UNIT ONE

Topic One: Introduction to surgery:

Definitions; types of surgery; surgical divisions
Topic Objectives
By end of this topic, you should be able to:-
· Define surgery
· Classify types of surgery
· Classify surgical conditions
· Define surgical terminologies
. Identify the main surgical divisions

Topic 1: Definition, types of surgery, surgical conditions

Definition
· Surgery is a medical specialty that uses operative, manual and instrumental techniques on a
patient to investigate and / or treat a pathological condition such as disease or injury, to help
improve bodily
function or appearance.
· An act of performing surgery may be called a surgical procedure, operation, or simply surgery.
· To operate means to perform surgery
· Surgical means pertaining to surgery
· As a general rule, a procedure is considered surgical if it involves cutting of a patient’s tissues or
closure of a previously sustained wound.
· Surgery can be used to repair broken bones, stop uncontrolled bleeding, remove injured or
diseased tissue and organs, and reattach severed limbs.
· Surgeons are doctors who do operations – cutting tissue to treat disease.
· Surgery is an art or craft as well as a science.
· It involves making judgment, coping under pressure, taking decisive action when necessary, and
teaching & training skills

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Types of surgery
Based on timing:
1. Elective surgery – done to correct a non-life-threatening condition. It is subject to the surgeon’s and surgical
facility’s availability.
2. Emergency surgery – surgery which must be done promptly to save life, limb, or functional capacity.
Based on purpose:

1. Exploratory surgery – performed to aid or confirm a diagnosis.

2. Therapeutic surgery – treats a previously diagnosed condition.
3. Cosmetic surgery – done to improve the appearance of an otherwise normal structure.
Classification of surgical conditions
Surgery is classified according to whether it is vital to life, necessary for continued health, or desirable for medical
or personal reasons.
Surgical conditions can be classified into:
· Emergency surgical conditions
· Urgent surgical conditions
· Elective surgical conditions
Emergency surgical conditions
Unpredictable events that result in the need for immediate surgical attention are termed emergency surgeries. E.g.:
-
 Injury from:

 • An automobile accident
 • A fire
 • A violent assault
 A sudden change in a chronic medical problem such as a perforated peptic ulcer or a strangulated hernia.
 Emergency cases typically involve treatment of:

1. Gunshot and stab wounds

2. Fractures of the skull and other major bones
3. Head injury with intracranial hematoma and lateralizing signs
4. Severe eye injuries
5. Acute airway obstruction e.g. choking
6. Multiple injuries
7. Acute abdomen: presenting as acute onset severe pain in the abdominal area for which immediate surgery
might be the remedy.
8. Acute appendicitis
9. Intestinal obstruction
10. Intussusception
11. Testicular torsion, etc.
Urgent surgical conditions
Cases in which an operation is vital but can be postponed for a few days. E.g.
 Injury with minor bone fracture
 Acute cholecystitis, acute diverticulitis
 Kidney stones
 Cancer of a vital organ

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Elective surgical conditions
Elective surgery can be: required, selective, or optional.
1. Required surgery cases include physical ailments that are serious enough to need corrective surgery but that
can be scheduled weeks or months in advance.
2. Selective surgery covers a broad range of conditions that are of no real threat to the immediate physical
health of the patient, but nevertheless should be corrected by surgery in order to improve comfort and emotional
health. E.g. cleft lip and cleft palate, removal of certain cysts and benign fatty or fibrous tumors.
3. Optional surgery includes operations that are primarily of cosmetic benefit. E.g. removal of warts and other
non-malignant growths on the skin, blemishes on the skin, plastic surgery undertaken for cosmetic reasons.

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Terminology
-ectomy: Excision - starts with the name of the organ to be excised and ends in –ectomy. E.g. colectomy,
gastrectomy, lumpectomy.
-otomy: procedures involving cutting into an organ or tissue end in –otomy. E.g. laparotomy = cutting through the
abdominal wall to gain access into the abdominal cavity.
-ostomy: procedures for formation of a permanent or semi-permanent opening (stoma) in a body, end in –ostomy.
E.g. colostomy, ileostomy.
-oplasty: reconstruction, plastic or cosmetic surgery of a body part starts with the name of the body part to be
reconstructed and ends in –oplasty. E.g. rhinoplasty.
-rraphy: repair of damaged or congenital abnormal structure ends in – rraphy. E.g. herniorraphy.
-oscopy: minimally invasive procedures involving small incisions through which an endoscope is inserted. End in –
oscopy). E.g. laparoscopy.
Amputation: surgical removal of a limb or body part
A fistula

 • Implies a tunnel connecting two epithelial surfaces.

A sinus

 • Is a blind track opening on to the skin or a mucous surface

 • A fluid may discharge from a sinus or fistula.
 • The discharge should be examined and noted: is it blood, blood-stained, clear, bile-like, serous, faecal
or purulent?
 • The type of fluid may give a clue to the possible diagnosis.
Lymphangitis

 • Is inflammation within a lymphatic vessel and appears as a red line often leading to an inflamed
regional lymph node.
Thrombophlebitis

 • Is a thrombosed and inflamed vein – it is more usual in superficial veins often associated with
varicose veins, which are tender and hard.
Cellulitis

 • Is a spreading inflammation of tissues, usually superficial or subcutaneous tissue due to bacterial

infection, usually beta haemolytic streptococci or staphylococci
 • The part affected is swollen, tense and tender.
 • Later it becomes red, shiny and boggy.
 • It may progress to an abscess, which is the presence of pus in the tissue concerned.
Inflammation

 • Is the presence of redness, swelling, heat and tenderness, often associated with the loss of function
Translucency

 • There are occasions when swellings containing clear fluid lie adjacent to the skin.
 • When a torch is shone through the swelling it lightens the area, confirming translucency.

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Crepitus

 • Is a term used in a variety of conditions but in each having a fundamental diagnostic importance
 • Bone crepitus is noted as coarse grating on movement of a bone – it is very painful to the patient, and
an unmistakable diagnosis of a fracture of a bone.
 • Joint crepitus is elucidated by one hand on a joint and passively moving the joint with the other
hand: fine, evenly spaced crepitations are present in many subacute and chronic joint conditions.
 • Coarse, irregular crepitations signify osteoarthritis.
 • The crepitus of tenosynovitis is found over an inflamed tendon sheath when effusion has occurred
into the sheath.
 • The crepitus of subcutaneous emphysema is due to gas in the tissues; a peculiar crackling sensation
is imparted to the examining fingers.
Ballottement

 • Is when a swelling can be tapped away from the examining finger, often due to fluid adjacent to the
swelling
 • The term also describes the ability to palpate bimanually a renal swelling and to tap the kidney
forward from the loin to the examining fingers of the other hand on the abdomen.
 • A swelling may be balloted from the pelvis, by a finger in the vagina, to the examining abdominal
hand.
Fluctuation

 • Is a specific term to elucidate the presence of fluid

 • Two watching fingers are placed on either side of a swelling and a central displacing finger presses
momentarily.
 • An impulse is felt by the watching finger confirming the presence of fluid, provided the sign is
elicited in more than one place.
Surgical divisionsSurgical Divisions
1. General surgery:
 Is the broadest surgical division.

 Focuses on surgery of the abdomen, the breast, and the endocrine organs.

 General surgeons operate on the appendix, colon, small intestine, gallbladder, stomach,
pancreas, spleen, and liver.

2. Neurosurgery:
 Involves operations on the brain & spinal column.

 These procedures include excising, or cutting out, brain tumours and removing ruptured discs
in the spine, an operation known as laminectomy.

4. Orthopaedic surgery:

 Entails operations on bones, muscles, and joints.

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  Orthopaedic surgery allows for the replacement of hip and knee joints with artificial
joints made of special metals and plastics.

  Fractures in bones are repaired with the implantation of pins, metal plates, and screws.
  These techniques greatly reduce the time needed for healing and recuperation.
4. Plastic surgery:

  Encompasses cosmetic procedures to improve appearance and reconstruct damaged parts of the
body such as skin and underlying muscle.
  Cosmetic procedures include enlarging or reducing the size of the breasts; rhinoplasty (cosmetic
surgery of the nose); face lift (cosmetic surgery to tighten facial tissues); and blepharoplasty (cosmetic
surgery on the eyelids).
5. Cardiothoracic surgery:
 Deals with surgery of the lungs, chest wall, heart, and large blood vessels of the chest.
  Typical procedures include the removal of malignant cancers and correction of structural birth
defects in the heart, lungs and chest.
Topic One: Summary

In this topic, you have learnt the following;

1. Definitions of terms and concepts used in surgery

2. Types of surgery
3. Classification of surgical conditions
4. Main surgical divisions

Topic Two: Surgical Clerkship

Steps in surgical clerkship

1. Assemble all the available facts gathered from particulars (Bio data), chief complaints, history of
presenting illness and relevant history

2. Analyze and interpret the examination details to reach the provisional diagnosis (impression)

3. Make differential diagnoses

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4. Order for appropriate investigations

5. Select a closest possible diagnosis

6. Come up with an effective treatment plan

Components

1. Personal particulars (bio data)

2. Chief complaint(s)

3. History of presenting illness

4. Review of systems

5. Past medical and surgical history

6. Family history

7. Personal, social and economic history

8. General examination

9. Vital signs

10. Local examination

11. Other systems examination

12. Provisional diagnosis

13. Investigations

14. Final diagnosis

15. Treatment plan

Self-introduction

1. Greet the patient by name

2. Introduce yourself

3. Shake the patient`s hand

4. Ensure the patient is comfortable

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Personal Particulars

They include:

1. Patient’s name:

 To communicate with the patient

 To establish a rapport with the patient

 Record maintenance

 Psychological benefits

2. Age:

 Age related diseases

 For diagnosis

 Treatment planning

3. Sex:

 Certain diseases are gender specific

 Record maintenance

 Treatment planning

4. Residence/ address:

 For future correspondence

 View of socio-economic status

 Prevalence and geographical distribution

5. Occupation:

 To assess socio-economic status

 Prediction of different diseases in different occupations

6. Religion:

 Beliefs and customs that might impact on treatment modalities

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 To identify festive periods when religious people are reluctant to undergo treatment

7. Patients registration number:

 Maintain records

 Billing purposes

 Medico-legal aspects

Chief complaints

Chief complaint is usually the reason for the patient’s visit. It is stated in patient’s own words (no medical terms)
in chronological order of their appearance (Brief & duration). Chief complaint aids in diagnosis and treatment
hence should be given utmost priority.

Common chief complaints:

1. Pain
2. Swelling
3. Ulcer
4. Vomiting
5. Abdominal distension
6. Bleeding
7. Discharge
8. Deformity

History of presenting illness

Elaborate on chief complaints in detail. Symptoms can be elaborated in terms of:

  Mode and cause of onset

  Course and duration of disease
  Symptoms related and relation to constitutional factors
  Special character and effects- nearby structures
  Treatment taken
  Leading questions- to help the patient
  Negative answers- more valuable to exclude the disease

Review of systems

  Review all the systems that are not affected and thus not covered in the history of presenting
illness.
  Helps to discover any other problems the patient could be having.
  Ask specific questions in relation to each system

Past medical & surgical history

  Note the past history in chronological order

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   All diseases-previous to present noted: pay attention to diseases like diabetes, systemic
hypertension, heart diseases, bleeding disorders, tuberculosis, asthma, epilepsy etc.
  Previous operations or accidents
  Previous blood transfusions or fluid infusions
  Drug allergies and intolerances

Treatment or drug history

  Ask about the drugs the patient was on

  Special enquiry on steroids, antihypertensive drugs, contraceptives, antidiuretic drugs, ARVS etc.
  Treatment for current illness

Gynaecological and obstetric history

  For females
  Gynecological and obstetric history is important in determining pregnancy status
  Rules out or confirms certain conditions associated with pregnancy e.g. ectopic pregnancy.

Personal, social and economic history

  Marital status
  Occupation
  Education level
  Diet
  Habits of smoking and drinking alcohol
  Hobbies

Family history

  Family members share genes as well as their environment, lifestyle and habits
  Certain diseases run in families- diabetes, hypertension, piles, peptic ulcers, cancer (such as
breast, thyroid) etc. should be noted
  Enquire about family members- alive or dead/current illnesses among family members
 Examination
 General survey or examination
  Analyze the patient entering the clinic for gait, built & nutrition, attitude and mental status
  Check for pallor, jaundice, cyanosis, finger clubbing, oedema, dehydration, lymphadenopathy and
any skin eruptions
  Record the vital signs- blood pressure, pulse, respiration rate and temperature


 Local examination
 It is the most important part- definite clue to arrive at a diagnosis.
 It entails:
  Inspection- looking at affected part
  Palpation- feeling of affected part
  Percussion- listening to notes produced by tapping the affected part
  Auscultation- listening to the sounds produced
  Movements and measurements
  Lymph node examination

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 
 Inspection
  Make sure there is good lighting
  Position and expose body parts so that all surfaces can be viewed
  Inspect each area for size, shape, colour, symmetry, position and abnormalities
  If possible compare each area inspected with the same area on the opposite side of the body

 Palpation
  Use the pulp (palmar surface) of the fingers to palpate for:
 1. Texture- smooth, rough, moist or dry
 2. Masses- size, surface, edges, mobility, tenderness
 3. Fluid- fluctuancy
  Use the dorsum of hand to assess for local warmth or temperature
  Client should be relaxed and positioned comfortably

 Types of palpations
 1. Light palpation
 2. Deep palpation
 3. Bimanual palpation

 Percussion
  Used to evaluate for presence of air or fluid in body tissues
  Sound waves are heard as percussion notes
  Percussion notes can be: -
 1. Dull
 2. Stony-dull
 3. Resonant (chest)
 4. Hyper-resonant (chest)
 5. Tympanic (abdomen)


 Types of percussion
  Direct percussion- by tapping the affected area directly using flexed finger
  Indirect percussion- by placing the left middle finger over the area and its middle phalanx is
tapped with the tip of the right middle or index finger
  Fist percussion- placing one hand flat against the body and striking the back of the hand with a
clenched fist of the other hand

 Auscultation
  Done using a stethoscope
  Note the following characteristics of sounds:
 • Pitch
 • Loud or soft
 • Duration
 • Quality

Examination of systems

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1. Head and neck

 • Cranial nerves- iii,iv,v,vi,vii,ix,xi and xii examined

 • Eyes – visual field, pupil, movement
 • Mouth and pharynx- teeth and gum, tongue, and tonsils
 • Movement of neck, neck veins, lymph nodes, carotid pulse and thyroid gland

2. Musculoskeletal system

Upper limbs

 • Arms and hands- power, tone, reflexes and sensations

 • Axillae and lymph nodes
 • Joints
 • Finger nails

Lower limbs

 • Legs and feet- power, tone, reflexes and sensations

 • Varicose veins
 • Joints
 • Oedema

Spine

 • Curvature – lordosis, kyphosis and scoliosis

 • Swellings
 • Pain and tenderness
 • Movements

3. Thorax – RS, CVS, Breasts

Examine the respiratory and cardiovascular systems using the format of inspection, palpation, percussion, and
auscultation.

 • Chest symmetry
 • Dilated vessels and pulsations
 • Position of trachea
 • Apex beat
 • Lungs - percussion notes, breath sounds, air entry, ...
 • Heart - sounds, murmurs, ...
 • Breasts

4. Abdomen

Follow the formats of inspection, auscultation, palpation, and percussion.

 • Abdominal wall- umbilicus, scars, dilated vessels

 • Symmetry and movement with respiration
 • Masses, tenderness, percussion
 • Hernias
 • Inguinal lymph nodes
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  • Bowel sounds
 • Rectal examination
 • Gynecological examination- if required

Provisional diagnosis

 • Also referred to as tentative or working diagnosis

 • It is formed after evaluating the case history and performing the physical examination

 Investigations
 Investigations are requested/ performed to:
 1. Confirm the diagnosis
 2. Rule out differential diagnosis
 3. Aid in management of the patient
 4. To monitor success of treatment

 Types of investigations:

1. Laboratory investigations:

Blood tests

 • Full blood count (complete blood count)

 • Erythrocyte sedimentation rate (ESR)
 • Renal function tests- electrolytes, urea & createnine levels
 • Liver function tests- bilirubin, liver enzyme (alanine transaminase, aspartate transaminase) serum
proteins, alkaline phosphatase
 • Blood for grouping and cross matching
 • Random blood sugar
 • C-reactive proteins- elevated acute infections/inflammatory conditions
 • Coagulation tests- prothrombin test, thrombin time etc

Aspirates/swabs- microscopy, culture and sensitivity

Fine needle aspirate cytology (FNAC) for cytology
Open biopsy for histology
Urinalysis
2. Radiological investigations

 • Plain radiographs (X-rays)

 • Computerized tomographic scans (CT Scans)
 • Magnetic resonance imaging (MRI)
 • Ultrasound
 • Doppler ultrasound

 3. Endoscopies

 Differential diagnosis
 • The process of listing two or more diseases having similar signs and symptoms with the
provisional diagnosis


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 Treatment plan
 • Formulation of treatment plan depends on knowledge & experience of a competent clinician and
nature and extent of treatment facilities available
 • Medical assessment is needed to identify the need of medical consultation and to recognize
significant deviation from normal health that may affect management

Topic Two: Summary

In summary, surgical clerkship consists of:

  Components of a surgical history

  Chief complaints
  History of presenting illness; expounding on symptoms
  General examination
  Local examination
  Examination of systems
  Investigations
  Provisional diagnosis
  Treatment plan

Topic 3: Medical Conditions that Affect Surgical Treatment

Introduction

A number of medical conditions can affect the outcome of surgical treatment. These are discussed below:

Diabetes mellitus

  Blood sugar levels must be under control before surgery.

  Uncontrolled diabetes can slow the healing of surgical wound
  It also makes one to be more susceptible to post-operative infection
  Surgery can cause increased stress to the body and higher blood sugar.
  Insulin dose may need to be adjusted.

Patients with diabetes mellitus are at special risk from general anaesthesia and surgery for the following reasons:

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  1. Certain complications of diabetes are associated with a higher post-operative risk
 2. Stress (e.g. surgery, trauma & infection) causes increased production of catabolic hormones which oppose
the action of insulin. This makes diabetic control more difficult.
 3. General anaesthesia, surgery, deprivation of oral intake and post-operative vomiting disrupt the delicate
balance between dietary intake, exercise (energy utilization) and diabetic therapy.
 4. Diabetic ketoacidosis may cause an elevated leucocyte count and raised amylase level, which may confuse
the diagnosis of acute abdomen. DKA may sometimes present with abdominal pain.
 5. Diabetic patients are at greater risk of hospital-acquired infection.

Perioperative management of insulin dependent diabetics:

 1) Establish good diabetic control before operation

 2) Give soluble insulin as a continuous intravenous infusion during the operative period
 3) Give an infusion of dextrose throughout the operative period to balance the insulin given and to make up
for lack of dietary intake
 4) Add potassium to the dextrose infusion
 5) Monitor blood glucose and electrolytes frequently throughout the operative and early post-operative
period.

Diabetics controlled on oral hypoglycaemic drugs:

 1. Maintain on short-acting sulphonylureas such as glipizide [omit dose on the morning of the operation]
 2. Patients on long-acting drugs such as metformin should be changed to a short acting sulphonylurea several
days before the operation
 3. If this fails to provide adequate control, an insulin regimen can be used

Diabetics controlled by diet alone:

 These do not require special preoperative measures as they do not become hypoglycemic and blood glucose rarely
drifts above acceptable levels

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Anaemia

  Anaemia increases the risk of cardiac and wound complications during surgery.
  Full blood count should be done before surgery. Haemoglobin level must be checked.
Haemoglobinopathies

  Patients with sickle-cell disease and beta thalassaemia have a high operative morbidity and
mortality.
  They require intensive perioperative management with particular attention to avoiding hypoxia,
infection, acidosis, dehydration and hypothermia.
Bleeding disorders
1. Thrombocytopenia
2. Haemophilia
3. Von-Willebrands disease

  Can cause uncontrolled bleeding intra-operatively

Most surgical bleeding problems are caused by:

1. Poorly controlled anticoagulant therapy

2. Liver disease
3. Aspirin therapy
4. Vitamin K malabsorption such as in obstructive jaundice
Varicose veins, leg swelling, DVT

  Surgery and post-operative immobility increases the risk of DVT.

  Blood clots can be dislodged leading to embolism to the lungs.
Hypertension

  Blood pressure control is necessary before surgery.

  High blood pressure can lead to excessive haemorrhage during surgery.
Jaundice

  Jaundice delays post-operative wound healing.

  Vitamin K malabsorption in obstructive jaundice can lead to excessive bleeding.
Obesity

Overweight and obese patients are at increased risk of medical and surgical complications, including wound infections,
pneumonia, blood clots and heart attack. Losing weight before surgery would improve the outcome of surgery.
Surgical complications of obesity:
 Cardiopulmonary complications such as cardiac failure and chest infections

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 Wound complications such as infection, wound dehiscence and burst abdomen
 Venous thromboembolism – increased risk of deep venous thrombosis and pulmonary embolism
 General anaesthesia complications:

 • Anatomical problems, e.g. intravenous canulae are difficult to insert and intubation is more difficult.
Clinical signs of dehydration and hypovolaemia are more difficult to elicit.
 • Physiological problems: metabolic problems, e.g. altered distribution of drugs

 Predisposition to various medical disorders:

 • Hypertension
 • Ischaemic heart disease
 • Type 2 diabetes
 • Gallstones
 • Gout

 Operative difficulties:

 • Operations take longer to perform because of difficult access and vital structures obscured by fat.
 • This leads to a higher incidence of anaesthetic and surgical complications, particularly involving the
wound.

 Problems of manual handling of patients who are markedly overweight:

 • Weight and size limitations of standard equipment, e.g. CT scanners, operating tables, beds.
 • Risks to staff involved in lifting and handling

Thyrotoxicosis

  Thyroid or non-thyroid surgery for a patient with uncontrolled thyrotoxicosis carries a risk of thyrotoxic
crisis with attendant high mortality.
  It can increase the risk of cardiac complications.
  Hyperthyroidism must be controlled before surgery.
  The patient should be rendered euthyroid before operation using antithyroid drugs and beta-blocking drugs
  Non-selective beta-blocking drugs rapidly control the cardiovascular effects of thyrotoxicosis and can be
used for urgent perioperative preparation.

Hypothyroidism

  Have moderate risk when undergoing surgery

  They are more sensitive to CNS depressants, have a decreased cardiovascular reserve, and are also
susceptible to electrolyte disorders e.g. water retention.
  If clinical suspicion of hypothyroidism, operation should be delayed or postponed until oral replacement is
commenced.

Arrhythmias

  A problem with the rate or rhythm of the heartbeat.

 o Tachycardia
 o Bradycardia

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  o Irregular heart beat
  Can lead to operative and post-operative cardiac complications.

Adrenal insufficiency

  Patients with potential adrenal insufficiency must be given steroid cover during the perioperative period.
I.V. hydrocortisone 25-50mg prior to operation and 50mg daily until recovery.
  Lack of additional adrenal response to the stresses of surgery or trauma may cause acute postoperative
cardiovascular collapse with hypotension and shock (Addisonian crisis)

Cushing’s syndrome

  Results from excess secretion of cortisol.

  Long term steroid therapy for conditions such as rheumatoid arthritis or asthma is the most common cause
of cushingoid features.
  The main surgical problems in cushingoid patients are hypertension, hyperglycemia, poor wound healing,
infection and peptic ulceration.

Topic 3: Summary

You have learnt how some medical conditions can affect surgical treatment. The conditions could complicate the
surgery intra-operatively, could make surgery technically difficult, could lead to anaesthesia complications, and
also post-operative complications, among others. You have also learnt how to manage some of these conditions
in preparation for surgery.

UNIT TWO: INTRODUCTORY TO ORTHOPAEDICS AND

TRAUMATOLOGY
Topic 1: Diagnosis of orthopaedic disorders

Introduction

Orthopaedics is the branch of surgery that deals with diseases and injuries of the trunk and limbs. It deals with
conditions affecting bones, joints, muscles, tendons, ligaments, bursae, nerves, and blood vessels. The term
“Orthopaedic” is derived from Greek words meaning ‘straight child’. Orthopaedics originally dealt with the art
of correcting deformities in children.

DIAGNOSIS OF ORTHOPAEDIC DISORDERS

Depends first upon an accurate determination of all the abnormal features from

 1. History

 2. Clinical examination

 3. Radiographic examination/ imaging

 4. Special investigations

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Secondly, upon a correct interpretation of the findings.

HISTORY

Except in the most obvious conditions, a detailed history is always required, the exact nature of the patient’s
complaint being determined. The development of symptoms is traced step by step from their earliest beginning
up to the present. It is important to take into consideration the patient’s own views on the cause of the symptoms.
They are often correct.

 Pay attention to the following:

 • Relieving and aggravating factors/activities

 • Effect of any previous treatment

 • Presence or absence of symptoms in other parts of the body

 • Whether the general health of patient affected

 • History of previous illnesses

 Facts that often have an important bearing on the condition/problem are:

 1. Age

 2. Present occupation

 3. Previous occupation

 4. Hobbies and recreational activities

 5. Previous injuries.

 In cases that seem trivial, inquire tactfully as to why patient decided to seek advice, and to what extent he
is worried by his disability.

CLINICAL EXAMINATION

The clinical examination should include:

 1. Examination of the part complained of

 2. Investigation of possible sources of referred symptoms

 3. General examination of the body as a whole

Examination of the part complained of

Exposure for examination

19
The part to be examined should be adequately exposed and in good light, and when a limb is being examined, the
sound limb should always be exposed for comparison.

Inspection

  The bones – general alignment and position of the parts to detect any deformity, shortening, or unusual
posture.
  The soft tissues – observe soft tissue contours. Compare the two sides. Note swelling and muscle wasting.
  Color and texture of the skin – look for redness, cyanosis, pigmentation, shininess and loss of hair.
  Scars or sinuses – if a scar is present, determine from its appearance whether it was caused by:
 1. Operation (linear scar with suture marks)
 2. Injury (irregular scar), or
 3. Suppuration (broad, adherent, puckered skin).

Palpation

 Four points should be considered:

 1. Skin temperature
 2. The bones – general shape and outline.
 • Feel for thickening, abnormal prominence, and disturbed relationship of the normal landmarks.
 3. The soft tissues
 • Muscles
 • Joint tissues: thickened synovial membrane; effusion
 • Local swelling: ? Cyst; ? Tumor; General swelling of the part.
 4. Local tenderness.
 • The exact site of any local tenderness should be mapped out and an attempt made to relate it to a particular
structure.

Measurements

 Measurement of limb length is often necessary especially in the lower limbs, where discrepancy between the two
sides is important.
 Measurement of limb circumference (compare two sides at the same site) provides an index of: muscle wasting,
soft tissue wasting, and bony thickening.

Estimation of fixed deformity

Fixed deformity exists when a joint cannot be placed in the neutral (anatomical) position. The degree of fixed
deformity at a joint is determined by bringing the joint as near as it will come to the neutral (anatomical) position
and then measuring the angle by which it falls short.

Movements

The following should be sought in the examination of joint movement:

 • What is the range of active movement?

 • Is passive movement greater than active?
 • Is movement painful?
 • Is movement accompanied by crepitation?
 • Is there any spasticity (stiff resistance of free movement)?

It is wise always to use the unaffected limb for comparison. Limitation of movement in all directions suggests
some form of arthritis. Selective limitation of movements in some directions with free movement in others is
more suggestive of a mechanical derangement.

20
The passive range will exceed the active range only in the following circumstances: -

 1. When the muscles responsible for the movements are paralyzed.

 2. When the muscles or their tendons are torn, severed or unduly slack.

Stability

The stability of a joint depends partly upon the integrity of its articulating surfaces and partly upon intact
ligaments, and to some extent upon healthy muscles. When a joint is unstable, there is abnormal mobility; for
instance, lateral mobility in a hinge joint.

Power

The power of the muscles responsible for each movement of a joint is determined by instructing the patient to
move the joint against the resistance of the examiner. Compare the two sides.

 Power 0 - no contraction
 Power 1 - a flicker of contraction
 Power 2 - slight power, sufficient to move the joint only with gravity eliminated.
 Power 3 - power sufficient to move the joint against gravity.
 Power 4 - power to move the joint against gravity plus added resistance.
 Power 5 - normal power.

Sensation

 Test for sensibility to light touch and to pin prick throughout the affected area.
 In unilateral affection the opposite side should be similarly tested.
 Any blunting or loss of sensibility should be carefully mapped out.
 Identify the nerves affected (dermatomes).

Peripheral circulation

Examine for the following: -

 1. The color of the skin – normal pink or pale, cyanosed.

 2. The temperature of the skin – cold in impaired arterial supply
 3. The texture of the skin and nails – ischaemia causes loss of hair, thin & inelastic skin, coarse,
thickened, irregular nails
 4. The arterial pulses – lower limb (dorsalis pedis, posterior tibial, popliteal, femoral)
 5. Capillary return

Reflexes

Deep reflexes: Determine the integrity of central nervous system or peripheral nervous system. They are
exaggerated in CNS problem and depressed in PNS problem.

Superficial reflexes: motor responses to scraping of the skin, e.g. abdominal reflex; Cremasteric reflex; plantar
reflex.

Tests of function

21
Assess how much the disorder affects the part in its fulfillment of everyday activities. E.g. observe the patient
standing, walking, running, jumping, ascending and descending stairs.

INVESTIGATION OF THE POSSIBLE SOURCES OF REFERRED SYMPTOMS

Think of possible extrinsic disorders with referred symptoms. E.g.:

 1. For shoulder pain, examine the neck (Brachial plexus), thorax, abdomen (diaphragmatic
irritation).
 2. For hip pain, examine the back (spine) and sacro-iliac joints.
 3. Pain in the thigh – examine the spine, abdomen, pelvis, genito-urinary system, or hip

GENERAL EXAMINATION

 1. Examine the patient as a whole.

 2. Assess the general physical condition and psychological outlook of the patient.
 3. Do systemic examination

Diagnostic Imaging & Special Investigations

DIAGNOSTIC IMAGING

You can carry out the following investigations: -

 1. Radiography
 2. Ultrasound scanning
 3. Computerized tomography (CT) scanning
 4. Magnetic resonance imaging (MRI)
 5. Radioisotope scanning
 6. Positron emission tomography (PET CT)

Radiography

Plain radiography – X-rays

 At least two projections in planes at right angles to one another – usually AP & Lateral views
 The films should always include a good length of bone above and below the site of the injury or lesion, including
the adjacent joints.

Contrast radiography

 • Myelography – in which the spinal theca is outlined with an oily non-absorbable contrast medium (fluid).
 • Radiculography – in which water-soluble absorbable contrast medium allows visualization of the nerve
sleeves, as well as the spinal theca itself. (Especially used for lumbar spine).
 • Arthrography – outlines the cavity of a joint.
 • Arteriography or angiography- to show the arterial tree.
 • Venography – shows network of veins.
 • Lymphangiography – shows lymphatic network
 • Sinography – defines the course and ramifications of a sinus.

SPECIAL INVESTIGATIONS

Depend on the condition you are dealing with.

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  • Haematological – e.g. haemogram, ESR
 • Serological – e.g. Widal test, V.D.R.L
 • Bacteriological – E.g. Gram stain, Culture and sensitivity
 • Biochemical – upon urine, plasma, cerebrospinal fluid
 • Histological - biopsy

Assignment

 Outline the steps taken in reading and correctly interpreting a plain radiograph in orthopaedics.

Summary

In this topic we have seen that:

Diagnosis of orthopaedic disorders depends:

  First, upon an accurate determination of all the abnormal features from

1. History
2. Clinical examination
3. Radiographic examination/ imaging
4. Special investigations

  Secondly, upon a correct interpretation of the findings.

Topic Two: TREATMENT OF ORTHOPAEDIC DISORDERS

Orthopaedic treatment falls into three categories: -

1. No treatment – simply reassurance and advice

2. Non-operative treatment

3. Operative treatment

NON-OPERATIVE TREATMENT METHODS

REST

 • Is one of the mainstays of orthopaedic treatment

 • This may be in the form of bed rest or immobilization of the diseased part

SUPPORT

• Rest and support often go together

• Support can be used to:

23
  1. Stabilize a joint rendered insecure by muscle paralysis

 2. Prevent the development of deformity

 3. Support can be provided by cast, splint or orthosis

• Examples of orthoses include:

 1. Spinal braces or corsets

 2. Cervical collars

 3. Wrist supports

 4. Walking calipers

 5. Knee and ankle orthoses, and devices to control foot drop.

PHYSIOTHERAPY

Is very useful in non-operative and post-operative management of orthopaedic conditions.

Physiotherapy can be:

 1. Active

 2. Passive

 3. A combination of active and passive

Passive approaches are carried out on the patient by the physiotherapist

Active approaches require active involvement by the patient, either by exercising or changing behaviour.

Active interventions include: Exercises and Physical fitness.

Exercises aim to: Strengthen specific muscles; Stretch soft tissues; Mobilize joints; and Improve co-ordination of
muscles.

Physical fitness programmes include aerobic exercise with an aim to improve overall cardiovascular fitness, as
well as specific exercises.

Hydrotherapy is a way of allowing active pain-free movements of all joints in warm water.

Passive interventions

Are carried out by the therapist and do not require any active participation by the patient.

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The chief use of passive movements or mobilization is to preserve full mobility when the patient is unable to
move the joint actively, e.g. when muscles are paralyzed or severed.

Passive interventions include: Manual therapy; Soft tissue techniques; Traction; Electrotherapy; and Ultrasound.

LOCAL INJECTIONS

Indicated in two scenarios:

 1. In joint affections that require intra-articular injection of drugs

 E.g. injection of hydrocortisone or other steroid into the joint in osteoarthritis or rheumatoid arthritis

 2. In extra-articular lesions ascribed to chronic strain such as tennis elbow, tendonitis about the
shoulder, and certain types of back pain

Treatment of Orthopaedic conditions - Drugs

DRUGS

Categories of drugs used include:

• Antibacterial agents

• Analgesics

• Sedatives

• Anti-inflammatory drugs

• Hormone-like drugs

• Anti-osteoporosis drugs

• Specific drugs

• Cytotoxic drugs

Antibacterial agents

Are used in infective lesions such as: Acute osteomyelitis; acute pyogenic arthritis; and Tuberculosis.

Treatment must be started early for best outcomes.

Analgesics and sedatives

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Analgesics should be used as sparingly as possible

It is undesirable to prescribe analgesics continuously for prolonged periods

Sedatives may be given if needed to promote sleep, but should not be overprescribed.

Anti-inflammatory drugs

These are drugs that dampen excessive inflammatory response by inhibiting the cyclooxygenase enzymes
responsible for prostaglandin formation. Non-steroidal anti-inflammatory drugs are to be preferred. Many of
these drugs also have analgesic action.

Steroids such as cortisone, prednisolone, and their analogues should be used with extreme caution due to possible
adverse effects.

Hormone-like drugs

These include:

 i. Corticosteroids

 ii. Sex hormones or analogues used for prevention of osteoporosis in post-menopausal women, and
for the control of certain metastatic tumours such as hormone-dependent breast and prostatic tumours.

 iii. Biphosphonates – drugs which block the resorption of bone mineral.

Specific drugs

• Vitamin C for scurvy

• Vitamin D for rickets

• Salicylates for arthritis of rheumatic fever

Cytotoxic drugs

Form the basis of chemotherapy for malignant tumours. These anticancer drugs include: Cyclophosphamide,
Melphalan, Vincristine, Doxorubicin, and Methotrexate. They have serious side effects and are used only under
expert supervision.

MANIPULATION

This is the passive movements of joints, bones, or soft tissues carried out by the surgeon – with or without
anaesthesia, and often forcefully – as a deliberate step in treatment. This method has three main uses:

 i. Manipulation for correction of deformity – e.g. reduction of fractures and dislocations; correction
of deformity from contracted or short soft tissues e.g. CTEV.

 ii. Manipulation to improve the range of movements at a stiff joint

 iii. Manipulation for relief of chronic pain in or about a joint, especially in the neck or spine.

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RADIOTHERAPY

Radiotherapy by X-rays or by the gamma rays of radio-active substances may be used for certain benign
conditions or for malignant disease.

OPERATIVE TREATMENT

Includes:

 1. Synovectomy

 2. Osteotomy

 3. Arthrodesis

 4. Arthroplasty

 5. Bone grafting operations

 6. Tendon transfer operations

 7. Tendon grafting operations

 8. Equalization of leg length

 9. Amputation

Synovectomy

Is the operation for removal of the inflamed lining of a joint (synovial membrane), while leaving the capsule
intact.

Useful in early rheumatoid arthritis and in some types of chronic infective arthritis.

Osteotomy

Is the operation of cutting bone or creating a surgical fracture

Indications include: -

 1. Correction of excessive angulation, bowing or rotation of a long bone.

 2. To permit angulation of a bone so as to compensate for mal-alignment at a joint

 3. To allow for lengthening or shortening of a bone in the lower limb in order to correct length
discrepancy.

27
  4. To improve stability of the hip by altering the line of weight transmission (abduction osteotomy)

 5. To improve containment in transient avascular necrosis of the epiphysis of a long bone

 6. To relieve the pain of an osteoarthritic hip.

Arthrodesis

This is an operation to fuse a joint

Indications:

 1. Advanced osteoarthritis or rheumatoid arthritis with disabling pain, especially when confined to a
single joint

 2. Quiescent tuberculous arthritis with destruction of the joint surfaces, to eliminate risk of
recrudescence and to prevent deformity

 3. Instability from muscle paralysis, as after poliomyelitis

 4. For permanent correction of deformity, as in hammer toe

Arthroplasty

Arthroplasty is the operation for the reconstruction of a new movable joint. It can be carried out in the following
joints: Hip, Knee, Ankle, Shoulder, Elbow, Hand joints, First metatarso-phalangeal joint.

Indications of Arthroplasty include:

 1. Advanced osteoarthritis or rheumatoid arthritis with disabling pain, especially in the hip, knee, ankle,
shoulder, elbow, hand and metatarso-phalangeal joints.
 2. Quiescent destructive tuberculous arthritis especially of the elbow or hip
 3. For the correction of certain types of deformity, especially hallux valgus
 4. Certain ununited fractures of the neck of the femur

Methods of arthroplasty:

 • Excision arthroplasty: Excision of one end or both of the articular ends so that a gap is created between
them, creating a false joint or pseudoarthrosis.
 • Hemiarthroplasty or half-joint replacement: Only one of the articulating surfaces is removed and replaced
with a prosthesis of similar shape.
 • Total replacement arthroplasty: Both of the articular ends are excised and replaced by prosthetic
components.

Bone grafting operations

Types of bone grafts:

 • Autogenous grafts or autografts: are bone grafts obtained from another part of the patient`s own body
 • Allografts or homogenous grafts or homografts: are bone graft obtained from another human subject
 • Xenografts or hetrogenous grafts or heterografts: are grafts obtained from animals

28
Indications

 • In non-union of fractures to promote union

 • In arthrodesis of joints, either to supplement an intra-articular arthrodesis or to promote extra-articular
fusion
 • To fill a defect or cavity in a bone

Techniques / Methods

Strut grafts
Are obtained from strong cortical bone such as the subcutaneous part of the tibia. The graft is fixed to the
recipient bone by internal fixation or by inlaying. It serves as an internal splint as well as providing a framework
for the growth of new bone.

Strip grafts
Sliver or strip grafts are obtained from spongy cancellous bone – especially from the iliac crest. Commonly used
for ununited fractures. They are laid about the fracture, deep to the periosteum.

Chip grafts
Are obtained from cancellous bone; are smaller pieces than sliver grafts. They are used for non-united fractures;
the chips are packed firmly into or around the recipient bone and held in place by suture of the soft tissues over
them.

Vascularised grafts
Require a suitable donor site such as the fibula, rib, or iliac crest. Anastomosis of nutrient vessels is meticulously
done at the new site.

Topic Two: Summary

In this topic we have learned that;

Orthopaedic treatment falls into three categories: -

 1. No treatment – simply reassurance and advice

 2. Non-operative treatment
 3. Operative treatment

We have also discussed the various non-operative methods of treatment and the operative methods of treatment.

UNIT 3. PATHOLOGY OF FRACTURES AND FRACTURE HEALING

29
Definition of fracture
A bone fracture (#) is a break in the continuity of the bone. It may be a complete break or an incomplete break of
the bone.

A bone fracture can be the result of:

 • High force impact or stress, or

 • Trivial injury as a result of certain medical conditions that weaken the bones, where the fracture is then
properly termed a pathological fracture.

Classification of fractures
Fractures can be classified according to:

 1. Aetiology
 2. Whether open or closed
 3. Fracture pattern

CLASSIFICATION BY AETIOLOGY

Fractures may be classified, according to their aetiology, into four groups:

 1) Traumatic fractures
 2) Fragility fractures
 3) Fatigue or stress fractures
 4) Pathological fractures

Traumatic fracture - This is a fracture due to sudden injury or trauma. e.g. - Fractures caused by a fall, road
traffic accident, fight etc. They occur through bone that was previously free from disease. May occur by direct
violence or by indirect violence.

Fragility fractures – these are fractures associated with generalized bone weakness due to osteoporosis. Seen
most commonly in elderly patients

Fatigue or stress fractures – occur from oft-repeated stress and not from a single violent injury. Commonly
occur in athletes or new military recruits. They occur when the rate of microdamage exceeds the rate of repair.
The microdamage accumulates and progresses to a complete fracture across the full width of the bone. Mostly
occur in the metatarsals (mostly 2nd and 3rd). May also occur in the shaft of fibula, tibia and neck of femur.

Pathological fractures – fractures through bone already weakened by disease. Occur following trivial violence,
or even spontaneously. Usually occur in conditions that weaken the bones, such as bone cancer, osteogenesis
imperfecta, bone cysts, chronic bone infection.

CLOSED AND OPEN FRACTURES

All fractures can be broadly described as:

 1. Closed (simple) fractures: Are those in which the skin is intact, and therefore no communication between
the site of fracture and the exterior of the body.
 2. Open (compound) fractures: There is a wound on the skin surface that communicates with the fracture.
May thus expose bone to contamination. Open injuries carry a higher risk of infection.
 PATTERNS OF FRACTURE

 Fractures can be designated by descriptive terms denoting the shape or pattern of the fracture.

30
 The following are the terms in common use:

 1. Transverse fracture: A fracture that is at a right angle to the bone's long axis.

 2. Oblique fracture: A fracture that is diagonal to a bone's long axis.

 3. Spiral fracture: A fracture where at least one part of the bone has been twisted.

 4. Comminuted fracture: A fracture in which the bone has broken into several pieces (more than

 5. Compression or crush fracture: usually occurs in the vertebrae, for example when the front
portion of a vertebra in the spine collapses due to osteoporosis

31
  6. Greenstick fractures – A greenstick fracture occurs when a bone bends and cracks, instead of
breaking completely into separate pieces. They are peculiar to children below 10 years. Their bones are
springy and resilient like branches of a young tree (a green stick)

 7. Impacted fractures – the bone fragments are driven so firmly together that they become
interlocked and there is no movement between them.

 8. Segmental fracture - is a fracture composed of at least two fracture lines that together isolate a
segment of bone, usually a portion of the diaphysis of a long bone. It is a comminuted fracture with
middle fragment having the full circumference intact.

 9. Avulsion fracture: A fracture where a fragment of bone is separated from the main mass as a
result of a tendon or ligament pulling off a piece of the bone.

 10. Linear fracture: A fracture that is parallel to the bone's long axis.

HEALING OF FRACTURES

A fracture begins to heal as soon as the bone is broken. Healing proceeds through several stages until the bone is
consolidated. Fracture healing, is a proliferative physiological process in which the body facilitates the repair of a
bone fracture.

REPAIR OF TUBULAR BONE

Occurs in five stages:

 1. Stage of haematoma
 2. Stage of subperiosteal and endosteal cellular proliferation
 3. Stage of callus
 4. Stage of consolidation
 5. Remodeling

Stage of haematoma

 • Bleeding torn vessels form a haematoma between and around the fracture surfaces
 • Haematoma is contained by the periosteum, which may be stripped up
 • Where the periosteum is torn, the haematoma extravasates into soft tissues and is contained by muscles,
fascia and skin.
 • Deprived of blood supply, about 1or 2 millimeters of bone at the fracture surfaces dies.

Stage of subperiosteal and endosteal cellular proliferation

 • Within 8 hours of the fracture there is an acute inflammatory reaction with migration of inflammatory cells
and the initiation of proliferation and differentiation of mesenchymal stem cells.
 • Cells proliferate from the deep surface of the periosteum and the breeched medullary canal [in the
endosteum and marrow tissue].
 • The cells are precursors of osteoblasts, which later lay down the intercellular substance.

32
  • The cellular tissue form a collar of active tissue around each fragment, which grows out towards the other
fragment and this creates a scaffold across the fracture site.
 • The clotted haematoma is gradually absorbed and fine new capillaries grow into the area.

Stage of callus

The differentiating stem cells give rise to osteoblasts and chondroblasts.

 • The osteoblasts lay down an intercellular matrix of collagen and polysaccharide, which soon becomes
impregnated with calcium salts to form the immature bone or osteoid of fracture callus.
 • Osteoclasts also begin to mop up dead bone.
 • As the immature fibre bone [woven bone] becomes more densely mineralized, movement at the fracture
site decreases progressively and the fracture becomes rigid.
 • At about 4 weeks after injury the fracture fragments unite and the fracture is said to be ‘sticky’.
 • The callus may be felt as a hard mass surrounding the fracture.
 • The mass of callus is also visible in radiographs and gives the first indication of union.

Stage of consolidation

 •With continuing osteoclastic and osteoblastic activity, the woven bone is transformed into lamellar bone [a more
mature bone with a typical lamellar structure]

33
Stage of remodeling

 • Newly formed bone often forms a bulbous collar which surrounds the bone and obliterates the medullary
canal.
 • The mass of callus tends to be large when:

1. There is marked periosteal stripping

2. The fracture haematoma has been large
3. There is marked displacement of the fragments.

 • The mass tends to be small when:

1. Bone fragments are in exact anatomical apposition

2. The fragments are rigidly fixed in close apposition by a metal plate with screws or by an intramedullary nail.

 • Callus is usually profuse in children because the periosteum is easily stripped from the bone by
extravasated blood, allowing bone to form beneath it.
 • In the months that follow, the bone is gradually strengthened along the lines of stress, and surplus bone
outside the line of stress is slowly removed. The medullary cavity is gradually reformed, and eventually the
bone assumes a shape as close to normal as possible.
 • In children, remodeling is usually so perfect that eventually the site of the fracture becomes
indistinguishable on radiographs.
 • In adults the site of fracture is usually permanently marked by an area of thickening or sclerosis.

REPAIR OF CANCELLOUS BONE

 • Healing of cancellous bone follows a different pattern from that of tubular bone.
 • Because the bone is of uniform spongy texture and has no medullary canal, there is a relatively much
broader area of contact between the fragments, and the open meshwork of trabeculae allows easier
penetration by bone forming tissue.
 • Union can occur directly between the bone surfaces and it does not have to take place through the medium
of external callus.
 • The first stage of healing is the formation of a haematoma, into which new blood vessels and proliferating
osteogenic cells from the fracture surfaces penetrate until they meet and fuse with similar tissue growing out
from the opposing fragment.
 • Osteoblasts then lay down the intercellular matrix, which becomes calcified to form woven bone.

Assignment

 1. Discuss the rate of union of fractures, outlining factors that influence the speed of union.
 2. Classify the common causes of pathological fractures.
Summary
In this topic you have learnt that:
Fractures can be classified according to:
1. Aetiology
2. Whether open or closed
3. Fracture pattern
Healing of tubular bone occurs in five stages:
1. Stage of haematoma
2. Stage of subperiosteal and endosteal cellular proliferation

34
  3. Stage of callus
 4. Stage of consolidation
 5. Remodeling

Topic Four: PRINCIPLES OF FRACTURE MANAGEMENT

PRINCIPLES OF FRACTURE MANAGEMENT

Learning objectives

 • Outline the steps in the initial management of a patient with fracture.

 • Outline the priorities of management of a patient with multiple injuries
 • Discuss the three fundamental principles of fracture treatment: Reduction; Immobilization; and
Rehabilitation

Initial management

First Aid and Clinical Assessment

First Aid

At accident site:

 • Clear the airway

 • Control any external bleeding
 • Cover wounds with clean dressing
 • Immobilize fractured limbs
 • Make patient comfortable

Moving the patient:

 • If fracture of long bone, apply traction while the limb is being moved
 • If spinal column fracture/dislocation is suspected, avoid flexion of the spine. In some cases also avoid
extension. Patient should be lifted bodily (straight) on to a firm surface, and the neck protected with a
cervical collar.

Temporary immobilization of limbs:

 • Bandage the two lower limbs together (sound limb acts as a splint)
 • Bandage arm to chest
 • Apply a sling for forearm

Control haemorrhage:

 • Apply firm bandage over a pad

 • Application of tourniquet (if profuse pulsatile bleeding despite pressure). Time of application must be
indicated
 • Apply firm manual pressure over the main artery at the root of the limb

35
Clinical assessment

 • Follow the priorities of management of a multiple injury patient.

 • Primary survey – ABC
 • Secondary survey
 1. Re-examine ABC
 2. Investigate as per injury
 3. Physical examination of all systems
 4. Drug treatment (analgesics, antibiotics, tetanus toxoid)

Examination of the limb should determine:

 • Whether there is a wound communicating with the fracture

 • Evidence of vascular injury
 • Evidence of nerve injury
 • Evidence of visceral injury

Resuscitation
Is done during primary survey

 • Airway
 • Breathing
 • Circulation
 Many of the severe trauma patients (multiple fractures with visceral injury) have problem with circulation. They
are usually in shock.

Correction of shock:

1. Immediate replenishment of circulating blood volume

2. Infuse electrolyte fluids to establish intravenous infusion: Normal saline; Ringer’s lactate.
3. Plasma expanders (colloids) to replace the lost volume: Dextran – a high molecular weight polysaccharide;
Hemacel – a gelatin solution.
4. Transfusion only for severe haemorrhage > 1 liter

Topic Four: Priorities of management of multiple injury patient

Priorities of management of a patient with multiple injuries

Advanced trauma life support (ATLS)

Steps in the ATLS philosophy:

 1. Primary survey with simultaneous resuscitation – identify and treat what is killing the patient.
 2. Secondary survey – proceed to identify all other injuries.
 3. Definitive care – develop a definitive management plan.

On arrival:

 • Take a brief history

 • Do Primary survey – ABC

• Airway:

 1. The airway must be evaluated first

36
  2. Check verbal response. If present, the airway is not immediately at risk.
 3. Ensure the airway is clear. Clear the mouth and airway with a large-bore sucker. Inspect for any FBs.
 4. Stabilize the neck to protect the cervical spine.

• Breathing:

 1. Make sure the patient is ventilating and if not, assist (Ambu bag, oxygen)
 2. Give 100% oxygen at high flow
 3. Check for tension pneumothorax
 4. Decompress at once if tension pneumothorax is suspected (needle in the second intercostal space mid-
clavicular line)

• Circulation:

 1. Assess consciousness level – compromised cerebral perfusion; Assess skin colour for pallor; Asses the
pulse; BP
 2. Secure an intravenous line
 3. Give I.V. fluids to restore blood volume
 4. Stop obvious bleeding
 5. Blood for GXM, Hb, haematocrit, blood gases

Secondary survey

Secondary survey involves:

 1. Re-examine ABC
 2. Investigate as per suspected injuries
 • Skull x-ray
 • Chest x-ray
 • Spinal x-ray
 • Pelvic x-ray
 3. Perform a physical examination of body systems even if you think they are not injured
 4. Give analgesics
 5. Administer tetanus toxoid in case of open wounds
 6. Give antibiotics in case of open wounds
 7. Splint the fractures
 8. Admit or refer the patient

Definitive care
There should be as little delay as possible in reaching this stage. A definitive management of the injuries
identified is carefully planned and carried out.

Fundamental principles of fracture treatment

Fundamental principles of fracture treatment

Are three:

 1. Reduction
 2. Immobilization
 3. Rehabilitation – preservation of function

Reduction

37
Reduction is done if necessary. In some cases there is no displacement, or displacement may be immaterial to the
final result. Imperfect apposition of the fragments can be accepted, e.g. a loss of contact of half the diameter in
fracture femur. Imperfect alignment may not be accepted, e.g. angulation (angular deformity of more than 20
degrees in fracture femur). Fractures involving joint surfaces must be reduced as accurately as possible. The
articular fragments must always be restored as nearly as possible to normal to lessen the risk of osteoarthritis.

Methods of reduction

Three methods:

 1. Closed manipulation
 • Manipulative reduction usually under anaesthesia or sedation and strong analgesia.
 2. Mechanical traction (with or without manipulation)
 • To overcome contraction of large muscles that exert a strong displacing force.
 3. Operative reduction (open reduction)

Immobilization
If necessary

Indications for immobilization:

 • To prevent displacement or angulation of the fragments – in order to maintain correct alignment

 • To prevent movement that might interfere with union
 • To relieve pain

Prevention of displacement or angulation:

 • Immobilize to prevent displacement or angulation of the fragments – in order to maintain correct alignment

Prevention of movement:

 • Movement is undesirable when it might shear the delicate capillaries bridging the fracture, e.g. rotation
movements.

• Fractures that constantly demand immobilization to ensure their union are:

 1. Fracture of the neck of femur

 2. Fracture of the scaphoid bone
 3. Fracture of the shaft of ulna

• Fractures that heal well without immobilization include:

 1. Fracture of the ribs

 2. Fracture of the clavicle
 3. Fractures of the scapula
 4. Stable fractures of the pelvic ring

• Immobilization may be unnecessary for certain fractures of the humerus, femur, metacarpals, metatarsals and
phalanges.
• Injured fingers poorly tolerate prolonged immobilization. Leads to stiffness.
Relief of pain:

 • Relief of pain is an important reason for immobilization

38
  • The limb is made comfortable
 • It is possible to use the limb without causing movement at the fracture site, therefore causing no pain

Methods of immobilization

Four methods:

 1. Plaster of Paris cast (P.O.P), Dyna cast or other external splint, e.g. cervical collar, malleable strips of
aluminium.
 2. Continuous traction
 3. External fixation
 4. Internal fixation

Immobilization by plaster /cast

 Assignment:
 1. Write down the requirements and procedure of application of plaster of Paris.
 2. Describe the use of:
 a) Plaster-cutting shears
 b) Powered oscillating plaster saw
 c) Plaster spreader
 3. What complications may follow application of P.O.P, and how do you prevent/manage them?
Immobilization by sustained traction

• Used mainly for fractures that are difficult or impossible to hold in proper position by plaster or external
splint alone. E.g. fractures of shaft of femur.
• Also used when the fragments are difficult to hold in position particularly when the fracture is oblique or
spiral because the elastic pull of muscles tends to draw the distal fragment proximally so that it overlaps
the proximal fragment.
• The pull of muscles must be balanced by sustained traction upon the distal fragment, by a weight or other
mechanical device.
• Angular deformity is prevented by use of a splint e.g. Thomas’s splint for femur and Braun’s splint/frame
for tibia.

Skeletal traction

Traction is applied to pins passed through the bone. They allow substantial loads to be applied accurately to the
bone itself. Common sites for application are:

 1. Upper end of the tibia (tibial tuberosity)

 2. Distal femur
 3. Calcaneum
 4. Olecranon
 5. The skull
 6. Pelvis
 7. Greater trochanter

Types of pin used in skeletal traction

Two types of pin are in common use:

 1) Steinmann pin
 • Has a trocar and smooth sides

39
  • Easy to insert, but it can slip sideways after being in position for some time
 2) Threaded pins, e.g. Denham pin
 • Have threads which grip the bone and prevent lateral slippage
 • Are harder to insert

Skin traction

 • Is applied by means of adhesive strapping stuck directly onto the skin.

 • They pull the bone indirectly through the overlying skin and muscles (soft tissues)
 • The soft tissues can be disrupted if too much weight is applied.
 • The usual upper limit is 5 kg (12 lb)
 • Skin traction is suitable for children and the elderly, and as a temporary measure in adults until definitive
treatment is instituted.

Types of traction

 1. Skeletal or skin traction

 2. Fixed or sliding
 3. Fixed traction with a splint e.g. fixed to a Thomas's splint.
 4. Fixed traction using gravity e.g. gallows traction.
 5. Sliding traction uses a system of pulleys and weights. E.g. Hamilton-Russell traction.
 6. Sliding traction can be balanced or not balanced.
 7. In a balanced traction, one weight applies longitudinal traction and others are applied to the upper and

lower ends of the limb so that it ‘floats’ in a gravity-free field.

Complications of traction

1. Over-distraction with resultant: -

• Circulatory embarrassment
• Stretched or damaged nerves
• Non-union or delayed union as fragments are held apart and do not join
2. Loss of position
• Slipped, angulated or overlapped
3. Pressure sores
4. Pin track infection
5. Allergy to adhesive strapping

Assignment:

 1) Describe the procedure of application of skin traction

 2) State the indications, contraindications, and complications of skin traction
 3) Describe the procedure of application of skeletal traction for fractures of the femur
 4) State the indications, contraindications, and complications of skeletal traction
 5) Name the various traction arrangements (e.g. Russell's traction) and their indications
 6) Name the various parts of an orthopaedic bed and traction apparatus.

40
41
Topic Four: Immobilization by External Fixation

Immobilization by external fixation

• External fixation implies anchorage of the bone fragments to an external device such as a metal bar
through the medium of pins inserted into the proximal and distal fragments of a long bone

fracture.
• Threaded pins are inserted into the bone from one side.
• Two or three pins are inserted into each fragment and the protruding ends of the pins are clamped to the
rigid body of the fixator, which lies just clear of the skin surface parallel with the fractured bone.

Indications of External Fixation

1. Stabilization of severe open fractures

2. Stabilization of fractures associated with infection or nonunion
3. Severely comminuted diaphyseal and peri-articular fractures
4. Closed fracture with associated severe soft tissue injuries
5. Severely comminuted and unstable fractures
6. Pelvic ring disruptions
7. Arthrodesis
8. Fractures that are associated with bony deficits
9. Limb-lengthening procedures
10. Osteotomies

Immobilization by internal fixation

Indications:

1. To provide early control of limb fractures when conservative methods would interfere with the
management of other severe injuries, for instance of the head, thorax or abdomen.

42
2. As a method of choice in certain fractures, to secure immobilization of the fracture and to allow early
mobility of the patient, e.g. in the elderly patient with trochanteric hip fracture
3. When it has been necessary to operate upon a fracture to secure adequate reduction
4. If it is impossible in a closed fracture to maintain an acceptable position by splintage alone.
5. Fractures that cannot be controlled in any other way
6. Patients with fractures in more than one bone
7. Fractures in which the blood supply to the limb is jeopardized and the vessels must be protected
8. Intra-articular, displaced fractures

Methods of internal fixation

1) Metal plate held by screws or locking plate (with screws fixed to the plate by threaded holes)
2) Intramedullary nail – plain [e.g. K-nail] or interlocking i.e. with locking screws [e.g. Sign nail]
3) Dynamic compression screw-plate [dynamic hip screw]
4) Condylar screw-plate
5) Tension band wiring
6) Transfixion screws
7) Kirschner wire fixation

Metals for internal fixation

 • Must be resistant to corrosion in the tissues.

 • A special stainless steel containing chromium, nickel and molybdenum is widely used.
 • A non-ferrous alloy containing chromium, cobalt and molybdenum has even better resistance to corrosion
in the body and is used for all types of internal appliance except wire.
 • Titanium and its alloys are also resistant to corrosion and are used for the manufacture of prostheses and
internal fixation devices.

The place of operative fixation

Operative fixation is accepted as the best routine method of treating fractures of the neck and trochanteric region
of the femur in the elderly. Intramedullary nailing is used for most fractures of the shaft of femur or tibia, and
many fractures of the upper limb are also now routinely operated on.

Advantages of internal fixation

1. Substantial reduction in hospital stay and time away from work

2. Function of the limb, and particularly of the joints, may be restored earlier
3. By providing rigid fixation of the fracture, complications such as delayed union and non-union will be
reduced.

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Rehabilitation

Rehabilitation is always essential, and should begin as soon as the fracture is under definitive treatment. The
purpose of rehabilitation is to: -

1. Preserve function while the fracture is uniting;

2. Restore function to normal when the fracture is united.

This is achieved by encouraging the patient to help himself by active use and active exercises. Supervision of a
physiotherapist is required.

Topic Four: Summary

In this topic you have learnt steps in the initial management of a patient with fracture (First aid); Priorities of
management of a patient with multiple injuries (Primary survey, Secondary survey); and Fundamental principles
of fracture treatment, which are three:

 1) Reduction
 2) Immobilization
 3) Rehabilitation – preservation of function

44
Topic Five: OPEN FRACTURES

OPEN FRACTURES

Definition:
A fracture is open or compound when there is a wound of the skin surface leading down to the site of fracture. A
fracture is classed as open only when a direct communication exists between the body surface and the fractured
bone ends.

Gustilo-Anderson Classification of open fractures

The Gustilo–Anderson classification divides open fractures into three types – I, II & III.

Type I:
Clean wound smaller than 1 cm in diameter, Appears clean, Simple fracture pattern, No skin crushing.

Type II:
A laceration larger than 1 cm but without significant soft tissue crushing: No flaps, No degloving, No contusion
[a bruise]. Simple fracture pattern

Type III:
High-energy injury with extensive soft tissue damage; or an open segmental fracture or multifragmentary
fracture, or bone loss irrespective of the size of skin wound; or Severe crush injuries; or vascular injury requiring
repair. Also included are injuries older than 8 hours or severe contamination.

45
Type III injuries are subdivided into three types:

1. Type III A: Adequate soft tissue coverage of the fracture despite high energy trauma or extensive laceration or skin
flaps.
2. Type III B: Inadequate soft tissue coverage with periosteal stripping. Soft tissue reconstruction is necessary.
3. Type III C: Any open fracture that is associated with vascular injury that requires repair.

Treatment of open fractures

46
An open fracture requires urgent attention. The sooner the wound can be dealt with, the smaller is the risk of infection
arising from contaminating organisms. Initial management at the emergency department includes carrying out a primary
survey – ABC: -
1. AIRWAY: Ensure airway is clear
2. BREATHING: Make sure the patient is ventilating and if not assist (Ambu bag, oxygen)
3. CIRCULATION:

 • Assess for bleeding – inspect, pulse, BP

 • Start an IV line
 • Give IV fluids to restore volume
 • Stop obvious bleeding
 • Blood for grouping and cross-match, Hb, haematocrit, blood gases.

Principles of treatment

1) Clean the wound by performing a thorough surgical toilet.

 • Remove all dead and devitalized tissue

 • Remove all extraneous material
 • Aim at leaving healthy, well-vascularized tissues that are able to fight infection from any remaining
contaminating organisms.

2) The wound should not be subjected to repeated examination, but should be covered with sterile
dressing.
3) Avoid immediate skin closure.

Topic Five: Treatment of open fractures ...

Technique of operation for major wounds

 1. Enlarge the skin wound to display clearly the extent of the underlying damage
 2. Flush the wound with copious quantities of water or saline to remove all contaminating dirt.
 3. Pick out with forceps any foreign matter e.g. shreds (pieces) of clothing.
 4. Excise any tissues that are obviously dead
 5. Remove dead or devascularized muscle in order to reduce the risk of gas gangrene.

47
  6. Remove bone fragments that are small and completely detached.
 7. Large bone fragments, which usually retain some soft tissue attachments, should be preserved.
 8. The bone ends must be inspected.
 9. When debriding bone, the fracture edges are curetted and all dirt and non-viable bone are removed.
 10. Damage to major blood vessels is dealt with by:
 • Ligation
 • Suture
 • Or vein grafting
 11. The ends of severed nerve trunks may be tucked lightly together with one or two sutures to facilitate later
definitive repair.
 12. Tourniquets should be avoided when possible to prevent additional ischemic injury to the soft tissues.
 13. Necrotic tissue is removed and only viable tissue is left behind. The exception is skin, where none is
removed unless obviously necrotic.
 14. The quality of the muscle tissue is assessed using the classic 4 C’s:
 • Color (red or brown)
 • Consistency (how does the muscle feel)
 • Capillary Circulation (does it bleed?)
 • Contractility (responds to pinch or electro-cautery)

Skin closure
The wound should be left unsutured after surgical toilet and dressed with sterile covering. Delayed closure
should be done as soon as infection has been aborted or overcome (delayed primary suture).

Methods of skin closure

Direct suture of the skin edges if feasible, depending upon the amount of skin destroyed and lost in the injury. If
the skin loss is negligible and the skin edges can be brought together without tension, direct suture should be
done. A free split-skin graft is used if the skin edges will not come together easily (full-thickness skin graft).
Soft-tissue flaps can also be done.

Treatment of the fracture

Once the wound has been dealt with, the fracture itself should be treated following the general principles of
managing closed fractures.

There should be greater reluctance to resort to operative methods of fixation, due to increased risk of infection.

If the fracture is unstable and unsuitable for treatment by traction or by simple splintage, external
fixation should be done. This provides temporary stabilization and minimizes additional soft-tissue injury. This
fixation facilitates access to the wound for inspection between debridements.

Once the wound has healed, the fracture can be immobilized in plaster for the remaining duration of treatment.
Other treatment
1. Antibiotics:

• A course of treatment with a broad-spectrum antibiotic, such as a third generation cephalosporin, should be
begun immediately and continued until the danger of infection is past.

• Antibiotics should be given intravenously.

2. Prophylaxis against tetanus:

• Tetanus toxoid should be given and repeated 6 weeks later or a booster should be given if the patient was
already immunized previously.
3. Analgesics
4. Monitor vital signs

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The end! Topic Five: Summary

In this topic you have learnt the definition of open fracture, Gustilo-Anderson Classification of open fractures and
the principles of treatment of open fractures, including:

1. Primary survey
2. Wound management
3. Fracture management
4. Prevention of infection/tetanus

Topic Six: COMPLICATIONS OF FRACTURES

COMPLICATIONS OF FRACTURES

Complications of fractures can be classified into three broad groups depending upon their time of occurrence.
These are as follows -

 1. Immediate complications - occurs at the time of the fracture.

 2. Early complications - occurring in the initial few days after the fracture.
 3. Late complications - occurring a long time after the fracture.

Immediate complications

Systemic

 • Hypovolaemic shock due to haemorrhage

Local

 • Injury to major blood vessels

 • Injury to nerves
 • Injury to muscles and tendons
 • Injury to joints
 • Injury to viscera

Early complications

Systemic

 • Fat embolism syndrome

 • Deep vein thrombosis
 • Disseminated intravascular coagulation [DIC]
 • Septicemia (in open fracture)
 • ARDS - Adult respiratory distress syndrome [shock lung or wet lung]

Local

 • Infection
 • Compartment syndrome

Late complications

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Imperfect union of the fracture

 • Delayed union
 • Non union
 • Mal union
 • Cross union

Others

 • Avascular necrosis
 • Shortening
 • Joint stiffness
 • Sudeck's dystrophy
 • Osteomyelitis
 • Ischaemic contracture
 • Myositis ossificans
 • Osteoarthritis

Complications of fractures can also be classified as follows:

Related to the # itself

 • Infection
 • Delayed union
 • Non-union
 • Avascular necrosis
 • Mal-union
 • Shortening

Due to associated injury

 • Injury to major blood vessels

 • Injury to nerves
 • Injury to viscera
 • Injury to tendons
 • Injuries and post-traumatic affections of joints
 • Fat embolism
 • Compartment syndrome

Infection

 • Is common in open fractures contaminated by organisms carried in from outside.

 • Could also follow operative treatment of a closed fracture
 • Very rarely occurs in some closed fractures due to bacteraemia
 • Infection often leads to osteomyelitis
 • The infection of bone tends to become chronic.

Treatment:

 • Acute infection is treated by:

1. Establishing free drainage

2. Antibacterial medication – choice depends on sensitivity of the organisms.

 • Chronic infection:

50
  Sequestrectomy and saucerization and chiseling away bone with small pus containing cavities

Mal-union

 • Refers to a fractured bone that has united soundly but in the wrong position (imperfect position).
 • Results from improper or imperfect reduction
 • Commonly presents as angulation, rotation, loss of end-to-end apposition, or overlap and consequent
shortening.
 • Treatment of clinically significant mal-union is by dividing the bone, correcting the deformity, and fixing
the fragments by the appropriate means.

Shortening

Shortening of a bone after a fracture may occur from the following causes:

 • Mal-union with overlap

 • Mal-union with marked angulation
 • Crushing of bone as in severely comminuted compression fractures
 • Loss of bone as in gunshot wound with a piece of bone shot away
 • Interference with epiphyseal growth plate in children

Topic Six: Delayed union; Non-union

Delayed union

 • A fracture with delayed union takes longer than expected to unite, but eventually does so.
 • Union is usually deemed to be delayed if the fracture is still mobile 3 or 4 months after the injury.
 • In delayed union, there is nothing in the condition of the bones to indicate that union will fail altogether.

Non-union

 • Healing process fails

 • Bone ends do not unite and remain separate
 • The bone ends at the site of the fracture become dense and rounded.
 • The fracture line becomes increasingly clear-cut.

 • Two types of non-union are seen:

 1. Hypertrophic non-union
 2. Atrophic non-union
Hypertrophic non-union:

 • Occurs due to excessive movement at the fracture site, with abundant callus formation but failure to unite
due to instability.
 • Characterized by a massive cuff of bone around the ends of the fractures that looks like an elephant’s foot.
 • These fractures are trying desperately to heal.
 • Healing can be enhanced by realigning the limb and preventing movement between the bone ends.
 • Prevention of movement can be done by rigid internal fixation

Atrophic non-union:

 • The fracture gap is filled by fibrous tissue and the bone fragments remain mobile.
 • Shows rounding of the bone ends, sometimes so marked that the tips of the bone ends resemble pencils,
and the medullary cavity may be closed.
 • This is indicative of a poor blood supply to the bone ends.

51
  • A pseudoarthrosis forms in some patients.
 • Treatment aims to ‘kick start’ osteogenesis by bone grafting with fresh cancellous bone or marrow.

Causes of non-union include:

 1. Infection of the bone

 2. Incomplete reduction
 3. Excessive shearing movements between the fragments
 4. Interposition of soft tissues between the fragments
 5. Loss of the fracture haematoma in an open fracture
 6. Dissolution of fracture haematoma by synovial fluid (#s within joints)
 7. Destruction of bone as by a tumour

Treatment:

 • Bone grafting operation

 • Joint replacement operation e.g. Austin-Moore prosthesis in fracture of the neck of femur

Avascular necrosis; Post-traumatic ossification; Osteoarthritis

Avascular necrosis

This is death of bone from a deficient blood supply. It occurs when the blood supply to a bone or part of a bone is
interrupted by injury. It usually occurs as a complication of a fracture near the articular end of a bone, especially
where the terminal fragment is devoid of vascular soft tissue attachments and depends for its nutrition almost
entirely upon the intra-osseous vessels which may be torn by the injury. It often leads to non-union and
osteoarthritis. The avascular bone gradually loses its rigid trabecular structure and becomes granular or
gritty. The bone crumbles easily and may eventually collapse from pressure imposed by muscle tone or body
weight.

Sites of avascular necrosis:

• Head of the femur after # neck of femur or hip dislocation
• Proximal half of the scaphoid bone after a fracture through the waist of the scaphoid
• Body of the talus after a fracture through the neck of the talus
• Lunate bone may undergo avascular necrosis after its dislocation.

Diagnosis:
• May be recognized from radiographs about 1-3 months after injury
• The avascular fragment appears denser due to its not taking part in the osteoporosis of disuse affecting
surrounding bones.
• Fragment may have reduced height, with a shrunken crumbled appearance.

Treatment:

• Early operation to prevent joint disorganization

• Promote revascularization by drilling the avascular fragment, with or without bone grafting.
• Excision of the avascular fragment and replacing it with a prosthesis, (arthroplasty) or perform arthrodesis.

Post-traumatic ossification

Is a rare cause of joint stiffness after fracture or dislocation. It is Sometimes called myositis ossificans. It occurs
in severe injury to a joint, especially when the capsule and periosteum have been stripped from the bones by
violent displacement of the fragments. Blood colllects under the stripped soft tissues, forming a large haematoma

52
about the joint. Instead of being absorbed, the haematoma is invaded by osteoblasts and becomes ossified. This
leads to restriction of joint movement. It is encountered most commonly in the elbow after fracture-dislocation. It
also occurs in the hip after dislocation. There is greater risk of occurrence in children than in adults because the
periosteum is only loosely

Treatment
1) Gentle active exercises
2) Excise a mass of bone that is blocking movement.

Osteoarthritis

• Occurs due to roughening or irregularity of joint surface

• Is likely to develop sooner or later after any displaced fracture which involves an articular surface
• Even a slight step between the fragments may lead to serious subsequent disability from arthritis, esp. in a
weight bearing joint.
• Avascular necrosis is also an important cause of osteoarthritis.
• There is risk of osteoarthritis if fracture fragments unite with angular deformity because mal-alignment of
joint surfaces causes excessive stress at one part of the joint and accelerates wear-and-tear changes.

Compartment syndrome

This is a rise in hydrostatic pressure within a fascial compartment leading to compromised circulation within the
compartment, with resultant tissue ischaemia and eventually, necrosis.
Pathophysiology:
Muscles are contained within fascial compartments. If swelling occurs within a compartment as a consequence of
injury, the fascia resists the swelling, and pressure within the compartment rises greatly. Increased pressure
occludes the veins and small arteries supplying the muscles causing ischaemia. Muscle ischaemia in turn
promotes further swelling worsening the situation. Within a few hours, irreversible changes may occur:

1. The muscles may become necrotic

2. The nerves within the affected compartment lose their conductivity because of ischaemia
3. The muscles are eventually replaced by fibrous tissue, which contracts causing Volkmann’s ischaemic contracture.

Volkmann’s ischaemic contracture is seen most often in the flexor muscles of the forearm and lower leg.

Clinical features
• Severe pain in the limb
• Pain worsened by attempted passive extension of the digits
• Pallor of the limb
• Coldness of the limb
• Pulses may be absent if the relevant artery is contained within the affected compartment.

 A lack of pulse rarely occurs in patients, as pressures that cause compartment syndrome are often well below
arterial pressures. Therefore, in compartment syndrome the peripheral arterial pulses may still be present, and this
could cause confusion as to the true diagnosis.

• Tense and swollen shiny skin.

• Congestion of the digits with prolonged capillary refill time.
• Paraesthesia (altered sensation e.g., "pins & needles") in the cutaneous nerves of the affected compartment.
• Paralysis of the limb is usually a late finding.

53
Treatment
• Immediate operation to decompress the whole length of the affected compartment or compartments by fasciotomy.
• The fascial compartments and the skin must be divided so that the muscle can swell.
• The wound is left open until swelling has subsided, after which it may be closed or grafted.
Compartments
Forearm
There are two compartments in the forearm:
1) Ventral (flexor) compartment

 • Includes the median and ulnar nerves, and the radial and ulnar arteries.

2) Dorsal (extensor) compartment

 • Is less often damaged than the ventral

 • It includes the posterior interosseous nerve but no major vessels.
 • Consequences are less serious.

Lower limb
In the leg there are four compartments:
1) Anterior tibial compartment

 • Contains the anterior tibial artery and deep peroneal nerve

2) Superficial posterior compartment

 • Composed of gastrocnemius and soleus only

 • Has no important vessels or nerves

3) Deep posterior compartment

 • Contains the posterior tibial vessels and nerves and the peroneal artery
 • Consequences are serious

4) Lateral (peroneal) compartment

 • Contains the superficial peroneal nerve, but it is seldom affected by compression.

Fat embolism syndrome

 Is one of the most serious complications of fractures

 The essential feature is occlusion of small blood vessels by fat globules.

Pathology

Fat embolism syndrome mainly affects the lungs and brain. Occlusion of blood vessels leads to oedema and
haemorrhages in the alveoli of the lungs. Transfer of oxygen from the alveoli to arterioles is thus impaired. This

54
leads to hypoxaemia, which may be severe. In the brain there may be multiple petechial haemorrhages. Petechial
haemorrhages occur also in other organs and in the skin.

Clinical features

1. Occurs mainly after severe fractures in the lower limbs particularly those of the femur and tibia.
2. The onset is usually within two days of the injury
3. There is a symptom-free period between injury and onset. This distinguishes fat embolism from cerebral
contusion.
4. Breathlessness
5. Cerebral disturbance
6. Marked restlessness
7. Confusion
8. Drowsiness or coma
9. Cerebral symptoms may be caused partly by petechial haemorrhages in the brain, but in large measure
they are probably secondary to hypoxia from occlusion of small blood vessels in the lungs.
10. Tachypnoea
11. Dyspnoea
12. Petechial rash

 • On the front of the neck

 • On the anterior axillary folds or chest
 • In the conjunctiva
 The finding of such a rash strongly supports a diagnosis of fat embolism syndrome.

Diagnosis

1) Characteristic clinical features

2) Arterial blood gas analysis may show reduction of the partial pressure of oxygen in the blood well below
100mmHg and often below the critical level of 60mmHg at which respiratory failure is likely.
3) Chest radiographs show patchy consolidation
4) Platelet count is low
5) Serum lipase is low
6) Fat globules may be present in the urine

Treatment

Fat embolism is spontaneously reversible if the patient can be tided over the dangerous period of hypoxia.

• This may be achieved by administration of 100% oxygen with positive pressure ventilation if necessary.
Control oxygen requirement by repeated blood gas analysis
• Patient needs to be managed in the intensive care unit.
• The administration of methylprednisolone in patients with severe multiple injuries may help to prevent
and correct the adverse effects of fat embolism by maintaining blood oxygen tension and stabilizing the
free fatty acids.
• Heparin or Dextran 40 may also be administered intravenously to improve capillary flow

Topic Six: Reflex sympathetic dystrophy; Articular adhesions

Reflex sympathetic dystrophy

55
Also known as: Sudeck’s atrophy, Sudeck’s post-traumatic osteodystrophy, Post-traumatic painful osteoporosis,
Complex regional pain syndrome.

• It is characterized by pain, swelling and marked joint stiffness in the hand or foot of the injured limb.
• The cause and exact nature of the condition are unknown.
• Probably due to a disturbance of centrally mediated autonomic regulation with consequent increased
stimulation of sympathetic and motor efferent fibres.

Clinical features
• Symptoms are noticed about 2 months after the injury, or when the plaster is removed.
• The function of the limb is not regained as it should be with active use and exercises.
• Instead, the patient complains of severe pain in the affected hand or foot when attempting to use it.
• On examination:
1) The limb is swollen and may be hyperaemic.
2) The skin creases are obliterated, giving the surface a glossy appearance
3) The nails and hair of the hand or foot are atrophic.
4) The palmar aponeurosis may be thickened
5) Joint movements are severely impaired, esp. the metacarpophalangeal and interphalangeal joints (‘frozen
hand’)
6) Radiographs show spotty osteoporosis, often of severe degree.
Treatment
• Most cases respond slowly but surely to efficient conservative treatment.
• Mainstay of treatment is active exercise, with active use of the limb so far as the pain will allow.
• Periods of elevation and local heat (warm baths)
• Adequate recovery is usually gained in 2-4 months.
Intra-articular and peri-articular adhesions
• Joint stiffness after adhesions is common after fractures, esp. those that are near a joint.
• The knee, shoulder, elbow and finger joints stiffen easily and often suffer permanent impairment.
• The hip and wrist usually regain their full mobility without difficulty.
• Adhesions occur chiefly after a fracture that has involved the articular surface of a bone. Blood escapes
into the joint (haemarthrosis) and may leave residual strands of fibrin which later become organized into
fibrous adhesions between opposing folds of synovial membrane.
• Peri-articular changes are a more frequent cause of joint stiffness than intra-articular adhesions. Due to
the injury and possibly prolonged immobilization, oedema fluid collects in the tissues, binding together the
connective tissue fibers. This leads to loss of resilience of the peri-articular tissues such as joint capsule and
ligaments, and also impairs the free gliding of muscle fibres one upon another.
• Direct adhesion of muscle to the underlying bone at the site of fracture is another cause of stiffness.
Treatment
1) Active exercises preferably under supervision of physiotherapist
2) Manipulation:

 • Manipulation under anaesthesia may be considered if active exercises and use are not achieving steady
improvement.
 • Manipulation is more likely to be successful in overcoming stiffness from intra-articular adhesions.
3) Operation to release the adhesions
The end.
Topic Six: Summary

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In this topic you have learnt the classification of various complications of fractures -
• Immediate – local and systemic
• Early - Local and systemic
• Late - due to imperfect union of fracture or other causes
• Complications related to the fracture itself
• Complications due to associated injury
You have also learnt the management of the complications.

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Topic Seven: SPECIAL FEATURES OF FRACTURES IN CHILDREN

Special features of fractures in children

Injuries involving the growth plate

• Also known as epiphyseal injuries

• Each end of the long bones has a cartilaginous growth plate.
• Most growth occurs away from the elbow and towards the knee.
• The growth plate is a potentially weak point in the bone and is commonly injured in children.
• Epiphyseal injuries can be classified radiologically into five types as described by Salter and Harris.

• Designated as Salter-Harris classification.

Salter-Harris classification

• Type I injury: complete separation of epiphysis at the growth plate without damage to the
metaphysis or epiphysis.
• Type II injury: the most common type, with a characteristic triangular fragment of the metaphysis
attached to the displaced epiphysis.
• Type III injury: involves the articular surface with separation of an epiphyseal fragment.
• Type IV injury: fracture of the articular surface with extension across the growth plate into the
metaphysis.
• Type V injury: compression fracture involving part or all of the growth plate

Bone resilience
Bones in children are more resilient and springy, withstanding greater deflection without fracture. This explains
the predominance of incomplete fractures of the greenstick type in children.

Periosteum

The periosteum in children’s bones is attached only loosely to the diaphysis and is therefore easily stripped from
the bone over a considerable part of its length by blood collecting beneath it. This leads to abundance of callus
following injury, even with little displacement of the fragments.

58
Site of fracture

Certain fractures that are common in adults are uncommon in children; e.g. Fractures of: Scaphoid bone, Neck of
femur, Trochanteric region of femur. Some fractures are quite common in childhood: - Supracondylar fractures
of humerus, Fractures of the capitulum of the humerus

Healing

Healing of childhood fractures is usually rapid, the younger the child the more rapid the healing. In infancy a
fracture may be soundly united in 2 or 3 weeks; in later childhood the average time required for union gradually
increases. Remodeling is very active and complete in early childhood; so much so that all evidence of a past
fracture may be obliterated within a matter of months.

Effect on growth

After a fracture of a long bone in a child, growth is often accelerated for a time, perhaps from hyperaemia of the
neighbouring epiphyseal cartilage. Growth may be seriously disturbed if the growth plate is damaged. If the
whole area of the growth plate is fused, all growth ceases at that site.

The degree of consequent shortening will depend on the age at which premature fusion occurred; the younger the
patient at the time of fusion, the greater the eventual shortening.

If premature fusion occurs in only a part of the epiphyseal plate, further growth will be prevented at that point but
will continue in the undamaged part of the plate, leading to angulation deformity. Angulation will also occur if
there is premature arrest in one bone of a pair, as in the forearm or leg.

The end.

Topic Seven: Summary

In this topic you have learnt some of the special features of fractures in children:

 1) Salter-Harris classification of epiphyseal injuries

 2) Bone resilience
 3) Periosteum in children
 4) Rate of healing
 5) Effects of fractures on growth
Topic Eight: JOINT INJURIES

JOINT INJURIES

A Joint injury is dysfunction of a joint as a result of an injury, following either acute trauma or chronic
overuse. A joint injury can involve damage to the bones, ligaments or other tissues of the joint. The larger limb
joints tend to be the most utilized and are hence more prone to injuries. Severity of symptoms varies depending
on the type and location of injury and often the primary symptom is pain.

Symptoms of joint injury

 1. Joint pain
 2. Joint swelling
 3. Joint redness
 4. Joint discoloration
 5. Inability to move joint

59
  6. Movement problems
 7. Bruising around joint
 8. Broken bone in joint
 9. Deformed joint
 10. Joint tenderness
 11. Reduced range of joint motion
 12. Joint weakness
 13. Joint numbness
 14. Joint warmth

Mechanisms of injury

Joints are usually injured by twisting or tilting forces that stretch the ligaments and capsule. If the force is great
enough the ligaments may tear, or the bone to which they are attached may be pulled apart. The articular
cartilage may also be damaged if the joint surface is compressed or if there is a fracture into the joint. Forceful
angulation usually tears ligaments rather than crush the bone. However, in older people with osteoporosis, the
ligaments may hold and the bone on the opposite side of the joint is crushed. In children there may be a fracture-
separation of the epiphysis.

Common joint injuries

A joint injury can be:

 1. A sprain of the joint

 2. A strain of the ligaments
 3. A rupture of the ligaments
 4. A subluxation of the joint
 5. A dislocation of the joint

Topic Eight: Sprain; Strain; Rupture

Sprain/ Strain / Rupture

A sprain is any painful wrenching (twisting or pulling) movement of a joint that does not cause tearing of the
capsule or ligaments.
A strain is a physical effect of tensile stress associated with stretching of the ligaments, which involves tearing of
some fibers.
If the stretching or twisting force is severe enough, the ligament may be strained to the point of complete rupture.

Strained ligament
• Only some of the fibers in the ligament are torn and the joint remains stable.
• The injury occurs when a joint is momentarily twisted or bent into an abnormal position.
• The joint is painful and swollen and the tissues may be bruised.
• Tenderness is localized to the injured ligament and tensing the tissues on that side causes a sharp increase
in pain.

Treatment of a strained ligament

1. The joint should be firmly strapped and rested until the pain subsides.
2. Ice packs can be applied locally
3. Non-steroidal anti-inflammatory medication
4. Thereafter active movements are encouraged.
5. Muscle strengthening exercises are carried out.

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Ruptured ligament

The ligament is completely torn and the joint is unstable. Sometimes avulsion of the bone to which the ligament
is attached occurs if the ligament holds and fails to rupture. Treatment is easier in the case of avulsion because
the bone fragment can be securely reattached.
The mechanism of injury is a sudden forceful twist or bending of the joint into an abnormal position. The patient
might hear a snap sound during the injury.
Rupture most likely affects joints that are insecure by virtue of their shape or their being least well protected by
the surrounding muscles. They include: the knee; the ankle; and finger joints.

Clinical features
1) Severe pain
2) Bleeding under the skin (ecchymosis)
3) Swollen joint, probably due to a haemarthrosis
4) Very tender joint, patient does not want the joint to be disturbed
5) Examination under anaesthesia by stressing the joint demonstrates joint instability. This distinguishes the
lesion from a strain.
6) X-ray may show a detached flake of bone in the case of avulsion.

Treatment of Ruptured ligament

Torn ligaments heal by fibrous scarring.

1. Non-operative treatment is encouraged in the first instance.

 •The joint is splinted for 1-2 weeks and local measures taken to reduce swelling [elevation, cold compress]
 •Thereafter the splint is replaced with a functional brace that allows joint movement but prevents repeat injury to
the ligament.
 •Physiotherapy – muscle strengthening exercises.

2. In the case of an avulsion of bone with the ligament, reattachment of the ligament is indicated if the piece
of bone is large enough.

Dislocation and subluxation

• Dislocation means that the joint surfaces are completely displaced and are no longer in contact.
• Subluxation implies a lesser degree of displacement, such that the articular surfaces are still partly
apposed.

Clinical features

1. Severe joint pain

2. Patient avoids moving the joint
3. The shape of the joint is abnormal
4. Bony landmarks may be displaced
5. The limb is held in a characteristic position depending on the joint affected
6. Movement is painful and restricted

X-ray findings
Radiographs will clinch the diagnosis and will also show if there is any associated bony injury (fracture-
dislocation)

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Apprehension test
If the dislocation is reduced by the time the patient is seen, the joint can be tested by stressing it as if almost to
reproduce the suspected dislocation: the patient develops a sense of impending disaster and violently resists
further manipulation.

Recurrent dislocation
If the ligaments and joint margins are damaged, repeated dislocation may occur. This is termed recurrent
dislocation. This is especially common in the shoulder and the patella-femoral joint.

Treatment of dislocation/subluxation
1. The dislocation must be reduced as soon as possible by manipulation.
2. A general anaesthetic is usually required or an opioid analgesic [e.g. pethidine or morphine]
3. A muscle relaxant may also be required [e.g. diazepam]
4. The joint is then rested or immobilized until soft tissue swelling reduces – usually after 2 weeks.
5. Physiotherapy

Complications of dislocation/subluxation
1) Vascular injury
2) Nerve injury
3) Avascular necrosis of bone
4) Heterotopic ossification (post-traumatic ossification)
5) Joint stiffness
6) Secondary osteoarthritis

The end - Thank you.

TOPIC Eight: Summary

In this topic you have learnt about common joint injuries, their clinical presentation and their management.
1) A sprain of the joint
2) A strain of the ligaments
3) A rupture of the ligaments
4) A subluxation of the joint
5) A dislocation of the joint

UNIT THREE: PRE AND POST OPERATIVE SURGICAL CARE

Topic 1: PRE-OPERATIVE AND POST-OPERATIVE SURGICAL CARE

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INTRODUCTION

The care of the patient with a major surgical problem commonly involves distinct phases of management that
occur in the following sequence:

 1) Pre-operative care:
 • Diagnostic work-up.
 • Pre-operative evaluation.
 • Pre-operative preparation.
 2) Anaesthesia and operation.
 3) Post-operative care

PRE-OPERATIVE CARE

General Health Assessment:

1) A careful and accurate history should be taken to establish a correct diagnosis. The history should include
a review of the patient’s previous experiences with anaesthesia, including: Any allergic reactions; Delayed
awakening; or Prolonged paralysis from neuromuscular blocking agents.
2) Full clinical examination.

 • A thorough physical examination should be done. The cardiovascular system, lungs and upper airway
should be carefully examined. It should include measurements of heart rate and blood pressure and auscultation for
cardiac murmurs and abnormal breathing.
 • The airway, head and neck should be examined for factors that could make endotracheal intubation
difficult, e.g., fat or short neck or limited temporo-mandibular mobility.
 • If regional anaesthesia is planned, the proposed site of injection should be examined for abnormalities and
signs of infection.

3) Investigations:

 1. Urinalysis.
 2. Complete blood count: A haemoglobin of 10g/dL is considered to be physiologically safe for tissue oxygen
delivery.
 3. Urea, electrolytes and creatinine - kidney function
 4. Liver function tests
 5. Blood grouping and cross-matching.

NB: The adequacy of liver and kidney function should be tested if impairment is suspected, as both organs play a major
role in the response to and clearance of anaesthetic agents both preoperatively and intra-operatively.

4) Informed consent:

 Surgery is a frightening prospect for both patient and family. Informed consent involves advising the patient of
what to expect from administration of anaesthesia and of possible adverse effects and risks.
 Patient should be informed of the surgical procedure to be performed, benefits and risks and possible
consequences, in understandable terms. Their psychological preparation and reassurance should begin at the initial
contact with the surgeon. The potential need for blood transfusion must also be addressed.
 The patient or the legal guardian of the patient must sign (in advance) a consent form authorizing a major or minor
operation or a procedure

Summary:
The pre-operative evaluation should be comprehensive in order to:

63
1. Assess the patient’s overall state of health.
2. Determine the risk of the impending surgical treatment.
3. Guide the pre-operative preparation.
Topic 1: Specific factors affecting operative risk

SPECIFIC FACTORS AFFECTING OPERATIVE RISK

1) Chronic respiratory disease

 • Careful attention should be given to peri-operative management in patients with chronic respiratory
disease. Smoking cessation is important as this will decrease sputum production. Aim at stopping at least 2 months
before the planned procedure. Even a few days of abstinence from smoking will have a positive effect on sputum
production.
 • Oral or inhaled bronchodilators along with twice-daily chest physical therapy and postural drainage will
help clear inspissated secretions from the airway. Before surgery, patients should be instructed in techniques of
coughing and deep breathing.
 • Peri-operative strategies include the use of epidural anaesthesia, vigorous pulmonary toilet &
rehabilitation, and continued bronchodilator therapy. Early mobilization and treatment of infection is also
important.
 • The patient with compromised pulmonary function preoperatively is susceptible to post-operative
pulmonary complications, including hypoxia, atelectasis (lung collapse), and pneumonia.

2) Delayed wound healing:

 The following factors are of possible clinical significance in delaying wound healing:
 1. Protein depletion.
 2. Ascorbic acid deficiency.
 3. Marked dehydration or oedema.
 4. Severe anaemia.
 5. Large doses of corticosteroids.
 6. Cytotoxic drugs.
 7. Irradiation.

3) Drug effects:

 • Drug allergies, sensitivities and incompatibilities and adverse drug effects that may be precipitated by
operation must be foreseen and, if possible, prevented. A personal or strong family history of asthma, hay fever or
other allergic disorder should alert the surgeon to possible hypersensitivity to drugs.
 • Drugs currently being taken by the patient may require continuation, dosage adjustment, or
discontinuation. Medications such as digitalis, insulin and corticosteroids must usually be maintained and their
dosage carefully regulated during the operative and post-operative periods.
 • Prolonged use of corticosteroids may be associated with hypofunction of the adrenal cortex, which impairs
the physiologic responses to the stress of anaesthesia and operation.
 • Anticoagulant drugs are an example of a medication that is to be strictly monitored or eliminated pre-
operatively.

4) Risk of thromboembolism:

 Increased risk factors for deep vein thrombophlebitis and pulmonary embolus include:
 1. Cancer.
 2. Obesity.
 3. Myocardial dysfunction.
 4. Age over 45 years.
 5. A prior history of thrombosis.

64
5) The elderly patient:

 • Aged patients generally require smaller doses of strong narcotics and are frequently depressed by routine
doses. Sedative and hypnotic drugs often cause restlessness, mental confusion, and uncooperative behaviour in the
elderly and should be used cautiously.
 • Pre-anaesthetic medication should be limited to atropine or scopolamine in the debilitated elderly patient
and anaesthetic agents should be administered in minimal amounts.

6) The obese patient:

 • Obese patients have an increased frequency of concomitant disease and a high incidence of post-operative
wound complication.
 • Obesity increases both technical difficulties of operation and liability to post-operative chest complications
and venous thrombosis.
 • Obesity is also a risk factor for post-operative wound infection.
 • A controlled pre-operative weight loss program is often beneficial before elective procedures.

PRE-OPERATIVE ORDERS

On the day before operation, orders are written that assure completion of the final steps in the pre-operative
preparation of the patient.

These orders will usually include the following:

1. Diet:

 • Starve the patient, usually from midnight if the surgery is elective and is scheduled for the following
morning.
 • Omit solid foods for 6 hours and fluids for 4 hours pre-operatively.
 • Recently, there has been a shift to permit clear, non-fizzy fluids up to 2 hours pre-operatively.

2. Enema:

 • Need not be given routinely.

 • Given in cases of operations on the colon, rectum and anal regions or operations likely to be followed by
paralytic ileus and delayed bowel function.
 • Constipated patients and those scheduled for the above types of operations should be given a flushing
enema 8 – 12 hours pre-operatively with 500 – 1500ml of warm tap water or, preferably, physiologic saline, or
with 120 – 150ml of hypertonic sodium phosphate solution conveniently available in a commercial kit.
 • When thorough cleaning of the bowel is not essential, satisfactory evacuation on the evening before
operation can usually be accomplished by use of a 10mg bisacodyl (Dulcolax) rectal suppository.
 • A hypertonic sodium phosphate enema or bisacodyl rectal suppository, or both, may also be effective in the
rapid preparation of the colon and rectum for sigmoidoscopy.

3. Premedication:

 The anaesthetist will usually examine the patient and write the premedication order.
 The principal goals of pre-operative medication are:
 1) To relive anxiety and provide sedation.
 2) To induce amnesia.
 3) To decrease secretion of saliva and gastric juices.
 4) To elevate the gastric pH, and

65
  5) To prevent allergic reactions to anaesthetic drugs.
 Medication is usually given 30 min to 2 hours before the induction of anaesthesia. The selection of drugs is largely
subjective. Sedation can be achieved by:
 1) Barbiturates.
 2) Benzodiazepines or
 3) Narcotics.
 Gastric secretion can be decreased by H2receptor antagonists such as cimetidine. For reduction of anxiety, oral
short-acting benzodiazepines can be used 1 – 2 hours pre-operatively, especially for children.
 The anticholinergic agents, atropine, glycopyrronium and hyoscine, are used to reduce respiratory and oral
secretions. Atropine and glycopyrronium also protect against vagal dysrhythmias.
 If indicated, prophylactic antibiotic agents are given by the anaesthetist in concert with the surgeon, either with the
premedication or intravenously at induction of anaesthesia.

4. Special orders:

 a) Blood transfusion:
 If blood transfusion may be needed during or after operation, have the patient typed and arrange for a sufficient
number of units to be cross-matched and available prior to operation.

 b) Nasogastric tube:
 N/G tube for suction may be needed after operations on the GIT to prevent distension due to paralytic ileus. If the
patient has gastrointestinal obstruction with possible gastric residual secretions, a N/G tube is passed preoperatively
and the stomach aspirated or placed on continuous suction to reduce the possibility of regurgitation and aspiration
during induction of anaesthesia.

 c) Bladder catheter:
 If it appears the patient will need hourly monitoring of urinary output during or after operation or if post-operative
urinary retention is anticipated (as in spinal anaesthesia), a Foley catheter is inserted for constant bladder drainage.
If bladder distension will interfere with exposure in the pelvis, a catheter should be placed pre-operatively

PRE-OPERATIVE NOTE

When the diagnostic workup and pre-operative evaluation have been completed, all details should be reviewed
and a pre-operative note written in the chart. This is usually done on the day before the operation. The note
summarizes the pertinent findings and decisions, gives the indications for the operation proposed, and attests that
a discussion of the complications and the risks of operation has occurred between surgeon and patient (i.e.,
informed consent).

The following should also be noted and prominently displayed on the chart:
i. Bleeding tendencies.
ii. Medications currently being taken.
iii. Allergies and reactions to antibiotics and other agents.

Other preparations

 Shave the patient if necessary

 Gown the patient
 Label the patient
1. Name
2. Patient number
3. Ward number
4. Type of operation

66
 5. Part to be operated on [esp. limbs]
 Observe vital signs

POT-OPERATIVE MANAGEMENT

1) Observe vital signs – BP, temperature, pulse rate, respiratory rate – half hourly until the patient is fully
awake, then continue observation in the ward 4 hourly or 6 hourly as convenient.
2) Give intravenous fluids – normal saline and dextrose till bowel sounds return. 3 liters per day (1 liter
normal saline, 2 liters 5% dextrose)
3) Give analgesics in the first 48 hours – pethidine or morphine (or other strong analgesics)
4) Nil per oral till bowel sounds are heard, then start on oral sips (plain water) for 1 day.
5) On the second day after bowel sounds appear, start on water and then light diet – soup, porridge, rice,
mashed diet, etc. avoid fluids with plenty of gases e.g. soda.
6) Give antibiotic cover where appropriate
7) Can catheterize for the first 24 hours to monitor urine output.
8) Nasogastric tube suction, especially after abdominal surgery, until the volume of aspirate diminishes.
9) Monitor any surgical drains. Remove the drain when it ceases to discharge effluent.
10) If no complications, the wound need not be disturbed until the skin sutures have been removed.
11) Remove alternate sutures on the 6th day and all sutures on the 7th post-operative day.
12) Start counting 1st P.O.D 24 hours after the operation.

POST OPERATIVE COMPLICATIONS

Factors influencing post-operative complication
1) Type of surgery
2) Patient factor
3) Pre-existing co-morbid illness
4) Procedure-related complication

Immediate complications
1) Primary haemorrhage
2) Basal atelectasis: minor lung collapse
3) Hypoxia
4) Haemodynamic complication – Shock due to blood loss
5) Reduced urine output – due to inadequate fluid replacement intra- and post-operatively.

Early complications
1) Acute confusion: exclude dehydration and sepsis
2) Nausea and vomiting: analgesia or anaesthetic-related; paralytic ileus
3) Fever
4) Secondary haemorrhage: often as a result of infection
5) Pneumonia
6) Wound infection
7) Wound dehiscence
8) Anastomotic leakage
9) Deep venous thrombosis (DVT)
10) Embolism
11) Acute urinary retention
12) Urinary tract infection (UTI)
13) Paralytic ileus

Late complications
1) Bowel obstruction due to fibrous adhesions
67
2) Incisional hernia
3) Persistent sinus
4) Recurrence of reason for surgery e.g. malignancy

Haemorrhage

Haemorrhage can be classified as:

1. Primary: occurring when a vessel is cut during surgery
2. Reactionary: occurring when rises in blood pressure at the end of the operation cause vessels that had
previously not been bleeding to start to do so.
3. Secondary: normally due to infection which causes damage to a vessel days after surgery
Risk factors to haemorrhage include:
1) Drugs such as anticoagulants (heparin, warfarin), non-steroidal anti-inflammatory drugs, and antiplatelet
drugs.
2) Congenital bleeding disorders: haemophilia, von Willebrand disease
3) Acquired bleeding disorders: as a result of sepsis, liver disease, or disseminated intravascular coagulation.

Post-operative pyrexia

Post-operative pyrexia is commonly caused by inflammatory mediators released as the response to surgery. This
causes low-grade fever within 24 hours of surgery. Other common causes of pyrexia include the seven Cs:
· Cut wound (incisional) infection
· Collection of pus especially pelvic or subphrenic abscess
· Chest infection or pulmonary embolism
· Cannula infection
· Central venous catheter infection
· Catheter sepsis (urinary tract infection)
· Calves affection by deep venous thrombosis (DVT)
NB: Fever can also be due to blood transfusion or drug reaction
Infections
Post-operative infections can be classified by site and cause.
· Surgical site infection
· Central venous catheter infection
· Urinary tract infection
· Abdominal collections
· Infected cannula sites
· Pneumonia

Wound dehiscence
Wound dehiscence is disruption of any or all the layers in a post-operative wound. It is very distressing to the
patient. It occurs from the 5th to the 8th postoperative day when the strength of the wound is at its weakest. The
patient may have felt a popping sensation during straining or coughing.
General risk factors in wound dehiscence include:
· Malnutrition
· Diabetes mellitus
· Obesity
· Renal failure
· Jaundice
· Sepsis
· Cancer
· Treatment with steroids
Local risk factors include:

68
· Inadequate closure of wound
· Poor closure of wound
· Poor local wound healing due to infection or haematoma
· Increased intra-abdominal pressure due to: excessive coughing in chronic obstructive airway disease.
Most patients with wound dehiscence are taken back to theatre for re-suturing. In some patients, it may be
appropriate to leave the wound open and treat with dressings or vacuum-assisted closure pumps.

Topic 1: Summary

In this topic you have learnt about;

 Preoperative preparation of a surgical patient,

 Post-operative care, and
 Post-operative complications

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UNIT FOUR: SOFT TISSUE INJURY
a) Introduction
This unit deals with surgical conditions affecting soft tissues. These include burns, soft tissue infections, soft
tissue injuries, ulcers, and gangrene. The aim of this unit is to enable the learner to identify and manage these
conditions.

Unit Objectives
By the end of this unit, you will have achieved the following objectives;

1. Classify and manage burns

2. Identify and manage the various soft tissue infections
3. Identify and manage various types of soft tissue injury
4. Manage ulcers
5. Identify and manage gangrene

Topic 1: BURNS

Objectives

By the end of this topic you should be able to;

1. State the predisposing factors to burns

2. Outline the mechanisms of causation of burn injuries
3. Highlight the pathophysiology of burn injury
4. Classify burns according to depth
5. Outline the clinical features of burns
6. Determine the severity of burn injury
7. Assess the surface area and the depth of burns
8. State the indications for in-patient management of burns
9. Highlight the methods of management of burns
10. State the complications of burns

BURNS

DEFINITION
A burn is an injury due to a sudden drastic change of temperature resulting into tissue damage. It is an injury
caused by thermal, chemical or physical agents, such as heat, corrosive substances or irradiation.

PREDISPOSING FACTORS

An individual is more likely to suffer a burn injury under the following circumstances:
1) Epilepsy – fits, loss of consciousness near fire.
2) Age – toddlers and other children, elderly – impaired mobility, poor coordination and diminished
awareness of pain.
3) Unguarded fires – a threat to all children
4) Neuropathy – diminished awareness of pain.
5) Alcoholism.
6) Occupation – industrial workers – physicochemical burns.
7) Abuse of drugs (opium).

MECHANISMS OF INJURY

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• Most burns follow accidents in the home.
• Burns may be caused by flames, hot solids, hot liquids, steam, irradiation, electricity, chemicals (e.g.
acids, alkalis), or mechanical friction.
• Burns sustained in house fires are often accompanied by smoke inhalation, with injury to the lungs.
• Accidental or deliberate ingestion of corrosive chemicals also causes burns of the oropharynx and
oesophagus.
• Antibody-antigen (allergic) reactions also present like burns
• Exposure to hot sunlight (UV) can cause sunburn

I. SCALDS

 • Hot water produces a particularly well-defined type of skin damage. The temperature of boiling water
(1000C) or steam is constant and the major determinant of the severity of injury is the duration of contact. In the
home, spills from kettles or cooking pots are common injuries of childhood.
 • As with all burning accidents, those least able to protect themselves (the very young, the very old and the
very drunk) are particularly vulnerable. Children reaching up to grasp the flex of an electric kettle, or a pot handle,
can drench themselves in boiling water, and the larger the volume, the more severe the injury in terms of area and
depth.
 • Common areas involved are the face, neck and upper trunk or limbs.
 • Immersion in boiling water, or prolonged steam exposure (as in some industrial accidents where
superheated steam may have a temperature above 1000C) are particularly dangerous and likely to cause deeper
burns.

II. FAT BURNS

 Cooking fat or oil has a much higher temperature (18000C) than boiling water and hot fat cools slowly on the skin
surface. Spills therefore cause deep burns.

III. FLAME BURNS

 • Have a varied aetiology:

1. House fires.
2. Clothing fires.
3. Spills of petrol on the skin.
4. Butane gas fires.

 • They often occur in confined spaces and may be associated with inhalation injury.
 • It is important to know whether the clothing ignited and how the flames were extinguished (did clothing
burn away?). Generally, deep burns will result if clothing ignites, since there is a prolonged flame contact with the
skin.

IV. ELECTRIC BURNS

  The passage of electric current through the tissues causes heating that results in cellular damage. Heat
produced is a function of resistance of the tissue, the duration of contact and the square of the current.
  Bone is a poor conductor of electrical current, whereas blood vessels, nerves and muscles are good
conductors. Bone can therefore become very hot and cause secondary damage to tissues near to the bone.
  Low voltage (< 1000 V) such as from a domestic supply (240 V, 50 Hz) causes significant contact wounds
and may induce cardiac arrest, but no deep tissue damage. High voltage burns (> 1000 V) cause damage by two
mechanisms: -
 1.Flash &
 2.Current transmission.

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   The flash from an electric arc may cause a cutaneous burn and ignite clothing, but will not result in deep
damage. High-voltage current transmission will result in cutaneous entrance and exit wounds and deep damage.
  Lightning strikes cause very high-voltage, very short duration discharge. A direct strike has a high
mortality. A side strike may cause superficial burns to the skin and deep exit burns to the feet.
  Electrical injuries, unlike thermal burns, often cause massive tissue damage underneath intact skin.
Exposure of this tissue damage uncovers vital structures such as nerves, tendons and joints, which then require
coverage. These injuries remain a diagnostic and therapeutic challenge during the acute post-injury period.

V. COLD INJURY

 • Results from exposure to extreme cold. Severe cooling can freeze tissues and ice formation is particularly
likely to cause cellular disruption.
 • Tissue damage from cold can occur from industrial accidents due to spills of liquid nitrogen or similar
substances. The injuries cause acute cellular damage with the possibility of either a partial-thickness or full-
thickness burn.
 • Frost bite is due to prolonged exposure to cold and there is often an element of ischemic damage.
Vasoconstriction reduces the resistance of the tissue to cold exposure as the warming effect of the circulation is
reduced. There is therefore combined tissue damage from freezing, together with vasospasm.

VI. FRICTION BURNS

  The tissue damage in friction burns is due to a combination of heat and abrasion. There is generally a
superficial open wound that may progress to full-thickness skin loss. Friction burns may be associated with
degloving injuries where the damage is judged to be deep.
  Early surgical excision and skin cover is the best means of management.

VII. IONIZING RADIATION

  X-irradiation may lead to tissue necrosis. The tissue necrosis may not develop immediately. These injuries
are generally limited in area, and surgical excision and flap reconstruction may be appropriate management.

VIII. CHEMICAL BURNS

 • Numerous chemicals in industrial and domestic situations can cause burns. Tissue damage depends on the
strength and quantity of the agent and the duration of the contact. Some agents penetrate deeply or may have
specific toxic effects.
 • Chemicals cause local coagulation of proteins and necrosis, and some also have systemic effects (e.g. liver
and kidney damage with tannic, formic and picric acids).
 • The harmful effect will continue until the chemical is diluted or neutralized. The most important initial
treatment is dilution with running water.

 Classification of Injurious Chemicals
 1. Acids that cause burns are: Hydrochloric acid, Hydrofluoric acid, Sulfuric acid, Nitric acid, Phosphoric
acid, and Acetic acid.
 2. Bases - the common bases are: Hydroxides of calcium, sodium, potassium and ammonia.
 3. Organic compounds – these are the products (by) of petroleum and phenol.
 4. Inorganic agents – sodium sticks and chlorine gas are common examples.

 Mechanism of Action:

 When these chemicals come into contact with the skin various kinds of reactions occur, apart from the effect of
thermal burn due to the heat produced by the acid when in contact with the skin (exothermic reaction).
 • Protein denaturation occurs, resulting in corrosion of the skin.
 • Oxygen ions get into the cells and release highly reactive chemicals and these oxidation products result in
severe untoward effects on the skin.

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  • These corrosives are protoplasmic poisons; they form esters with the protein and by desiccation, result in
full-thickness burn of the skin.
 • By being vesicants, they are poisonous to the proliferating cells. Vesication also results in blister
formation. The severity of injury depends upon:
 1) Concentration of the chemical.
 2) Amount of the chemical in contact with the tissue.
 3) Duration of exposure.
 4) State of the lipid barrier of the skin.

 General Principles of Management of chemical burn:
  Rapid removal of all the clothing and washing with large volumes of clean cold water is very important.
Any dry chemical or powder adherent to the body should be brushed away and removed before washing. Normal
saline can also be used to wash the area. This procedure decreases the rate of reaction between the chemical and the
tissue.
  It must be borne in mind that time should not be wasted from receiving the patient with chemical burn to
initiation of treatment. The depth and magnitude of ongoing tissue necrosis is directly related to the time taken to
initiate the treatment. Hence, first aid should stress on continuous irrigation of the wound with water.

Topic 1: Pathophysiology of burn injury

PATHOPHYSIOLOGY OF BURN INJURY

Burns cause injury in a number of different ways, but by far the most common organ affected is the skin.
However, burns can also damage the airway and lungs, with life-threatening consequences.

Airway injuries occur when the face and neck are burned. Respiratory system injuries usually occur if a person is
trapped in a burning vehicle, house, or aeroplane and is forced to inhale the hot and poisonous gases.

I. INJURY TO THE AIRWAY AND LUNGS

Burn injury to the airway above the larynx:

Hot gases can physically burn the nose, mouth, tongue, palate and larynx. This will lead to swelling of the linings
of these structures, and in a few hours cause obstruction to the airway if action is not taken to secure the airway.

Burn injury to the airway below the larynx:

Steam can cause thermal damage to the lower airway. This causes rapid swelling and detachment of the
respiratory epithelium from the bronchial tree. This can lead to blockage of the main upper airway.

Metabolic poisoning:
Many poisonous gases can be emitted from a fire, the most common being carbon monoxide, a product of
incomplete combustion often produced by fires in enclosed spaces.

Carbon monoxide binds to haemoglobin with an affinity of 240 times greater than that of oxygen and thus blocks
the transport of oxygen. Levels of carboxyhaemoglobin concentration in the bloodstream above 10% is
dangerous and require treatment with pure oxygen for more than 24 hours. Death occurs with concentrations of
more than 60%.

Hydrogen cyanide is another metabolic toxin produced in house fires. It causes a metabolic acidosis by
interfering with mitochondrial respiration.

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Inhalational injury:
Inhalational injury is caused by the minute particles within thick smoke, which, because of their small size, are
not filtered by the upper airway, but are carried down to the lung parenchyma.

They stick to the moist lining, causing an intense reaction in the alveoli. This chemical pneumonitis causes
oedema within the alveolar sacs and decreasing gaseous exchange over the ensuing 24 hours, and often gives rise
to a bacterial pneumonia.

Mechanical block on rib movement:

Full-thickness burns across the chest can physically stop the ribs from moving due to thickness and stiffness of
the burned skin.

II. LOCAL EFFECTS OF BURN INJURY

The local effect of a burn depends on the temperature of the burning agent and the duration of contact with the
skin. The local effects result from destruction of the more superficial tissues and inflammation of the deeper
tissues.

1. Tissue Damage:

  Heating of tissue results in direct cell rupture or cell necrosis.

  In addition, collagen is denatured and damage to the peripheral microcirculation occurs.
  RBCs may be damaged in the burn & a greater number often show increased fragility and they are
destroyed over the next few days.
  The severity of the local response can vary from simple reddening to destruction and charring of tissues.
  With deeper injuries, the epidermis and dermis are converted into a coagulum of dead tissue known as
eschar.
  Compromise of circulation to a limb by circumferential burns acting as tourniquet as the limb swells

2. Inflammation:

  There is a marked and immediate inflammatory response. In the areas least damaged by burning, this is
manifest simply as erythema, the dermal inflammatory response consisting of capillary dilatation. Mild areas of
erythema resolve within a few hours.
  The inflammatory reaction produced by burns leads to markedly increased vascular permeability. Water,
solutes and proteins move from the intra- to the extravascular space. The volume of fluid lost is directly
proportional to the area of the burn. Above 15% of surface area, the loss of fluid produces shock.

3. Fluid loss:

  Occurs from the burn surface or is trapped in blisters.

  The magnitude of loss depends on the extent of injury.
  Loss is greatly increased by leakage of fluid from the circulation, where instead of the normal insensible
loss of 15 ml/m2 body surface per hour, as much as 200 ml/m2/hour may be lost in the first few hours.
  Damaged capillaries become permeable to protein, and an exudate forms with an electrolytic and protein
content only slightly less than that of plasma.
  Lymphatic drainage does not keep pace with the rate of exudation and interstitial oedema forms, with
resultant reduction in circulating fluid volume.

4. Infection:

  Destruction of the epidermis removes the barrier to bacterial invasion.

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   Cell-mediated immunity is significantly reduced in large burns, leaving them more susceptible to bacterial
and fungal infections.
  Sepsis may increase the amount of tissue destruction, delay healing or interfere with the `take` of skin
grafts.
  Severe sepsis may lead to septicaemia and death.
  Sepsis also increases energy needs.

III. GENERAL EFFECTS OF BURNS

  General effects of a burn depend upon its size. Large burns lead to water, salt, and protein loss,
hypovolaemia and increased catabolism.
  Plasma loss into the burned tissues leads to a marked reduction in blood volume. The blood becomes more
viscous as the loss of plasma through the capillaries is greater than that of red blood cells.
  The volume of plasma loss is roughly proportional to the extent of the body surface burned. A burn of
more than 10% of the body surface area in a child, or more than 15% in an adult, will cause hypovolaemic shock
within a few hours. Severe hypovolaemia can damage other organs (multiple organ failure), particularly the kidney.
  Severe loss of body protein often occurs, leading to serious weight loss, pressure sores, lowered resistance
to infection, delayed healing, and skin graft failure.
  Some red blood cells are destroyed immediately by a full-thickness burn, but many more are damaged and
die later. This could contribute to anaemia in burns.
  Large burns increase metabolic rate as water losses from the burned surface cause expenditure of calories
to provide the heat for evaporation.
  Malabsorption from the gut due to microvascular damage and ischaemia to gut mucosa, as a result of the
inflammatory stimulus and shock.

CLASSIFICATION OF BURNS

Burns are classified according to depth as follows:

1. Partial thickness burns

 • In a partial thickness burn, epithelial cells survive to restore the epidermis.

 • Divided into: -
 i. Superficial partial-thickness burns and
 ii. Deep partial-thickness burns

2. Full thickness burns

 • Destroy all the epithelial elements.

Superficial partial-thickness burns

• Involve only the epidermis and the superficial dermis. Damage goes no deeper than the papillary dermis.
• The clinical features are blistering and/or loss of the epidermis. The underlying dermis is pink and moist.
• The capillary return is clearly visible when blanched.
• Pinprick sensation is normal.
• Pain, swelling and fluid loss can be marked.
• New epithelial cover is provided by undamaged cells originating from the epidermal appendages.
• The burn usually heals in less than 3 weeks, with a perfect final cosmetic result.

Deep partial-thickness burns

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• The epidermis and much of the dermis are destroyed, damage involving the deeper parts of the reticular
dermis.
• Clinically, the epidermis is usually lost.
• Restoration of the epidermis depends on there being intact epithelial cells within the remaining
appendages.
• The colour does not blanch with pressure.
• Sensation is reduced, and the patient is unable to distinguish between pressure from the sharp and blunt
ends of a needle.
• Pain, swelling and fluid loss are marked.
• The burn takes longer than 3 weeks to heal, as fewer epithelial elements survive, and often leaves an ugly
hypertrophic scar.
• Infection often delays healing and can cause further tissue destruction, making the burn a full-thickness
one.

Full-thickness burns

• A full-thickness burn destroys the epidermis and dermis, including the epidermal appendages.
• Clinically they have a hard leathery feel.
• The destroyed tissues undergo coagulative necrosis and form an eschar.
• The eschar begins to lift after 2-3 weeks.
• There is no prospect of spontaneous epidermal cover unless the raw area is grafted.
• Fibrosis and ugly contracture is inevitable in all but small, ungrafted injuries

CLINICAL FEATURES OF BURNS

1. Pain:

 • Pain is immediate, acute and intense with superficial burns.

 • It is likely to persist until strong analgesia is administered.

 • With deep burns there may be surprisingly little pain.

2. Acute Anxiety:

 • The patient is often severely distressed at the time of injury.

 • It is frequent for patients to run about in pain or in an attempt to escape, and secondary injury may result.

3. Fluid Loss and Dehydration:

 • Fluid loss commences immediately and, if replacement is delayed or inadequate, the patient may be clinically
dehydrated.

 • There may initially be tachycardia from anxiety and later a tachycardia from fluid loss.

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4. Local Tissue Oedema:

 • Superficial burns will blister and deeper burns develop oedema in the subcutaneous spaces.

 • This may be marked in the head and neck, with severe swelling which may obstruct the airway.

 • Limb oedema may compromise the circulation.

5. Special Sites:

 • Burns of the eyes are uncommon in house fires as the eyes are tightly shut and relatively protected.

 • The eyes, however, may be involved in explosion injuries or chemical burns.

 • Burns of the nasal airways, the mouth and upper airway may occur in inhalation burns.

6. Coma:

 • Following house fires, the patient may be unconscious and the reason for this must be ascertained.

 • Asphyxiation or head injury must be excluded.

 • Burning furniture is particularly toxic and the patient may suffer from carbon monoxide or cyanide poisoning.

Determination of Severity of Injury

Illness and death are related to:

1. The size (surface area) and depth of the burn.

2. The age and prior state of health of the victim.
3. The location of the burn wound, and
4. The severity of associated injuries (if any) – particularly lung injury.

 Patients under age 2 years and over age 60 years have a significantly higher death rate for any given extent of
burn. The higher death rate in infants results from a number of factors:

1. The body surface area in children relative to body weight is much greater than in adults. Therefore, a burn of
comparable surface area has a greater physiologic impact on a child.
2. Immature kidneys and liver do not allow for removal of a high solute load from injured tissue or the rapid
restoration of adequate nutritional support.
3. The incompletely developed immune system increases susceptibility to infection.

 Associated conditions such as cardiac disease, diabetes or chronic obstructive pulmonary disease significantly
worsen the prognosis in elderly patients.
 Burns involving the hands, face, feet or perineum will result in permanent disability if not properly treated. Patients
with such burns should always be admitted to the hospital, preferably to a burn centre.
 Chemical and electrical burns or those involving the respiratory tract are invariably far more extensive than is
evident on initial inspection. Therefore, hospital admission is necessary in these cases also.

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Assessment of the Burn Area
A careful calculation of the percentage of total body burn is useful for several reasons:
1. There is a general tendency to under-estimate clinically the size of the burn and thus its severity.
2. Prognosis is directly related to the extent of injury.
3. The decision about who should be treated in a specialized burn facility or managed as an outpatient is based in part on
the estimate of burn size.
An approximate clinical rule in wide use is the Wallace’s ‘’rule of nines’’ which acts as a rough guide to body surface
area.
A useful guide for estimating burn surface area is that the patient’s hand (fingers and palm) is 1% body surface area.

Wallace’s ‘’rule of nines’’

AREA PERCENTAGE
Head and neck 9%
Left upper extremity 9%
Right upper extremity 9%
Anterior trunk 18%
Posterior trunk 18%
Left lower extremity 18%
Right lower extremity 18%
Perineum 1%
TOTAL 100%

Rule of 10 is used in children:

AREA PERCENTAGE
Head and neck 20%
Anterior trunk 20%
Posterior trunk 20%
Each limb (lower/upper) 10% (total 40%)
Total 100%
 The clinician should assess the total area involved and how much of the area is partial-thickness and how
much full-thickness.
 As a general rule, an adult with more than 15% of the body surface area involved or a child with more
than 10% of body surface area involved will require intravenous fluid replacement.
 However, an intravenous access line may be necessary for adequate analgesia for much smaller areas of
burn and many children in particular will require fluid replacement because of vomiting.
 For smaller percentages than the above, it is necessary to maintain an adequate oral intake of fluid.
 The prognosis depends upon the percentage body surface area burned.
 A rough guide is that if the age and percentage add together to a score of 100 then the burn is likely to be
fatal.
 A child may therefore survive a large burn, but even a small burn in an elderly patient is potentially fatal.

Assessment of Burn Depth

• Burn depth depends, in thermal injury, upon:

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  1) The temperature of the burning agent.
 2) The mode of transmission of heat.
 3) The duration of the contact.

• Much of this information can be obtained from taking a good history of the injury.
• Clinical examination of the burn wound may also show characteristic features.

First-Degree Burns:
Involve only the epidermis (epidermal burns). They are characterized by:
 Erythema (look red) & minor microscopic changes.
 Minimal tissue damage.
 Minimal skin oedema.
 Blisters are not present.
 Intact protective functions of the skin.
 Pain – the chief symptom, usually resolves in 48-72 hours.
 Rapid healing without sequelae
 Systemic effects are rare.
In 5-10 days, the damaged epithelium peels off in small scales, leaving no residual scarring. The most common
causes of first-degree burns are over-exposure to sunlight and brief scalding. The desiccated outer layers of
epidermis peels off in 1-2 weeks’ time & heals without any residual scar formation.

Second-Degree Burns (Partial-thickness burns):

Are deeper, involving the entire epidermis and part of the dermis. The systemic severity of the burn and the
quality of subsequent healing are directly related to the amount of undamaged dermis. Depending on the depth of
injury into the dermis they are divided into two subgroups namely:

 1. Superficial second-degree (superficial partial-thickness).

 2. Deep second-degree (deep partial-thickness)

Superficial Partial-thickness Burns:

 • Consist of severe erythematous appearance of the skin with blister formation.

 • Prominent oedema causes the wound surface to be elevated above the surrounding unburned skin.
 • Superficial dermal burns are blistered and painful.
 • The erythema is due to hyperaemia of superficial dermal capillaries with occasional extravasation of
erythrocytes.
 • In the absence of any complications these burns will heal spontaneously by epithelialisation within three
weeks with minimal or no scaring.

Deep Partial-Thickness Burns:

Are characterized by:

 • A blotchy red appearance or a layer of whitish nonviable dermis firmly adherent to the remaining viable
tissue.
 • A soft, dry, waxy, white appearance after devitalized material is removed.
 • No capillary return on pressure.
 • The tissue is not initially oedematous.
 • Absent sensation to pin prick, but perception of deep pressure is still intact.
 • May have blisters.
 • Blisters, when present, continue to increase in size in the past burn period as the osmotically active
particles in the blister fluid attract water.
 • Deep partial thickness burns may destroy some of the adnexa structures, but the capacity for spontaneous
healing though prolonged is still present.

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  • Deep dermal burns heal over a period of 25-35 days with a fragile epithelial covering that arises from the
residual uninjured epithelium of the deep dermal sweat glands and hair follicles.
 • Severe hypertrophic scarring occurs when such an injury heals, the resulting epithelial covering is prone to
blistering and breakdown.
 • Conversion to a full-thickness burn by bacteria is common.
 • Skin grafting of deep dermal burns, when feasible, improves physiologic quality and appearance of the
skin cover.

Full-thickness (Third-Degree) Burns:

 Have a characteristic white, waxy appearance and may be misdiagnosed by the untrained eye as unburned
skin. Burns caused by prolonged exposure, with involvement of fat and underlying tissue, may be brown, dark red
or black. The diagnostic findings of full-thickness burns are:
 1) Lack of sensation in the burned skin.
 2) Lack of capillary refill, and
 3) A leathery texture that is unlike normal skin.
 These burns are characterized by a white to black hard, ‘’leathery’’ inelastic eschar that may have a glistening,
apparently translucent surface.
 The wound is insensitive to all but deep pressure.
 Coagulative necrosis affects the entire thickness of the epidermis and dermis and usually extends into subcutaneous
fat. All epithelial elements are destroyed, leaving no potential for re-epithelialization

MANAGEMENT OF BURNS

First Aid:

1. Stop the Burning Process:

  Flames from burning clothing or from burning inflammable substances on the skin surface should be
extinguished by wrapping the patient in a fire blanket or any other readily available garment such as the
bystander’s own clothing.
  With electrical burns it is important that any live current is switched off.
  With chemical burns the first-aid worker must avoid contact with the chemical.
  Burned or water-soaked clothing should be removed.

2. Cool the Burn Surface:

  Patient continues burning for the next half hour following stopping flame.
  Therefore remove the heat already in the body using cold running tap water.
  Copious amount of clean cold water can be applied by sponges.
  It can also neutralise/dilute chemicals.
  Pain also gets reduced when cold water is applied.
  The secretion of histamine by the mast cells gets reduced by cooling, & this will reduce the oedema
formation.
  With scalds, irrigation with cold water under a tap is best and scald damage can successfully be limited.
  Immediate cooling of the part should continue for 20 minutes.
  Do not use ice or iced water to avoid hypothermia.
  The ideal temperature of cooling water is 150C, but 8-250C is effective.
  The burn should then be wrapped in any clean linen or plastic ‘’cling film’’ and the patient transported
immediately to hospital.

Emergency Examination and Treatment:

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The order of priorities in the management of a major burn injury is:

 Primary Survey:

 A: airway maintenance.
 B: breathing and ventilation.
 C: circulation.
 D: disability – neurological status.
 E: exposure and environment control – keep warm.
 F: fluid resuscitation.

 In severe facial and neck burns early endotracheal intubation or tracheostomy should be considered.
 Early escharotomy may be needed in circumferential chest or limb burns where respiratory or circulatory
disturbances is observed.
 An altered consciousness level may be caused by carbon monoxide poisoning.
 If there is a possibility that smoke inhalation has occurred – as suggested by exposure to a fire in an enclosed space
or burns of the face, nares, or upper torso – arterial blood gases and arterial oxygen saturation of haemoglobin and
carboxyhaemoglobin levels should be measured and oxygen should be administered.

 Endotracheal intubation is indicated if the patient is:

 1. Semicomatose.
 2. Has deep burns to the face and neck, or
 3. Is otherwise critically injured.

 If the burn exceeds 20% of body surface area, a urinary catheter should be inserted to monitor urine output.
 A large-bore intravenous catheter should be inserted, preferably into a large peripheral vein.
 Protect burned area in order to prevent infection and reduce pain.
 Place the patient in a comfortable position. On no account should patients with extensive burns be permitted to
walk about.
 Ensure warmth of the patient because he/she will be shocked and the peripheral blood vessels will have contracted
to increase central circulation.
 Give sedatives and analgesics.
 Give oral fluids in limited quantities.
 Secondary Survey:

 1. Assess the extent of burn.

 2. Assess the burn depth.
 3. Assess the sites (special areas like the eyes).
 4. Chart the area for calculation of the total body surface area burnt.
 5. Smoke inhalation injury and associated trauma, like head injuries and spinal cord injuries are taken care of
first.
 6. Then the management of burn wound must be initiated

Indications of admission:

1) Burns requiring fluid resuscitation (> 15% in adults & 10% in children).
2) Burns of special areas e.g. face, hands feet, perineum, genitalia and flexure surfaces.
3) Full-thickness burns > 5% body surface area.
4) Circumferential limb or chest burns.
5) Electric burns.
6) Chemical burns.
7) Inhalation burns.
8) Deep burns.
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9) Burns in children or the elderly.
10) Where non-accidental injury is suspected in the case of a child.
11) Associated medical conditions or pregnancy.
12) Associated other trauma e.g. fractures.

MANAGEMENT ON ADMISSION

I. Barrier Nursing

 • All patients with exposed areas of burn are nursed under aseptic conditions to prevent cross-infection.
 • Room temperature should be 24-270C.
 • Check on general condition of the patient, recording the following if possible:- pulse, blood pressure and
weight.
 • Remove dressings, linen coverings and clothes, so that the extent of the body surface burned can be
assessed.
 • In an extensive burn, set up an i.v. infusion if not already in position.
 • Keep the patient warm and comfortable. Use a cradle to protect the burned surfaces.
 • Burned arms and legs should be elevated to reduce the oedema.

II. Commence the following charts to assess progress of resuscitation:

 • Temperature 4 hourly.
 • Pulse – ½ hourly.
 • Blood pressure ½ hourly
 • Fluid in-put out-put chart: Urine output should be between 50-100ml/hr. < 30ml and > 150ml/hr. indicate
inadequate or excess respectively.

III. Investigations

 1. Haemoglobin and haematocrit.

 2. Urea and electrolytes.
 3. Blood cross-matching.
 4. Blood gases and blood analysis for carbon monoxide or cyanide poisoning in the unconscious patient.

IV. Fluid Replacement Therapy

 • Severe burns are characterized by large losses of intravascular fluid, which are greatest during the first 8-
12 hours, and are significantly diminished by 24 hours post-burn.
 • Initially, an isotonic crystalloid salt solution is infused to counterbalance the fluid loss.
 • Ringer’s Lactate (Hartmann`s solution) is commonly used, the rate being dictated by:
 1. Urine output.
 2. Pulse (character and rate).
 3. State of consciousness
 4. Blood pressure.
 • Burned patients are always thirsty, but gastric movements may be altered. It is therefore unwise to give too
much fluid by mouth in the first few hours or the patient may vomit.
 • Small quantities only should be given to correct the thirst, since vomiting would lead to loss of valuable
electrolytes.

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Fluid requirements
There are two fluid requirements:

 • Normal metabolic fluid intake. In an adult who is on fluids only, this should be 2000 ml/day. This is
usually taken by mouth even in an extensive burn. The rate of administration should be:
 30 ml per 30 min in 0-8 hrs, then increase to
 60 ml per 30 min from 8-36 hrs if there is no vomiting.
 • Replacement of fluid lost from the circulation - given intravenously.

Fluid replacement

Fluid Management of burns

Start:

 • Start replacement of fluids as at onset of burns, i.e. from 0 hours.

 • Start the fluids as if the patient presented soon after injury.
 • Stop at 48 hours when no more inflammatory response is expected.
 • Stop drips gradually over 12 hours.
 • Only reasons for giving beyond 48 hours are:

1. Infections.
2. Deep burns.
3. Diarrhoea and vomiting.
4. If patient cannot take orally antibiotics that are given in drips.

Amount of Fluid:
 The simplest formula (for adults) is:
Parkland’s Formula

  4ml x body weight in kg x % burn surface area in the first 24 hours.

  Half of this volume is given in the first 8 hours and the rest in the next 16 hours.
  Timings begin from the time of the burn, not the start of resuscitation.
  Hartmann`s solution is preferred, but other isotonic fluids may be used.
  Metabolic fluid requirements are also needed.

Parkland`s formula Example:

 • Burn surface area 20% of body surface

 • Patient`s weight 60kg
 • Total calculated fluid requirement for 24 hour period from time of burn
 4ml x 60 X 20 = 4800ml
 2400ml is given in the first 8 hours (from 0 hrs)
 2400ml is given in the next 16 hours
 Total duration 24 hours.

Formulae are only a guide and the adequacy of fluid resuscitation is monitored by regular clinical assessment. A
urinary catheter is essential. Urine output is the best guide to adequate tissue perfusion; in an adult one should
aim for 30-50 ml per hour

V. CARE OF THE BURN WOUND:

• In the management of first- and second-degree burns, one must provide as aseptic an environment as
possible to prevent infection.
• However, superficial burns generally do not require the use of topical antibiotics.

83
• Occlusive dressings to minimize exposure to air have been shown to increase the rate of re-
epithelialization and to decrease pain.
• If there is no infection burns will heal spontaneously.
• Goal of Management of Full-Thickness Burns:
1. To clean the wound and remove dead tissue.
2. To prevent invasive infection (i.e., burn wound sepsis).
3. To cover the wound with skin as soon as possible.
4. To prevent further destruction of tissue.
5. To provide an environment in the burned area which is conducive to the natural regeneration of
epithelium.
6. To aid the separation of slough and provide a suitable surface for grafting.
7. To maintain function in the affected parts.

Clean the wound

 Wound is washed with tepid water and a solution of chlorhexidine or mild soap.
 Then the excess water is sponged off with cotton sponges.
 With deep burns the eschar is firmly adherent and should not be separated, but the whole area wiped and
any loose material removed with fine dissecting forceps and scissors.
 Blisters are snipped so that the fluid escapes and all the loose skin removed.
 Great gentleness should be exercised so that any unburned tissue is not accidentally damaged.

Topical antibacterial agents

 • Silver sulfadiazine is the most widely used preparation today.

 • Mafenide
 • Silver nitrate
 • Povidone-iodine
 • Gentamicin ointment
 • For small superficial burns a soothening emollient like paraffin tulle gras will be comfortable to the patient
when applied to the surface.

Silver Sulfadiazine 1% (SS):

 • Is effective against a wide spectrum of Gram-negative organisms and is moderately effective in penetrating
the burn eschar.
 • Delays colonization by Gram-negative bacteria for 10-14 days.

Mafenide Acetate (Sulfamylon):

 • Is used to help prevent and treat wound infections in patients with severe burns.
 • Penetrates the burn eschar and is a more potent antibiotic
 • It is used chiefly on burns already infected or when silver sulfadiazine is no longer controlling bacterial
growth.
 • Used as a 10% concentration in a water soluble cream base.
 • Used to cover the burn wound as a thick cover.
 • Applied twice a day

Methods of wound treatment

Exposure Therapy:
No dressings are applied over the wound after application of the agent to the wound twice or three times daily.

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Advantages:

 • Bacterial growth is not enhanced, as the presence of light and the recommended room temperature of 24-
270C discourages bacterial growth.
 • The coagulation of exudate in the presence of air provides a hard, dry, impervious surface which is
resistant to external infection.
 • The wound remains visible and readily accessible. The presence of infection is immediately detected.
 • Heat is lost normally from the body by evaporation and radiation, unlike when bulky dressings are
applied.

Disadvantages:

 • Increased pain.
 • Increased heat loss as a result of the exposed wound.

Indications of exposure method:

 • Face burns.
 • Head burns.
 • Front or back trunk but not both.

Contraindications of exposure therapy:

 • Circumferential burns of the trunk – difficulty of keeping the undersurface dry.

 • Burns of the hand - difficulty of early restoration of function.
 • Circumferential burns of the neck because it is rarely possible to keep the area dry.
 • Circumferential full-thickness burns of the limbs because the eschar may produce a tourniquet effect.

Response to exposure therapy:

 • By about the 14th day after burning the superficial or partial thickness burn will have healed.
 • The deep dermal burn will have some areas healed, and the deeper areas will have firmly adherent slough.
 • The full-thickness burn will have thick adherent slough, just beginning to separate at the edges.
 • This must be removed in order to obtain a surface which will heal spontaneously or will be suitable for
grafting.

Closed Method:

 An occlusive dressing is applied over the agent and is usually changed once or twice daily.
 May be used from the beginning or may follow a period of exposure.
 Dressings are used on burn wounds in the acute stage.
 As the wounds are very sensitive to the external air, they become very painful when exposed due to
exposure of fine nerve terminals.
 Superficial burns and some hand burns feel more comfortable with dressings.

Dressing Technique:

 • The burn area is covered with a single layer of relatively non-greasy sofra-tulle gauze.
 • This is then covered with a sufficiently thick layer of gauze and wool to ensure absorption of all transudate.
 • The dressing is held in place with crepe bandage or tape.
 • The dressing should overlap normal skin sufficiently to avoid any accidental exposure of the burn by
slipping of the bandage.

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Advantages:

 • The wound is protected and the dressing prevents desiccation.

 • It absorbs most of the exudates.
 • Pain gets relieved to a greater extent.
 • Suitable method for use after eschar separates and is removed or excised, to prevent drying of the raw ulcer
bed.
 • Dressings protect the grafted areas, and immobilize the grafts.
 • Dressings also conserve body temperature by reducing evaporative water loss from the wound surface.

 Superficial dermal burns with blistering are usually dressed to:

 1) Absorb exudate.
 2) Prevent desiccation.
 3) Provide pain relief.
 4) Encourage epithelialisation and
 5) Prevent infection

COMPLICATIONS OF BURNS

Early Complications:
1) Anaemia – caused by:

  Direct injury.
  Reduced RBC survival time.
  Oozing of blood from burned areas and Curling’s ulcer may lead to acute haematemesis.
  Primary or secondary BM depression caused by a large raw area and hypoproteinaemia.
  Surface bleeding from: Surgery; Slough excision; and Cutting of skin grafts

2) Electrolyte imbalance
3) Infections – local sepsis; septicaemia
4) Organ failure – renal failure due to acute tubular necrosis following shock
5) Uraemia
6) Curling`s ulcer – acute duodenal ulceration – and multiple gastric erosions

Late Complications:

1) Keloids
2) Hypertrophic scars
3) Lid ectropion
4) Organ damage e.g., liver damage.
5) Infection and chest complications e.g., bronchitis and B/pneumonia.
6) Deformities/depigmentation/delayed healing/contractures.
7) Squamous cell carcinoma (Marjolin’s ulcer)

Non-specific complications include:

1) Urinary tract infection from catheterisation.
2) Deep vein thrombosis.
3) Pulmonary embolism.

The end.

Topic 1: Summary
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In this topic you have learnt the following about burns:

1. Predisposing factors to burns

2. Mechanisms of causation of burn injuries
3. The pathophysiology of burn injury
4. Classification of burns according to depth
5. Clinical features of burns
6. How to determine the severity of burn injury
7. Assessment of the surface area and the depth of burns
8. Indications for in-patient management of burns
9. Methods of management of burns
10. Complications of burns

Topic 2: FURUNCLE, CARBUNCLE AND HIDRADENITIS

FURUNCLE, CARBUNCLE AND HIDRADENITIS

INTRODUCTION

 • Furuncles and carbuncles are cutaneous abscesses that begin in skin glands and hair follicles.
 • Furuncles are the most common surgical infections, but carbuncles are rare.
 • Furuncles can be multiple and recurrent (furunculosis).
 • Furunculosis usually occurs in young adults and is associated with hormonal changes resulting in impaired
skin function.
 • The commonest organisms are staphylococci and anaerobic diphtheroids.
 • Hidradenitis suppurativa is a serious skin infection of the axillae or groin consisting of multiple abscesses
of the apocrine sweat glands.
 • The condition often becomes chronic and disabling.

PATHOGENESIS

• Furuncles usually start in infected hair follicles, although some are caused by retained foreign bodies and
other injuries.
• Hair follicles normally contain bacteria.
• If the pilosebaceous apparatus becomes occluded by skin disease or bacterial inflammation, the stage is
set for development of a furuncle.
• Because the base of the hair follicle may lie in subcutaneous tissue, the infection can spread as a cellulitis,
or it can form a subcutaneous abscess.
• If a furuncle results from confluent infection of hair follicles, a central core of skin may become necrotic
and will slough when the abscess is drained.
• Furuncles may take a phlegmonous form, i.e. extend into the subcutaneous tissue, forming a long, flat
abscess.

CLINICAL FINDINGS

Furuncles itch and cause pain. The skin first becomes red and then turns white and necrotic over the top of the
abscess. There is usually some surrounding erythema and induration. Regional nodes may become
enlarged. Systemic symptoms are rare.
Carbuncles usually start as furuncles, but the infection dissects through the dermis and subcutaneous tissue in a
myriad of connecting tunnels. Many of these small extensions open to the surface, giving the appearance of
large furuncles with many pustular openings.The affected area is swollen brawny and painful.The overlying

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skin is dusky red and exhibits characteristic sinuses which discharge small amounts of yellow
pus.Urine for sugar should be tested in all cases. As carbuncles enlarge, the blood supply to the skin
is destroyed and the central tissue becomes necrotic. Carbuncles on the back of the neck are seen almost
exclusively in diabetic patients. The patient is usually febrile and mildly toxic. This is a serious problem
that demands immediate surgical attention. Diabetes must be suspected and treated when a carbuncle is
found.

DIFFERENTIAL DIAGNOSIS

• When lesions are located near joints or over the tibia or when they are widely distributed, one must
consider:

 • Gout.
 • Bursitis.
 • Synovitis.
 • Erythema nodosum.
 • Fungal infections.
 • Some benign or malignant skin tumours.
 • Inflamed (but not usually infected) sebaceous or epithelial inclusion cysts.

• Hidradenitis is differentiated from furunculosis by skin biopsy, which shows typical involvement of the apocrine
sweat glands.
• One suspects hidradenitis when abscesses are concentrated in the apocrine gland areas, i.e. the axillae, groin and
perineum.
• Carbuncles are rarely confused with any other condition.

TREATMENT

 The classic therapy for furuncle is drainage, not antibiotics.

 Invasive carbuncles, however, must be treated by excision and antibiotics.
 Between these two extremes, the use of antibiotics depends on the location of the abscess and the extent
of infection.
 Patients with recurrent furunculosis may be diabetic or immune-deficient.
 Frequent washing with soaps containing hexachlorophene or other disinfectants is advisable.
 It may also be necessary to advise extensive laundering of all personal clothing and disinfection of the
patient’s living quarters in order to reduce the reservoirs of bacteria.
 Furunculosis associated with severe acne may benefit from tetracycline, 250mg orally once or twice
daily.
 When an abscess fails to resolve after a superficial incision, look for a small opening to a deeper and
larger subcutaneous abscess, i.e., a collar-button abscess.

Hidradenitis:

  Hidradenits is usually treated by drainage of the individual abscess followed by careful hygiene.
  The patient must avoid astringent antiperspirants and deodorants.
  Painting with mild disinfectants is sometimes helpful.
  Fungal infections should be searched for if healing after drainage does not occur promptly.
  If none of these measures are successful, the apocrine sweat-bearing skin must be excised and the deficit
filled with a skin graft.

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Carbuncles:
 Carbuncles are often more extensive than the external appearance indicates.
 Incision alone is almost always inadequate, and excision with electro-cautery is required.
 Excision is continued until the many sinus tracts are removed – usually far beyond the cutaneous
evidence of suppuration.
 It is sometimes necessary to produce a large open wound.
 This may appear to be drastic treatment, but it achieves rapid cure and prevents further spread.
 The large wound usually contracts to a small scar and does not usually require skin grafting, because
carbuncles tend to occur in loose skin on the back of the neck and on the buttocks, where contraction is the
predominant form of repair.

COMPLICATIONS

1. All these infections may cause suppurative phlebitis when located near major veins. This is particularly
important when the infection is located near the nose or eyes. Central venous thrombosis in the brain is a serious
complication, and abscesses on the face usually must be treated with antibiotics as well as prompt incision and
drainage.
2. Hidradenitis may disable the patient but rarely has systemic manifestations.
3. Carbuncles on the back of the neck may lead to epidural abscess and meningitis.

Topic 2: CELLULITIS

CELLULITIS

DEFINITION

Cellulitis is a spreading inflammation of connective tissues as a result of infection. The term usually refers to
subcutaneous infection.

CAUSATIVE ORGANISMS

The common organism is the beta-haemolytic streptococcus which usually gains entrance through a scratch or
prick. Staphylococcus aureus is also usually implicated. Clostridium perfringens is also a causative organism.

PATHOGENESIS

• Cellulitis is usually located at the point of injury and subsequent tissue infection. The microscopic picture
is one of severe inflammation of the dermal and subcutaneous tissues. There is no gross suppuration except
perhaps at the portal of entry. In addition to the cardinal signs of inflammation, there is poor localisation.
• Spreading infection is typical of organisms such as:

 1.β-haemolytic streptococci.
 2.Staphylococci and
 3.Clostridium perfringens.

• Tissue destruction and ulceration may follow, caused by release of streptokinase, hyaluronidase, and other
proteases. The spreading invasiveness of Streptococcus pyogenes is due to its ability to produce hyaluronidase which
dissolves the intercellular matrix, and a fibrinolysin called streptokinase which is able to destroy the fibrin inflammatory
barrier to bacterial spread.
• Systemic signs (toxaemia) are common and include chills, fever and rigors. These follow release of exotoxins and
cytokines but blood cultures are often negative.
• Cellulitis is frequently accompanied by lymphangitis and lymphadenitis, painful red streaks in affected lymphatic

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channels and the regional glands becoming enlarged and tender. Lymphangitis is often accompanied by painful lymph node
groups in the related drainage area.
• There is sometimes associated septicaemia, which originates either from a septic thrombophlebitis in the affected
area or from spread of bacteria from the lymphatics to the blood stream by way of the thoracic duct.

CLINICAL FEATURES

1. Cellulitis usually appears on an extremity as a brawny red or reddish-brown area of oedematous skin
2. It advances rapidly from its starting point, and the advancing edge may be vague or sharply defined (e.g.,
in erysipelas)
3. A surgical wound, puncture, skin ulcer, or patch of dermatitis is usually identifiable as a portal of entry
4. The disease often occurs in susceptible patients, e.g. alcoholics with post-phlebitic leg ulcers
5. A moderate or high fever is almost always present
6. Lymphangitis arising from cellulitis produces red, warm, tender streaks 3 or 4 mm wide leading from the
infection along lymphatic vessels to the regional lymph nodes
7. There is usually no suppuration
8. Cutaneous gangrene with ulceration occurs in advanced cases.

Summary of clinical features:

• Dusky red skin around the site of inoculation
• Local swelling
• Raised local temperature
• Severe pain and tenderness
• Vesicles may appear
• Fever
• Lymphangitis
• Cutaneous gangrene in advanced cases.

INVESTIGATIONS

1. Blood culture is sometimes positive.

2. Fluid exudate for culture and sensitivity
3. Full haemogram - leukocytosis

DIFFERENTIAL DIAGNOSIS

1. Thrombophlebitis is often difficult to differentiate from cellulitis, but phlebitic swelling is usually greater,
and tenderness may localize over a vein. Fever is usually greater with cellulitis, and pulmonary embolization
does not occur in cellulitis.
2. Contact allergy may mimic cellulitis in its early phase, but dense non-haemorrhagic vesiculation soon
discloses the allergic cause.
3. Chemical inflammation due to drug injection may also mimic streptococcal cellulitis.
4. The appearance of haemorrhagic bullae and skin necrosis suggests necrotizing fasciitis.

TREATMENT

1) Hot packs actually elevate subcutaneous temperature, and if regional blood supply is normal, they can
raise local oxygen tension (local heat by short-wave diathermy).
2) Rest – immobilisation of the affected part may necessitate bed rest.
3) Elevation
4) Antibiotics – Penicillin. Start with injectable drugs e.g. crystalline penicillin and gentamicin; could use
flucloxacillin, or a cephalosporin.

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5) Incision & drainage
6) Analgesia

NB: If a clear response has not occurred in 12-24 hours, one should suspect an abscess or consider the possibility
that the causative agent is a staphylococcus or other resistant organism. The patient must be examined one or more
times daily to detect a hidden abscess masquerading within or under cellulitis.
COMPLICATIONS

 1. Lymphangitis
 2. Lymphadenitis
 3. Septicaemia
 4. Osteomyelitis
 5. Gangrene and ulceration

Assignment Activity

Write a brief case summary of a patient who has been in the surgical ward with cellulitis.

 • Presenting complaints and progression up to date

 • Investigations done
 • Drug treatment
 • Supportive treatment
 • Any complications?

The end.

Topic 2: PYOMYOSITIS

PYOMYOSITIS

DEFINITION

Pyomyositis is an acute bacterial infection of skeletal muscles that results in localized abscess formation.

It usually affects gluteal, quadriceps or calf-muscles and occurs mostly in hot climates and after intense muscular
activity.

PREDISPOSING FACTORS

Skeletal muscle usually enjoy an immunity to pyogenic infections. Since normal muscle is very difficult to
infect, some predisposing event or condition is suspected. The factors which cause a break in this immunity may
be:

1. In the Patient:

 • Chronic ill health and debility.

 • Vitamin C deficiency.

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  • Septic spots – very common in the feet and legs of a largely shoeless population and provide a ready entry
for the staphylococcus.
 • Race.

2. In the Muscle:

 • Haematoma – after injury.

 • Toxic degeneration of Zenker’s type
 • Vascular change

3. In the Environment:

 • Filariasis – the death of these and similar parasites in muscles may provide a suitable focus of necrosis for
colonisation by staphylococcus.
 • Virus – Coxsackie virus can produce hyaline degeneration in skeletal muscle.

AETIOLOGY

Causative organisms include:

 1. Staphylococcus aureus - > 90% of the patients

 2. Staphylococcus albus
 3. Streptococci
 4. Escherichia coli.

PATHOGENESIS

Neither the pathogenesis nor the source of the bacteria is entirely clear. The usual portal for entry of bacteria is a
local injury, but spread via the bloodstream into a fatigued or injured muscle has also been postulated.

CLINICAL FEATURES

The most common form, usually due to Staphylococcus aureus, begins insidiously with

 • Localized pain progressing to

 • Fever
 • Induration, and
 • Abscess formation.
 • An acute variety, caused usually by streptococci, may progress in hours or days and resembles infection
with non-gas forming clostridial organisms.
 • Sex – more men than women.
 • Age – peak is during the 3rd and 4th decades, although it is often seen in children.

Site:
Pyomyositis can occur in any voluntary muscle but has a predilection for the heavy powerful muscles of the trunk and root
of the limbs, such as:

 1. Trapezius.
 2. Latissimus dorsi.
 3. Biceps.
 4. Brachialis.

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  5. Sacrospinalis.
 6. External and internal oblique.
 7. Quadriceps.
 8. Hamstring.
 9. Gastrocnemius.
 10. Soleus.

Pyomyositis typically demonstrates the progress of inflammation as follows:

1. The Invasive Stage:

 • The illness may start suddenly with pyrexia and cramp-like pains in the muscle which on palpation feels
tender and indurated. The condition may resolve or progress to suppuration.

2. The Suppurative Stage:

 • Presents with abscess formation and the classical signs of inflammation.

 • These may, however, be modified by the anatomical position of the muscle.
 • NB: redness as a sign of inflammation is replaced by shininess in dark skinned people.

3. The Late Stage:

 • Over a period of 2-3 months the signs of inflammation subside, the patient becomes bed-ridden and the
muscle is completely replaced by a large bag of pus.

Clinical Types:
1) Fulminating:
The patient is admitted with a high temperature in a semi-comatose condition; resents handling and especially resents
pressure on particular areas of muscles.

2) Pyrexia with Many Abscesses:

These patients are ill and abscesses appear in one muscle after another with much pain. Eventually most of them form pus
but some resolve.

3) Pyrexia with Minimal Abscesses:

These patients are not ill and rarely more than 3 muscles are affected. If seen early and treated, resolution may take place
without drainage.

4) Solitary Abscess:
This may simulate a traumatic muscle haematoma. Enlargement of the regional lymph glands is not normally a feature.
DIFFERENTIAL DIAGNOSIS

Right Upper Quadrant:

 • Hepatoma.
 • Kidney swelling.
 • Amoebic abscess.

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Left Upper Quadrant:

 • Splenic abscess.
 • Perinephric abscess.
 • Subphrenic abscess.

Right Lower Quadrant:

 • Appendix abscess.
 • Suppuration of iliac glands.
 • Psoas abscess.

Inguinal Region:

 • Lymphosarcoma.
 • Strangulated inguinal hernia.

Calf:

 • DVT.
 • Sickle cell crisis with acute infarction of bone.

Thigh:

 • Acute osteomyelitis
 • Osteosarcoma
 • Fibro-sarcoma
 • Pathological fracture.

INVESTIGATIONS

1. Ultrasound.
2. CT scan.
3. Aspiration – pus has often a pink colour due to the digestion of muscle, haemoglobin, and several
authorities have commented on the fact that it does not smell.
4. Haemoglobin estimation.
5. X-ray of the affected part

MANAGEMENT

Admit to hospital

 The Invasive Stage:

 • Rest in bed.
 • Tetracycline/cephalosporin (Duracef) + lincomycin
 • Avoid intramuscular injections.
 • Antibiotics effective against staphylococci and streptococci are given empirically until culture and
sensitivity test results are reported.
 • Prompt treatment may prevent abscess formation.

 Suppurative Stage:

 • Surgical drainage is usually required in the acute form (I & D under G/A).

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  • Delays in surgery have led to loss of limb or even to death due to sepsis.

 Late Stage:

 • Operation contraindicated until the anaemia – often profound, is corrected by transfusion.

 • I & D + antibiotics – 2nd place.
 • Pyrexia and rigors following I&D indicate the formation of new abscesses which should be looked for and
treated without delay.

COMPLICATIONS

1. Severe anaemia
2. Septicaemia
3. Multiple abscesses
4. Death – this is unusual except in the fulminant type.

The end

Topic 2: NECROTIZING FASCIITIS

NECTROTIZING FASCIITIS

DEFINITION

• Necrotising fasciitis is an invasive infection of fascia.

• Is usually due to multiple pathogens.
• Is characterized by infectious thrombosis of vessels passing between the skin and deep circulation,
producing skin necrosis superficially resembling ischemic vascular or clostridial gangrene.

BACTERIOLOGY

The infection usually involves a mixed microbial flora, often including:

• Microaerophilic streptococci
• Staphylococci
• Gram-negative bacteria
• Anaerobes, especially peptococci, peptostreptococci, and Bacteroides.
• Clostridia may be present, and the disease may clinically resemble clostridial cellulitis.

CLINICAL FEATURES

• Fasciitis usually begins in a localized area such as:

 o Puncture wound.
 o Leg ulcer, or
 o Surgical wound.

• The infection spreads along the relatively ischemic fascial planes, meanwhile causing the penetrating vessels to
thrombose.
• The skin is thus devascularized.

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• Externally, haemorrhagic bullae are usually the first sign of skin death.
• The fascial necrosis is usually wider than the skin appearance indicates.
• The bullae and skin necrosis are surrounded by oedema and inflammation.
• Crepitus is occasionally present, and the skin may be anaesthetic.
• The patient often seems alert and unconcerned but appears toxic and has fever and tachycardia.
INVESTIGATIONS

1. Blood for haemoglobin level

2. Blood glucose levels
3. Blood urea and electrolyte concentrations
4. Aspirates, swabs and excised tissue for Gram-stained smears and bacteriologic cultures are helpful for
diagnosis and treatment.
5. Blood for culture
6. At surgery, the finding of oedematous, dull-gray, and necrotic fascia and subcutaneous tissue confirms
the diagnosis. Thrombi in penetrating vessels are often visible.
7. Intra-operative frozen-section biopsy examination showing dense inflammation, arteritis, or obliterative
thrombosis of arteries and veins may confirm the diagnosis.

DIFFERENTIAL DIAGNOSIS

• Cellulitis
• Localized abscecess
• Phlebitis
• Clostridial myositis
• Vascular gangrene
• Meleney’s gangrene (progressive bacterial cutaneous gangrene) - advances slowly. Fasciitis advances
rapidly.

MANAGEMENT

Treatment consists of:

 • Surgical debridement.
 • Antibiotics, and
 • Support of the local and general circulation.

Surgical Treatment:

 • Debridement – under general or spinal anaesthesia – must be thorough, with removal of all avascular skin
and fascia.
 • This may require extensive denudation.
 • Where necrotic facia undermines viable skin, longitudinal skin incisions (not too close together) aid
debridement of facia without sacrificing excessive amounts of skin.
 • It is often difficult to distinguish necrotic from oedematous tissue.
 • Careful daily inspections of the wound will demonstrate whether repeated debridement will be necessary.
 • If possible, all obviously necrotic tissue should be removed the first time.
 • It is essential to avoid confusing fasciitis with deep gangrene.
 • It is a tragic error to amputate an extremity when removal of dead skin and fascia will suffice.
 • A functional extremity can usually be salvaged in fasciitis; if not, amputation can be safely performed later.
 • When viability of the remaining tissue is assured and the infection has been controlled, the resulting defect
in the skin and deep fascia, which is frequently very large, may require skin grafting.

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Antibiotics:

 • Benzylpenicillin, high-dose (20-40 million units/day) intravenously, is begun as soon as material has been
taken for smear and culture.
 • Metronidazole intravenous infusion 500mg 8-hourly to cater for anaerobes
 • An aminoglycoside (e.g., gentamicin, 5mg/kg/day; amikacin, 15mg/kg/day) should be added to eradicate
Gram-negative bacteria that are so often seen in this disease.
 • Antibiotic regime can be changed if indicated by reports of antibiotic sensitivity.

Circulatory Support:

 • Blood volume must be maintained.

 • Debridement often leaves a large raw surface that may bleed extensively.
 • Since tissue oxygenation is critical, early transfusion with fresh blood is a rational procedure.
 • Diabetes mellitus, if present, must be treated appropriately.

The end.

Topic 2: Summary

In this topic you have learnt about:

Soft tissue infections: furuncles, carbuncles, hidradenitis, cellulitis, pyomyositis, and necrotizing fasciitis.

 Their pathogenesis
 Their clinical features
 The management of each of the soft tissue infections
 The complications associated with these infections

Reading Assignment

Describe the procedure of treating an abscess

Topic 3: SOFT TISSUE INJURIES

OBJECTIVES

By the end of this topic you should be able to:-

1. Define a wound

2. Describe the phases of normal wound healing

3. Classify types of wound closure and healing

4. Highlight factors influencing wound healing

5. Identify the types of wounds

SURGICAL ASPECTS OF INJURY AND REPAIR

WOUNDS

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A wound may be defined as disruption of the normal continuity of bodily structures due to trauma, which may be
penetrating or non-penetrating.

Local Response to injury:

The local result of an injury is a wound. Healing depends upon the severity and extent of the wound. A clean-cut
incision will heal with minimal scarring (by first intention) provided that certain conditions are met:

 1) There is minimal damage to adjacent tissue

 2) Loss of tissue is minimal
 3) The wound is not contaminated by foreign material
 4) Bleeding is controlled
 5) Infection is prevented
 6) The edges of the wound are carefully apposed without tension

Principles of wound healing

Wound healing is a mechanism by which the body attempts to restore the integrity of the injured part.

Normal wound healing

Normal wound healing can be divided into three phases according to the development of tensile strength.

Phase 1 (Inflammatory, preparative or exudate phase; 2-3 days).

 • Following injury, the space between the edges of the wound quickly fills with blood clot and the wound is
sealed with fibrin.
 • This phase is characterized by an inflammatory response to injury, during which capillary permeability
increases and a protein-rich exudate accumulates. This occurs within a few hours after injury, and the exudate
quickly forms an impermeable coagulum.
 • Inflammatory cells (leucocytes and macrophages) invade the wound. Macrophages are activated to release
factors which stimulate the growth of fibroblasts and blood vessels. Macrophages remove devitalised tissue and
microorganisms.
 • At the same time there is a rapid increase in chondroitin sulphate in the wound which forms the ground
substance.

Phase 2 (Reparative or proliferative phase; 3 days -3 weeks):

 • This phase consists mainly of the production of collagen and ground substance by fibroblast activity, the
growth of new blood vessels and capillary loops (angioneogenesis), and the re-epithelialization of the wound
surface.
 • New capillaries sprout from the sides of existing ones, and fibroblasts appear and align themselves to the
capillaries.
 • The wound tissue formed in the early part of this phase is called granulation tissue; this becomes vascular,
bleeds easily but affords some protection against bacterial invasion.
 • Fine fibrils appear in the intercellular space and aggregate to form collagen fibres. Increase in collagen
contributes to an increase in tensile strength of the wound. The collagen is at first deposited randomly and is type
III collagen.
 • At the same time epithelialisation takes place.

Phase 3 (Remodelling or contraction or maturation phase; 3 -12 weeks, up to 6 months):

 • The remodelling phase is characterized by maturation of collagen, type I replacing type III until a ratio of
4:1 is reached. The hyperplastic wound tissue begins to be reabsorbed.
 • Collagen fibres become larger, longer and intertwined.

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  • There is realignment of collagen fibres along the lines of tension, decreased wound vascularity and wound
contraction due to fibroblast and myofibroblast activity.
 • The red scar of the wound is replaced by a silver, flat hairline one.
 • Tensile strength continues to increase and attains normal strength after about 3 months.

Classification of wound closure and healing

Wounds may heal by:

 1) Primary intention
 2) Secondary intention
 3) Tertiary (delayed primary) intention

Primary intention:
Wounds may heal by primary intention if the edges are closely approximated or apposed. This type of healing is
also known as healing by first intention. Because of minimal surrounding tissue trauma, it causes the least
inflammation and leaves the best scar.

Secondary intention:
Healing by secondary intention occurs if the wound is left open and allowed to heal by granulation, contraction
and epithelialization. The restoration of epidermal continuity takes much longer, and usually results in delayed
healing, excessive fibrosis and an ugly scar.

Tertiary / Delayed primary intention:

Healing by delayed primary intention occurs when the wound edges are not apposed immediately, and the wound
is left open initially. This may be the case in contaminated or untidy wounds. Later, when healing conditions are
favourable, often when the inflammatory and proliferative phases are well advanced, closure of the wound is
carried out by apposing its edges. It results in a less than satisfactory scar than after healing by primary intention.

Topic 3: Soft tissue injuries: Factors influencing wound healing

FACTORS INFLUENCING WOUND HEALING

1. Factors that Decrease Collagen Synthesis:

 • Starvation (protein depletion)

 • Steroids
 • Infection
 • Associated injuries
 • Hypoxia and hypovolemia
 • Radiation injury
 • Uraemia
 • Diabetes
 • Drugs:
 Dactinomycin
 Fluorouracil
 Methotrexate
 • Advanced age.

2. Operative Factors:

 • Tissue injury.
 • Poor blood supply – damage to an artery or suture of the wound under excessive tension.
 • Poor apposition of surrounding tissues:
 Inaccurate anastomosis.

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  Unreduced fracture.
 Unclosed dead space.

3. Factors that Increase Collagen Lysis:

 • Starvation
 • Severe trauma
 • Inflammation
 • Infection
 • Steroids.

4. Local factors:

 • Site of the wound and its orientation relative to tissue tension lines
 • Structures involved
 • Mechanism of wounding – incision; crush; crush with avulsion
 • Inaccurate skin apposition
 • Loss of tissue - a large tissue defect leaving a large gap to bridge
 • Presence of dead or damaged tissue
 • Presence of foreign bodies (contamination) or blood clot in the wound
 • Impaired blood supply - slows healing, inhibits fibroblasts and weakens the defence against infection.
 • Local infection
 • Increased mechanical stress / pressure on a wound e.g. abdominal distension after abdominal surgery.

5. General/ systemic factors

 • Protein deficiency – delayed repair due to lack of collagen in the wound.

 • Lack of vitamin C – leads to defective formation and maintenance of collagen
 • Zinc deficiency – retards healing. Zinc is a co-factor for important enzymes involved in healing.
 • Anaemia – delay occurs in association with hypoproteinaemia.
 • Age – the young heal better than the elderly
 • Presence of other disease – diabetes mellitus, uraemia, jaundice, Cushing`s disease and disseminated
neoplasia
 • Immune deficiencies (e.g. chemotherapy, AIDS)
 • Smoking

CLASSIFICATION OF WOUNDS

 1. Tidy Wounds
 2. Untidy wounds
 3. Bruise, contusion and haematoma.
 4. Puncture wounds
 5. Bites
 6. Abrasions and friction burns
 7. Laceration
 8. Degloving injuries
 9. Crush
 10. Incised wounds or cuts

TIDY WOUNDS

• Are inflicted by sharp instruments and contain no devitalised tissue.

• Such wounds can be closed primarily with the expectation of quiet primary healing.
• Examples are: Surgical incisions, cuts from glass and knife wounds.
• Skin wounds will usually be single and clean cut.

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• Tendons, arteries and nerves will commonly be injured in tidy wounds, but primary repair of these
structures is usually possible.
• Fractures are uncommon in tidy wounds.

UNTIDY WOUNDS

• Usually result from: Crushing, tearing, avulsion or burns. They are generally contaminated and contain
devitalised tissue. Skin wounds will often be multiple and irregular, and often there is tissue loss.
• Tendons, arteries and nerves may be exposed, and might be injured in continuity, but will usually not be
divided.
• Fractures are common and may be multi-fragmentary.
• Such wounds must not be closed primarily; if they are closed wound healing is unlikely to occur without
complications, such as: - Wound dehiscence, infection, delayed healing, and gas gangrene.
• The correct management of untidy wounds is excision of all devitalised tissue to create a tidy wound.
Once the untidy wound has been converted to a tidy wound by the process of wound excision it can be safely
closed (or allowed to heal by second intention).

BRUISE OR ECCHYMOSIS, CONTUSION & HAEMATOMA

• These result from a blunt force disrupting superficial capillaries, the overlying skin remaining intact.
There is bleeding into the tissues and visible discoloration. Where the amount of bleeding is sufficient to create a
localised collection in the tissues, this is described as a haematoma. Initially this will be fluid, but it will clot
within minutes or hours. Later, after a few days, the haematoma will again liquefy. There is a danger of
secondary infection.
• Bruises require no specific management, and no treatment is of proven value. The patient should be
advised that the time required for bruising to clear is extremely variable and in some individuals, in some sites,
discoloration may persist for months.
• A haematoma should be evacuated by open surgery if large or causing pressure effects (such as
intracranially), or aspirated by a large-bore needle if smaller or in a cosmetically sensitive site. It may be
necessary to await liquefaction (which may take several days) and to perform repeated aspirations, with
appropriate antiseptic precautions. A haematoma will generally reabsorb without scarring, but on occasions there
may be persistent tethering of the skin.

PUNCTURE WOUNDS

A Puncture Wound is an open injury caused by a pointed object that pierces or penetrates the skin, and through
which foreign material and organisms are likely to be carried deeply into the underlying tissues. Common causes
are standing on a nail or other sharp object. There may be little to see on the surface. Radiological examination
may detect metal fragments or glass.

Management of puncture wound:

• Wound irrigation
• Antibiotic treatment
• Tetanus prophylaxis
• Large foreign bodies should be removed, but small particles may be surprisingly difficult to find without
a destructive dissection and are better left undisturbed. A metal detector may be helpful during exploration.
• The danger of puncture injuries is that they may give rise to an abscess deep within the tissues and on
such occasions drainage may be required. It is likely that it will take 24-48 hours for an abscess to declare itself
and arrangement should be made for review.
• Needle-stick injuries are a particular cause for concern. Discarded needles from drug abuse are becoming
increasingly a cause of accidental injury in the community

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BITES

• Bites are a particular type of puncture wound associated with a high incidence of infection, presumably
from mouth organisms.
• Animal bites may result in small, sharp, incised wounds or in severe tissue crushing as in horse bites.
• Dog bites may also be associated with a degree of tissue avulsion, and often there are puncture wounds
from upper and lower teeth and contusion of the intervening tissue.
• Human bites may be associated with avulsion of pieces of the nose or ear. An accidental type of ‘’bite’’
injury may result from an attacker striking the victim’s incisor teeth with the knuckles. This injury presents with
a puncture wound over the metacarpophalangeal (MP) joints. It is important to recognize the nature of the injury
as the history is often less than truthful.

Management:
• Open surgical exploration and excision of skin margins.
• Thorough cleaning of the wound and irrigation of any involved joint.
• Antibiotic therapy.
• Tetanus toxoid injection

ABRASIONS & FRICTION BURNS

 An abrasion or graze is a shearing injury in which the surface is rubbed off.

 Most are superficial and will heal by epithelialisation, but some may result in full-thickness skin loss.
 Abrasions may be dirt-ingrained and if this dirt is not removed at the time of primary treatment
permanent tattooing of the skin will result.
 Treatment is by cleaning with a scrubbing brush, gently brushing along the grain of the scratch lines.
 A friction burn is similar, but there will be an element of thermal damage as well as abrasion.
 Treatment is as for other types of burn.

LACERATION

• A laceration is a cut produced as a result blunt forces that tear, shear or crush skin and soft tissues.
• The wound edges are irregular and often abraded or contused, as are the surrounding tissues. They are
characterized by jagged edges and possible bruising or bleeding.
• The clinical examination must therefore assess the integrity of all structures in the area:

 Arteries.
 Nerves.
 Muscles.
 Tendons &
 Ligaments.

• As a general rule, the damage to nerves and tendons is generally greater than suspected pre-operatively.
• Once all of the damaged layers have been identified, each structure must be repaired individually by the
appropriate technique.
• Haemostasis must be ensured throughout the exploration.
• There are precise suture placement techniques for nerves, tendons and blood vessels.
• Muscles can be apposed in layers by mattress sutures and fascia, and subcutaneous fat should be opposed by
interrupted absorbable sutures to allow a firm platform for skin closure in such a way that the skin margins do not invert.
• It is an important principle to prevent collections of blood or other fluids in a wound as they separate tissues and
act as a nidus for infection.
• A corrugated or suction drain may be required.
• All patients sustaining open wounds should have prophylaxis against tetanus, and antibiotics should be

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administered where there is significant contamination, commencing generally with a broad-spectrum antibiotic active
against Gram-positive organisms.
INCISED WOUNDS OR CUTS

These are produced by sharp edges, such as knives or glass shards, and have characteristically clean edges with
clear margins. The greatest dimension of an incised wound is its length.

• The ideal form of management of an incised wound is:

1. Surgical inspection.
2. Cleaning &
3. Closure.

• The wound must be thoroughly inspected to ensure that there is no damage to deep structures or, where
encountered, these must be repaired.
• In a simple incised laceration, a method of wound closure should be selected which is appropriate for the needs of
function and appearance.
• On the face, fine (5 / 0 or 6 / 0) nylon sutures should be placed near to the wound margins, to be removed on the
fifth day.
• Alternatively, subcuticular (intradermal) sutures avoid suture marks and can be left in place longer (2 weeks or
more).
• An alternative to suturing is the application of adhesive tape strips.
• It is necessary to apply these with the same care as sutures ensuring that all bleeding has stopped and that the skin
is dry.
• For limb and trunk wounds, a heavier suture is required but it is rarely necessary to use more than 4 / 0 or 3 / 0
sutures for skin closure.
• Monofilament sutures, such as nylon, leave less obvious suture marks than braided material such as silk, but other
factors also contribute to stitch marks, such as:

 Inflammation (from infection or reaction to organic material such as silk),

 Wound tension and
 Late removal

DEGLOVING INJURIES

• These result from shearing forces that cause parallel tissue planes to move against each other. Such
injuries occur when hands or limbs are trapped in moving machinery, such as in rollers, producing a degloving
injury.
• Degloving is caused by shearing forces that separate tissue planes, rupturing their vascular
interconnections and causing tissue ischemia.
• Degloving soft tissue injuries are a form of avulsion of soft tissue, in which an extensive portion of skin
and subcutaneous tissue detaches from the underlying fascia and muscles. This most frequently occurs between
the subcutaneous fat and deep fascia. Degloving injuries can be open or closed.
• Similar injuries occur as a result of run-over road traffic accident injuries where friction from rubber tyres
will avulse skin and subcutaneous tissue from the underlying deep fascia.
• The history should raise the examiner’s suspicion and it is often possible to pinch the skin and lift it
upwards revealing its detachment from the normal anchorage.
• The danger of degloving or avulsion injuries is that there is devascularisation of tissue and skin necrosis
may become slowly apparent in the following few days.
• Even tissue that initially demonstrates venous bleeding may subsequently undergo necrosis if the
circulation is insufficient.

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Management:
• Identify the area of devitalised skin.
• Carefully assess the extent of the devitalized tissue and the blood supply to the affected tissues
• Remove the skin.
• Defat the skin.
• Reapply it as a full-thickness skin graft.
• Avulsion injuries of hands or feet may require immediate flap cover using a one-stage microvascular
tissue transfer of skin and/or muscle.

CRUSH INJURIES

• Crush injuries are a further variant of blunt injury and are often accompanied by degloving and
compartment syndrome.
• Injury to tissues within a closed fascial compartment leads to bleeding, exudate and swelling of these
tissues, and increased interstitial pressure. As the interstitial pressure rises above capillary perfusion pressure the
blood supply to the viable tissues is reduced, resulting in further ischemic tissue injury and swelling. This cycle
causes a worsening compartment syndrome with muscle ischemia and nerve ischemia progressing to muscle
necrosis, skin necrosis and limb loss.
• This process can be arrested by early recognition and decompression of the affected compartment(s) by
fasciotomy.
• The most reliable clinical sign of compartment syndrome is pain worsened by passive stretching of
affected muscles.
• Loss of peripheral pulses is not a sign of compartment syndrome, but indicates major vessel damage.
• Where compartment syndrome is suspected or confirmed fasciotomy is advised. Longitudinal incisions
are made in the deep fascia and it may also be necessary to make extensive longitudinal releases in the skin.
• It is important to release the fascia over each individual compartment in a limb.

Topic 3: Summary

In this topic you have learnt the following:

1. Definition of wound

2. The phases of normal wound healing

3. Classification of types of wound closure and healing

4. Factors influencing wound healing

5. The types of wounds and their management.

Topic 4: ULCERS

DECUBITUS SORES /PRESSURE SORES

DEFINITION
A decubitus sore is a lesion of cutaneous & subcutaneous tissues, which occurs in bed-ridden persons as a result
of pressure.

PREDISPOSING FACTORS

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1. Diminished/absent sensation.
2. Debilitation
3. Emaciation
4. Paralysis (e.g. spinal cord injuries/ degenerative neurological diseases)
5. Prolonged bed-riddenness.

AETIOLOGY

• Prolonged debilitating illnesses.

• Cachexia due to malnutrition.
• Old age.
• General shock following lesions of the nervous system – in particular, spinal cord injuries.

Plaster & splint sores:

• Careless moulding of the plaster & using plaster slab which is not sloppy but has already began to harden.
• Inadequate protection of bony prominences. This is especially disastrous in lesions of peripheral nerves &
of the spinal cord.
• Movement of a joint during the application of plaster, causing ridge formation & preventing smooth
adaptation of the plaster to the contour of the limb. This occurs especially in patients with paraplegia of spastic
type, accompanied by marked reflex spasms.
• Allowing the plaster to take the weight of the patient’s limb or trunk before it has completely hardened,
thus producing flattening of the plaster, especially over the bony prominences.
• Friction at the edges of cock-up plaster splints for paralysed feet, & at the edges of bivalved walking
plasters.
• Pressure or friction by the iron & leather bands of callipers.
• In cases of cauda equina & spinal-cord lesions, if the thigh band of the calliper is too long, its upper edge
will cause pressure in the region of the ischial tuberosity.

MECHANISM

I. Intrinsic factors:
The most important is the lowering of tissue vitality & tissue resistance to pressure, as the result of:
1) Circulatory disturbances in the peripheral vascular system
2) Disuse atrophy
3) Loss of vasomotor control, caused by paralysis of the nervous pathways
4) Malnutrition
5) Anaemia
6) Infection
7) Sensory loss in spinal lesions, as afferent impulses from a pressed area, which normally elicit discomfort
& thus incite change of posture, are abolished.

II. Extrinsic factors:

1. Pressure, especially over the bony prominences can result in obstruction of blood capillaries, depriving
tissues of oxygen and nutrients, causing ischaemia, hypoxia, oedema, inflammation, and, finally, necrosis and
ulcer formation.
2. Friction occurring when two surfaces rub against each other, damages superficial blood vessels directly
under the skin. This can occur when patients are pulled or slid over bed sheets while being moved up in bed.
3. Shearing or separation of the skin from underlying tissues. Occurs when two surfaces move in the
opposite direction. E.g. patient sliding down when the head of the bed is elevated.
4. Moisture: sweat, urine, faeces, or excessive wound drainage can exacerbate the damage caused by
pressure, friction and shearing, and contribute to maceration of surrounding skin.

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BACTERIOLOGY

• Bedsores always become infected, & the infection may become generalized.
• The micro-organisms most commonly found are:

 1. Streptococcus pyogenes (Beta-haemolytic streptococcus)

 2. Staphylococcus aureus
 3. Proteus mirabilis
 4. Escherichia coli
 5. Streptococcus faecalis
 6. Pseudomonas aeruginosa
 7. Bacteroides

Topic 4: ULCERS: Decubitus sores

CLINICAL FEATURES

Sites – commonly occurs in areas over bony (skeletal) prominences, especially the:

 1) Sacrum
 2) Greater trochanters
 3) Heels
 4) Lateral malleoli
 5) Ischial tuberosities
 6) Shoulder blades
 7) Elbows
 8) Knees
 9) Occipital area of head.

Warning signs of bedsores are:

  Unusual changes in skin colour or texture

  Swelling
  Pus-like draining
  An area of skin that feels cooler or warmer to the touch than other areas
  Tender areas

Stages of bedsores:
Stage (I) of transient circulatory disturbance

 • Pressure has been sufficient merely to cause reddening of the skin, without destruction of the tissues.
 • It promptly disappears if the pressure is relieved, & with massage (the skin and underlying tissues are still
soft).

Stage (II) of permanent superficial circulatory & tissue damage

 • Characterized by reddening & oedema/congestion of the pressed area, which does not disappear after
decompression, & which leads to induration of the tissues (at times with epidermal blistering or desquamation).

Stage III

 • The superficial layers of the skin have been killed & may be excoriated, exposing the weeping corium
(exposure of fat).

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Stage IV

 • Necrosis extends through the skin & fat to muscle.

Stage V

 – further fat & muscle necrosis.

State VI
– bone destruction begins, with periostitis & osteitis, progressing finally to osteomyelitis, with possibility of
septic arthritis, pathological # & septicaemia.

Stage of penetrating necrosis (malignant sore)

 • The destruction also involves the subcutaneous tissues, including fasciae, muscles and bones.
 • It leads to gangrene & later to a deep ulcer.
 • Often the necrosis of the deeper tissues is more extensive than that of the skin, which accounts for the
undermining character of the sore & the formation of deep sinuses.

Topic 4: ULCERS: Decubitus sores - management; complications

MANAGEMENT

I. Prophylactic.

 • Remove hard objects from the patient’s pockets

 • Pad bony prominences
 • Manage spinal injuries in special centres or hospitals
 • Skin inspection of pressure prone areas
 • Avoid over-sedation & encourage activity
 • Physiotherapy when practicable.

Protect the skin:

 • Change of posture. As a rule, turn the patient at 2 hourly intervals, day & night.
 • Keep the skin clean and dry.
 • Use moisture barrier creams to protect the skin from urine and stool
 • Change bedding and clothing frequently
 • Watch for buttons on clothing that could cause pressure to the skin.
 • Creases & crumbs in the bed-clothes that could irritate the skin must be scrupulously avoided.
 • Inspect the skin daily for warning signs of pressure sores
 • Redistribution of pressure by nursing the patient on a rigid bed equipped with a pressure-redistributing
mattress. Plenty of small pillows are also needed to support the limbs & trunk in the various positions adopted as
the result of turnings.
 • Promote good circulation by frequent gentle massage to the compressed areas.
 • Maintenance of a good general condition of the patient also helps in preventing bedsores e.g. proper
nutrition, correction of anaemia.

II. Curative:

 • Once bed sores have developed, the principles of prophylaxis should be enforced & every effort made to
remove pressure from them.
 • In certain cases, it may be necessary to turn the patient even more frequently than every 2 hours.
 1. Superficial sores with excoriation of the skin:

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  • 1st cleaned with soap & water.
 • Followed by sterile sulphanilamide powder dressing.
 • Later, sofratulle can be used in dressing.
 2. If a blister is present, the elevated epithelium is removed aseptically before the application of
sulphanilamide powder.
 3. Superficial, indolent ulcers are scraped & the pigmented border is excised. This is followed by daily saline
dressings.
 4. In malignant sores with penetrating gangrene:
 • Excision of the necrotic tissues.
 • Cleansing with hydrogen peroxide & saline solution or soap & water.
 • Routine culture and sensitivity of wound swabs.
 • Antiseptics are applied to the devitalized tissue cautiously, as they have an inhibitory action on the
granulations which play a vital part in the healing of deep sores in the early stages.

Complications of pressure sores

 1. Cellulitis
 2. Bone and joint infections – septic arthritis and osteomyelitis
 3. Cancer – long-term non-healing wounds can develop into squamous cell carcinoma
 4. Septicaemia
 5. Necrotizing fasciitis
 6. Gas gangrene

Topic 4: Summary

In this topic you have learnt the following:

1. Definition of decubitus sores

2. The predisposing factors and aetiology
3. Mechanisms of causation of decubitus sores
4. Microorganisms impicated in pressure sores
5. Clinical features of pressure sores
6. Management of decubitus sores
7. Complications of pressure sores

Topic 5: GANGRENE


 OBJECTIVES
 By the end of this topic, you should be able to:

1. Define gangrene
2. Outline the causes / aetiology of gangrene
3. Describe the clinical features of gangrene and the clinical types of gangrene
4. Outline the management of gangrene
5. Describe diabetic gangrene and its management
6. Describe gas gangrene and its management

Topic 5: GANGRENE: Definition; Aetiology

GANGRENE

DEFINITION
Gangrene implies death with putrefaction of macroscopic portions of tissues.

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It is commonly seen affecting:

1. The distal part of a limb.

2. The appendix or loop of small intestine and sometimes organs such as
3. The gall bladder.
4. The testis.

The term necrosis applies mainly to the death of groups of cells, although it is extended to include bone, i.e., a
sequestrum. A slough is a piece of dead, soft tissue, e.g., skin, fascia or tendon.

AETIOLOGY OF GANGRENE
1. Secondary to arterial obstruction from disease, e.g.:

 • Thrombosis of an atherosclerotic artery.

 • Embolus from the heart in atrial fibrillation or after coronary thrombosis.
 • Arteritis with neuropathy in diabetes.
 • Buerger’s disease.
 • Arterial shutdown in Raynaud’s disease or ergotism.
 • Effect of intra-arterial injections – thiopentone and cytotoxic substances.

2. Infective:

 • Boils and carbuncles.

 • Gas gangrene.
 • Gangrene of the scrotum (Fournier’s gangrene).

3. Traumatic:

 • Direct, such as:

 Crushes.
 Pressure sores and
 The constriction groove of strangulated bowel.
 • Indirect due to injury of vessels at some distance from the site of gangrene, e.g., pressure on the popliteal
artery by the lower end of a fractured femur.

4. Physical, e.g.

 • Burns.
 • Scalds.
 • Frostbite.
 • Chemicals.
 • Irradiation and
 • Electricity.

5. Venous gangrene.
CLINICAL FEATURES

A gangrenous part lacks:

 • Arterial pulsation.

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  • Venous return.
 • Capillary response to pressure (colour return).
 • Sensation.
 • Warmth and
 • Function.

The colour of the part changes through a variety of shades according to circumstances (pallor, dusky grey,
mottled, purple) until finally taking on the characteristic dark brown, greenish black or black appearance, which
is due to the disintegration of haemoglobin and the formation of iron sulphide.

Clinical types:
1) Dry Gangrene:

 • Occurs when the tissues are desiccated by gradual slowing of the bloodstream.
 • It is typically the result of atherosclerosis.
 • The affected part becomes dry and wrinkled, discoloured from disintegration of haemoglobin and greasy to
the touch.

2) Moist (wet) Gangrene:

 • Occurs:
 When venous as well as arterial obstruction is present.
 When an artery is suddenly occluded, as by a ligature or embolus, and
 In diabetes.
 • Infection and putrefaction are always present.
 • The affected part becomes swollen and discoloured.
 • The epidermis may be raised in blebs.
 • Crepitus may be palpated, owing to infection by gas-forming organisms.
 • Moist gangrene is manifest also in such conditions as:
 - Acute appendicitis and
 - Strangulated bowel

SEPARATION OF GANGRENE
Separation by Demarcation:
• A zone of demarcation between the truly viable and the dead or dying tissue appears first.
• It is indicated on the surface by a band of hyperaemia and hyperaesthesia.
• Separation is achieved by the development of layer of granulation tissue which forms between the dead
and the living parts.
• These granulations extend into the dead tissue until those which have penetrated farthest are unable to
derive adequate nourishment.
• Ulceration follows and thus a final line of demarcation (separation) forms which separates the gangrenous
mass from healthy tissue.

Dry Gangrene:

 • If the blood supply of the proximal tissues is adequate, the final line of demarcation appears in a matter of
days and separation begins to take place neatly and with the minimum of infection (so-called separation by aseptic
ulceration).
 • Where bone is involved, complete separation takes longer than when soft tissues alone are affected, and the
stump tends to be conical as the bone has a better blood supply than its coverings.

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Moist Gangrene:

 • There is more infection and suppuration extends into the neighbouring living tissue, thereby causing the
final line of demarcation to be more proximal than in dry gangrene (separation by septic ulceration).
 • This is why dry gangrene must be kept as dry and aseptic as possible, and why every effort should be made
to convert moist gangrene into the dry type.

Vague Demarcation; Spread of Gangrene; Skipping and Die-Back:

 • In many cases of gangrene from atherosclerosis and embolism, the line of final demarcation is very slow to
form or does not develop.
 • Unless the arterial supply to the living tissues can be improved forthwith, the gangrene will spread to
adjacent tissues or toes, or will suddenly appear as ‘’skip’’ areas further up the limb.
 • Signs of skipping should always be carefully looked for.
 • Black patches suddenly appear, perhaps:
 On the other side of the foot.
 On the heel.
 On the dorsum of the foot or
 Even in the calf.
 • Infection, another cause of the spread of gangrene, may spread upwards beyond the line of separation along
the lymphatic vessels or cellular tissue into healthy parts; extensive inflammation then results.
 • Except in diabetic gangrene without concomitant atherosclerotic obstruction, these forms of spread do not
usually respond to efforts to save the limb and an above-knee amputation becomes necessary.
 • To attempt local amputation in the phase of vague demarcation is to court failure, as gangrene reappears in
the skin-flaps (‘’die-back’’)

MANAGEMENT

General Principles:
• A limb-saving attitude is needed in most cases of symptomatic gangrene affecting hands and feet.
• The surgeon is concerned with how much can be preserved or salvaged.
• With arterial disease all depends upon there being a good blood supply to the limb above the gangrene, or whether
a poor blood supply can be improved by such measures as percutaneous transluminal angioplasty or direct arterial surgery.
• A good or an improved blood supply indicates that a conservative excision is likely to be successful and a major
amputation may be avoided.
• A life-saving amputation is required for:

 A badly crushed limb.

 Rapidly spreading symptomatic gangrene
 Gas gangrene.

General treatment includes that of:

 • Cardiac failure.
 • Atrial fibrillation and
 • Anaemia, to improve the tissue oxygenation.
 • A nutritious diet, essential in all forms of gangrene
 • The control of diabetes when present
 • Pain relief (night pain, may be difficult to relieve)
 • Non-addictive drugs should be used whenever possible.

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Local Treatment:
1. Care of the affected part
includes keeping it absolutely dry. Exposure and the use of a fan may assist in the desiccation and may relieve pain.
2. Protection of local
pressure areas, e.g., the skin of the heel or the malleoli, is required otherwise fresh patches of gangrene are likely to occur
in these places.
3. A bed-cradle, padded
rings, foam blocks and air beds are useful preventive aids.
4. Careful observation of a
gangrenous part will show whether the lifting of a crust, or the removal of hard or desiccated skin, will assist in
demarcation, the release of pus and the relief of pain.
Topic 5: DIABETIC GANGRENE


 DIABETIC GRANGRENE


 PATHOGENESIS


  Trophic changes that lead to diabetic gangrene result from:

1. Peripheral neuritis;
2. Atheroma of the arteries resulting in ischemia;
3. Excess of sugar in the tissues which lowers resistance to infection, including fungal infection.


  The neuropathic factor impairs sensation and thus favours the neglect of minor injuries and infection, so
that inflammation and damage to tissues are ignored.
  Muscular involvement is frequently accompanied by loss of reflexes & deformities.
  In some cases, the feet are splayed and deformed (neuropathic joints).
  Thick callosities develop on the sole and are the means whereby infection gains entry, often following
amateur chiropody.
  Infection involving fascia, tendon and bone can spread proximally with speed via sub-fascial planes.
  Palpable dorsalis pedis and posterior tibial pulses, and the absence of rest pain and intermittent
claudication, imply that there is no associated major arterial disease.

 INVESTIGATIONS
 1. Urinalysis.
 2. Random blood sugar.
 3. Pus swab for C/S.
 4. A radiograph may help to reveal the extent of any osteomyelitis.

 MANAGEMENT
 1) Control diabetes with diet and appropriate drugs.
 2) The gangrene is treated along the lines already described, the accent being on conservatism if there is no
major arterial obstruction.
 3) A rapid spread of infection requires drainage of the area by incision and the removal of any obvious dead
tissue. This may often involve free and extensive laying open of infected tissue planes. Adequate surgical drainage of pus
and the control of infection due to bacteria and fungi may then be followed by rapid healing.
 4) After healing, protection of the affected part is essential.

Topic 5: GAS GANGRENE

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GAS GANGRENE

INTRODUCTION

• Clostridia are saprophytes (live and feed on dead or decaying organic matter).

• Vegetative and spore forms are widespread in soil, sand, clothing and faeces.
• Wounds allowing the patient’s own faecal flora, or clostridial spores in the soil, to enter the tissues can
give rise to anaerobic gas-producing infections.
• Surgery around the hip joint and leg amputations are at high risk from this post-operative complication, as
are the wounds of warfare

PATHOPHYSIOLOGY AND BACTERIOLOGY

Bacteriology:
1) Clostridium perfringens (welchii) is the principal cause (about 80%) of clostridial myonecrosis or gas
gangrene. Other causative clostridia, include:
2) Cl. novyi (Cl.oedematiens) in 40%.
3) Cl. histolyticum
4) Cl. bifermentans &
5) Cl. septicum

Clostridium perfringens:
• The Gram-positive, spore-bearing bacilli are widely found in nature, particularly in soil and faeces
• Clostridium perfringens is found in stool and therefore is also found on the perineum and, occasionally, as normal
flora in the vagina.
• The clostridia produce numerous toxins, including α-toxin believed to be important in the pathogenesis of gas
gangrene.
• Patients who are immunocompromised, diabetic or have malignant disease are at risk, particularly when anaerobic
wound conditions are present with necrotic or foreign material.
• Clostridia are, generally fastidious/strict anaerobes requiring a low redox potential to grow and to initiate
conversion of the spores to vegetative, toxin-producing pathogens.
• Their growth is favoured by failure to debride contaminated wounds.
• Tissue redox potential are diminished by:

  Impaired blood supply.

  Muscle injury.
  Pressure from casts.
  Severe local oedema.
  Foreign bodies, or
  Oxygen-consuming organisms.

• Clostridial infections frequently occur in the presence of other bacteria, especially Gram-negative bacilli.
• Clostridia proliferate and produce toxins that diffuse into the surrounding tissue.
• The toxins destroy local microcirculation.
• This allows further invasion, which can advance at an astonishing rate.
• The alpha toxin, a necrotizing lecithinase, is thought to be particularly important in this sequence.
• Other toxins that also contribute include:

  Collagenase.

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   Hyaluronidase.
  Leukocidin.
  Protease.
  Lipase and
  Hemolysin.

Pathophysiology:
• Clostridial invasion of a traumatised muscle affects the whole of that muscle from origin to insertion, producing a
foul-smelling necrosis of the bundles which lose contractibility and become dull red, green or black in appearance.
• Oedema and spreading gangrene follow the release of collagenase, hyaluronidase, other proteases and α-toxin.
• One of the patient’s muscles may be involved, or more often a group of them, or a whole limb, or part of it.
• Infection spreads up and down a muscle, and has less tendency to spread from one muscle to another.
• As infection progresses along a muscle it changes from brick red to purplish black.
• At first the wound is relatively dry; later, you can express from its edges a thin exudate with droplets of fat and gas
bubbles, which becomes increasingly offensive.
• Subcutaneous tissues alone can be infected; the foul-smelling necrosis, often spreading extensively.
• Severe wound pain, signs of spreading inflammation with crepitus and smell lead on to widespread gangrene.
• The extent of subdermal spread of gangrene is always much more extensive than at first is apparent.
• The progress of the local lesion can be judged by the general state of the patient as well as by the local signs.
• If septicaemia occurs, gas is produced in many organs, notably the liver
• Systemic complications with circulatory collapse often follows.

Topic 5: GAS GANGRENE: Clinical features / types

CLINICAL FEATURES

1. Sudden deterioration in a patient whose wound has been progressing satisfactorily.

2. Over a few hours the patient becomes anxious and frightened.
3. Raised pulse rate; becomes feeble with fall in blood pressure.
4. Patient develops fever, becomes apathetic and may have anorexia and vomiting.
5. Locally, the wound is under tension.
6. There is severe local wound pain and crepitus (gas in the tissues). Large blisters often form. Gas bubbles
may be visible within the blister.
7. Between the sutures the pouting edges exude a brownish and foul-smelling fluid, from which bacteria can
be recognised on Gram staining.
8. The skin becomes discoloured – a khaki colour – owing to associated haemolysis.
9. When the disease has advanced sufficiently, toxins enter the systemic circulation, causing:

 • Pallor & jaundice due to haemolytic anaemia.

 • Anxiety.
 • Restlessness.
 • Delirium.
 • Severe tachycardia.
 • Shock and death.

10. The patient, although toxic and pale, with raised pulse, misleadingly appears mentally clear.
11. The temperature is raised at first but becomes subnormal as the condition progresses.

Spectrum of infection:
The spectrum of infection extends from superficial contamination of an open wound to clostridial myonecrosis and gas
gangrene. Clostridial infections are classified, in ascending order of lethal potential, as:
1) Simple contamination.
2) Gas abscess.

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3) Clostridial cellulitis.
4) Localized clostridial myositis.
5) Diffuse clostridial myositis, and
6) Oedematous gangrene.
The term gas gangrene is reserved to denote clostridial myositis with gas production.

Simple Contamination:
• Many open wounds are superficially infected or contaminated with clostridia without developing significant
infections.
• There is often a brown seropurulent exudate.
• The condition is not invasive, because the surrounding tissue is basically healthy and the clostridia are confined to
necrotic surface tissue.
• Debridement of dead surface tissue is usually the only treatment necessary.
• Simple clostridial contamination can change to invasive gangrene if a severe hemodynamic abnormality or further
injury decreases the oxidation-reduction potential of the surrounding tissue and allows invasion.

Gas Abscess (Welch’s Abscess):

• Gas abscess is a localized infection not usually thought of as invasive.
• Muscle is not involved.
• The incubation period is usually a week or more.
• There is usually little pain.
• The oedema is moderate.
• The patient does not appear toxic, though fever and tachycardia may be present.
• The wound, however, has the characteristic autopsy room odour, and gas may be present.
• Except for the involved area, the tissue appears well perfused.
• Treatment usually consists of incision and drainage and administration of penicillin.

Crepitant Clostridial Cellulitis:

• This type (‘’anaerobic cellulitis’’) is an invasive infection of subcutaneous tissue that has been made susceptible by
injury or ischemia.
• It usually follows appendectomy.
• Invasion is superficial to the deep fascia and may spread very fast, often producing discolouration of the skin and
oedema as well as crepitus.
• The systemic symptoms and signs are much less pronounced than the surface appearance and extent of gas
production might indicate, and this picture distinguishes cellulitis from myositis.
• The differentiation is important, since adequate therapy for cellulitis is far less aggressive than that for myositis.

Localized Clostridial Myositis:

• Is rare.
• The injury and infection involve muscle, but the infection is not invasive.
• The wound has the characteristic odour, oedema, crepitation, and appearance, but the changes are localized and the
region appears well perfused, with intact pulse.
• The systemic reaction may include fever and tachycardia but not severe prostration, delirium, and other signs of
toxaemia.

Diffuse Clostridial Myositis (Gas Gangrene):

• Usually begins less than 3 days after the injury, with rapid increase of pain in the wound, oedema, and a brown
seropurulent exudate, often containing bubbles.
• There is marked tachycardia, but fever is variable.
• Crepitus may or may not be present.
• Profound toxaemia often appears early and progresses to delirium and haemolytic jaundice.
• The surface oedema, necrosis, and discolouration are usually less extensive than the underlying muscle necrosis.
• The disease characteristically progresses rapidly with loss of blood supply to the infected muscle.
• The swelling and oedema may produce ischemia under tight dressings or plaster casts.
• Delayed or inadequate debridement of injured tissue after devascularizing injury is the most common setting.
• Since gas gangrene often develops under plaster casts, a sudden deterioration within 3-4 days after injury, an
autopsy room odour, and a brown exudate are indications that removal or windowing of the cast is necessary.
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Oedematous Gangrene:
• Is a variant caused by Cl. novyi (Cl. oedematiens).
• No gas is produced, but oedema of muscle is prominent.
• This is a particularly aggressive and often fatal infection requiring rapid and aggressive therapy.

GAS GANGRENE: Differential diagnosis; Management

DIFFERENTIAL DIAGNOSIS

1. Surgical emphysema.
2. Ischemic gangrene.
• There is no toxaemia, unless the gangrenous tissue becomes secondarily infected.
3. Anaerobic cellulitis:
• Infection is limited to the patient’s subcutaneous tissues.
• Spread may be rapid and there may be much subcutaneous gas.
• Sometimes the whole abdominal wall is involved.
• When you remove the affected tissue, the muscle underneath appears healthy, and bleeds and contracts
normally.
• Remove the necrotic tissue, and drain the wound.
4. Anaerobic Streptococcal Myositis:
• Spreading redness and swelling originating in a stinking discharging wound with Gram-positive cocci and
pus cells in its exudate.
• The patient’s muscles are boggy and pale at first, then bright red and later pale and friable.
• The characteristic toxaemia of gas gangrene does not develop.
• Make radical incisions through his deep fascia to relieve tension and provide drainage.

INVESTIGATIONS

1. Exudate from the wound for Gram Stain and look for Gram positive rods.
2. Culture and sensitivity of the exudate.
3. A radiograph will show the gas in the muscles or under the skin.

MANAGEMENT

 Management to be effective, requires immediate action.

 The major emphasis in treatment is inevitably surgical.
 Antibiotics are often essential but are ineffective without surgical control of the disease.
 Once established, large doses of intravenous antibiotics and aggressive debridement of affected tissues
are required.
 Wide-spectrum antibiotic therapy must be combined with aggressive circulatory support and wide
excision and laying open of affected tissue.
 Debridement may need to be extensive.
 Patients who survive need large areas of skin grafting.
 The use of hyperbaric oxygen in a pressure chamber may have a role.

Surgical Treatment:
 The wound must be opened, and dead and severely damaged tissue must be excised.
 Tight fascial compartments must be decompressed.
 Immediate amputation is necessary when there is diffuse myositis with complete loss of blood supply or
when adequate debridement would leave a useless limb.
 Surgical treatment for clostridial cellulitis must often be aggressive, but amputation is not necessary.
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 Extensive debridement may be performed, with excision of necrotic skin or subcutaneous tissue, or both.
 Wide-open drainage is essential.
 One must be careful to determine whether muscle is involved, because myositis and cellulitis may
coexist.
 Daily debridement under anaesthetic may be required, since these lesions are extensive.
 If skin is viable, surprising amounts can be saved after debridement of subcutaneous tissue.

Hyperbaric Oxygen:
 Is beneficial in treating clostridial infections, but it cannot replace surgical therapy.
 Early use of hyperbaric oxygen, sometimes prior to debridement, can reduce tissue losses.
 Because even hyperbarically administered oxygen will fail to reach the tissues in hypovolemic patients,
vigorous support of blood volume is necessary.

Antibiotics:
 High dose antibiotic therapy is essential.
 Penicillin is given intravenously in very high dosage, together with metronidazole or clindamycin to
control other anaerobes.
 Combinations of beta-lactam inhibitor antibiotics such as ampicillin together with sulbactam or ticarcillin
plus clavulanate are other alternatives.
 In mixed infection, imipenem could be used.

Nursing:
 Isolate him from the other surgical patients.
 If possible, barrier nurse him.

Antitoxin:
 There should be no need to use this in most wounds.
 If you give it, do a skin sensitivity test first.
 Then give him pentavalent gas gangrene antiserum intravenously and repeat it after 4 to 6 hours.

Blood transfusion.
 Many patients with gas gangrene and extensive injuries require multiple blood transfusions.
 Fresh blood should be given early, and serum phosphate levels should be kept within the normal range.

PREVENTION

Almost all clostridial infections are preventable by:

  Cleaning wounds thoroughly

  Removing foreign objects and dead tissue from wounds (early debridement of dead tissue)
  Giving antibiotics intravenously before, during, and after abdominal surgery to prevent infection.
  Early antibiotic treatment after injury

PROGNOSIS

 Clostridial cellulitis and myositis are potentially lethal diseases.

 With adequate treatment, deaths should occur only when treatment is delayed or when patients are
already severely ill with other diseases or have advanced invasion of vital structures.
 The death rate is currently about 20%.
 The prognosis for salvage of functioning limbs is not so favourable.

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 When clostridial myonecrosis is added to injury, affected limbs often become useless and must be
amputated to save life.

opic 5: Summary

In this topic you have learnt the following about gangrene:

1. Definition of gangrene
2. The causes / aetiology of gangrene
3. Clinical features of gangrene and the clinical types of gangrene
4. Management of gangrene
5. Diabetic gangrene and its management
6. Gas gangrene and its management

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UNIT FIVE: CHEST CONDITIONS
a) Introduction
This unit deals with surgical conditions affecting the chest or thorax. These include obstruction of the airway, chest injuries
such as rib fractures and flail chest, pneumothorax, haemothorax, cardiac tamponade, surgical emphysema, empyema, lung
tumours and breast conditions. The aim of this unit is to enable the learner to identify and manage these conditions.

Topic 1: Obstruction of the Airway

OBSTRUCTION OF THE AIRWAY

Objectives
• State the causes
• Describe the pathology
• Outline the clinical features
• state the investigations
• State the management

CAUSES

1. Intraluminal:

 • Inhaled foreign body.

 • Neoplasm.

2. Intramural:

 • Congenital stenosis.
 • Fibrous stricture (post-intubation or tuberculosis)

3. Extramural:

 • Neoplasm (thyroid cancer, 2o deposits).

 • Aortic arch aneurysm.

PATHOLOGY

Inhaled foreign bodies are a common occurrence in small children. Surprisingly large objects can be inhaled and
become lodged in the wider calibre and more vertically placed right main bronchus. If not removed, an
obstructive emphysema may result but, if there is total occlusion of the bronchus, the air distally will be absorbed
and the secretions may become infected.

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CLINICAL FEATURES

 In upper airway:

 1. Choking which may be persistent or come to pass

 2. Cyanosis

 There are three possible presentations of lower airway obstruction:

 1. Asymptomatic.
 2. Wheezing (from airway narrowing) with a persistent cough and signs of obstructive emphysema.
 3. Pyrexia with a productive cough from pulmonary suppuration.

INVESTIGATIONS

1. Chest x-ray

 Is vital as the object may be radio-opaque. Often it is not or is obscured by the cardiac shadow or the inflammatory
response.

2. Bronchoscopy

 May be both diagnostic and therapeutic.

MANAGEMENT

1. Upper airway obstruction

 Heimlich manoeuvre: Give 5 back blows between the shoulders using the heel of your hand. If the foreign body
does not dislodge, do abdominal thrust

2. Failed upper Heimlich manoeuvre and lower airway obstruction

  Remove foreign body by bronchoscopy

  Bronchotomy: If bronchoscopy fails
  If the object has caused chronic lung damage it may be necessary to remove the affected lobe.

Topic 1: Empyema Thoracis

EMPYEMA THORACIS (Pyothorax)

DEFINITION
Empyema is a collection of pus within the pleural cavity.

AETIOLOGY
• Underlying lung diseases such as bronchiectasis, pneumonia, carcinoma of the lungs and rarely
tuberculosis
• Penetrating wound on the chest wall or following a transthoracic operation
• Perforation of the oesophagus
• Trans-diaphragmatic infection from sub-phrenic abscess
• Haematogenous from distant focus
• Repeated aspiration of pleural effusion

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• Secondary infection of a clotted haemothorax
 Common causative organisms include:
1. Pneumococcus
2. Streptococcus
3. Staphylococcus

PATHOLOGY
• Empyema commonly follows a pneumonia due to infection of a reactive parapneumonic effusion.
• The infected fluid is initially thin and may be completely evacuated by a low intercostal drain.
• The empyema quickly becomes thick and loculated due to fibrin deposition. This stage requires formal
surgical drainage.
• The pus collection is typically placed posteriorly towards the base of the pleural cavity and causes a D-
shaped shadow on the lateral chest X-ray.

CLINICAL FEATURES
1. Chest pain (pleuritic pain).
2. Shortness of breath – respirations may be grunting.
3. Fever – temperatures may reach 40.6°C
4. Weakness.
5. Haemoptysis.
6. Weight loss
7. Cyanosis.
8. Chronic ill health.
9. Finger clubbing
10. Anaemia
11. Physical signs of pleural effusion are common.

INVESTIGATIONS
1) Full haemogram: reveals leukocytosis
2) Chest X-ray: demonstrates an effusion and there may evidence of underlying lung disease
3) Bronchoscopy: it is vital in determining the primary pathology
4) Aspiration of the chest: confirms diagnosis and identifies the causative organism through microscopy
culture & sensitivity

MANAGEMENT
• Repeated aspiration with antibiotic therapy given both systemically and into the pleural cavity (in early
acute cases)
• If above fails: Drainage is done by means of excision of a segment of rib overlying the lowest part of the
empyema, an intercostal tube is inserted and suctioning and curetting the cavity clean is done.
• In more chronic cases: Decortication (excision of the fibrous wall of empyema cavity) is done through
open thoracotomy.

COMPLICATIONS
1. Empyema necessitatis (invasion of the chest wall).
2. Bronchopleural fistula.
3. Pericardial extension.
4. Mediastinal abscess.
5. Osteomyelitis of the ribs.
6. Septicaemia.
7. Chronicity.
8. Metastatic abscesses, particularly to the brain –unusual when antibiotic coverage is adequate.
9. Amyloid deposition, particularly in the liver and kidneys – 2o to prolonged suppuration.

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Topic 1: Summary

In this topic you have learnt the following about 1. Obstruction of the airway and 2. Empyema thoracis:

1. Definition
2. Causes / aetiology
3. Pathology
4. Clinical features
5. Investigations
6. Management
7. Complications of empyema

Topic 2: CHEST INJURIES

CHEST INJURIES

INTRODUCTION

Ventilation of the lungs depends on a patent airway and pulmonary alveoli, a rigid rib bony skeleton of the
thorax, and integrity of nerves and muscles that control the movement of the ribs and the diaphragm. Traumatic
disruption of the chest wall is likely to be lethal unless treatment is instituted rapidly. Chest injuries commonly
involve rib fractures, injuries to the pleura and lung parenchyma.

Dangerous complications of chest injuries include:

  Flail chest: paradoxical breathing

  Pneumothorax
  Haemothorax
  Penetrating lung injury
  Cardiac tamponade due to laceration of the heart
  Damage to large blood vessel

FRACTURES OF THE RIBS

 Mostly caused by direct blow on the chest

 The most commonly affected are the 7th, 8th and 9th ribs in which fractures occur on the region of mid
axillary line

CLINICAL FEATURES

 Pain in the chest overlying the fracture which is aggravated by breathing or movement
 Shortness of breath
 Tenderness

INVESTIGATIONS

1. CHEST X-RAY

 Confirms the fracture/s

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  Identifies underlying lung damage or haemorrhage

2. BONE SCAN

 More sensitive at detecting fractures especially pathological fractures where it reveals metastatic deposits

TREATMENT
• Pain relief by:

 Analgesics esp. NSAIDs

 Injection of local anaesthetic in the paravertebral region to block the intercostal nerves or by thoracic epidural
block

• Vigorous physiotherapy encourage deep breathing

• Strapping of the chest- but discouraged since it inhibits thoracic movement and encourage pulmonary collapse
FLAIL CHEST

DEFINITION

Flail chest is a life-threatening surgical condition that occurs when a segment of the rib cage breaks due to
trauma and becomes detached from the rest of the chest wall. It occurs when multiple adjacent ribs are fractured
in multiple places, separating a segment, so a part of the chest wall moves independently. Flail chest occurs when
three or more adjacent ribs are fractured in at least two locations; when several adjacent ribs are fractured in two
places either on one side of the chest (segmental) or either side of the sternum.

PATHOLOGY

The flail segment moves in opposite direction to the rest of the chest wall; it moves inwards during inspiration
while the rest of the chest is moving out, and vice versa. This is called paradoxical breathing. Flail chest is
usually accompanied by pulmonary contusion, a bruise of the lung tissue. Hypoxia is caused by restricted chest
wall movement and underlying lung contusion.

CLINICAL FEATURES

Symptoms

1. History of blunt chest trauma

2. Severe chest pain
3. Difficulty in breathing
4. Uneven chest movement when breathing

Signs
1. PARADOXICAL BREATHING

  On inspiration, the flail part of the chest becomes indrawn by the negative intrathoracic pressure
  On expiration, the flail part of the chest is pushed out whilst the rest of the bony cage becomes contracted

2. Dyspnoea with resultant:

  Hypoxia

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   Cyanosis
  Hypercapnoea
  Acidosis

2. Cardiovascular embarrassment:

  Patient gets rapidly and progressively shocked

3. Tenderness over the fracture sites on the chest

INVESTIGATIONS

1. Chest X-ray

 Will show fractured ribs, lung collapse on the flail side, and hyperventilated opposite lung.

2. Arterial blood gas analysis- for severely anoxic patients

TREATMENT

1. Support the flail segment in an emergency by means of firm pad held by strapping- it stops paradoxical breathing
and air shunting
2. On admission: endotracheal intubation and positive-pressure ventilation which stops the paradoxical movement as
the chest wall moves as one unit.
3. Positive pressure ventilation is continued for 10 days until fixation of the chest wall occurs
4. In cases of gross instability, wire fixation of the chest wall may be necessary
5. Tracheostomy- may be indicated for prolonged periods of intubation
6. Pain management – analgesics e.g. morphine

PNEUMOTHORAX

DEFINITION

Pneumothorax is the accumulation of air or gas in the pleural cavity (potential space between the visceral and
parietal pleura) with secondary lung collapse. It occurs through either an external chest wound or an internal air
leak. It is referred to as ‘closed’ when the chest wall is intact or ‘open’ when a breach in the chest wall exists.

CLASSIFICATION

1. Spontaneous

 • Primary
 • Secondary

2. Traumatic
3. Iatrogenic

SPONTANEOUS PNEUMOTHORAX

Occurs due to spontaneous rupture of lung alveoli and the visceral pleura with escape of air into the pleural
space. It may occur in any age but is most common in males 15-35 years of age, especially young tall male

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smokers. A high incidence is reported in patients with Marfan’s syndrome. Spontaneous pneumothorax is more
common on the right side. Less than 10% are bilateral.

Spontaneous pneumothorax is described as primary or secondary. Primary spontaneous pneumothorax is one that
occurs without an apparent cause and in the absence of significant lung disease. Secondary spontaneous
pneumothorax occurs in the presence of existing lung disease.

Primary pneumothorax typically occurs in young individuals (15-35 years) with essentially normal lungs apart
from a few apical bullae or blebs. Secondary pneumothorax is common in elderly patients with emphysema and
chronic obstructive pulmonary disease. It is caused by rupture of a large bulla.

Causes of secondary spontaneous pneumothorax

1. Diseases of the airways:

 • Chronic obstructive pulmonary disease (COPD) - most common cause of 20 pneumothorax.

 • Acute severe asthma
 • Cystic fibrosis

2. Infections of the lung, including:

 • Staphylococcal pneumonia.
 • Lung abscess.
 • Tuberculosis
 • Pneumocystis pneumonia

3. Malignancy

 • Bronchogenic carcinoma.
 • Metastatic lung cancer (sarcoma and lymphoma)

4. Interstitial lung disease

 • Sarcoidosis
 • Histiocytosis X.
 • Lymphangioleiomyomatosis.
 • Idiopathic pulmonary fibrosis

5. Connective tissue /Collagen diseases:

 • Systemic sclerosis
 • Ehlers-Danlos syndrome
 • Scleroderma.
 • Marfan’s syndrome

6. Miscellaneous

 • Endometriosis (Catamenial pneumothorax)

TRAUMATIC PNEUMOTHORAX

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A traumatic pneumothorax may result from either blunt trauma or penetrating injury to the chest wall. The most
common mechanism is due to penetration by the sharp ends of a fractured rib, which damages lung tissue. It may
be classified as open or closed.

Open pneumothorax:
There is a passage from the external environment into the pleural space through the chest wall.
When air is drawn into the pleural space through the opening, it is referred to as a sucking chest wound.

Closed pneumothorax:
This is when the chest wall remains intact.

Causes of Traumatic pneumothorax

1. Blunt trauma to the chest wall may result in a lung laceration from a rib fracture i.e. fracture ribs with
lung puncture/valvular lung puncture causing tension pneumothorax.
2. Ruptured trachea or main bronchus causing tension pneumothorax.
3. Rupture of the oesophagus or stomach.
4. Penetrating/open chest wound causing a sucking pneumothorax.
5. Surgical operations of the thorax causing iatrogenic pneumothorax.

IATROGENIC PNEUMOTHORAX

Procedures often complicated by pneumothorax include:

1) Thoracocentesis.
2) Placement of a percutaneous vein catheter (subclavian, internal jugular) for central venous pressure
monitoring or hyperalimentation.
3) Operations on the chest wall, neck, back or upper abdomen.
4) Lung or pleural biopsy.
5) Brachial plexus block
6) Arteriography
7) Intercostal nerve block
8) Assisted/artificial ventilation

CLINICAL FEATURES OF PNEUMOTHORAX

1. Sudden onset of chest pain referred to the shoulder or arm of the involved side.
2. Dyspnoea (sudden onset).
3. Tachypnoea.
4. Cough.
5. Hyper-resonant affected hemithorax/increased percussion note.
6. Ipsilateral decreased chest wall motion/movement.
7. Air in the tissues (surgical emphysema) affecting the chest wall, neck and face.
8. Decreased/absent breath sounds on the affected side.
9. Decreased vocal resonance and vocal fremitus.
10. Pleural rub.
11. Tachycardia
12. Mediastinal shift away from the involved side in the case of tension pneumothorax.
13. The trachea may be pushed over to the opposite side

INVESTIGATIONS

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1. P/A chest x-ray usually diagnostic - reveals retraction of the lung from the parietal pleura.
2. CT scan gives an accurate estimate of size of pneumothorax and is useful for assessment of remaining
lung parenchyma and contralateral lung.

TENSION PNEUMOTHORAX

• Results if the pleural tear is valvular allowing air to be sucked into the pleural cavity at each inspiration
but preventing air returning to the bronchi on expiration
• May occur as a result of: fractured rib, ruptured trachea or bronchus, or penetrating wound on the chest
producing sucking wound

See the radiograph of Tension pneumothorax Clinical Features

1. Rapidly increasing dyspnoea

2. Tracheal deviation to the opposite sidet3. Displacement
of the apex beat
4. Reduced chest expansion on the affected side
5. Bulging of intercostal space on the affected side
6. Hyper-resonant percussion note on the affected side
7. Reduced/ absent air entry on the affected side

TREATMENT OF PNEUMOTHORAX

1. Emergency Treatment (esp. for tension pneumothorax)

 • Treat with immediate decompression.

 • Pad and strap the sucking wound to prevent more air from entering the pleural cavity
 • Don’t wait for an X-ray
 • Take a 12G cannula/the largest needle you can find and insert into 2nd or 3rd intercostal space mid
clavicular line
 • The air will hiss out of the needle, trachea will return to the midline, and the patient will immediately
breathe more easily.

2. Underwater seal drainage (chest drain)

 • Inserted into 5th intercostal space mid axillary line

 • In most cases of primary pneumothorax, air leakage stops within 48 hours or so, after which the drain can
be removed.
 • Secondary pneumothorax may not settle rapidly due to poor quality of the underlying lung tissue.
 • Observe for 1-2 weeks to see if the air leak stops spontaneously.
 • Videothoracoscopy is done if leakage does not stop, to inspect the lung for a leaking bulla and to close it
by stapling.

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 3. Antibiotic
4. Analgesics
5. Chest physiotherapy to encourage deep breathing
6. Thoracotomy and repair is performed if
pneumothorax persists

Topic 2: Haemothorax

HAEMOTHORAX

DEFINITION

Haemothorax is the accumulation of blood in the pleural cavity. Massive haemothorax is accumulation of ≥
1500ml of blood in the pleural cavity.

AETIOLOGY (CAUSES)

• The primary cause of haemothorax is sharp or blunt trauma to the chest.

• Iatrogenic haemothorax often occurs as a complications of:

 1. Cardiopulmonary surgery,
 2. Placement of subclavian or jugular catheters and
 3. Pleural biopsies.

• Spontaneous haemothorax is generally caused by:

 1. Rupture of pleural adhesions,

 2. Neoplasms invading the pleural cavity,
 3. Pleural metastases, and
 4. As a complication of anticoagulant therapy.

The bleeding may be as a result of: -

 1. Rupture of parietal vessels (intercostal, internal mammary), when continued haemorrhage is likely.
 2. Rupture of pulmonary vessels in association with lung trauma, when low pressure haemorrhage usually
ceases spontaneously.

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  3. Diaphragmatic and sub-diaphragmatic trauma, when blood from a ruptured diaphragm and/or upper
abdominal viscera is sucked into the pleural cavity.
 4. Rarely due to an unusual manifestation of endometriosis.
 5. Other benign reasons for haemothorax include:
  Ruptured pulmonary cysts
  Rupture of pulmonary arteriovenous fistulae
  Ruptures of aneurysmal disease within the subclavian
  Rupture of the innominate and aortic vessels
  Rupture of aortic aneurysm.

CLINICAL FEATURES

If a patient has a large haemothorax, the patient will have the following features:
• Breathlessness (difficulty in breathing)
• Chest pain
• Shock:

  Sweaty, pale, cool and clammy skin.

  Rapid, thready pulse.
  Collapsed neck veins
  Cyanosis

• Affected side of chest is stony dull to percussion.

• Reduced chest movement and expansion on the affected side
• Reduced or absent breath sounds.

INVESTIGATIONS/Diagnosis

1. Chest x-ray

  A diffuse opacity of the affected half of the thorax, more clearly seen in an erect film.
  Obliteration /blunting of the costophrenic angle

2. Ultrasonography: is more sensitive than chest X-ray in detecting haemothorax. Can provide rapid, reliable results at
the bedside
3. CT scan: can detect much smaller amounts of fluid than plain chest X-ray.
4. MRI can be used to differentiate between a haemothorax and other forms of pleural effusion.
5. Thoracocentesis:

  The diagnosis is established by thoracocentesis (aspiration of the pleural fluid)

  A haemothorax is defined as having a haematocrit of at least 50% of that found in the patient`s blood.

MANAGEMENT

• Simultaneous restoration of blood volume (fluid resuscitation) and decompression with a chest drain
(tube thoracostomy)
• Continuing blood loss in excess of 200ml/hour and need for persistent blood transfusion may require
urgent thoracotomy within the first few hours, or a video-assisted thoracoscopic surgery (VATS)
• If blood is not drained urgently, it will clot, organize, and prevent lung re-expanding. When this happens,
it can only be made to expand again by decorticating it at thoracotomy.
• Additional treatment options include:
• Antibiotics to reduce the risk of infection

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• Fibrinolytic therapy to break down clotted blood within the pleural space. Streptokinase or urokinase is
given directly into the pleural space 7 to 10 days after the injury.
• Thoracostomy
• This is the insertion of a drain (chest tube) into the pleural cavity to remove the blood.
• Large-bore chest drain with a diameter of 24 -36 F should be used so as to reduce the risk of blood clots
obstructing the tube.
• Drainage is essential because re-expansion of the lacerated lung compresses the torn vessels and reduces
further blood loss.
• Drainage will also allow the mediastinal structures to return to the midline and relieve compression of the
contralateral lung.

COMPLICATIONS

1) Are more likely to occur if blood is not adequately drained from the pleural cavity.
2) If infected, empyema will result.
3) A dense fibrothorax will result, if retained blood irritates the pleura causing scar tissue formation.
4) Entrapped lung results from fibrothorax

Topic 2: Cardiac Tamponade

CARDIAC TAMPONADE

DEFINITION
• Cardiac tamponade is compression of the heart caused by fluid collecting in the pericardium (e.g.
bleeding into the patient’s pericardial cavity).
• Cardiac tamponade puts pressure on the heart and keeps it from filling properly, with resultant dramatic
drop in blood pressure that can be fatal.

CAUSES
• Penetrating chest injury - usually.
• Blunt chest injury – occasionally.

PATHOLOGY
• As blood leaks out of the injured heart, it accumulates in the pericardial sac. Because the pericardium is
not acutely distensible, the pressure in the pericardial sac will rise to match that of the injured chamber. Since
this pressure is usually greater than that of the right atrium, right atrial filling is impaired and right ventricular
preload is reduced.
• This leads to decreased right ventricular output and increased central venous pressure (CVP).
• Increased intrapericardial pressure also impedes myocardial blood flow, which leads to sub-endocardial
ischaemia and a further reduction in cardiac output.
• This vicious cycle may progress insidiously with injury of vena cava or atria, or precipitously with injury
of either ventricle.
• With acute tamponade, as little as 100ml of blood within the pericardial sac can produce life-threatening
haemodynamic compromise.

CLINICAL FEATURES
• Patients usually present with a penetrating injury in proximity to the heart.
• Hypotension/shock (rapid weak pulse).
• Grossly distended neck veins (raised JVP).
• Elevated central venous pressure (CVP).
• Severe distress.
• Apex beat can neither be felt nor seen (faint heart sounds).

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• The classic findings of Beck’s triad –
1. Hypotension
2. Distended neck veins
3. Muffled/faint heart sounds and sometimes pulsus paradoxus (abnormally large decrease in stroke volume,
systolic blood pressure and pulse wave during inspiration)
 Normally, the peripheral pulse becomes stronger on inspiration, because the lower intrathoracic pressure
increases the venous return.
 In pulsus paradoxus the peripheral pulse is stronger on expiration.

INVESTIGATIONS
• Ultrasonography using a subxiphoid of parasternal view is extremely helpful if the finding is clearly
positive; shows diminished excursion of the borders of the heart.
• X-ray shows a widening of the heart shadow, especially in the cardiophrenic angle.
• CT Scan/MRI

MANAGEMENT
• If critically ill with suspected temponade perform ‘blind’ pericardiocentesis and call cardiothoracic or
general surgeons to consider emergency thoracotomy.
Insert a needle into the patient’s pericardial cavity from just under his xiphoid.
Alternatively, and less satisfactorily, approach it through the 4th left intercostal space 5cm from the
midline, so as to avoid his internal mammary vessels.
• Refer the patient for urgent thoracotomy
• Pericardial sac is opened and blood is evacuated
• Cardiac laceration is repaired

Topic 2: Surgical Emphysema

SURGICAL EMPHYSEMA

DEFINITION
Surgical Emphysema is a pathological accumulation of air in the tissues.
GENERAL CONSIDERATIONS
Surgical emphysema is common, but it is rarely serious in itself, and soon disappears.
Air in the mediastinum is much more serious and may indicate the rupture of a bronchus.

CAUSES
1. Chest trauma
2. Rib fracture – when a fractured rib punctures a lung
3. Pneumothorax
4. Bowel perforation

CLINICAL FEATURES
Surgical emphysema is manifested by:
• Alarming swelling of the face.
• Crepitant swelling under the skin and muscles of the neck.
• Sometimes swelling may extend upwards from the pelvis to the forehead.

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MANAGEMENT
1. If the eyelids are swollen and the patient has difficulty seeing, he can milk the air out of them.
2. Where necessary, treat the underlying cause – this may be a leak from a lung that requires an underwater seal.
3. Small quantities of air can be removed by massaging it into a few pockets, and then aspirating it with a syringe and
needle.
4. If surgical emphysema spreads or is life-threatening, tracheostomy can be performed. This abolishes coughing and
the large rises in intrathoracic pressure it causes.
5. If air escapes into the mediastinum and pleura from tears in the trachea, oesophagus, or bronchi, it may press on the
veins at the base of the neck and congest the veins of the head.
6. Insert an underwater seal drain and remove the air trapped in the pleura. This may cure the patient

Topic 2: Summary

In this topic you have learnt the following:

1. Fractures of the ribs: clinical features, treatment

2. Flail chest: pathology, clinical features and management
3. Pneumothorax: types, clinical features, management
4. Haemothorax: causes, clinical features, management
5. Cardiac tamponate: causes, pathology, clinical presentation, and management
6. Surgical emphysema: causes, clinical features and management

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Topic 3: LUNG TUMOURS

LUNG TUMOURS

Learning objectives

1) Classify lung tumours

2) State the aetiological factors for lung cancer
3) Describe the pathology of lung cancer
4) Outline the clinical features of lung cancer
5) State the differential diagnosis of lung cancer
6) Investigate lung cancer
7) Outline the treatment of lung cancer

CLASSIFICATION

1. BENIGN TUMOURS

  Adenoma
  Carcinoid (sometimes malignant)
  Hamartoma
  Haemangioma

2. MALIGNANT TUMOURS
a) Primary

  Squamous cell carcinoma

  Adenocarcinoma
  Small cell carcinoma
  Large cell carcinoma
  Carcinoid

(b) Secondary

  Carcinoma (esp. from breast and kidneys)

  Sarcomas (esp. from the bone)
  Melanoma

Topic 3: LUNG CANCER

LUNG CANCER

AETIOGICAL/RISK FACTORS

1. Cigarette smoking: strongly positive association with cigarette smoking (polycyclic aromatic
hydrocarbons plus nicotine related carcinogens).
2. Radon exposure.
3. Genetic predisposition.
4. Occupational factors e.g. exposure to: -

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  i. Polycyclic aromatic hydrocarbons
 ii. Asbestos
 iii. Arsenic
 iv. Nickel
 v. Silica
 vi. Coal tar
 vii. Aluminium production
 viii. Coal gasification
 ix. Exposure to paints
 x. Chromium compounds
 xi. Bischloromethyl ether

PATHOLOGY

I. MACROSCOPIC APPERANCE

  About half arise from the main bronchi (particularly squamous cell carcinoma) and 75% are visible at
bronchoscopy
  The growth may arise peripherally (particularly adenocarcinoma) and some appear to be multifocal
  The bronchial wall is narrowed & ulcerated
  Surrounding tissue is invaded by pale tumour mass which may undergo necrosis, haemorrhage and abscess
formation
  The lung segment distal to the occlusion may show collapse, bronchiectasis or abscess formation

II. MICROSCOPIC APPEARANCE

a) Squamous cell carcinoma

  Accounts for 40%

  Mostly poorly differentiated
  Arises in an area of squamous metaplasia of bronchial epithelium

b) Adenocarcinoma

  Accounts for 30%

  Very fast growing tumour
  Often found in the periphery of the lung
  Associated with a large fibrotic (desmo-plastic) reaction
  Often occurs in non-smokers

c) Small cell carcinoma

  Also known as oat cell carcinoma

  Account for 20%
  Has neuro-endocrine properties and produces peptides giving rise to Paraneoplastic syndromes
  Tumour comprises of small cells with little cytoplasm
  Has poor prognosis; has general spread by the time of diagnosis
  Best treated by chemotherapy

d) Large cell carcinoma

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   Accounts for 10%
  Large cells containing abundant cytoplasm and without evidence of squamous or glandular metaplasia

SPREAD
1. LOCAL SPREAD

  Pleura
  Left recurrent laryngeal nerve
  Pericardium
  Oesophagus (Bronchio-oesophageal fistula)
  Sympathetic chain (Horner’s syndrome)
  Brachial plexus (Pancoast’s syndrome)

2. LYMPHATIC SPREAD

  Mediastinal and cervical lymph nodes

  Compression of superior vena cava by massive mediastinal L/nodes produces gross oedema and cyanosis
of the face and upper limbs (superior vena cava syndrome)

3. HAEMATOGENOUS

  Brain, liver and suprarenal glands

4. TRANS-COELOMIC

  Pleural seedlings and effusion

Topic 3: LUNG CANCER - Clinical Features

CLINICAL FEATURES

 Predominance in males compared to females (6:1) but the ratio is decreasing as women tend to smoke
more
 When the tumour arises in a large bronchus, symptoms arise early, but tumours originating in a peripheral
bronchus can attain a very large size without producing symptoms.
Lung cancer presents in many different ways. Most commonly, symptoms reflect:
 Local involvement of the bronchus
 Spread to the chest wall or mediastinum
 Distant blood-borne spread
 Non-metastatic paraneoplastic syndromes

SYMPTOMS
1. Cough

  Is the most common early symptom.

  It is often dry but sputum may be purulent if there is secondary bacterial infection.
  A change in the character of the ‘regular’ cough of a smoker, particularly if it is associated with other new
respiratory symptoms, should always alert the clinician to the possibility of bronchial carcinoma.

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2. Haemoptysis

  Is a common symptom, especially in tumours arising in central bronchi

  Occasionally, central tumours invade large vessels, causing massive haemoptysis which may be fatal.
  Repeated episodes of scanty haemoptysis or blood-streaking of sputum in a smoker are highly suggestive
of bronchial carcinoma and should always be investigated.

3. Pneumonia 2o Bronchial Obstruction

  Is often the first clinical manifestation of a lung cancer, even when the degree of obstruction is insufficient
to cause collapse
  Recurrent pneumonia at the same site or pneumonia which is slow to respond to treatment, particularly in a
smoker, should immediately suggest the possibility of bronchial carcinoma.

4. Lung abscess 2o to Bronchial Obstruction

  May sometimes develop behind an obstructive lesion.

5. Breathlessness/Dyspnoea

  May reflect occlusion of a large bronchus, resulting in collapse of a lobe or lung or the development of a
large pleural effusion.
  In other circumstances is a late symptom unless the patient is coincidentally suffering from chronic
bronchitis and emphysema

6. Stridor (a harsh inspiratory noise)

  Occurs when the lower trachea, carina of main bronchi are narrowed by the primary tumour or by
compression from malignant enlargement of the subcarinal and paratracheal lymph nodes.

7. Pleural pain

  Usually indicates malignant invasion of the pleura, although it can occur with distal infection/infective
pleurisy.
  Involvement of the intercostal nerves/the brachial plexus may cause pain in the chest along the appropriate
nerve root distribution/an upper limb.

8. Pancoast’s syndrome

  Pain in the shoulder and inner aspect of the arm caused by involvement of the lower part of the brachial
plexus.

9. Dysphagia

  Due to mediastinal spread.

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10. Blood-borne metastases

  Focal neurological defects.

  Headaches & epileptic seizures.
  Hepatomegaly, jaundice, ascites and liver failure.
  Anorexia.
  Bone pain & pathological fractures.
  Skin nodules which may be tender.
  Haematuria.

11.Endocrine

  Inappropriate ADH secretion causing hyponatraemia (small cell carcinoma).

  Ectopic ACTH secretion (small cell carcinoma).
  Hypercalcaemia due to secretion of PTH-related peptides (small cell carcinoma).
  Carcinoid syndrome (flushing, diarrhoea, heart failure, emesis and bronchoconstriction) due to production
of serotonin & kallikrein
  Gynaecomastia.

Non-metastatic extrapulmonary symptoms

12. Neurological

  Polyneuropathy
  Myelopathy
  Cerebellar degeneration
  Neurological headache.
  Blurred vision.
  Nausea.
  Diplopia.
  Decreased consciousness.
  Ataxia.

SIGNS
Examination is usually normal unless there is significant bronchial obstruction, or the tumour has spread to:

  Pleura.
  Mediastinum or
  Supraclavicular nodes.

• A tumour obstructing a large bronchus produces the physical signs of collapse (or occasionally obstructive
emphysema) and may give rise to pneumonia that is characterised by a relative absence of physical signs and a slow
response to treatment.
• Wheeze

 A monophonic or unilateral wheeze which fails to clear with coughing suggests the presence of a fixed bronchial
obstruction.

• Stridor

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  The presence of stridor indicates obstruction at or above the main carina.

• A hoarse voice associated with an ineffectual or ‘bovine’ cough usually indicates left recurrent laryngeal nerve
palsy.
• Phrenic nerve paralysis causes unilateral diaphragmatic palsy and hence dullness to percussion and absent breath
sounds at a lung base.
• Involvement of the pleura may produce a pleural rub or signs of pleural effusion.
• Bronchial carcinoma is also the most common cause of the superior vena cava syndrome, which presents initially
as:

 i. Bilateral engorgement of the jugular veins and later as

 ii. Oedema affecting the face, arms and conjunctivae.

• Horner’s syndrome

 Caused by cancer in the apex of the lung (‘superior sulcus tumour’) manifesting as:
 i. Ipsilateral partial ptosis
 ii. A small pupil and
 iii. Anihypohydrosis of (loss of facial sweating on one side) due to involvement of the sympathetic chain
at or above the stellate ganglion.
• Digital clubbing is often seen and may be associated with a syndrome called Hypertrophic Pulmonary
Osteoarthropathy (HPOA), characterised by periostitis of the long bones, most commonly the distal tibia, fibula, radius and
ulna: This gives rise to pain and tenderness over the affected bones and often pitting oedema over the anterior aspect of the
shin.
• Other general features of cancers such as:

  Cachexia
  Anaemia

Topic 3: LUNG CANCER - DDx, Investigations & Treatment

DIFFERENTIAL DIAGNOSIS

1. Infections:

  Pulmonary tuberculosis.
  Primary lung abscess (e.g., due to aspiration).
  Secondary lung abscess (e.g., preceding pneumonia, pyaemia, sepsis).
  Bronchiectasis
  Fungal infections (e.g., aspergillosis, mucormycosis)

2. Non-infectious Causes:

  Pneumoconiosis (e.g., simple coal-worker’s pneumoconiosis, silicosis, asbestosis).

  Metastatic lung tumours.
  Wegener’s granulomatosis.
  Pulmonary infarction.
  Congenital cysts.
  Idiopathic pulmonary fibrosis.

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3. Others

  Pulmonary thromboembolism.
  Left ventricular failure.
  Mitral stenosis.
  Trauma.
  Foreign bodies.
  Primary pulmonary hypertension.
  Haemorrhagic diathesis.

INVESTIGATIONS

1. Chest X-ray and thoracic CT scans/MRI may show:

  Opacities in the lungs & enlargement of the hilar L/nodes

  Paralysis of one side of the diaphragm due to involvement of the phrenic nerve

2. Abdominal CT scan/MRI to detect liver and suprarenal glands metastasis

3. Cytology of the sputum may identify malignant cells
4. Bronchoscopy and biopsy: bronchoscopy may reveal an ulcerating or exuberant growth & involved L/nodes may
widen the carina. Brushings and washings may be taken for cytology in addition to biopsy
5. Fine needle aspirate cytology (FNAC) of peripherally placed tumours under X-ray guidance
6. Mediastinoscopy: performed through a small suprasternal incision. May be indicated to remove L/nodes from the
region of the carina for histological examination to aid in staging
7. Pulmonary function tests to determine lung reserve and hence capacity to withstand surgery
TREATMENT

1. SURGERY
Possibility of curative surgery is assessed by:

  Biopsy of all suspicious L/nodes to exclude spread

  Radiological imaging
  Bronchoscopy
  Pulmonary function tests

Surgery is performed in small tumours with no spread. Interventions include:

• Removal of a lobe or
• Removal of a whole lung

2. RADIOTHERAPY
May give useful palliation though may not prolong life. However it can:

 1) Stop distressing haemoptysis

 2) Relieve pain from bone metastasis
 3) Give relief to patients with irritating cough
 4) Produce improvement in patients with acute superior vena cava obstruction

Topic 3: Summary

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In this topic you have learnt the following about lung tumours:
1) Classification of lung tumours
2) Aetiological factors for lung cancer
3) The pathology of lung cancer
4) The clinical features of lung cancer
5) The differential diagnosis of lung cancer
6) Investigations carried out in lung cancer
7) Treatment of lung cancer

Topic 4: BREAST CONDITIONS


 OBJECTIVES
 By the end of this topic, you should be able to:

 1. Take a comprehensive history of a patient with a breast condition
 2. Demonstrate understanding of breast examination techniques
 3. Outline the types of nipple discharges
 4. state the investigations for breast conditions
 5. Describe presentation and management of mastitis
 6. Describe benign breast swellings
 7. Describe the predisposing factors, clinical features, and management of carcinoma of the breast

BREAST CONDITIONS

CONTENT

1. History taking
2. Breast examination
3. Types of nipple discharges
4. Investigations
5. Mastitis
6. Benign breast swellings
7. Carcinoma of the breast

HISTORY TAKING

1. AGE: Young women will only very rarely have cancer, but over the age of 70 most breast lumps turn out to be
malignant.
2. ONSET: Inflammatory breast swelling have an acute onset whereas tumours have an insidious onset
3. PAIN: Inflammatory conditions are painful at an early stage whereas tumours are painless at an early stage
4. BREAST FEEDING: lactating mothers are more likely to suffer from breast engorgement mastitis and breast
abscess compared to non-breast feeding women
5. NIPPLE DISCHARGE: Colour and if bloody or blood stained
6. PREVIOUS PREGNANCIES:

 • How many children has the patient had?

 • Were the children breast-fed and, if so, for how long?
 • Parity and breast-feeding reduce the incidence of breast cancer e.g. mother of five who breastfed all her
children is less likely to have breast cancer than a nulliparous woman of the same age.

7. MENESTRUAL PATTERN:

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   What is the menstrual pattern? (Regularity, duration and quantity of bleeding).
  Breast symptoms which alter with the menstrual cycle are highly likely to be associated with benign
disease.

8. MEDICATIONS/HORMONES

 Exposure to estrogen increases risk of development of breast cancer:

  Early menarche
  Late menopause
  Nulliparity or first child after the age of 30 years
  Hormonal Replacement Therapy
 NB: Oophorectomy is protective against cancer of the breast

9. DIET AND LIFESTYLE

  Some studies and historical data suggest that high fat diets increase breast cancer risk, but the results of
controlled studies are inconsistent

10. RADIATION

  Radiation exposure from nuclear explosion or medical diagnostic or therapeutic procedures prior to age 40
  Women with mantle radiation/chemo for Hodgkin's before age 15 have markedly increased risk of
developing cancer of the breast

11. FAMILY HISTORY (Familial breast cancer genes)

  Family Characteristics
 • 2 or more family members under age 50 with breast cancer
 • Both breast and ovarian cancers in family
 • Male breast cancer

Topic 4: Breast Examination

EXAMINATION

 Routine breast examination especially in women above the age of 30 is vital to detect any breast
pathology, most importantly, carcinoma. The inspection and palpation of the breast are the mainstays of the
breast examination.
 The physical examination provides an ideal time to teach the patient how to perform breast self-
examination. The patient should be advised to examine herself in the mirror, looking for skin changes or
dimpling, and then carefully palpate all quadrants of the breast.
 The examination should be repeated at the same time each month, preferably 1 week after the initiation of
the menses, when the breasts are least nodular. Postmenopausal women should perform self-examination on the
same day each month.

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 POSITIONS for
breast examination

 The patient must be fully undressed to the waist, resting comfortably on an examination couch with her
upper body raised at 450 to the legs.
 This position is the best compromise between lying flat, which makes the breasts fall sideways, and
sitting upright, which makes the breasts pendulous.

1. Patient is sitting, arms at sides.

 Perform visual inspection in good light, looking for lumps or for dimpling or wrinkling of skin.

2. Patient is sitting, hands pressing on hips so that pectoralis muscles are tensed.

  The patient places her hands on her hips and stretches her elbows backwards so as to tighten the muscles
across the chest.
  Pressing on the hips and contracting pectoralis major may accentuate attachment of the lump.
  This may reveal a previously invisible swelling.
  Repeat visual inspection

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3. Patient is sitting, arms above head/raising the arms above the head. Ask the patient to slowly raise her arms
above her head.

  This may accentuate or make obvious lumps or dimples

  Skin changes may then become more apparent, particularly tethering to a carcinoma.
  Inspect the axillae

4. Patient is sitting and leaning forward.

  The patient stretches her arms out in front of her and leans forward so that the breasts may be inspected in
the dependent position.
  Hands on examiner’s shoulders, the stirrups, or her own knees.
  Bending forward: deep attachment may cause failure of breasts to “fall away” equally from anterior chest
wall.

5. Patient is supine, arms relaxed at sides

INSPECTION

Stand or sit directly in front of the patient “square”, inspect both breasts and look for the following features:

  Breast skin colour.

  Breast contour - size, symmetry, lumps & dimples.
  Nipple levels.
  Nipple retraction.
  Nipple & areolar eczema & ulceration.
  Areolar pigmentation.
  Peau d’orange – late sign of breast cancer.
  Cancer en cuirass – rigidity of the entire skin of the breast and sometimes the chest wall and neck – late
sign of breast cancer

BREAST SKIN CHANGES

1. Redness – inflammatory conditions
2. Ecchymosis – breast trauma
3. Ulcerations – due to direct invasion of the skin by cancer
4. Peau d’orange- oedema caused by obstruction of skin lymphatics by cancer cells

Peau d’orange

BREAST CONTOUR
1. Size and symmetry

  It is quite normal for there to be a difference between the sides.

  Usually one breast (often the left one) is larger than the other.
  However, any marked size difference of recent onset is likely to be caused by significant pathology.

2. Other Changes

  Dimpling, skin retraction

  Abnormal contour or depressions
  Any deviation of the nipples from their normal position.

Asymmetrical breasts

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AREOLAR AND NIPPLES
 The colour of the nipples and areolae changes with age, and there is darkening during pregnancy.
 The areolar skin is naturally corrugated with small nodules known as Montgomery’s tubercles.
 Nipple inversion
 Bilateral nipple inversion with transverse slit is a sign of duct ectasia
 Evidence of nipple discharge or bleeding
 Duplication: There may be accessory nipples along the mammary line from axilla to groin, or visible
ectopic breast tissue in the anterior axillary fold.

Nipple inversion

Topic 4: Breast Examination

PALPATION

 The breast should be palpated with the flat of the fingers and not with the palm of the hand.
 The patient is supine and the body is rotated so that the nipple is at the highest point on the chest wall.
 To accomplish this the arm and shoulder of the potentially affected side are placed on a pillow.

 The examination is performed in some orderly sequence such as:

 1. Affected breast.
 2. Potentially affected axilla.
 3. Potentially affected side of neck and deep cervical lymph chain.
 4. Opposite breast.
 5. Opposite axilla.
 6. Opposite side of the neck.

 Breast palpation is performed quadrant for quadrant initially with the flat of the hand and any lump felt in this way
must be considered highly suspicious of malignancy until proven otherwise.
 Next palpation with fingers and thumb is performed for any lump, not only in the breast, and is accurately
described as follows: Site, Shape, Size, Local temperature, Surface, Mobility (Tethering /attachments), Edges, Consistency,
Tenderness, and Transillumination.

THE NIPPLE
 If there is nipple inversion, it may be possible to evert it by gentle squeezing its base or by asking the
patient to do it for you.
 Nipple inversion that is easily everted is not an abnormality.
 If the nipple will not evert, there is likely to be underlying disease.
 Unilateral inversion is more significant than bilateral inversion.
 If there is said to be a discharge, it may be possible to express it by gently pressing the areola around the
base of the nipple and observing whether any fluid comes from one or many duct orifices.
 The character of the fluid should be noted.
 Nipple discharges may be: Red, White, Creamy yellow or Watery.

THE AXILLA
 Stand on the patient’s right side.
 Take hold of her right elbow with your right hand and let her forearm rest on your right forearm.
 Place your left hand flat against the chest wall and feel for any glands that may lie in the central or medial
aspects of the right axilla by sweeping the tips of your fingers across and from the top to the base of the axilla to
catch the glands against the chest wall.

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 To reach the apex of the axilla you will have to push the tips of your fingers upwards and inwards.
 Explain to the patient that you must push firmly to examine the axilla thoroughly and that this may cause
discomfort
 Next move your left hand anteriorly over the edge to the pectoralis minor muscle and downwards into the
axillary tail and behind the edge of the pectoralis major muscle.
 Turn your hand (or change hands) to feel the subscapular glands on the posterior wall of the axilla, and
finally feel the lateral aspect of the axilla in case there are any brachial glands level with the neck of the humerus.
 To palpate the left axilla, lean across the patient, hold her left elbow with your left hand and use your
right hand to feel the axilla.
 If it is difficult to feel the axilla in this way, move round to her left side.

NB: Local examination of the breast must always be accompanied by the usual general examination but
particular emphasis is placed on the skeleton, lungs and liver.

TYPES OF NIPPLE DISCHARGES

1. BLOOD STAINED

  Duct papilloma, when blood arises from a single duct

  Intraductal carcinoma
  Paget’s disease
  Invasive carcinoma

2. CLEAR

  Intraductal papilloma

3. MULTICOLOURED

  Duct ectasia (discharge commonly yellow, brown or green)

4. MILKY

  Galactorrhoea- may follow lactation

  Can be drug induced
  Manifestation of hyperprolactinaemia

5. PURULENT

  Breast abscess

INVESTIGATIONS

IMAGING
Mammography
• Requires compression of the breast between two plates and is uncomfortable.
• Two views are usually obtained: Oblique and Craniocaudal
• Mammography allows the detection of mass lesions, areas of parenchymal distortion, and
microcalcification.
• Mammography is recommended for women above 35 years old because the breasts in women below 35
years of age are relatively radiodense.

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Ultrasonography
• Cysts show up as transparent objects
• Other benign lesions tend to have well-demarcated edges
• Cancers usually have an indistinct outline and absorb sound, resulting in a posterior acoustic shadow.

Magnetic resonance imaging (MRI)

• MRI is an accurate way of imaging the breast
• It has a high sensitivity for breast cancer
• Is of value in demonstrating the extent of invasion of the cancer.
• Useful in determining whether a mammographic lesion at the site of previous surgery in a conserved
breast is due to scar or recurrence.

CYTOLOGY AND BIOPSY

Fine-needle aspiration cytology (FNAC)
• Needle aspiration can differentiate between solid and cystic lesions
• If the lesion is cystic, the fluid is aspirated, and if not blood-stained, discarded.
• Aspiration of solid lesions is performed with a 21- or 23-gauge needle attached to a syringe. The needle is
introduced into the lesion and suction applied. Multiple passes are made through the lesion.
• The plunger is then released and the material spread on to microscope slides. These are either air-dried or
fixed in alcohol and then stained for microscopy.

Core biopsy
• A core biopsy is a procedure where a wide bore needle (14-gauge) is used to take a sample of suspicious
tissue from a mass or lump.
• A special mechanical gun is used in combination with the needle.
• Core biopsy can be guided by hand palpation, or ultrasound guided (mass lesions), or stereotactic-guided
(impalpable calcifications).
• Stereotactic uses x-ray equipment and a computer to guide the needle.
• Image-guided core biopsy is the most accurate and efficient technique for diagnosis of breast masses.

Open biopsy
• Involves cutting into the breast and removing all or part of the abnormal tissue or lump and often a small
amount of normal-looking tissue (margin).
• Often involves wide local excision or lumpectomy.
• An open biopsy should only be done in patients who have already been investigated by imaging, FNAC
and core biopsy.

Topic 4: Breast conditions -Mastitis

MASTITIS

Overview

Mastitis is an inflammation of breast tissue that sometimes involves an infection. The inflammation results in
breast pain, swelling, warmth and redness. It might also present with fever and chills.
Mastitis most commonly affects women who are breast-feeding (lactation mastitis). But mastitis can occur in
women who aren't breast-feeding and in men.
Lactation mastitis poses difficulty in caring for the baby. Sometimes mastitis leads a mother to wean her baby

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before she intends to. But continuing to breast-feed, even while taking an antibiotic to treat mastitis, is better for

the mother and her baby.

Causes

Milk that is trapped in the breast is the main cause of mastitis.

A blocked milk duct. If a breast doesn't completely empty at feedings, one of the milk ducts can become clogged.
The blockage causes milk to back up, leading to breast infection.
Bacteria entering the breast. Bacteria from the skin's surface and baby's mouth can enter the milk ducts through a
crack in the skin of the nipple or through a milk duct opening. Stagnant milk in a breast that isn't emptied
provides a breeding ground for the bacteria. Most cases are caused by Staphylococcus aureus.

Risk factors

Risk factors for mastitis include:

• Previous bout of mastitis while breast-feeding
• Sore or cracked nipples — although mastitis can develop without broken skin
• Wearing a tightfitting bra or putting pressure on your breast when using a seat belt or carrying a heavy
bag, which may restrict milk flow
• Improper nursing technique
• Becoming overly tired or stressed
• Poor nutrition
• Smoking

Clinical features

Signs and symptoms of mastitis can appear suddenly. They may include:
• Pain or a burning sensation continuously or while breast-feeding
• Breast swelling
• Generally feeling ill
• Skin redness, often in a wedge-shaped pattern
• Breast tenderness or warmth to the touch
• Thickening of breast tissue, or a breast lump
• Fever of 38 degrees Celsius or greater
• Presents first as a generalized cellulitis but later an abscess will form.

Treatment

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 During the
cellulitic stage,
the patient
should be
treated with an
appropriate
antibiotic, for
example
flucloxacillin
or co-amoxiclav.
Support of the
breast, local
heat and
analgesia will
help to relieve
pain. Breast
feeding may continue if the patient can manage.
If pus is present, repeated aspiration under antibiotic cover
should be performed. This often allows resolution
without the need for an incision scar, and also allows the patient to continue breastfeeding.
The presence of pus can be confirmed by needle aspiration. A sample should be taken for culture and sensitivity.

Complications
Mastitis that isn't adequately treated or that is due to a blocked duct can cause a collection of pus (abscess) to
develop in the breast. An abscess usually requires surgical drainage.
To avoid this complication, treatment should be given as soon as signs or symptoms of mastitis are detected.

Prevention
• Fully drain the milk from your breasts while breast-feeding.
• Allow your baby to completely empty one breast before switching to the other breast during feeding.
• Change the position you use to breast-feed from one feeding to the next.
• Make sure your baby latches on properly during feedings.
• If you smoke, ask your doctor about smoking cessation.

Topic 4: Benign Breast Swellings

BENIGN BREAST SWELLINGS

There are many possible causes of non-cancerous (benign) breast lumps. Two of the most common causes of
benign single breast lumps are cysts and fibroadenomas. In addition, several other conditions can present
themselves as lumps.

Breast Abscess

A breast abscess is a pocket of pus that causes inflammation and a sore lump in the breast. Other symptoms
include fever, and tiredness.
Operative drainage of a breast abscess is carried out if there is marked skin thinning and can be done under local
anaesthesia.
The usual incision is sited radially over the affected segment. Circumareolar incision is preferred if it allows
adequate access to the abscess, because it gives a better cosmetic result.
The incision should pass through the skin and superficial fascia. A long artery forceps is then inserted into the
abscess cavity, and passed into every part of the abscess, and its jaws opened. A finger is then inserted after

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withdrawal of the forceps, to disrupt any remaining septa. The wound is then lightly packed with ribbon gauze or
a drain inserted to allow dependent drainage.

Breast Cysts

A cyst is a fluid-filled sac that develops in the breast tissue. They most often happen in women between the ages
of 35 and 50 and are common in those nearing menopause. The cysts often enlarge and become sore just before
menstrual period. They may seem to appear overnight. Cysts are rarely cancerous and may be caused by blocked
breast glands.
Cysts can feel either soft or hard. When close to the surface of the breast, cysts can feel fluctuant and smooth on
the surface. When they are deep in breast tissue, cysts will feel like hard lumps because they are covered with
tissue.

Diagnosis:
A cyst may be detected during a physical examination of the breast. Confirmation of the diagnosis is with a
mammogram or ultrasound. A fine-needle aspiration may also be done. This involves guiding a very fine needle
into the cyst and drawing fluid from it.

Treatment:
Cysts are treated by aspiration. Once the fluid is aspirated, the cyst collapses and disappears. But, cysts can
reappear later, in which case they are simply drained again. However, if there is a residual lump or if the fluid is
blood-stained, a core biopsy or local excision for histology is done. This will exclude cystadenocarcinoma.

Fibroadenoma

Fibroadenomas are solid, smooth, firm, benign lumps that are most commonly found in women in the ages 15 to
25 years. They occur in the fully developed breast and are the most common benign lumps in women.
Fibroadenomas can occur at any age, and are increasingly being seen in postmenopausal women who are taking
hormone therapy.
Fibroadenomas arise from hyperplasia of a single lobule and usually grow up to 2-3 cm in size. They are
surrounded by a well-marked capsule. Some fibroadenomas can grow quite big and can exceed 5 cm in diameter.
The painless lump feels rubbery and moves around freely. Fibroadenomas can grow anywhere in the breast
tissue.
Diagnosis is made by palpation of the lump, but confirmation of the diagnosis can be done with a mammogram
or ultrasound and fine-needle aspiration.

Treatment:
A fibroadenoma does not require removal unless associated with suspicious cytology, becomes very large or the
patient desires to have it removed. The fibroadenoma should be enucleated through a cosmetically appropriate
submammary incision.

Fat Necrosis

Fat necrosis is a condition in which painless, round, firm lumps caused by damaged and disintegrating fatty
tissues form in the breast tissue. Fat necrosis often occurs in women with very large breasts or who have had a
bruise or blow to the breast. Fat necrosis may mimic a carcinoma, even displaying skin tethering and nipple
retraction. Biopsy is required for diagnosis.

Galactocele

Galactocele is a fluid-filled mass usually caused by a blocked milk duct. It presents as a solitary sub-areolar cyst
that contains milk. It arises during lactation.

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Sclerosing Adenosis

Sclerosing adenosis is excess growth of tissues in the breast's lobules. This often causes breast pain. While these
changes in the breast tissue are very small, they may show up on mammograms as calcifications and can make
lumps. Usually a biopsy is needed to rule out cancer. In addition, because the condition can be mistaken for
cancer, the lumps are usually removed through surgical biopsy.

Topic 4: CARCINOMA OF THE BREAST - Epidemiology; Risk factors

Learning Objectives:

By the end of this lesson, you should be able to;

1. State the risk factors for breast cancer

2. Classify the types of breast cancer
3. Briefly describe the pathology of breast cancer
4. Outline the clinical features of breast cancer
5. State the differential diagnoses of breast cancer
6. State the investigations useful in confirming or staging breast cancer
7. Outline the management of breast cancer

CARCINOMA OF THE FEMALE BREAST

EPIDEMIOLOGY
 Breast cancer is among the commonest of human cancers throughout the world. It is the most common
malignancy in women.
 Over 1 million new cases are diagnosed each year world-wide. Incidence and mortality are particularly
high in developed countries. It is the most common cause of death in middle-aged women in western countries.
 Women who start menstruating early in life, or who have a late menopause, have a slightly increased risk
of developing breast cancer. Young age at first delivery protects against breast cancer. Risk of breast cancer in
women whose first delivery was after age 30 is twice that of women whose first delivery was before age 20.
Highest risk is in women who have their first pregnancy over the age of 40 years.
 The incidence of breast cancer increases with age, doubling every 10 years until the menopause, when the
rate of increase slows markedly. The incidence of breast cancer is highest in the peri-menopausal age group and
is uncommon before the age of 25 years. Breast cancer is also increased in nulliparous women. Breast feeding
has a small protective effect.

RISK FACTORS FOR BREAST CANCER

1. Geography
The incidence of breast cancer is about six times higher in developed countries than the developing countries,
with the notable exception of Japan. These geographic differences are considered to be related to consumption of
large amounts of animal fat and high caloric diet by Western populations than the Asians (including Japanese)
and Africans.

2. Genetic factors
Family history – first-degree relatives (mother, sister, or daughter) of women with breast cancer have 2-6 fold
higher risk of development of breast cancer. The risk is proportionate to the following factors:

 • Number of blood relatives with breast cancer.

 • Younger age at the time of development of breast cancer.
 • High risk cancer families having breast and ovarian cancer.

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Pointers to an inherited disposition are:

 • A first degree relative who developed breast cancer, particularly bilateral cancer, under the age of 40 years
 • Numerous female relatives with breast cancer
 • A close female relative who has had ovarian cancer.

3. Endocrine – oestrogen excess

There is sufficient evidence to suggest that excess endogenous oestrogen or exogenously administered oestrogen
for prolonged duration is an important factor in the development of breast cancer. Evidences in support of
increased risk with oestrogen excess are as follows:

  Women with prolonged reproductive life, menarche setting in at an early age, and who have menopause
relatively late have greater risk.
  Higher risk in unmarried and nulliparous women than in married and multiparous women.
  Women with first childbirth at a late age (over 30 years) are at greater risk.
  Lactation is said to reduce the risk of breast cancer.
  Bilateral oophorectomy reduces the risk of development of breast cancer.
  Hormone replacement therapy (HRT) increases breast cancer risk. Combined oestrogen and progesterone
HRT is associated with a greater risk than preparations containing oestrogen alone.
  Men who have been treated with oestrogen for prostatic cancer have increased risk of developing cancer of
the male breast.

4. Environmental and dietary factors

  Consumption of large amounts of animal (saturated) fats and high calorie foods.
  Cigarette smoking
  A high alcohol intake.

5. Fibrocystic change
Women with severe atypical hyperplasia have about 5-fold higher risk of developing breast cancer than women
who have no proliferative changes.

6. Age
Carcinoma of the breast is extremely rare below the age of 20 years but, thereafter, the incidence steadily rises so
that by the age of 90 years nearly 20% of women are affected.

7. Gender
Females are more at risk of developing breast cancer than males. Less than 0.5% of patients with breast cancer
are male.

8. Previous radiation
Women treated by radiation therapy for lymphoma during adolescence and teenage years are at significant risk of
developing early-onset breast cancer. The risk appears about a decade after treatment and is higher if
radiotherapy occurred during breast development.

TYPES OF BREAST CANCER

 Breast cancers are derived from the epithelial cells that line the terminal duct lobular unit.
 Cancer cells that remain within the basement membrane of the lobule and the draining ducts are classified
as in situ or non-invasive.
 An invasive cancer is one in which cells have moved outside the basement membrane of the ducts and
lobules into the surrounding adjacent normal tissue.

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CLASSIFICATION

1. Non-invasive (in-situ) carcinoma

  Ductal carcinoma in situ - DCIS

  Lobular carcinoma in situ - LCIS

2. Invasive carcinoma

  Infiltrating (invasive) duct carcinoma

  Infiltrating (invasive) lobular carcinoma.
  Medullary carcinoma.
  Colloid (mucinous) carcinoma.
  Papillary carcinoma.
  Tubular carcinoma
  Adenoid cystic (invasive cribriform) carcinoma.
  Secretory (juvenile) carcinoma.
  Inflammatory carcinoma.
  Carcinoma with metaplasia.

3. Paget’s disease of the nipple.

PATHOLOGY

 Normal breast epithelium possesses oestrogen and progesterone receptors. The breast cancer cells secrete
many growth factors which are oestrogen-dependent. In this way, the interplay of high circulating levels of
oestrogen, oestrogen receptors and growth factors brings about progression of breast cancer.

 Cancer of the breast occurs more often in left breast than the right and is bilateral in about 4% cases.
Carcinoma of the breast arises from the ductal epithelium in 90% cases while the remaining 10% originate from
the lobular epithelium. For variable period of time, the tumour cells remain confined within the ducts or lobules
(non-invasive carcinoma) before they invade the breast stroma (invasive ca)

A. NON-INVASIVE (IN-SITU) CARCINOMA

Characterised histologically by presence of tumour cells within the ducts or lobules without evidence of invasion.

1. Ductal Carcinoma in situ (Intraductal carcinoma)

Confined within the larger mammary ducts. Initially begins with atypical hyperplasia of ductal epithelium,
followed by filling of the duct with tumour cells.

Clinically:
• It produces a palpable mass in 30-75% of cases.
• Presence of nipple discharge in about 30% patients.
Approximately ¼ of patients of intraductal carcinoma treated with excisional biopsy alone develop ipsilateral
invasive carcinoma during a follow-up period of 10 years. The chance of a contralateral breast cancer developing
in patients with intraductal carcinoma is far less than that associated with in situ lobular carcinoma.

Grossly – the tumour may vary from a small poorly-defined focus to 3-5cm diameter mass.

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2. Lobular carcinoma in-situ
Is not a palpable or grossly visible tumour. Patients of in situ lobular carcinoma treated with excisional biopsy
alone develop invasive cancer of the ipsilateral breast in about 25% cases in 10 years as in intraductal carcinoma
but, in addition, have a much higher incidence of developing a contralateral breast cancer (30%).

Topic 4: CARCINOMA OF THE BREAST - Types

B. INVASIVE CARCINOMA

In general, 90% of breast cancers are of larger ductal origin, while the remaining 10% arise from lobular
epithelium.

1. Invasive (Infiltrating) ductal carcinoma

 Is the classic breast cancer.
 It is the most common histologic pattern accounting for 70% cases of breast cancer.
 Clinically, majority of infiltrating ductal carcinomas have a hard consistency due to dense collagenous
stroma (scirrhous carcinoma).
 They are found more frequently in the left breast, often in the upper outer quadrant.
 Retraction of the nipple and attachment of the tumour to underlying chest wall may be present.

2. Invasive (Infiltrating) lobular carcinoma

Comprise about 5% of all breast cancers. This peculiar morphological form differs from other invasive cancers in
being more frequently bilateral; and within the same breast, it may have multicentric origin.

3. Medullary Carcinoma
Is a variant of ductal carcinoma, and comprises about 1% of all breast cancer. The tumour has a significantly
better prognosis than the usual infiltrating duct carcinoma, probably due to good host immune response in the
form of lymphoid infiltrate in the tumour stroma. Grossly – the tumour is characterised by a large, well-
circumscribed, rounded mass that is typically soft and fleshy or brain-like and hence the alternative name of
‘encephaloid carcinoma’. Cut section shows areas of haemorrhages and necrosis.

4. Colloid (mucinous) carcinoma

This is an uncommon pattern of breast cancer occurring more frequently in older women and is slow-growing.
Colloid carcinoma has better prognosis than the usual infiltrating duct carcinoma. Grossly – the tumour is usually
a soft and gelatinous mass with well-demarcated borders.

5. Papillary Carcinoma
Is a rare variety of infiltrating duct carcinoma in which the stromal invasion is in the form of papillary structures

6. Tubular Carcinoma
This is another uncommon variant of invasive ductal carcinoma which has more favourable prognosis.
Histologically – the tumour is highly well-differentiated and has an orderly pattern. The tumour cells are regular
and form a single layer in well-defined tubules. The tubules are quite even and distributed in dense fibrous
stroma.

7. Adenoid Cystic (invasive cribriform) carcinoma

This is a unique histologic pattern of breast cancer with excellent prognosis. Histologically – there is stromal
invasion by islands of cells having characteristic cribriform (fenestrated) appearance.

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8. Secretory (juvenile) Carcinoma
This pattern is found more frequently in children and has a better prognosis. The tumour is generally
circumscribed and slow growing. On histologic examination it shows abundant intra- and extra-cellular PAS-
positive clear spaces due to secretory activity of tumour cells.

9. Inflammatory Carcinoma
Is a clinical entity and does not constitute a histological type. It is a rare, highly aggressive cancer. The term has
been used for breast cancers in which there is:

 • Redness.
 • Cutaneous oedema
 • Tenderness/pain.
 • Rapid enlargement &
 • Swelling of the breast.
 Usually involves at least 1/3 of the breast and may mimic a breast abscess. Inflammatory carcinoma is associated
with extensive invasion of dermal lymphatics.

10. Carcinoma with metaplasia

Rarely, invasive ductal carcinoma may have various types of metaplastic alterations such as:

 • Squamous metaplasia.
 • Cartilagenous and
 • Osseous metaplasia, or their combinations.

C. PAGET’S DISEASE OF THE NIPPLE

Definition:
It is an eczematoid lesion of the nipple, often associated with an invasive or non-invasive ductal carcinoma of the
underlying breast. It is a superficial manifestation of an underlying breast carcinoma. It presents as an eczema-
like condition of the nipple and areola, which persists despite local treatment.

Pathology
Most of the patients with palpable mass are found to have infiltrating duct carcinoma, while those with non-
palpable breast lump are usually subsequently found to have intraductal carcinoma.
Grossly – the skin of the nipple and areola is crusted, fissured and ulcerated with oozing of sero-sanguinous fluid
from the erosions.

Clinical features
The nipple bears a crusted, scaly and eczematoid lesion with a palpable subareolar mass in about ½ the cases. The nipple is
eroded slowly and eventually disappears.
If left, the underlying carcinoma will sooner or later become clinically evident. Nipple eczema should be biopsied if there is
any doubt about its cause.
Prognosis
Prognosis of patients with ductal carcinoma having Paget’s disease is less favourable than of those who have
ductal carcinoma without Paget’s disease.

THE SPREAD OF BREAST CANCER

1. Local Spread
The tumour increases in size and invades other portions of the breast. It tends to involve the skin and to penetrate
the pectoral muscles and even the chest wall if diagnosed late.

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2. Lymphatic Metastases
Occurs primarily to the axillary and the internal mammary lymph nodes. Tumours in the posterior 1/3 of the
breast are more likely to drain to the internal mammary nodes. Involvement of supraclavicular nodes and of any
contralateral lymph nodes represents advanced disease.

3. Haematogenous
It is by this route that skeletal metastases occur, although the initial spread may be via the lymphatic system. In
order of frequency the following are affected:

 1) The lumber vertebrae

 2) Femur
 3) Thoracic vertebrae
 4) Rib &
 5) Skull.
 6) These deposits are generally osteolytic.
 Metastases may also commonly occur in the liver, lungs, brain and, occasionally, the adrenal glands and ovaries

CLINICAL FEATURES OF BREAST CANCER

60% present as symptomatic disease; 40% during screening. Take note of: Family history; Parity.

Symptoms

1) Age - extremely rare in teenagers and rare in the twenties.

  From the thirties onwards there is a progressively increasing incidence which peaks in the late fifties. It
remains common into old age.

2) Breast lump.

  Commonest presenting symptom.

  Usually painless (unless inflammatory carcinoma).
  Hard and gritty feeling.
  May be immobile (held within breast tissue), tethered (attached to surrounding breast tissue or skin), or
fixed (attached to chest wall).
  Ill-defined; irregular with poorly defined edges.

3) A pricking sensation occasionally draws the patient’s attention to the spot when she feels the lump in the
symptomatic area.
4) Skin changes.

  Carcinoma beneath skin causes dimpling, puckering, or colour changes.

  Late presentation may be with skin ulceration or fungation of the carcinoma through the skin.
  Lymphoedema of the skin (peau d’orange) suggests local lymph node involvement.

5) Nipple abnormalities.

  Nipple may be prime site of disease (Bowen’s disease) presenting as eczema.

  Nipple may be affected by an underlying cancer: -
 Destroyed; Retracted; Inverted; Deviated;

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  Associated bloody discharge.

6) The breast may be noticed to be harder or to have changed shape.

7) Swelling of the arm, caused by lymphatic or venous obstruction in the axilla is a significant presentation.
8) Backache.
9) Pathological fractures.
Signs

1. Site – ½ of carcinomata of the breast occur in the upper outer quadrant, which includes the axillary tail.
2. Colour – if the tumour is close to the surface, the overlying skin may be discoloured.

 Tumours fixed to the skin first give the skin a smooth, reddened appearance, but as the process advances and
ulceration is imminent, the skin becomes paler.

3. Tenderness – most carcinomata are not tender, but palpation may produce a mild discomfort, often because of the
patient’s fear of the consequences of the surgeon finding a lump.
4. Temperature – only the very rare ‘inflammatory’ type of breast cancer feels warm.
5. Shape – a carcinoma of the breast may grow into any shape but in the early stages it is roughly spherical.

 The disease may also be multifocal, & it is not that unusual to find two separate primary tumours.

6. Surface – the surface is usually indistinct, which makes it difficult to define the shape except when the lesion is
small.

 However, a few cancers are encapsulated and have a smooth surface, mimicking cysts and fibroadenomata.
7. Composition – carcinomata are solid, so they do not fluctuate, transilluminate or have a fluid thrill.

  Their consistence is normally quite firm and regular.

  However, some tumours are soft, almost as soft as a lipoma, so do not attribute too much significance to
the absence of a textbook ‘stony hard’ consistence.
8. Fixation of lump to the skin is almost diagnostic of a carcinoma. The only other condition producing
fixation is traumatic fat necrosis.
9. Frank ulceration fixation to the chest wall – called cancer-en-cuirasse.
10. Orange-peel appearance (peau d’orange).
11. Lymph glands containing metastases are usually hard and discrete. As they enlarge, they may mat together and
become adherent to nearby structures such as the skin, axillary vessels and nerves.
12. Lymphoedema of the arm or venous thrombosis and oedema.
13. Reduced spinal movements/paraplegia
14. Signs of pleural effusion.
15. Jaundice & hepatomegaly.
16. Skin – may have multiple hard nodules; usually in the skin of the breast containing the cancer, but may be seen in
the neck, trunk and further away.

Systemic features
1. Weight loss.
2. Anorexia.
3. Bone pain.
4. Jaundice. 5. Malignant pleural and pericardial effusions.
6. Anaemia.
DIFFERENTIAL DIAGNOSIS
I. Causes of nipple retraction:
  Congenital
  Schirrus cancer
  Following fibrosis due to breast abscess or TB breast

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   Following irradiation
  Rarely in chronic mastitis.
II. Causes of nipple discharge:
a) Blood stained –

 Paget’s disease
 Duct papilloma
 Duct cancer
 Chronic cystic mastitis(rare)
b) Serous – retention cysts usually with fibroadenosis.
c) Brown/green – this green discharge may be just an altered blood or from a retention cyst in association with the
fibroadenosis.

III. Fat necrosis – occurs in the elderly.


 After an injury, not necessarily noticed by the patient, there may be a focal necrosis of subcutaneous fat
with local scarring which causes skin tethering.
  There may be a history of trauma or of bruising.
  The condition resolves spontaneously.
IV. Mondor’s disease – is a thrombo-phlebitis of the lateral thoracic vein which produces a cord-like, linear skin
puckering that can alarm patient and clinician. It resolves spontaneously
INVESTIGATIONS
1. Open excisional biopsy – the most reliable diagnostic test for breast cancer.
2. Large-needle (core needle) biopsy.
3. FNAC
4. Ultrasonography
5. Transillumination.
6. Thermography.
7. Mammography useful particularly ˃35yrs; mammographic localization biopsy.
8. Xero-radiography.
9. Computerized stereotactic modifications
• Techniques like FNAC, stereotactic biopsy & frozen section are immensely valuable to the surgeon for
immediate pathological diagnosis.

Staging investigations
Systemic staging is usually reserved for breast cancer patients who are at risk of systemic disease or have symptoms
suggestive of systemic disease.

 Liver ultrasound.
 Chest x-ray.
 Bone scan.
 Specific investigations for organ-specific suspected metastases.
AJC CLINICAL STAGING
Stage TIS: in situ carcinoma (in situ lobular, intraductal, Paget’s disease of the nipple without palpable lump).
Stage I: Tumour ≤2cm in diameter. No nodal spread.
Stage II: Tumour 2-5cm in diameter. Regional lymph nodes involved.
Stage III A: Tumour ≥ 5cm in diameter. Regional lymph nodes involved on same side.
Stage III B: Tumour ≥ 5cm in diameter. Supraclavicular and infraclavicular lymph nodes involved.
Stage IV: Tumour of any size, with or without regional spread but with distant metastasis
MANAGEMENT

SURGERY
Surgery is the mainstay of non-metastatic disease. Options for treatment of the primary tumour are as follows:
 1. Wide local excision
 • To ensure clear margins.

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  • Breast conserving provided breast is adequate size and tumour location appropriate (not central/retro-
areolar).
 • Usually combined with local radiotherapy to residual breast to reduce risk of local recurrence.
 2. Lumpectomy.
 3. Quadrantectomy
 4. Patey mastectomy.
 5. Simple mastectomy.
MEDICAL TREATMENT
In non-metastatic disease medical therapy is adjuvant to reduce the risk of systemic relapse usually after primary
surgery. It is occasionally used as treatment of choice in elderly or those unfit/inappropriate for surgery.
Endocrine therapy: Most effective in ER +ve tumours (tumours in which the cancer cells grow in response to
estrogen).
 1. Anti-oestrogen, e.g. Tamoxifen;
 2. LHRH antagonists;
 3. Aromatase inhibitors.
Chemotherapy: Offered to patients with high risk features (+ve nodes, poor grade)
 1. Anthracyclines,
 2. Cyclophosphamide,
 3. 5-FU
 4. Methotrexate.
In metastatic disease, medical therapy is palliative to increase survival time and includes:
1. Endocrine therapy – as above
2. Chemotherapy (e.g. Anthracyclines, tanaxest);
3. Radiotherapy – to reduce pain of bony metastases or symptoms from cerebral or liver disease.

PREVENTION
1. Breast Self-Examination:
  Physicians who treat women should educate patients on the technique of self-examination, because the
well-prepared patient is one of the most accurate screening methods for breast disease.
2. Physician examination.
3. Mammography:

  The frequency of mammography or the earlier use of mammography depends on both the individual
woman and her family history.
  Patients with a positive family history of breast cancer should have a mammogram at an earlier age,
particularly those whose mother, aunt, or sister developed premenopausal breast cancer.
  In general, a mammogram should be obtained every 1-2years from ages 40-50 years and annually
thereafter.
4. Ultrasonography:

  Can now reliably differentiate solid from cystic lesions; this technique complements but does not supplant
mammography.
All the above are complementary, and all should be used for the early detection of breast cancer.
Topic 4: Summary
In this topic you have learnt the following about breast conditions:
 History taking
 Clinical examination
 Nipple discharges
 Investigations
 Mastitis
 Benign Breast Swellings
 Carcinoma of the breast
Reading Assignment

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