for a tracheostomy include:

• Respiratory failure where long-term ventilation may be required
(e.g., after an acquired brain injury)
• Prolonged weaning from mechanical ventilation (e.g., ICU patients
that are weak after critical illness)
• Upper airway obstruction (e.g., by a tumour or head and neck
surgery)
• Management of respiratory secretions (e.g., in patients with
paralysis)
• Reducing the risk of aspiration (e.g., in patients with an unsafe
swallow or absent cough reflex)

Tracheostomy tubes are short and curved. There are quite a few
variations of tubes, depending on their use. They usually have an outer
tube that stays in place, with an inner tube that can be removed to be
cleaned or changed. They can have inflatable cuffs to hold them in place
and seal the airway, similar to endotracheal tubes.
 Difficult Airway

The Difficult Airway Society (DAS) have published guidelines on the

steps to take in the case of unanticipated difficulty intubating a patient
(DAS guidelines 2015).

There are four stages (summarised):

• Plan A - laryngoscopy with tracheal intubation
• Plan B - supraglottic airway device
• Plan C - face mask ventilation and wake the patient up
• Plan D - cricothyroidotomy

Arterial Line
 An arterial line is a special type of cannula inserted into an artery
(e.g., the radial artery). The blood pressure can be accurately
monitored in real-time using an arterial line. Arterial blood samples (for
ABG monitoring) can be taken from the line. Medications are never given
through an arterial line.

Central Line

A central line is also called a central venous catheter (CVC). This is

essentially a long thin tube with several lumens (usually 3-5) that is
inserted into a large vein, with the tip located in the vena cava. They may
be inserted into the:
• Internal jugular vein
• Subclavian vein
• Femoral vein

They have separate lumens (tubes), which can be used for giving
medications or taking blood samples. They last longer and are more
reliable than peripheral cannulas. They can also be used for medications
that would be too irritating to be given through a peripheral cannula (e.g.,
inotropes, amiodarone or fluids with a high potassium concentration).

Vas Cath

A Vas Cath is a type of central venous catheter inserted on a

temporary basis, usually into the internal jugular or femoral vein. It has
two or three lumens. It may be used for short-term haemodialysis (in
renal failure).

PICC Line

A peripherally inserted central catheter (PICC line) is a type of

central venous catheter. A long, thin tube is inserted into a peripheral
vein (e.g., in the arm) and fed through the venous system until the tip is in
a central vein (the vena cava or right atrium). They contain one or two
lumens that are a narrower diameter than a standard central line.
 Tunnelled Central Venous Catheter

A Hickman line is a type of tunnelled central venous catheter. It is a

long, thin catheter that enters the skin on the chest, travels through the
subcutaneous tissue (“tunnelled”), then enters into
the subclavian or jugular vein, with a tip that sits in the superior vena
cava or right atrium.

There is a cuff (sleeve) that surrounds the catheter. It promotes

healing and adhesion of tissue to the cuff, making the catheter more
permanent and providing a barrier to bacterial infection. They can stay in
longer-term and be used for regular IV treatment (e.g., chemotherapy or
haemodialysis).

Pulmonary Artery Catheter

Pulmonary artery catheters are also known as Swan-Ganz catheters.

A pulmonary artery catheter is inserted through the central venous
system, right atrium, right ventricle and into a pulmonary artery. It has a
balloon on the end that can be inflated to “wedge” the catheter in a
branch of the pulmonary artery. The pressure distal to the wedged
balloon can be measured. This gives the pulmonary artery wedge
pressure, which gives an indication of the pressures in the left atrium.
This is mostly used in specialist cardiac centres for close monitoring of
cardiac function and response to treatment.

Portacath

A Portacath is a type of central venous catheter. There is a small

chamber (port) under the skin at the top of the chest that is used to
access the device. This chamber is connected to a catheter that travels
through the subcutaneous tissue and into the subclavian vein, with a tip
that sits in the superior vena cava or right atrium.

When nothing is attached to the port, the skin remains intact, and
there are no lines outside the body. The port can be seen as a bump on
the chest wall and felt through the skin (similar to palpitating a
pacemaker). When the catheter needs to be accessed, a needle is
inserted through the skin into the port, allowing injections to be given or
infusions to be set up. They remain long-term and can be used for regular
IV treatment (e.g., chemotherapy or haemodialysis).
 Pain Management
The International Association for the Study of Pain (IASP)
published a definition of pain (2020):

“An unpleasant sensory and emotional experience associated with, or

resembling that associated with, actual or potential tissue damage”

It is important to distinguish between two categories of pain:

• Acute pain - new onset of pain
• Chronic pain - pain present for 3 months or more

When managing pain, see local guidelines and seek advice from
seniors and pain or palliative care specialists when in doubt. This section
aims to help students prepare for exams and should not be used as a
reference for managing pain in patients.

Basic Pain Physiology

There are two aspects to the experience of pain:

• Sensory - the sensory signal transmitted from the pain receptor (“it
is a sharp sensation, likely a needle”)
• Affective - the unpleasant emotional reaction to the pain (“it is
excruciating, I can’t bear it”)

Pain is supposed to indicate underlying or potential damage to

tissues, but it can occur without tissue damage. The physiology of pain is
very complex. There is still a lot that is not fully understood about the
experience of pain.

Pain is subjective, meaning that when someone indicates they are in

pain, we need to accept their experience, even when there is no apparent
underlying cause.

Pain threshold refers to the point at which sensory input is reported

as painful. For example, different temperatures can be applied to the skin
to measure the point at which the heat is interpreted as pain. A higher
temperature indicates a higher sensory threshold for pain. Allodynia
refers to when pain is experienced with sensory inputs that do not
normally cause pain (e.g., light touch).

Pain tolerance is different to pain threshold. It is more difficult to

define and generally refers to a person’s response to pain. One person
may experience pain but think little of it and carry on with their activities
as usual. Another person may experience a similar pain and worry that it
indicates a serious underlying illness, take time away from work, and seek
medical investigations and treatment. Pain tolerance varies massively
between individuals and is influenced by many biological,
psychological and social factors.

At the most basic level, pain receptors (nociceptors) at the ends of

nerves detect damage or potential damage to tissues. Nerve signals are
transmitted along the afferent nerves to the spinal cord. Afferent
sensory nerves that transmit pain signals are part of the peripheral
nervous system and are called primary afferent nociceptors.

Two groups of nerve fibres transmit pain:

• C fibres (unmyelinated and small diameter) - transmit signals
slowly and produce dull and diffuse pain sensations
• A-delta fibres (myelinated and larger diameter) - transmit signals
fast and produce sharp and localised pain sensations

The signal then travels in the central nervous system, up the spinal
cord (mainly in the spinothalamic tract and spinoreticular tract) to the
brain where it is interpreted as pain, mainly in the thalamus and cortex.

The main sensory inputs that generate a pain signal are:

• Mechanical (e.g., pressure)
• Heat
• Chemical (e.g., prostaglandins)

However, when directly measuring activity in the peripheral afferent

sensory nerves:
• Pain can be experienced without activity in the primary afferent
nociceptors
 • Activity in the primary afferent nociceptors can be detected without
the patient experiencing any pain

Referred pain refers to pain experienced in a location away from the

site of tissue damage. For example, patients with a heart attack may have
pain in their left arm. There are several possible explanations for referred
pain, including:
• Nerves may share the innervation of multiple parts of the body
(e.g., the heart and left arm)
• Pain in one area amplifies the sensitivity in the spinal cord to
signals coming from other areas
• Activation of the sympathetic nervous system in response to pain
results in pain in other areas

Neuropathic pain is caused by abnormal functioning or damage of

the sensory nerves, resulting in pain signals being transmitted to the
brain. Typical features suggestive of neuropathic pain are:
• Burning
• Tingling
• Pins and needles
• Electric shocks
• Loss of sensation to stimulation of the affected area

Measuring Pain

There are no reliable ways to objectively measure the pain someone

is experiencing. As it is a subjective experience, pain is measured by
asking the patient about their perception of pain.

The two ways commonly used to measure pain are the visual
analogue scale (VAS) and numerical rating scale (NRS).

The visual analogue scale (VAS) involves asking the patient to rate
their pain along a horizontal line, where the left end indicates no pain and
the right end indicates the worst pain imaginable. The distance along that
line can be measured to get a numerical value to represent the pain (e.g.,
75mm along a 100mm line).
 The numerical rating scale (NRS) involves asking the patient to rate
their pain on a numerical scale of 0 - 10, with:
• 0 being no pain at all
• 10 being the worst pain imaginable

Pain can also be rated on a graphical rating scale, with a series of

faces going from happy to very unhappy. This may be helpful in children
or patients with learning disability.

Analgesic Ladder

The World Health Organisation (WHO) analgesic ladder was

originally developed to help manage cancer-related pain. It is also often
used for acute and chronic painful conditions. The idea is that patients
with mild pain start on the first step, and when pain is more severe or
does not respond to the lower steps, higher steps on the ladder are used
until the pain is adequately managed.

There are three steps to the analgesic ladder:

• Step 1: Non-opioid medications such as paracetamol and NSAIDs
• Step 2: Weak opioids such as codeine and tramadol
• Step 3: Strong opioids such as morphine, oxycodone, fentanyl and
buprenorphine

Other medications may be combined with the analgesic ladder for

additional effect (called adjuvants) or used separately to manage
neuropathic pain. These are:
• Amitriptyline - a tricyclic antidepressant
• Duloxetine - an SNRI antidepressant
• Gabapentin - an anticonvulsant
• Pregabalin - an anticonvulsant
• Capsaicin cream (topical) - from chilli peppers

Side-Effects

Medication overuse headache is a common side-effect of the long-

term use of analgesic medication.

The key side effects of NSAIDs are:

 • Gastritis with dyspepsia (indigestion)
• Stomach ulcers
• Exacerbation of asthma
• Hypertension
• Renal impairment
• Coronary artery disease, heart failure and strokes (rarely)

NSAIDs may be inappropriate or contraindicated in patients with:

• Asthma
• Renal impairment
• Heart disease
• Uncontrolled hypertension
• Stomach ulcers

Proton pump inhibitors (e.g., omeprazole or lansoprazole) are often

co-prescribed with NSAIDs to reduce the risk of gastrointestinal side
effects (e.g., acid reflux, gastritis and stomach ulcers).

The key side effects of opioids are:

• Constipation
• Skin itching (pruritus)
• Nausea
• Altered mental state (sedation, cognitive impairment or confusion)
• Respiratory depression (usually only with larger doses in opioid-
naive patients)

Naloxone is used to reverse the effects of opioids in life-threatening

overdose (usually due to respiratory depression).

Opioids in Palliative Care

Using opioids to control pain in palliative patients is a specific scenario

where the doses are titrated and optimised over time. This involves using
a combination of:
• Background opioids (e.g., 12-hourly modified-release oral
morphine)
• Rescue doses for breakthrough pain (e.g., immediate-release oral
morphine solution)
 The rescue dose is usually 1/6 of the background 24-hour dose. For
example, if the patient is getting 30mg in 24 hours of modified-release
morphine (15mg every 12 hours), each rescue dose will be 5mg, given
every 2-4 hours as required.

If the patient requires regular rescue doses for breakthrough pain, the
dose of the background opioid can be increased. The rescue doses will
also need increasing so that they remain 1/6 of the background 24-hour
dose.

TOM TIP: Remember that each rescue dose is 1/6 of the 24-hour
background dose. This is a very common exam question and
something that seniors will commonly ask to test your knowledge.
The question may be something like, “this patient is on 30mg of
modified-release morphine every 12 hours; what would be the
correct breakthrough dose?” In this scenario, 10mg is the correct
answer, as the patient is getting 60mg background morphine every
24 hours (30mg twice a day).

Opioid Conversion

The information here is from the BNF, which gives approximate

conversions between different opiates. It is helpful to remember the doses
equivalent to 10mg of oral morphine. The conversions are not exact, and
patients can respond differently to different opioids. Always check the
BNF or other official reference material for accurate conversion figures
(the information here may not be up to date or accurate and is only
intended for study purposes):

Opioid Route Equivalent Dose

Morphine Oral 10mg
Codeine Oral 100mg
Tramadol Oral 100mg
Oxycodone Oral 6.6mg
Morphine IV / IM / SC 5mg
Diamorphine IV / IM / SC 3mg
 It is also possible to use opioid patches for background analgesia:
• Buprenorphine patches (5 mcg/hour patches are roughly
equivalent to 12 mg/24 hours of oral morphine)
• Fentanyl patches (12 mcg/hour patches are roughly equivalent to
30mg/24 hours of oral morphine)

Post-Operative Analgesia

Adequate analgesia in the post-operative period is vital to encourage

the patient to:
• Mobilise
• Ventilate their lungs fully (reducing the risk of chest infections and
atelectasis)
• Have an adequate oral intake

Analgesia is usually started in theatre by the anaesthetist, with regular

paracetamol, NSAIDs and opiates if required (e.g., regular modified-
release oxycodone with immediate-release oxycodone as required for
breakthrough pain). The surgeon may put a local anaesthetic into the
wound to help with the initial pain after the procedure. Analgesia should
be reduced and stopped as symptoms improve.

Patient-Controlled Analgesia

Patient-controlled analgesia (PCA) involves an intravenous infusion

of a strong opioid (e.g., morphine, oxycodone or fentanyl) attached to a
patient-controlled pump. A PCA involves the patient pressing a button as
pain develops to administer a bolus of opioid medication. The button will
stop responding for a set time after administering a bolus to prevent over-
use. Only the patient should press the button (not a nurse or doctor).

Patient-controlled analgesia requires careful monitoring. There needs

to be input from an anaesthetist and facilities in place if adverse events
occur. This includes access to naloxone for respiratory depression,
antiemetics for nausea, and atropine for bradycardia. The anaesthetist
may prescribe background opiates (e.g., patches) in addition to a PCA.
Other “as required” opioids need to be avoided whilst a PCA is in use.
The machine is locked to prevent tampering.
 Chronic Pain

Chronic pain can be diagnosed when pain has been present or

reoccurs in one or more areas over more than 3 months.

Some studies suggest up to 50% of the adults in the UK are affected

by chronic pain. Common areas of chronic pain include:

• Headaches
• Lower back pain
• Neck pain
• Joint pain (e.g., knees or hips)

The NICE guidelines on chronic pain (April 2021) separates chronic

pain into:
• Chronic primary pain - where no underlying condition can
adequately explain the pain
• Chronic secondary pain - where an underlying condition can
explain the pain

There is a long list of causes of chronic secondary pain, which could

take up the entire page. A few examples are:
• Osteoarthritis
• Lasting pain after a traumatic injury (e.g., bone fracture)
• Migraines
• Irritable bowel syndrome
• Endometriosis
• Cancer
• Neuropathic pain (e.g., due to diabetes, nerve impingement,
multiple sclerosis or post-herpetic neuralgia)
• Complex regional pain syndrome

Biological, psychological and social factors contribute to the

persistence of the pain. The physical processes that can lead to chronic
pain include:
• Sensitisation of the primary afferent nociceptors by frequent
stimulation
• Increased activity of the sympathetic nervous system
• Increased muscle contraction in response to pain
 Chronic pain is a complex condition that can be challenging to
manage. Analgesia is often inadequate and can lead to side effects and
dependence.

Good communication and building a relationship with the patient is an

important part of managing chronic pain. In chronic primary pain, an
underlying physical cause of the pain may never be found. Chronic pain
may not improve and may get worse with time. It often fluctuates, with
flare-ups where the pain gets worse. A big part of management is
maintaining and improving the quality of life despite the pain.

Patients require a holistic, person-centred approach to assessing and

managing their condition. This involves:
• Exploring the impact on their life
• Discussing what they already do to manage their pain
• Their ideas, concerns and expectations about the pain

Options for managing chronic pain detailed in the NICE guidelines

(2021) are:
• Supervised group exercise programs
• Acceptance and commitment therapy (ACT)
• Cognitive behavioural therapy (CBT)
• Acupuncture
• Antidepressants (e.g., amitriptyline, duloxetine or an SSRI)

It is worth noting that the NICE guidelines (2021) advise that for
chronic primary pain (where no underlying condition can adequately
explain the pain), patients should not be started on:
• Paracetamol
• NSAIDs
• Opiates
• Pregabalin
• Gabapentin

In chronic secondary pain, analgesia may be helpful depending on

the underlying cause. For example, in patients with pain caused by
osteoarthritis, the use of analgesia involves a stepwise approach to
control symptoms:
 1. Oral paracetamol and topical NSAIDs

2. Oral NSAIDs (consider co-prescribing a proton pump

inhibitor, such as omeprazole, to protect the stomach)
3. Consider opioids such as codeine

TOM TIP: Chronic pain is incredibly common. It is worth noting

these recent guidelines that clearly state to avoid basically all forms
of analgesia (other than antidepressants) in patients with chronic
primary pain. These guidelines may come up in exams, potentially
asking you the most appropriate medication for a patient with
chronic primary pain (antidepressants). This is different to chronic
secondary pain, where there is an underlying condition that explains
the pain.

Neuropathic Pain

The DN4 questionnaire can be used to assess the characteristics of

the pain and the likelihood of neuropathic pain. Patients are scored out of
10. A score of 4 or more indicates neuropathic pain.

There are four first-line treatments for neuropathic pain:

• Amitriptyline - a tricyclic antidepressant
• Duloxetine - an SNRI antidepressant
• Gabapentin - an anticonvulsant
• Pregabalin - an anticonvulsant

NICE recommend using one of these four medications to control

neuropathic pain. If it does not help, it can be slowly withdrawn, and an
alternative can be tried. All four can be tried in turn. Only one neuropathic
medication should be used at a time.

Other options for managing neuropathic pain are:

• Tramadol only as a rescue for short term control of flares
• Capsaicin cream (chilli pepper cream) for localised areas of pain
• Physiotherapy to maintain strength
• Psychological input to help with understanding and coping
 Trigeminal neuralgia is a type of neuropathic pain. However, NICE
recommend carbamazepine as the first-line medication for trigeminal
neuralgia, and if that does not work to refer to a specialist.
 Intensive Care Unit
The high dependency unit (HDU) and intensive care unit (ICU) are
specialised hospital wards that manage severely unwell patients.
Generally:
• Level 1 patients are managed on a general acute ward
• Level 2 patients are managed on the high dependency unit
• Level 3 patients are managed on the intensive care unit (the
highest level of support)

ICUs are run by intensive care specialists and specialist intensive care
nurses. Each nurse only cares for one or two patients at a time. Patients
admitted to the unit usually have some form of organ failure, requiring
organ support and intensive monitoring.

Common reasons patients are admitted to intensive care are:

• Following major surgery (e.g., aortic aneurysm repair)
• Severe sepsis
• Major trauma
• Following cardiopulmonary resuscitation
• Organ failure (acute respiratory, renal or liver failure)

In the intensive care unit, patients can have advanced organ support.
This includes:

• Respiratory support
• Cardiovascular support
• Renal support
• Nutritional support
• Neurological support
• Dermatological support
• Liver support

Admission
 Whether to admit someone to the intensive care unit is the decision of
the intensive care specialists. The capacity of intensive care units is often
low, and the impact of intensive therapy on patients is very high, meaning
that careful thought and consideration need to be put into deciding
whether a patient will benefit from admission. The two main factors that
are considered are the potential to reverse the acute condition and the
baseline physiological reserve (their baseline health).

For example, in patients with a 90% probability of dying from their

current illness and an underlying terminal condition, it does not make
sense to admit them for extensive invasive interventions. A palliative care
approach on a general ward or at home would be much more appropriate.

There are scoring systems that can help predict mortality at the time of
admission to ICU:
• APACHE (Acute Physiology and Chronic Health Evaluation)
• SAPS (Simplified Acute Physiology Score)
• MPM (Mortality Prediction Model)

Nutritional Support

Nutrition is really important in critically ill patients. They are in a

hypermetabolic state and have increased nutritional requirements.
There is a high risk of malnutrition, which can contribute to worse
outcomes. Dieticians are involved in helping ensure patients meet their
nutritional requirements.

Where possible, patients should get their nutrition via their

gastrointestinal tract. Having nutrition via the GI tract is called enteral
nutrition. This could be by:
• Mouth
• Nasogastric (NG) tube
• Percutaneous endoscopic gastrostomy (PEG) - a tube from the
surface of the abdomen to the stomach

Total parenteral nutrition (TPN) involves meeting the complete

nutritional requirements of the patient using an intravenous infusion of a
solution of carbohydrates, fats, proteins, vitamins and minerals. This is
used where it is not possible to use the gastrointestinal tract for nutrition.
It is prescribed under the guidance of a dietician. TPN is very irritant to
veins and can cause thrombophlebitis, so it is normally given through a
central line rather than a peripheral cannula.

Complications

There are various complications associated with admission and

treatment in ICU. These include:
• Ventilator-associated lung injury
• Ventilator-associated pneumonia
• Catheter-related bloodstream infections (e.g., from central
venous catheters)
• Catheter-associated urinary tract infections
• Stress-related mucosal disease (erosion of the upper
gastrointestinal tract)
• Delirium
• Venous thromboembolism
• Critical illness myopathy
• Critical illness neuropathy

Ventilator-associated lung injury is a common complication of

mechanical ventilation. Forcefully blowing air into the lungs can cause
volutrauma (damage from over-inflating the alveoli), barotrauma
(damage from pressure changes) and inflammation. It can lead to short
term pulmonary oedema and hypoxia. Long-term, it can lead to fibrosis of
lung tissue, reduced lung function, recurrent infections and cor-
pulmonale. Using optimal settings and pressures during mechanical
ventilation helps reduce the risk of lung injury.

Ventilator-associated pneumonia is a common complication of

mechanical ventilation (up to 25%) and carries a high risk of death (up to
25%). Being ventilated increases the risk of bacteria being aspirated into
the lungs. Positioning the bed at a 30-degree angle with the patient’s head
elevated reduces the risk of aspirating secretions from the stomach. Good
oral care with regular mouth cleaning is also important to reduce the risk
of ventilator-associated pneumonia.
 Catheter-related bloodstream infections can be introduced by
invasive lines, such as central venous catheters. These are also common
(up to 25%) and carry a high risk of death (up to 25%). The risk may be
reduced by using antibiotic-impregnated or silver-impregnated
catheters, and keeping them in for the shortest time possible.

Catheter-associated urinary tract infections are common. The risk

can be reduced by only using urinary catheters when necessary and
keeping them in for the shortest time possible.

Stress-related mucosal disease is common in critically unwell

patients. Damage to the stomach mucosa occurs mainly due to impaired
blood flow. It increases the risk of upper gastrointestinal bleeding, which
can be life-threatening. The risk may be reduced by suppressing acid
secretion in the stomach using proton pump inhibitors (e.g.,
omeprazole) or H2 receptor antagonists (e.g., ranitidine). Starting NG
feeding early in patients that cannot eat normally also has a protective
effect, even if only small volumes are used (trophic feeds are small
volumes used for gastrointestinal benefits but are insufficient to meet
nutritional requirements).

Delirium (impaired mental state) is a very common complication of

both critical illness and intensive care. A long list of things can cause
acute confusion, including pain, infection, hypoxia, electrolyte
disturbances, renal failure, and medications. Usually, patients in ICU will
have many of these occurring at the same time. The Confusion
Assessment Method (CAM) can be used as a scoring system for
identifying delirium. Dexmedetomidine is a medication used in the
intensive care unit to sedate agitated patients.

Venous thromboembolism (VTE) includes deep vein thrombosis

and pulmonary embolism. Critically ill patients are at higher risk of VTE.
Every patient will have a risk assessment to determine whether they
require prophylaxis. The main preventative measures are low molecular
weight heparin (e.g., enoxaparin) and intermittent pneumatic
compression devices (e.g., Flowtrons) that regularly inflate to squeeze
the legs and promote blood flow.
 Critical illness myopathy refers to muscle wasting and weakness
during critical illness and treatment in the ICU. The weakness mostly
affects the limbs and respiratory muscles. The use of corticosteroids or
muscle relaxants is an important cause. Short-term, it can lead to
difficulty weaning the patient off mechanical ventilation. Long-term, it can
result in reduced exercise capacity and quality of life. It can take years to
recover.

Critical illness polyneuropathy refers to degeneration of the

sensory and motor nerve axons during critical illness and treatment in the
ICU. It often occurs alongside critical illness myopathy. There is a wide
range of pathological processes that result in degeneration of the nerves.
Having optimal control of blood sugar levels (glycaemic control) is
important in reducing the risk. It causes symmetrical weakness,
decreased muscle tone and reduced reflexes. It often makes it difficult to
wean patients off mechanical ventilation.
 Arterial Blood Gases
Arterial blood gases (ABGs) are very commonly used for monitoring
in the intensive care unit. Arterial lines make it easy to obtain an arterial
blood sample. ABGs give useful information about the acid-base balance,
blood gases (O2 and CO2 in the blood), bicarbonate, lactate, haemoglobin
and electrolytes.

Normal Values

Marker Normal Values

pH 7.35 - 7.45
PaO2 (oxygen in the blood) 10.7 - 13.3 kPa
PaCO2 (carbon dioxide in the blood) 4.7 - 6.0 kPa
HCO3 (bicarbonate) 22 - 28 mmol/L
Base excess -2 - +2
Lactate 0.5 - 1 mmol/L

Respiratory Failure

The first step when analysing an ABG is determining if the patient is

hypoxic. Look at the PaO2, which is the partial pressure of oxygen,
meaning the amount of oxygen dissolved in the blood. A low PaO2
indicates hypoxia.

Check the FiO2. FiO2 is the fraction of inhaled oxygen. Room air
has an FiO2 of 21%, meaning the concentration of oxygen in room air is
21%. Venturi masks can be used to control the FiO2. Other masks only
give an approximate FiO2.

It is important to be able to distinguish the types of respiratory

failure:
• Low PaO2 indicates hypoxia and respiratory failure
 • Normal pCO2 with low PaO2 indicates type 1 respiratory failure
(only one is affected)
• Raised pCO2 with low PaO2 indicates type 2 respiratory failure
(two are affected)

Acid-Base Balance

The next step when analysing an ABG is to check the acid-base

balance.

pH Acid-Base Balance
Under 7.35 Acidosis
7.35 - 7.45 Normal
Above 7.45 Alkalosis

Once you identify an acidosis or alkalosis, you need to determine

whether the cause is respiratory or metabolic.

Respiratory Acidosis

Remember that carbon dioxide (CO2) makes blood acidotic by

breaking down into carbonic acid (H2CO3).

Low pH (acidosis) with a raised PaCO2 indicates a respiratory

acidosis. This suggests the patient is acutely retaining CO2 (unable to
get rid of it), and their blood has become acidotic.

Bicarbonate

Bicarbonate is produced by the kidneys. It acts as a buffer to

neutralise the acid in the blood and helps maintain a normal pH. It takes a
while for the kidneys to produce bicarbonate. In an acute episode of
respiratory acidosis, the bicarbonate cannot be produced fast enough to
compensate for the rising carbon dioxide.

Raised bicarbonate indicates that the patient chronically retains

CO2. Their kidneys have responded by producing additional bicarbonate
to balance the acidic CO2 and maintain a normal pH. This is usually seen
in patients with chronic obstructive pulmonary disease (COPD). In an
acute exacerbation of COPD, the kidneys cannot keep up with the rising
level of CO2, so the patient becomes acidotic despite having higher
bicarbonate than someone without COPD.

Respiratory Alkalosis

Respiratory alkalosis occurs when a patient has a raised respiratory

rate and “blows off” too much CO2. There will be a high pH (alkalosis)
and a low PaCO2.

TOM TIP: The most common scenarios where you will see a
respiratory alkalosis in exams are hyperventilation syndrome (e.g.,
due to anxiety) and patients with a pulmonary embolism. Patients
with a PE will have a low PaO2, whereas patients with
hyperventilation syndrome will have a high PaO2.

Metabolic Acidosis

In metabolic acidosis, there is a:

• Low pH
• Low bicarbonate

Causes of metabolic acidosis include:

• Raised lactate - lactate is released during anaerobic respiration
(indicating tissue hypoxia)
• Raised ketones - typically in diabetic ketoacidosis
• Increased hydrogen ions - due to renal failure, type 1 renal tubular
acidosis or rhabdomyolysis
• Reduced bicarbonate - due to diarrhoea (stools contain
bicarbonate), renal failure or type 2 renal tubular acidosis

Metabolic Alkalosis

In metabolic alkalosis, there is a:

• Raised pH
• Raised bicarbonate
 Metabolic alkalosis results from the loss of hydrogen (H+) ions.
Hydrogen ions can be lost from the:
• Gastrointestinal tract - due to vomiting (the stomach produces
hydrochloric acid)
• Kidneys - usually due to increased activity of aldosterone, which
results in increased hydrogen ion excretion

Increased activity of aldosterone can be due to:

• Conn’s syndrome (primary hyperaldosteronism)
• Liver cirrhosis
• Heart failure
• Loop diuretics
• Thiazide diuretics
 Respiratory Support
There are several options for supporting a patient’s respiratory
system. These can be escalated as required. From least to most invasive,
the options are:
• Oxygen therapy
• High-flow nasal cannula
• Non-invasive ventilation
• Intubation and mechanical ventilation
• Extracorporeal membrane oxygenation (ECMO)

Additionally, chest physiotherapy and suction can be used to help

clear secretions and improve respiratory function.

Respiratory support does not fix the underlying problem. It buys time
while the underlying problem is managed.

Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome occurs due to a severe

inflammatory reaction in the lungs, often secondary to sepsis or trauma.
There is an acute onset of:
• Collapse of the alveoli and lung tissue (atelectasis)
• Pulmonary oedema
• Decreased lung compliance (how much the lungs inflate when
ventilated with a given pressure)
• Fibrosis of the lung tissue (typically after 10 days or more)

Clinically there is:

• Acute respiratory distress
• Hypoxia not responding to oxygen therapy
• Bilateral infiltrates on a chest x-ray

Management of ARDS is supportive. This includes:

• Respiratory support
• Prone positioning (lying on their front)
 • Careful fluid management to avoid excess fluid collecting in the
lungs

In ARDS, only a small portion of the total lung volume is aerated and
has functional alveoli. The remainder of the lungs are collapsed and non-
aerated. During mechanical ventilation, low volumes and pressures are
used to avoid over-inflating the small functional portion of the lungs (lung
protective ventilation). Positive end-expiratory pressure (PEEP) is
used to prevent the lungs from collapsing further (see below for more on
PEEP).

Prone positioning has several benefits:

• Reducing compression of the lungs by other organs
• Improving blood flow to the lungs, particularly the well-ventilated
areas
• Improving clearance of secretions
• Improving overall oxygenation
• Reducing the required assistance from mechanical ventilation

Oxygen Therapy

Oxygen can be delivered by several methods. The FiO2

(concentration of oxygen) will depend on the oxygen flow rate:
• Nasal cannula: 24 - 44% oxygen
• Simple face mask: 40 - 60% oxygen
• Venturi masks: 24 - 60% oxygen
• Face mask with reservoir (non-rebreather mask): 60 - 95%
oxygen
 Oxygen flow rate Approximate
Device
(L/min) FiO2
1 24%
Nasal Cannula 2 28%
4 36%
5 40%
Simple Face Mask
8 60%
Face Mask With 8 80%
Reservoir
(Non-Rebreather
10 95%
Mask)

Venturi masks can be used to deliver exact concentrations of oxygen.

The most common use for these is in patients with COPD who are at risk
of retaining carbon dioxide if the FiO2 is too high:

Venturi Mask Colour Oxygen flow rate (L/min) FiO2

Blue 2 24%
White 4 28%
Orange 6 31%
Yellow 8 35%
Red 10 40%
Green 15 60%
 Positive End-Expiratory Pressure

Positive end-expiratory pressure (PEEP) is an important term you

are likely to come across while working in a respiratory ward or intensive
care.

End-expiratory pressure refers to the pressure that remains in the

airways at the end of exhalation.

Additional pressure in the airways at the end of exhalation stops the

airways from collapsing. Forms of respiratory support that add positive
end-expiratory pressure help keep the airways from collapsing and
improve ventilation. It reduces atelectasis, improves ventilation of the
alveoli, opens more areas for gas exchange and decreases the effort of
breathing.

Positive end-expiratory pressure is added by:

• High-flow nasal cannula
• Non-invasive ventilation (NIV)
• Mechanical ventilation

High-Flow Nasal Cannula

Using a high-flow nasal cannula allows for carefully controlled flow

rates of up to 60 L/min of humidified and warmed oxygen.

Having a high flow rate reduces the amount of room air that the patient
inhales alongside the supplementary oxygen, increasing the
concentration of oxygen inhaled with each breath.

It also adds some positive end-expiratory pressure to help prevent

the airways from collapsing at the end of exhalation (although this effect
is reduced if the patient opens their mouth).

Finally, having a high flow of oxygen into the airways provides dead
space washout. The physiological dead space is the air that does not
contribute to gas exchange because it never reaches the alveoli. Dead
space air remains in the airways and oropharynx, not adding anything to
respiration and collecting carbon dioxide. High-flow oxygen clears this
and replaces it with oxygen, improving patient oxygenation.

Non-Invasive Ventilation

Non-invasive ventilation (NIV) involves using a full face mask, hood

(covering the entire head) or a tight-fitting nasal mask to blow air
forcefully into the lungs and ventilate them. It is not pleasant for the
patient but is much less invasive than intubation and ventilation. It is a
valuable middle-point between basic oxygen therapy and mechanical
ventilation.

Non-invasive ventilation can either be:

• CPAP (continuous positive airway pressure)
• BiPAP (bilevel positive airway pressure)

CPAP involves a constant pressure added to the lungs to keep the

airways expanded. It is used to maintain the patient’s airways in
conditions where they are likely to collapse (adding positive end-
expiratory pressure).

BiPAP involves a cycle of high and low pressure to correspond to the

patient's inspiration and expiration:
• IPAP (inspiratory positive airway pressure) is the pressure during
inspiration - where air is forced into the lungs
• EPAP (expiratory positive airway pressure) is the pressure during
expiration - stopping the airways from collapsing

Mechanical Ventilation

Mechanical ventilation is used where other forms of respiratory

support (e.g., oxygen and NIV) are inadequate or contraindicated. A
ventilator machine is used to move air into and out of the lungs. Patients
generally require a level of sedation whilst on a ventilator, as it can be
uncomfortable and distressing. Mechanical ventilation has several
adverse effects and is only used for the shortest time necessary.

An endotracheal tube (ETT) or tracheostomy is required to connect

the ventilator to the lungs. There should be no leaks in the circuit to
enable the ventilator to deliver controlled pressures and volumes into the
lungs.

The basic settings used for mechanical ventilation are:

• FiO2 (concentration of oxygen)
• Respiratory rate (breaths per minute)
• Tidal volume (volume of air pushed in per breath)
• Inspiratory:expiratory ratio (the ratio of time spent in inspiration
and expiration)
• Peak flow rate (the maximum rate of air flow during inspiration)
• Peak inspiratory pressure (the maximum pressure during
inspiration)
• Positive end-expiratory pressure (the positive pressure applied
at the end of expiration to prevent airway collapse)

The modes of mechanical ventilation can be quite complicated. Some

key modes to be aware of are:
• Volume controlled ventilation (VC) - the machine is set to deliver
a specific tidal volume per breath
• Pressure controlled ventilation (PC) - the machine is set to
deliver a specific pressure per breath
• Assist control (AC) - breaths are triggered by the patient (or by
the machine if there is no respiratory effort)
• Continuous positive airway pressure (CPAP) - the patient
breathes while the machine adds constant pressure

Extracorporeal Membrane Oxygenation

Extracorporeal membrane oxygenation (ECMO) is the most extreme

form of respiratory support and is very rarely used. It is used where
respiratory failure is not adequately managed by intubation and
ventilation.

Blood is removed from the body, passed through a machine where

oxygen is added and carbon dioxide is removed, then pumped back
into the body. The process is similar to haemodialysis but for respiratory
support rather than renal support.
 ECMO is only used short-term, where there is a potentially reversible
cause of respiratory failure. It is not a long-term treatment. It is only
provided in specialist ECMO centres and is not available in most
intensive care units. Patients need to be transferred to a specialist centre
for ECMO.
 Cardiovascular Support
Cardiac Function

Overall cardiac function (cardiac output) is the result of a

combination of four things:
• Preload
• Afterload
• Contractility
• Heart rate

Preload is the amount that the heart muscle is stretched when filled
with blood just before a contraction. You can think of preload as the load
or stretch in the ventricle pre contraction. It is related to the volume of
blood in the ventricle at the end of diastole, just before the ventricle
contracts.

Afterload is the resistance that the heart must overcome to eject

blood from the left ventricle, through the aortic valve and into the aorta.
You can think of afterload as being the load or resistance after the
aortic valve - how much resistance there is to pushing blood through the
aortic valve. Common causes of raised afterload are hypertension and
aortic stenosis.

Contractility refers to the strength of the heart muscle contraction.

Heart rate is the number of heartbeats per minute.

Systemic vascular resistance is the resistance in the systemic

circulation that the heart must overcome to pump blood around the body.

Stroke volume is the volume of blood ejected during each beat.

Cardiac output is the volume of blood ejected by the heart per

minute. The formula is:

Cardiac output = stroke volume x heart rate

 Mean arterial pressure (MAP) is the average blood pressure
throughout the entire cardiac cycle, including both systole and diastole.
Mean arterial pressure is a product of cardiac output and systemic
vascular resistance. Low arterial pressure may be the result of low
cardiac output or low systemic vascular resistance.

An adequate mean arterial pressure is essential for tissue perfusion

throughout the body. Low mean arterial pressure results in tissue
hypoperfusion, leading to hypoxia, anaerobic respiration, lactate
production and damage to the tissue.

Monitoring

Cardiac function can be monitored closely in the intensive care unit.

The extent of monitoring depends on the individual patient and clinical
problems.

Basic non-invasive monitoring involves:

• Heart rate
• Peripheral blood pressure
• Pulse oximetry (oxygen saturations)
• Continuous ECG monitoring

More intense monitoring can involve:

• Invasive blood pressure monitoring via an arterial line (a
special cannula inserted into an artery)
• Arterial blood gas analysis taken from an arterial line
• Central venous pressure via a central venous catheter in the
vena cava/right atrium
• Central venous oxygen saturation measured using blood
samples from a central venous catheter
• Pulmonary wedge pressure via a pulmonary artery catheter
(indicates the left atrial pressure) (rarely done)
• Pulmonary artery oxygen saturation via a pulmonary artery
catheter (rarely done)
• Echocardiogram (transoesophageal or transthoracic)

Cardiac output monitoring can involve:

 • Pulse contour cardiac output (PiCCO) measures the cardiac
output via a central venous catheter and a thermodilution arterial line
• Oesophageal Doppler monitor assesses the blood flow through
the thoracic aorta to estimate stroke volume and cardiac output

Fluid Status

An important part of maintaining cardiac function is optimising the fluid

status. This is the first step before considering inotrope and
vasopressor medications.

The central venous pressure is often used as an estimate of

preload. In simple terms, it shows how much blood is available to fill the
heart before a ventricular contraction. If the central venous pressure is
low, the heart has less blood filling the ventricles for each contraction.

The central venous pressure helps guide fluid resuscitation. Giving

additional IV fluids helps increase the central venous pressure, helping
the heart fill with blood during diastole. Preload and stroke volume are
improved, ultimately improving the cardiac output.

Too much fluid can lead to fluid overload, creating congestion in the
circulation. This results in congestive heart failure, pulmonary oedema
and increased mortality. Therefore, fluid balance needs to be carefully
monitored and optimised.

Inotropes

Inotropes are medications that alter the contractility of the heart.

Positive inotropes act to increase the contractility of the heart.

This increases cardiac output (CO) and mean arterial pressure (MAP).
They are used in patients with a low cardiac output, for example, due to
heart failure, recent myocardial infarction or following heart surgery.

Most positive inotropes are catecholamines. Catecholamines

stimulate the sympathetic nervous system via alpha and beta-
adrenergic receptors.
 Examples of positive inotropes that are catecholamines are:
• Adrenaline
• Dobutamine
• Isoprenaline
• Noradrenaline (weak inotrope and mostly a vasopressor)
• Dopamine (not an inotrope at lower infusion rates)

Milrinone is a positive inotrope that works as a

phosphodiesterase-3 inhibitor.

Levosimendan is another positive inotrope that works by increasing

the heart muscle’s sensitivity to calcium.

Positive inotropes are given through a central venous catheter.

They are only used where patients can be closely monitored (e.g., ICU).
Doses are titrated in response to changes in the patient’s clinical
condition, mean arterial pressure, central venous pressure and cardiac
output.

Negative inotropes act to reduce the contractility of the heart.

Examples are:
• Beta-blockers
• Calcium channel blockers
• Flecainide

Vasopressors

Vasopressors are medications that cause vasoconstriction

(narrowing of blood vessels). This increases the systemic vascular
resistance and consequently mean arterial pressure (MAP).

Vasopressors are commonly used by anaesthetists as a bolus dose or

in ICU as an infusion to improve patient’s blood pressure and, therefore,
tissue perfusion. Severe sepsis is a common example of a condition
where they may be used.

Common vasopressors are:

• Noradrenaline (given as an infusion via a central line)
• Vasopressin (given as an infusion via a central line)
 • Adrenaline (given as an infusion via a central line or as a bolus in
an emergency)
• Metaraminol (given as a bolus or an infusion)
• Ephedrine (given as a bolus)
• Phenylephrine (given as a bolus or an infusion)

Vasopressin is antidiuretic hormone (ADH). It acts as a

vasopressor by causing contraction of smooth muscle in blood vessels. It
also stimulates water reabsorption from the collecting ducts in the
kidneys.

Antimuscarinic Medication

Glycopyronium is an antimuscarinic medication used to treat

bradycardia (slow heart rate), often during operations. Antimuscarinic
medication work by blocking acetylcholine receptors.

Atropine is another antimuscarinic medication used to treat

bradycardia.

Intra-Aortic Balloon Pump

An intra-aortic balloon pump is a device used in a number of cardiac

conditions, such as:
• Cardiogenic shock
• Acute coronary syndrome (unstable angina and myocardial
infarction)
• Immediately following heart surgery

An intra-aortic balloon pump is a temporary measure used while the

underlying condition is managed.

A catheter is inserted into the arterial system, usually via the femoral
artery, up to the descending thoracic aorta. At the tip of the catheter is
an inflatable balloon. The balloon is intermittently inflated and deflated by
a special machine, synchronised to the heart contractions. Helium is used
to inflate the balloon.
 During diastole, when the heart is relaxing, the balloon is inflated.
This pushes blood backwards into the coronary arteries, improving
coronary perfusion.

During systole, when the heart is contracting, the balloon is deflated.

Deflating the balloon creates a vacuum effect, as empty space is created
that the balloon previously filled. This reduces the afterload and increases
cardiac output.

In summary, an intra-aortic balloon pump:

• Increases coronary blood flow
• Reduces afterload
• Increases cardiac output
 Renal Support
Acute kidney injury (renal failure) requiring dialysis is a common
reason for admission to the intensive care unit and a common
complication seen in patients in ICU for other conditions. It is a life-
threatening condition with high mortality.

Dialysis is a method for performing the filtration tasks of the kidneys

artificially. It involves removing excess fluid, solutes and waste products.

Indications for Acute Dialysis

The mnemonic AEIOU can be used to remember the indications for

acute dialysis in patients with a severe acute kidney injury:
• A - Acidosis (severe and not responding to treatment)
• E - Electrolyte abnormalities (particularly treatment-resistant
hyperkalaemia)
• I - Intoxication (overdose of certain medications)
• O - Oedema (severe and unresponsive pulmonary oedema)
• U - Uraemia symptoms such as seizures or reduced consciousness

Options

There are two options for dialysis in patients with renal failure:
• Peritoneal dialysis (rarely used in acute renal failure)
• Haemodialysis

Peritoneal dialysis is very rarely used in acute kidney injury and is

generally limited to use in patients with chronic kidney disease.

Haemodialysis

With haemodialysis, patients have their blood filtered by a

haemodialysis machine. Blood is taken out of the body, passed through
the dialysis machine, then pumped back into the body. Inside the dialysis
machine, the blood passes along a series of semipermeable
membranes. Solutes filter out of the blood, across the membrane and
into a fluid called dialysate. The concentration gradient between the
blood and the dialysate fluid causes water and solutes to diffuse out of the
blood and across the membrane.

Haemodialysis requires good access to an abundant blood supply.

This can be done in the acute setting with a Vas Cath (a type of central
venous catheter). Two lumens are required on the catheter, one to
remove the blood and one to put the blood back in. Anticoagulation with
citrate or heparin is necessary to prevent blood clotting in the machine
and during the process.

The amount of water and solutes removed from the blood can be
controlled depending on the patient’s clinical condition and reason for
dialysis.

There are two options for haemodialysis:

• Continuous renal replacement therapy (CRRT)
• Intermittent haemodialysis (IHD)

Continuous renal replacement therapy involves continuously

performing dialysis 24 hours a day. Most patients requiring haemodialysis
in ICU will be on CRRT.

Intermittent haemodialysis involves running the machine and

performing dialysis for set periods, for example, 3-12 hours, before taking
a break from dialysis.