DISORDERS OF THE INTESTINES

ACUTE ABDOMEN

Def: Acute abdomen refers to conditions that have a sudden onset and affect the abdomen or
abdominal organs and usually require immediate or urgent surgical intervention.

 This is an acute intra-abdominal condition of abrupt onset, usually associated with pain due to
inflammation, perforation, obstruction, infarction or rupture of abdominal organs and usually requiring
emergency surgical intervention
 Any part of the lower GIT is susceptible to acute inflammation caused bacterial, viral or fungal
diseases.
 Some of the conditions of acute abdomen may not be diseases by themselves, such as intestinal
obstruction but would eventually lead to inflammatory diseases such as peritonitis or appendicitis.
 Most common acute abdomen conditions are;

 Appendicitis
 Ruptured ectopic pregnancy
 Peritonitis
 Diverticulitis
 Small bowel obstruction
 Large bowel obstruction
 Strangulated hernia
 Volvulus
 Intussusception
 Ruptured spleen

Common causes of acute abdomen

 Inflammation e.g;
- Acute appendicitis- where the appendix is inflamed. There is sudden severe abdominal
pain such that if inflammation continues without treatment the appendix can rapture
- Acute diverticulitis- acute inflammation of the diverticulum (pouch or pocket of any
portion e.g. of the G.I.T).
This commonly occurs in the large intestine. There is severe pain and tenderness usually in the
lower left part of the abdomen among others
- Acute cholecystitis- acute inflammation of the gall bladder
- Acute salpingitis- acute inflammation of the fallopian tubes

 Acute intestinal obstruction

- May be a mechanical obstruction where the blockage could completely stop or seriously
impair the passage of intestinal contents. The part above the obstruction may swell up when
filled with food, fluid, digestive secretions, etc. Mechanical obstruction is commonly caused by:
- Volvulus-Which is the twisting of the intestine causing obstruction. In the this case,
blood supply is cut off to the affected part and gangrene may occur if not managed properly
- Intussusceptions-prolapsed of one of the intestine into another part immediately
adjacent to the part
- Intestinal obstruction can be non mechanical e.g. in paralytic ileus-where the normal
contractile movement of the intestinal wall temporarily stops.

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  Peritonitis

- Inflammation is usually caused by an infection or inflammation of the lining of the

abdominal cavity (peritoneum). Usually infection spreads from an infected organ in the
abdomen. Common sources are:
- Perforation of the stomach/ intestine (e.g. perforated peptic ulcers), gall bladder,
appendix), also perforation of the fallopian tube (e.g. ruptured ectopic pregnancy)

 Ischemia

- This is where there is deficiency in blood supply which could be as a result of:

 Strangulated hernia- This is a hernia of the bowel in which the neck of the sac containing the bowel is
so constricted that the blood supply is impeded and gangrene may result if not managed promptly.
 Volvulus- the blood supply is cut off and gangrene may result if not managed promptly
 Torsion of the ovarian cyst- This is where the long pedicles of an ovarian cyst twists leading to
impaired blood supply to the affected part, gangrene may result if not managed promptly.

 Ruptured arterial aneurysm

 This is the rupture of an aneurysm (bulge or dilatation in the wall of an artery) usually the abdominal
aortic aneurysm
 There s excruciating pain in the lower abdomen and back, also tenderness over the aneurysm
 With severe internal bleeding, a person may rapidly go into shock

PREOPERATIVE MANAGEMENT

Emergency care

 The management is emergency pre-operative

 Patient should be nil orally because if patient eats may aspirate the food under the influence of
anesthesia
 Inset a nasal gastric tube in order to empty the stomach (especially if the patient has eaten within 4-6
hours.
 If there is blood loss, or if patient has vomited a lot ( causing circulatory failure or dehydration or
where these are anticipated), Intravenous fluids are given
 A fluid balance chart is monitored in all cases
 In case patient is in shock or urinary retention is suspected, a catheter is put up
 Vitale signs are monitored regularly e.g. 2 hourly depending on condition, low Bp, fast and feeble
pulse indicate patient going in shock. High temperature will show that there is infection.
 Blood is collected for grouping and cross match since the patient may need blood transfusion.

GENERAL CARE

 Remove any dentures, jewelers, etc

 Will explain to the patient the type of operation and why is going to theatre
 Thereafter, patient will be asked to sign the consent form for operation

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 The abdomen will be trimmed up to the vulva
 I will put an identification band on the wrist
 Theater nurse will be informed of the patient going for laparotomy
 When ready will take the patient and handover to the theatre nurse
 Will come back to the ward to prepare the environment including the post –operative bed.

IEC

 IEC is given on the importance of good nutrition; high protein and vitamin diet. Proteins help in the
building of worn out tissues, while vitamins help in healing of the wound and boosting of the immunity.
Also need roughage in the diet to help in making the stool bulk and promote peristalsis thereby
preventing constipation. Constipation leads to staining while opening bowels and this would cause
pressure on the incision site which may open up.
 The patient will also be given IEC on the importance of not touching the incision site with dirty hands
as they may introduce microorganisms which may cause infection
 She will also be advised on not lifting heavy objects as this can cause strain on the incision site
thereby on the importance of coming back to the hospital for review so that the progress could be
assessed. However, she would be told that in case of having problems. Should come back even before
the review date.
 Drug compliance- advise the patient on the importance of drug compliance

Intestinal obstruction

Def: Intestinal obstruction occurs when the contents of the intestines or the lumen of the intestines
blocks the normal flow of bowel contents

 It is a partial or complete blokage of the intestinal lumen resulting from mechanical or non
mechanical obstruction characterised by abdominal distension, vomiting and constipation.

 Bowel obstruction (or intestinal obstruction) is a mechanical or functional obstruction of the

intestines, preventing the normal transit of the products of digestion which can occur at any level distal
to the duodenum of the small intestine and is a medical emergency.

- The obstruction can be partial or complete, with the severity depending on the degree
of obstruction, the degree to which vascular supply is disturbed and the lumen affected
- It can also be temporal due to manipulation during surgery {paralytic ileus}
- Most bowel obstruction occurs in the small intestines with adhesions as the top cause
followed by hernias and neoplasm.

Causes

There are basically two processes that can cause intestinal obstruction

 Mechanical obstruction
 Functional/Neurological obstruction

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 Mechanical obstruction

 This occurs when there is an intraluminal or a mural obstruction from pressure on the intestinal walls.
This may cause constriction resulting in partial obstruction but may suddenly become complete
obstruction.

Examples of mechanical obstruction would result from:

 Intussusception (invagination) – one part of the intestine invaginates/slips into part loacated below it
thereby narrowing the lumen.
 Polypoid tumors and neoplasm
 Stenosis
 Colon atresia
 endometriosis
 Strictures
 Adhesions – loop of the intestines becomes adherent to areas that heal slowly or scar after
abdominal surgery producing a kinking of the intestinal loop leading to narrowing of the lumen.
 Hernias – protrusion of the abdominal organs/intestines through a weak area in the abdominal
muscle or wall leading to complete obstruction of bowel and blood flow.
 Abscess
 Volvulus – bowel twists and turns on itself leading to obstruction of the lumen.
 Diverticulitis (crohns disease)
 Pressure from tumors outside the lumen like uterine fibroids
 Fecal impaction
 Inflamatory bowel diseases
 fecaloma

 Non mechanical/Functional obstruction

 This is where the intestinal musculature cannot propel the contents along the bowel and could be as
a result of amylidosis, muscular dystrophy, endocrine disorders such as diabetes or Neurological
disorders such as Parkinson’s syndrome.

Paralytic ileus is the most common cause of paralysis.

Obstruction may be as a result of vascular obstruction to a segment of the bowel where blood supply
will be cut off and ischemia results followed by infarction, gangrene and total obstruction. The vascular
causes may be a result of embolism, arthromatous changes in blood vessels and thrombosis

Patho- physiology of obstruction

The intestinal contents, fluid and gas accumulate above the intestinal obstruction. This causes
abdominal distension. Irritation of the nerves by the distension also causes acute abdominal pains.

The abdominal distention and retention of fluid reduces the absorption of the fluids and thus stimulate
more gastric secretions.

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With the Increase in distension, pressure within the intestinal lumen also increases thus causing a
decrease in the venous and arterial capillary pressure .this causes edema congestion ,necrosis and
eventually rapture or perforation of the bowel with resultant peritonitis.

Reflux vomiting may be cause by abdominal distension.

The vomiting causes loss of hydrogen ions and potassium from the stomach leading to a reduction o f
chlorides and potassium in the blood and eventually metabolic alkalosis.

Dehydration and acidosis follows from loss of water and sodium. With all these fluid losses
hypovolaemic shock occurs

Clinical picture

 The initial picture or symptom is usually

 Crampy pain that is wave- like and colicky.
 The patient may pass blood and mucous but no fecal matter or flatus
- If obstruction is complete the peristaltic movements initially become very vigorous and eventually
assume a reverse direction where the intestinal contents propel towards the mouth instead of the
rectum. If the obstruction is in the ileum;

 Fecal vomiting may occur. First the patient vomits the stomach contents then the bile-stained
contents from the jejunum and duodenum and finally the fecal like contents of the ileum
 Dehydrations becomes evident
 There is intense thirsty
 Drowsiness
 Generalized malaise
 aching and parched tongue
 Abdominal distension
 Hypovolaemic shock

SIGNS AND SYMPTOMS

MECHANICAL (Small bowel) MECHANICAL (Large bowel) NON MECHANICAL
Colicky pain Costipation Diffused abdominal discomfort
Nausea and vomiting Vomiting in a later stage Abdominal distension
Constipation Constant hypostatic pain Hiccups
Distended abdomen Nausea Constipation
Borborgymin and rashes Sudden onset of colicky abdominal Frequent vomiting (gastric and
bowel sounds pains after constipation bowel contnts
Abdominal tenderness Distended abdomen Decreased bowel sounds
Rebound tenderness Vissible loops of large bowels
Loud, high pitched borborygmi

Diagnosis

Based on the symptoms presented by the patient {subjective and objective history taking

 Physical examination of patient may review abdominal distension

 Abdominal X-ray findings show abnormal quantities of gases, fluid or both in the bowels

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 Laboratory findings review electrolyte imbalances
 FBC plus a complete blood cell count needs to be done and these will review a picture of dehydration
 Loss of plasma volume and possible infection with an increases
 ESR
 Barium meal/swallow/ enema
 Sigmoidoscopy
 Abdominal Scan
 Stool for occult blood
 Stool examination for worms

Medical Management

Objectives

 To correct the electrolyte imbalance

 To relieve abdominal distension
 To relieve pain
 To treat the cause
 Prevent complications

Decompression of bowel through a naso gastric tube is successful a most cases

 If obstruction is complete, it will warrant surgical intervention.

The surgical intervention is mostly dependent on the cause of obstruction i.e. hernia or adhesions will
involve repairing the hernia or dividing the adhesions to which the intestine is attached.

 In some cases a portion of the intestines will have to be removed and an anastomosis done

Appendicitis

Def: This is the inflammation of the vermiform appendix which may result from obstruction of the
appendiceal lumen charecterized by progressive sever generalised or upper abdominal pains that
becomes localised in the right lower quadrant of the abdomen.

Incidence;

 About 7% of the population has appendicitis within their lives.

 Males are affected more then females and teenagers more than adults
 Occurs more frequently between ages of 10 and 30.

Causes

 Tumor
 Fecalith (hard mass of stool)
 Foreign bodies
 Viruses
 Bacteria

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 Intestinal worms
 Lymphodenitis

Path physiology

The appendix becomes inflamed and edematous as a result of either becoming kinked or occluded by
fecal matter {a harden mass of stool} It can also be occluded by foreign matter or by mural causes such
as tumors

The inflammatory process initiates a progressively severe generalized or upper abdominal pain and
becomes localized in the right lower quadrant of the abdomen within a few hours eventually the
inflamed appendix fills with pus.

Clinical Picture

 There is vague epigastric pain or peri umbilical pain which progress to the right lower quadrant.
 The pain is usually accompanied by low-grade fever
 Nausea and vomiting sometimes occur
 Loss of appetite is common
 Local tenderness is elicited at Mc Burney’s point when pressure is applied
 Rebound tenderness
 Constipation/Diarrhea
 Pain in the lumber if appendix curls along the caecum
 If the tip is in the pelvis theses signs may only be elicited on rectal examination
 Pain on defecation suggests that the tip is in the pelvis or resting against the rectum
 Pain on urination suggests that the tip is near the bladder or impinges the urethra
 Rovsing sing may be elicited by palpating the left lower quadrant. This paradoxically causes pain to be
felt on the right side
 Pain becomes more diffuse if appendix has ruptured followed by abdominal distension
 Patient’s condition deteriorates art this time.

Note;

 Roving’s sign is pain felt on the right lower quadrant when the left lower quadrant is palpated
 The Mc Burney’s point is between the umbilicus and the anterior superior iliac spine

Diagnosis

This is based on a complete

 History taking,
 Physical examination
 Laboratory examination
 Complete Cell count demonstratives an elevated white blood cell count
 The leukocyte count may exceed 10 000 cells/mm3
 The nuetrophil count may exceeds 75%
 X-ray findings
 Abdominal examination/x-rays, C.T and ultra sound may reveal a right lower quadrant density or
localized distention of the bowel

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Medical Management

Objectives

 To ensure that Surgery is performed as soon as possible in order to decrease the risk of perforation.
 To correct or prevent fluid and electrolyte imbalance and dehydration by giving antibiotics and
intravenous fluids before surgery
 To relieve pain by giving analgesia, as patient awaits surgery (after the diagnosis has been made).
 To prevent development and spread of infection by giving antibiotics.

Surgical Management

 Appendectomy, which is a surgical removal of the appendis, is performed

 This may be done as an abdominal operation or via a laparascopy

Complications

The major complication is

 Perforation of the appendix {10% to 32%} This may occur about 24 hrs after the onset of pain thus
the need for urgent surgery
 Peritonitis
 Peritoneal abscess
 Pelvic abscess
 Intestinal obstruction
 Paralytic ileus
 Subphrenic abscess (abscess under the diaphram)

Hernia

Definition

A hernia occurs when the contents of a body cavity bulge out of the area where they are
normally contained.

These contents, usually portions of intestine or abdominal fatty tissue, are enclosed in the thin
membrane that naturally lines the inside of the cavity. Although the term hernia can be used for
bulges in other areas, it most often is used to describe hernias of the lower torso (abdominal
wall hernias).
Hernias by themselves may be asymptomatic, but nearly all have a potential risk of having their
blood supply cut off (becoming strangulated). If the hernia sac contents have their blood supply
cut off at the hernia opening in the abdominal wall, it becomes a medical and surgical
emergency.
Types of abdominal hernias
Different types of abdominal wall hernias include the following:

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1. Inguinal (groin) hernia: Making up 75% of all abdominal wall hernias and occurring up to 25
times more often in men than women, these hernias are divided into two different types, direct
and indirect. Both occur in the groin area above where the skin crease at the top of the thigh
joins the torso (the inguinal crease), but they have slightly different origins. Both of these types
of hernias can similarly appear as a bulge in the inguinal area. Distinguishing between the direct
and indirect hernia, however, is important as a clinical diagnosis.

 Indirect inguinal hernia: An indirect hernia follows the pathway that the testicles made
during prebirth development. It descends from the abdomen into the scrotum. This pathway
normally closes before birth but may remain a possible place for a hernia. Sometimes the hernia
sac may protrude into the scrotum. An indirect inguinal hernia may occur at any age.

 Direct inguinal hernia: The direct inguinal hernia occurs slightly to the inside of the site of
the indirect hernia, in a place where the abdominal wall is naturally slightly thinner. It rarely will
protrude into the scrotum. Unlike the indirect hernia, which can occur at any age, the direct
hernia tends to occur in the middle-aged and elderly because their abdominal walls weaken as
they age.

2. Femoral hernia: The femoral canal is the path through which the femoral artery, vein, and
nerve leave the abdominal cavity to enter the thigh. Although normally a tight space, sometimes
it becomes large enough to allow abdominal contents (usually intestine) into the canal. A
femoral hernia causes a bulge just below the inguinal crease in roughly the mid-thigh area.
Usually occurring in women, femoral hernias are particularly at risk of becoming irreducible (not
able to be pushed back into place) and strangulated.

3. Umbilical hernia: These common hernias (10-30%) are often noted at birth as a protrusion
at the bellybutton (the umbilicus). This is caused when an opening in the abdominal wall, which
normally closes before birth, doesn't close completely. If small (less than half an inch) this type
of hernia usually closes gradually by age 2. Larger hernias and those that do not close by
themselves usually require surgery at age 2-4 years. Even if the area is closed at birth, umbilical
hernias can appear later in life because this spot may remain a weaker place in the abdominal
wall. Umbilical hernias can appear later in life or in women who are having or have had children.

Other types of hernia

1. Incisional hernia: Abdominal surgery causes a flaw in the abdominal wall. This flaw can
create an area of weakness where a hernia may develop. This occurs after 2-10% of all
abdominal surgeries, although some people are more at risk. Even after surgical repair,
incisional hernias may return.

2. Spigelian hernia: This rare hernia occurs along the edge of the rectus abdominus muscle,
which is several inches to the side of the middle of the abdomen.

3. Obturator hernia: This extremely rare abdominal hernia develops mostly in women. This
hernia protrudes from the pelvic cavity through an opening in the pelvic bone (obturator
foramen). This will not show any bulge but can act like a bowel obstruction and cause nausea
and vomiting.

4. Epigastric hernia: Occurring between the navel and the lower part of the rib cage in the
midline of the abdomen, epigastric hernias are composed usually of fatty tissue and rarely
contain intestine. Formed in an area of relative weakness of the abdominal wall, these hernias
are often painless and unable to be pushed back into the abdomen when first discovered.

Causes of hernia

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Although abdominal hernias can be present at birth, others develop later in life. Some involve
pathways formed during fetal development, existing openings in the abdominal cavity, or areas
of abdominal wall weakness.

 Any condition that increases the pressure of the abdominal cavity may contribute to the
formation or worsening of a hernia. Examples include:

 Obesity

 Heavy lifting

 Coughing

 Straining during a bowel movement or urination

 Chronic lung disease

 Fluid in the abdominal cavity

 A family history of hernias can make you more likely to develop a hernia.

Diagnosis of Hernia
If you have an obvious hernia, the doctor may not require any other tests (if you are healthy
otherwise). If you have symptoms of a hernia (dull ache in groin or other body area with lifting or
straining but without an obvious lump), the doctor may feel the area while increasing abdominal
pressure (having you stand or cough). This action may make the hernia able to be felt. If you
have an inguinal hernia, the doctor will feel for the potential pathway and look for a hernia by
inverting the skin of the scrotum with his or her finger.

Hernia Treatment

Medical Treatment

Treatment of a hernia depends on whether it is reducible or irreducible and possibly

strangulated.

 Reducible hernia

 In general, all hernias should be repaired to avoid the possibility of future intestinal
strangulation.

 If you have pre-existing medical conditions that would make surgery unsafe, your doctor may
not repair your hernia but will watch it closely.

 Rarely, your doctor may advise against surgery because of the special condition of your
hernia.

 Some hernias have or develop very large openings in the abdominal wall, and closing the
opening is complicated because of its large size.

 These kinds of hernias may be treated without surgery, perhaps using abdominal binders.

 Some doctors feel that the hernias with large openings have a very low risk of strangulation.

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 The treatment of every hernia is individualized, and a discussion of the risks and benefits of
surgical versus nonsurgical management needs to take place.

 Irreducible hernia

 All acutely irreducible hernias need emergency treatment because of the risk of strangulation.

 An attempt to reduce (push back) the hernia will generally be made, often with medicine for
pain and muscle relaxation.

 If unsuccessful, emergency surgery is needed.

 If successful, however, treatment depends on the length of the time that the hernia was
irreducible.

 If the intestinal contents of the hernia had the blood supply cut off, the development of dead
(gangrenous) bowel is possible in as little as 6 hours.

 In cases where the hernia has been strangulated for an extended time, surgery is performed
to check whether the intestine has died and to repair the hernia.

 In cases where the length of time that the hernia was irreducible was short and gangrenous
bowel is not suspected, you may be discharged.

Because a hernia that was irreducible and is reduced has a dramatically increased risk of doing
so again, , you should therefore have surgical correction sooner rather than later.

Occasionally, the long-term irreducible hernia is not a surgical emergency. These hernias,
having passed the test of time without signs of strangulation, may be repaired electively.

Self-Care at Home

In general, all hernias should be repaired unless severe pre-existing medical conditions make
surgery unsafe. The possible exception to this is a hernia with a large opening. Trusses and
surgical belts or bindings may be helpful in holding back the protrusion of selected hernias when
surgery is not possible or must be delayed. However, they should never be used in the case of
femoral hernias.

Avoid activities that increase intra-abdominal pressure (lifting, coughing, or straining) that may
cause the hernia to increase in size.

Prevention

You can do little to prevent areas of the abdominal wall from being or becoming weak, which
can potentially become a site for a hernia.

Peritonitis

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Def: is the inflammation of the peritoneum (the serous and visceral membranes lining the abdominal
cavity) resulting from infection e.g bacterial or spresding from other organ characterised by fever,
abdominal tenderness.

Causes

 Usually this is as a result of bacterial infection with organisms mainly coming from the GIT.
 The common bacteria implicated here are E. coli, Klebsiella, proteus and pseudomonas.
 In women such organisms may come from as far as the internal reproductive organs
 Peritonitis can also be as a result of external source such as trauma and injury from gunshots stab
wound etc.
 It may be as a result of extension of inflammation from organs outside the peritoneum such as
kidneys
 Other secondary causes include appendicitis, perforated ulcers, Diverticulitis, bowel perforation and
abdominal surgical procedures and peritoneal dialysis

Primary causes

o Bacteria

o Trauma

o Gun shot wounds

o Talk or starch powder on surgeon’s gloves

Secondary causes

o Perforated ulcer

o Perforated intestines

o Perforated gull blader

o Raptured appendix

o Peritoneal dialysis

o PID

o Diverticulitis

o Abdominal surgical procedures

Path physiology

Peritonitis results from a leakage of abdominal contents into the abdominal cavity.

This is usually as result of infection causing inflammation and peroration, ischemia and trauma.

Bacteria proliferation occurs as a result of this leakage.

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 This brings about oedema of the tissue and exudates formation. Fluid develops within a short time and
collects in the peritoneal cavity.

The immediate response to this is hyper motility of the intestinal; tract followed by paralytic ileus.

The distension is as a result of air accumulation and fluid collection

Clinical picture

 Diffuse type of pain initially, later becoming constant and localized.

 Abdominal tenderness
 Abdominal distension
 Rebound tenderness
 Paralytic ileus with diminished peristalsis
 Increased temperature and pulse rate
 Elevation of WBC
 Nausea and vomiting

Diagnosis

 FBC shows elevated Leukocyte count, Low hemoglobin and haematocrit count, serum electrolyte may
review altered potassium, sodium and chlorides
 Abdominal x-ray reveals fluid and air collection
 CT - scan may show an abdominal abscess
 Peritoneal aspiration for culture and sensitivity studies to isolate causative organisms
 Blood culture

Medical management

Objectives

 Replacement of electrolytes to correct the imbalance

 Prevention of completion

 The fluid colloid and electrolyte replace is of primary importance therefore IV fluids will
be administered
 Analgesia are given for the abdominal pain
 Antiemetic are given to reduce vomiting and nausea
 Suction of the stomach and intestines helps to relieve the distension and promotes
intestinal motility
 The patient is put on massive antibiotic therapy with large doses of broad-spectrum
antibiotics administered until culture sensitivity results are available

Surgical management includes

 Removing the infected material

 Correcting the cause (appendectomy).

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Complications

 Generalized sepsis
 Shock from septicemia
 Hypovolaemic shock
 Intestinal obstruction
 Respiratory distress
 The post op complication include;
 evisceration abscess formation,
 adhesion formation wound dehiscence

Colostomy/iloestomy

Def: is a surgical creation of an opening called a stoma into the colon through the abdominal wall.

Indication

To allow drainage of evacuation of the contents outside the body

Nursing Management of Colostomy

The colostomy begins to function usually 3 to 6 days after surgery.

- Before this time the nurse should do the following;

 The stoma should be monitored for swelling (slight oedema from surgical manipulation is expected)
 Monitor the color of the stoma a health stoma should appear pink or red
 Check the discharge from the stoma (a small amount oozing is normal).
 Check for excessive bleeding
- The nurse begins to mange the colostomy and begins to teach the client how she/he
wound care for the colostomy in readiness for the patient to take control of his own care.
- The teaching includes skin care, how to apply and remove the drainage pouch.
- There is a particular danger to the excoriation of the personal skin where ulcers easily
develop. This is as a result of irritation from the adhering ostomy appliance.
- The effluent discharge from the ostomy may also contribute to this irritation particularly
with a transverse colon, which produces a mushy, and soft like discharge.
- The patient needs s to keep this area dry all the time.
- Use of deodorants and powder is encouraged.

 The other skin condition to worry about is the yeast infection and allergic dermatitis
- A micro pore tape should be applied if the patient wants to take a bath. This help s to
secure the pouch in place while bathing
- In order to remove the pouch, the patient should assume a comfortable sitting or
standing position and gently push the skin down from the face plate while pulling the pouch up
and away from the stoma.
- Gentle pressure prevents the skin from being traumatized and any liquid fecal matter
from spilling out.
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 - The patient is then instructed to wash the peristomal skin gently using a moist warm
cloth and a mild soap.
- The patient should move any excessive skin barrier.
- While cleaning the skin the stoma should be covered by a piece of gauze or a vaginal
tampon can be inserted gently to absorb excess drainage.
- After cleaning, the patient pats dry completely the area around the skin with a dry gauze
taking care not to rub the area.
- The patient can lightly rub nystatin powder around to prevent yeast growth.
- A drainage appliance is then secured
- The patient should always change the drainage pouch when it is one third full so that its
weight does not cause the appliance to separate from the adhesive disk and spill the contents
- Use of disposable and odor resistant appliances is encouraged.

Colostomy Irrigation

 A colostomy irrigation is done to empty the colon of faecal matter gas or mucous
cleanse the lower intestinal tract and to establish a regular pattern of evacuation so that normal
life activities can be pursued. A suitable time for irrigation is selected and if should be performed
at the same time each day.
 Before the procedure the patient sits on a chair in front of a toilet or on the toilet its
self. An irrigation reservoir of 500 to 1500 mls of lukewarm tap water is hung to 45 to 50 cm
above the stoma i.e. shoulder height when patient is sitted. The patient then removes the
drainage pouch and fluid allowed to run into the ostomy

Volvulus

Def: this occurs when a loop of the bowel twists through 180 degrees cutting off its blood supply.

 This ultimately causes gangrene and obstruction. Volvulus occurs in parts of the intestines that are
attached to the posterior abdominal wall by a long double fold of visceral peritoneum, the mesentery.

 The most common site for Volvulus in adults id the sigmoid colon and in children it’s the small
intestines

Causes

The causes are often unknown but the following are some of the predisposing factors

 An usually long mesocolon or mesentery

 Heavy loading of pelvic colon with feacal
 A slight of the loop of the bowel causing gas and fluid to accumulate and thus promote further
twisting
 Adhesions formed after surgery of peritonitis

Intussusception

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Def: this is invagination of the loop of intestine into itself.

Cause

 In adults tumors that bulge in the lumen i.e. polyps together with strong peristaltic
movement could be responsible for this.
 It mostly occurs in children when loop of the terminal ileum is pushed through the
ileocaecal valve.
 The overlying Mucosa bulges into the lumen creating a partial obstruction and rise in
pressure of the intestine proximal to the swelling.
 Strong peristaltic movements develop in an attempt to overcome this partial pressure
this unfortunately pushes the swollen part of bowel into the lumen of the section immediately
distal to it creating an invagination portion called Intussusception.
 The pressure on the veins is increased causing swelling congestion and ischemia with
possible gangrene formation.

Complete obstruction may occur.

Cancer of the colon

Colorectal cancer, also called colon cancer or large bowel cancer, includes cancerous growths in the
colon, rectum and appendix.

 Colorectal cancers arise from adenomatous polyps in the colon.

 These mushroom-shaped growths are usually benign, but some develop into cancer over time.

 Invasive cancers that are confined within the wall of the colon (TNM stages I and II) are curable with
surgery.

 If untreated, they spread to regional lymph nodes (stage III), where up to 73% are curable by surgery
and chemotherapy. Cancer that metastasizes to distant sites (stage IV) is usually not curable, although

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chemotherapy can extend survival, and in rare cases, surgery and chemotherapy together have seen
patients through to a cure.

 Radiation is used with rectal cancer.

Signs and symptoms

- The symptoms of colorectal cancer depend on the location of tumor in the bowel, and whether it has
spread elsewhere in the body (metastasis).

- Symptoms and signs are divided into local, constitutional (affecting the whole body) and metastatic
(caused by spread to other organs).

Local

Local symptoms are more likely if the tumor is located closer to the anus.

- There may be a change in bowel habit (new-onset constipation or diarrhea in the absence of another
cause),

- A feeling of incomplete defecation (rectal tenesmus)

- Reduction in diameter of stool;

- Tenesmus

- Change in stool shape is a characteristic of rectal cancer.

- Lower gastrointestinal bleeding,

- Passage of bright red blood in the stool, may indicate colorectal cancer, as may the increased
presence of mucus.

- Melena, black stool with a tarry appearance, normally occurs in upper gastrointestinal bleeding (such
as from a duodenal ulcer), but is sometimes encountered in colorectal cancer when the disease is
located in the beginning of the large bowel.

 A tumor that is large enough to fill the entire lumen of the bowel may cause bowel obstruction.

- This situation is characterized by constipation, abdominal pain, abdominal distension and vomiting.

- This occasionally leads to the obstructed and distended bowel perforating and causing peritonitis.

- A large left colonic tumor may compress the left ureter and cause hydronephrosis.

Constitutional

If a tumor has caused chronic occult bleeding, iron deficiency anemia may occur; this may be
experienced as:

- Fatigue,

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- Heart palpitations

- Pallor (pale appearance of the skin).

- Weight loss, generally due to a decreased appetite.

- An unexplained fever

- Thrombosis, usually deep vein thrombosis.

Risk factors

Certain factors increase a person's risk of developing the disease. These include:

 Age: The risk of developing colorectal cancer increases with age. Most cases occur in the 60s and 70s,
while cases before age 50 are uncommon unless a family history of early colon cancer is present.
 Polyps of the colon, particularly adenomatous polyps, are a risk factor for colon cancer. The removal
of colon polyps at the time of colonoscopy reduces the subsequent risk of colon cancer.
 History of cancer. Individuals who have previously been diagnosed and treated for colon cancer are
at risk for developing colon cancer in the future. Women who have had cancer of the ovary, uterus, or
breast are at higher risk of developing colorectal cancer.
 Heredity:
o Family history of colon cancer, especially in a close relative before the age of 55 or multiple relatives.
o Familial adenomatous polyposis (FAP) carries a near 100% risk of developing colorectal cancer by the
age of 40 if untreated
o Hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome
o Gardner syndrome
 Smoking: Smokers are more likely to die of colorectal cancer than nonsmokers. An American Cancer
Society study found "Women who smoked were more than 40% more likely to die from colorectal
cancer than women who never had smoked. Male smokers had more than a 30% increase in risk of
dying from the disease compared to men who never had smoked.
 Diet: Studies show that a diet high in red meat and low in fresh fruit, vegetables, poultry and fish
increases the risk of colorectal cancer. In June 2005, a study by the European Prospective Investigation
into Cancer and Nutrition suggested that diets high in red and processed meat, as well as those low in
fiber, are associated with an increased risk of colorectal cancer. Individuals who frequently eat fish
showed a decreased risk. However, other studies have cast doubt on the claim that diets high in fiber
decrease the risk of colorectal cancer; rather, low-fiber diet was associated with other risk factors,
leading to confounding. The nature of the relationship between dietary fiber and risk of colorectal
cancer remains controversial.
 Lithocholic acid: Lithocholic acid is a bile acid that acts as a detergent to solubilize fats for absorption.
It is made from chenodeoxycholic acid by bacterial action in the colon. It has been implicated in human
and experimental animal carcinogenesis. Carbonic acid type surfactants easily combine with calcium ion
and become detoxication products.
 Physical inactivity: People who are physically active are at lower risk of developing colorectal cancer.
 Viruses: Exposure to some viruses (such as particular strains of human papilloma virus) may be
associated with colorectal cancer.
 Primary sclerosing cholangitis offers a risk independent to ulcerative colitis.
 Low levels of selenium
 Inflammatory bowel disease: About one percent of colorectal cancer patients have a history of chronic
ulcerative colitis. The risk of developing colorectal cancer varies inversely with the age of onset of the
colitis and directly with the extent of colonic involvement and the duration of active disease. Patients

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with colorectal Crohn's disease have a more than average risk of colorectal cancer, but less than that of
patients with ulcerative colitis
 Environmental factors: Industrialized countries are at a relatively increased risk compared to less
developed countries that traditionally had high-fiber/low-fat diets. Studies of migrant populations have
revealed a role for environmental factors, particularly dietary, in the etiology of colorectal cancers.
 Exogenous hormones: The differences in the time trends in colorectal cancer in males and females
could be explained by cohort effects in exposure to some gender-specific risk factor; one possibility that
has been suggested is exposure to estrogens. There is, however, little evidence of an influence of
endogenous hormones on the risk of colorectal cancer. In contrast, there is evidence that exogenous
estrogens such as hormone replacement therapy (HRT), tamoxifen, or oral contraceptives might be
associated with colorectal tumors.
 Alcohol: Drinking, especially heavily, may be a risk factor.
 Vitamin B6 intake is inversely associated with the risk of colorectal cancer.

Pathogenesis

Colorectal cancer is a disease originating from the epithelial cells lining the colon or rectum of the
gastrointestinal tract, as a result of mutations along the Wnt signaling pathway. Some of the mutations
are inherited, and others are acquired. The most commonly mutated gene in all colorectal cancer is the
APC gene, which produces the APC protein. The APC protein is the "brake" on the β-catenin protein.
Without APC, β-catenin translocates (moves) into the nucleus, binds to DNA, and activates the
expression of more proteins. (If APC is not mutated in colorectal cancer, then β-catenin itself is.)

Beyond the defects in the Wnt-APC-beta-catenin signaling pathway, other mutations must occur for the
cell to become cancerous. The p53 protein, produced by the TP53 gene, normally monitors cell division
and kills cells if they have Wnt pathway defects. Eventually, a cell line acquires a mutation in the TP53
gene and transforms the tissue from an adenoma into an invasive carcinoma. (Sometimes the gene
encoding p53 is not mutated, but another protective protein named BAX is.) [3]

Other apoptotic proteins commonly deactivated in colorectal cancers are TGF-β and DCC (Deleted in
Colorectal Cancer). TGF-β has a deactivating mutation in at least half of colorectal cancers. Sometimes
TGF-β is not deactivated, but a downstream protein named SMAD is. DCC commonly has deletion of its
chromosome segment in colorectal cancer.

Some genes are oncogenes -- they are overexpressed in colorectal cancer. For example, genes encoding
the proteins KRAS, RAF, and PI3K, which normally stimulate the cell to divide in response to growth
factors, can acquire mutations that result in over-activation of cell proliferation. PTEN, a tumor
suppressor, normally inhibits PI3K, but can sometimes become mutated and deactivated.

Diagnosis

 Endoscopic image of colon cancer identified in sigmoid colon on screening colonoscopy in the setting
of Crohn's disease.

 Digital rectal exam (DRE): The doctor inserts a lubricated, gloved finger into the rectum to feel for
abnormal areas. It only detects tumors large enough to be felt in the distal part of the rectum but is
useful as an initial screening test.
 Fecal occult blood test (FOBT): a test for blood in the stool. Two types of tests can be used for
detecting occult blood in stools i.e. guaiac based (chemical test) and immunochemical. The sensitivity of

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immunochemical testing is superior to that of chemical testing without an unacceptable reduction in
specifity.
 Endoscopy:
o Sigmoidoscopy: A lighted probe (sigmoidoscope) is inserted into the rectum and lower colon to check
for polyps and other abnormalities.
o Colonoscopy: A lighted probe called a colonoscope is inserted into the rectum and the entire colon to
look for polyps and other abnormalities that may be caused by cancer. A colonoscopy has the advantage
that if polyps are found during the procedure they can be removed immediately. Tissue can also be
taken for biopsy.

Other screening methods

 Double contrast barium enema (DCBE): First, an overnight preparation is taken to cleanse the colon.
An enema containing barium sulfate is administered, then air is insufflated into the colon, distending it.
The result is a thin layer of barium over the inner lining of the colon which is visible on X-ray films. A
cancer or a precancerous polyp can be detected this way. This technique can miss the (less common) flat
polyp.
 Virtual colonoscopy replaces X-ray films in the double contrast barium enema (above) with a special
computed tomography scan and requires special workstation software in order for the radiologist to
interpret. This technique is approaching colonoscopy in sensitivity for polyps. However, any polyps
found must still be removed by standard colonoscopy.
 Standard computed axial tomography is an x-ray method that can be used to determine the degree of
spread of cancer, but is not sensitive enough to use for screening. Some cancers are found in CAT scans
performed for other reasons.
 Blood tests: Measurement of the patient's blood for elevated levels of certain proteins can give an
indication of tumor load. In particular, high levels of carcinoembryonic antigen (CEA) in the blood can
indicate metastasis of adenocarcinoma. These tests are frequently false positive or false negative, and
are not recommended for screening, it can be useful to assess disease recurrence. CA19-9 and CA 242
biomarkers can indicate e-selectin related metastatic risks, help follow therapeutic progress, and assess
disease recurrence.
 Genetic counseling and genetic testing for families who may have a hereditary form of colon cancer,
such as hereditary nonpolyposis colorectal cancer (HNPCC) or familial adenomatous polyposis (FAP).
 Positron emission tomography (PET) is a 3-dimensional scanning technology where a radioactive sugar
is injected into the patient, the sugar collects in tissues with high metabolic activity, and an image is
formed by measuring the emission of radiation from the sugar. Because cancer cells often have very
high metabolic rates, this can be used to differentiate benign and malignant tumors. PET is not used for
screening and does not (yet) have a place in routine workup of colorectal cancer cases.
 Whole-body PET imaging is the most accurate diagnostic test for detection of recurrent colorectal
cancer, and is a cost-effective way to differentiate resectable from nonresectable disease. A PET scan is
indicated whenever a major management decision depends upon accurate evaluation of tumour
presence and extent.
 Stool DNA testing is an emerging technology in screening for colorectal cancer. Premalignant
adenomas and cancers shed DNA markers from their cells which are not degraded during the digestive
process and remain stable in the stool. Capture, followed by PCR amplifies the DNA to detectable levels
for assay. Clinical studies have shown a cancer detection sensitivity of 71%–91%.
 High C-Reactive Protein levels is risk marker
 miRNA-profiling-based screening for detection of early-stage colorectal cancer: The life science and
research company Exiqon A/S has developed a novel plasma miRNA screening assay for identifying
early-stage colorectal cancer. Plasma miRNA has been shown to be a promising biomarker for many
diseases including cancer. The goal of this technique is to select individuals for colonoscopy rather than
to replace colonoscopy as the gold standard of colorectal cancer diagnosis. Blood plasma samples
collected from patients with early, resectable (Stage II) colorectal cancer and sex-and age-matched
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healthy volunteers were profiled. So far potential biomarkers have shown promising specificity and
sensitivity. The same technology can also be applied to patients who may be at higher risk of relapse and
therefore in need for more aggressive adjuvant chemotherapy... [41][42][43]

Staging

- Colon cancer staging is an estimate of the amount of penetration of a particular cancer.

- It is performed for diagnostic and research purposes, and to determine the best method of
treatment.

- The systems for staging colorectal cancers depend on the extent of local invasion, the degree of
lymph node involvement and whether there is distant metastasis.

Definitive staging can only be done after surgery has been performed and pathology reports reviewed.
An exception to this principle would be after a colonoscopic polypectomy of a malignant pedunculated
polyp with minimal invasion. Preoperative staging of rectal cancers may be done with endoscopic
ultrasound. Adjunct staging of metastasis include Abdominal Ultrasound, CT, PET scanning, and other
imaging studies.

The most common staging system is the TNM (for tumors/nodes/metastases) system, from the
American Joint Committee on Cancer (AJCC). The TNM system assigns a number based on three
categories. "T" denotes the degree of invasion of the intestinal wall, "N" the degree of lymphatic node
involvement, and "M" the degree of metastasis. The broader stage of a cancer is usually quoted as a
number I, II, III, IV derived from the TNM value grouped by prognosis; a higher number indicates a more
advanced cancer and likely a worse outcome. Details of this system are in the graph below:

AJCC stage TNM stage TNM stage criteria for colorectal cancer

Stage 0 Tis N0 M0 Tis: Tumor confined to mucosa; cancer-in-situ

Stage I T1 N0 M0 T1: Tumor invades submucosa

Stage I T2 N0 M0 T2: Tumor invades muscularis propria

Stage II-A T3 N0 M0 T3: Tumor invades subserosa or beyond (without other organs involved)

Stage II-B T4 N0 M0 T4: Tumor invades adjacent organs or perforates the visceral peritoneum

Stage III-A T1-2 N1 M0 N1: Metastasis to 1 to 3 regional lymph nodes. T1 or T2.

Stage III-B T3-4 N1 M0 N1: Metastasis to 1 to 3 regional lymph nodes. T3 or T4.

Stage III-C any T, N2 M0 N2: Metastasis to 4 or more regional lymph nodes. Any T.

Stage IV any T, any N, M1 M1: Distant metastases present. Any T, any N.

 Dukes’ classification is an older and less complicated staging system that predates the TNM system. It
identifies the stages as:

 A - Tumour confined to the intestinal wall

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 B - Tumour invading through the intestinal wall
 C - With lymph node(s) involvement (this is further subdivided into C1 lymph node involvement
where the apical node is not involved and C2 where the apical lymph node is involved)
 D - With distant metastasis

 A: Tumor limited to mucosa; carcinoma in situ

 B1: Tumor grows through muscularis mucosae but not through muscularis propria

 B2: Tumor grows beyond muscularis propria

 C1: Stage B1 with regional lymph node metastases

 C2: Stage B2 with regional lymph node metastases

 D: Distant metastases.

Additional Staging

Venous invasion (v)

 v0 no venous invasion
 v1 microscopic venous invasion
 v2 macroscopic venous invasion

Lymphatic invasion (l)

 l0 no lymphatic vessel invasion

 l1 lymphatic vessel invasion

Histologic grade (G)

 g1 well differentiated
 g2 moderately differentiated
 g3 poorly differentiated
 g4 undiffererentiated

Prevention

Most colorectal cancers should be preventable, through increased surveillance, improved lifestyle, and
the use of dietary chemopreventative agents.

Surveillance

Most colorectal cancers arise from adenomatous polyps. These lesions can be detected and removed
during colonoscopy.

Lifestyle and nutrition

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The comparison of colorectal cancer incidence in various countries strongly suggests that sedentarity,
overeating (i.e., high caloric intake), and perhaps a diet high in meat (red or processed) could increase
the risk of colorectal cancer.

Chemoprevention

- Other food components like calcium or folic acid (a B vitamin), and NSAIDs like aspirin are able to
decrease carcinogenesis in pre-clinical development models:

Aspirin chemoprophylaxis

- Aspirin should not be taken routinely to prevent colorectal cancer, even in people with a family
history of the disease, because the risk of bleeding and kidney failure from high dose aspirin (300 mg or
more) outweighs the possible benefits.

Calcium

- Calcium supplementation might contribute to a moderate degree to the prevention of colorectal

adenomatous polyps, this does not constitute sufficient evidence to recommend the general use of
calcium supplements to prevent colorectal cancer.

Vitamin D

- Vitamin D was beneficial in preventing colorectal cancer, which showed an inverse relationship with
blood levels of 80 nmol/L or higher associated with a 72% risk reduction compared with lower than 50
nmol/L.

- A possible mechanism is inhibition of Hedgehog signal transduction.

Management

- The treatment depends on the stage of the cancer.

- When colorectal cancer is caught at early stages (with little spread), it can be curable.

- Surgery remains the primary treatment, while chemotherapy and/or radiotherapy may be
recommended depending on the individual patient's staging and other medical factors.

Surgery

Surgeries can be categorised into curative, palliative, bypass, fecal diversion, or open-and-close.

Curative surgical treatment can be offered if the tumor is localized.

 Very early cancer that develops within a polyp can often be cured by removing the polyp (i.e.,
polypectomy) at the time of colonoscopy.
 In colon cancer, a more advanced tumor typically requires surgical removal of the section of colon
containing the tumor with sufficient margins, and radical en-bloc resection of mesentery and lymph
nodes to reduce local recurrence (i.e., colectomy). If possible, the remaining parts of colon are
anastomosed to create a functioning colon. In cases when anastomosis is not possible, a stoma (artificial
orifice) is created.
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 Curative surgery on rectal cancer includes total mesorectal excision (lower anterior resection) or
abdominoperineal excision.

- In case of multiple metastases, palliative (noncurative) resection of the primary tumor is still offered
to reduce further morbidity caused by tumor bleeding, invasion, and its catabolic effect.

- Surgical removal of isolated liver metastases is, however, common and may be curative in selected
patients;

- Improved chemotherapy has increased the number of patients who are offered surgical removal of
isolated liver metastases.

- If the tumor invaded into adjacent vital structures, which makes excision technically difficult, the
surgeons may prefer to bypass the tumor (ileotransverse bypass) or to do a proximal fecal diversion
through a stoma.

The worst case would be an "open-and-close" surgery, when surgeons find the tumor unresectable and
the small bowel involved; any more procedures are thought by some to do more harm than good to the
patient. This is uncommon with the advent of laparoscopy and better radiological imaging. Most of
these cases formerly subjected to "open and close" procedures are now diagnosed in advance and
surgery avoided.

- Laparoscopic-assisted colectomy is a minimally invasive technique that can reduce the size of the
incision and may reduce postoperative pain.

As with any surgical procedure, colorectal surgery may result in complications, including

 wound infection, dehiscence (bursting of wound) or hernia,

 anastomosis breakdown, leading to abscess or fistula formation, and/or peritonitis,
 bleeding with or without hematoma formation,
 Adhesions resulting in bowel obstruction. A 5-year study of patients who had surgery in 1997 found
the risk of hospital readmission to be 15% after panproctocolectomy, 9% after total colectomy, and 11%
after ileostomy[63]
 adjacent organ injury; most commonly to the small intestine, ureters, spleen, or bladder, and
 Cardiorespiratory complications, such as myocardial infarction, pneumonia, arrythmia, pulmonary
embolism, etc.

Chemotherapy

- Chemotherapy is used to reduce the likelihood of metastasis developing, shrink tumor size, or slow
tumor growth.

- Chemotherapy is often applied after surgery (adjuvant), before surgery (neoadjuvant), or as the
primary therapy (palliative).

- In colon cancer, chemotherapy after surgery is usually only given if the cancer has spread to the
lymph nodes (Stage III).

 Adjuvant (after surgery) chemotherapy

o 5-fluorouracil (5-FU) or capecitabine (Xeloda)
o Leucovorin (LV, folinic Acid)

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o Oxaliplatin (Eloxatin)

 Chemotherapy for metastatic disease. Commonly used first line chemotherapy regimens involve the
combination of infusional 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) with bevacizumab or
infusional 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI) with bevacizumab or the same
chemotherapy drug combinations with cetuximab in KRAS wild type tumors
o 5-fluorouracil (5-FU) or capecitabine
o UFT or Tegafur-uracil
o Leucovorin (LV, folinic Acid)
o Irinotecan (Camptosar)
o Oxaliplatin (Eloxatin)
o Bevacizumab (Avastin)
o Cetuximab (Erbitux)
o Panitumumab (Vectibix)

 In clinical trials for treated/untreated metastatic disease. [64]

o Bortezomib (Velcade)
o Oblimersen (Genasense, G3139)
o Gefitinib and erlotinib (Tarceva)
o Topotecan (Hycamtin)

Radiation therapy

Radiotherapy is not used routinely in colon cancer, as it could lead to radiation enteritis, and it is difficult
to target specific portions of the colon. It is more common for radiation to be used in rectal cancer, since
the rectum does not move as much as the colon and is thus easier to target. Indications include:

 Colon cancer
o pain relief and palliation - targeted at metastatic tumor deposits if they compress vital structures
and/or cause pain
 Rectal cancer
o neoadjuvant - given before surgery in patients with tumors that extend outside the rectum or have
spread to regional lymph nodes, to decrease the risk of recurrence following surgery or to allow for less
invasive surgical approaches (such as a low anterior resection instead of an abdominoperineal
resection). In locally advanced adenocarcinoma of middle and lower rectum, regional hyperthermia
added to chemoradiotherapy achieved good results in terms of rate of sphincter-sparing surgery.

o adjuvant - where a tumor perforates the rectum or involves regional lymph nodes (AJCC T3 or T4
tumors or Duke's B or C tumors)
o palliative - to decrease the tumor burden to relieve or prevent symptoms

Sometimes chemotherapy agents are used to increase the effectiveness of radiation by sensitizing tumor
cells, if present.

Immunotherapy

Bacillus Calmette-Guérin (BCG) is being investigated as an adjuvant mixed with autologous tumor cells in
immunotherapy for colorectal cancer.

Cancer Vaccine

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TroVax, a cancer vaccine, produced by Oxford BioMedica, is in Phase III trials for renal cancers, and
phase III trials are planned for colon cancers.

Support therapies

- Cancer diagnosis very often results in an enormous change in the patient's psychological wellbeing.

- Various support resources are available from hospitals and other agencies, which provide

 counseling,

 social service support,

 Cancer support groups, and other services.

 These services help to mitigate some of the difficulties of integrating patients' medical complications
into other parts of their lives.

Management of acute abdominal conditions

The following conditions fall under acute abdomen and take a similar approach in their management.

 Appendicitis/Appendectomy
 Intestinal Obstruction/Bowel obstruction
 Peritonitis
 Volvulus
 Intussusception
 Strangulated hernia
 Ruptured spleen
 Ectopic pregnancy
 Perforated peptic ulcer
 Burst abdomen

Pre operative Objectives (Surgical Management)

 To ensure that Surgery is performed as soon as possible in order to decrease the risk of
complications.
 To correct or prevent fluid and electrolyte imbalance and dehydration by giving antibiotics and
intravenous fluids before surgery
 To relieve pain by giving analgesia, as patient awaits surgery
 To prepare the patient physically, emotionally, psychologically so as to enable him withstand the
effects of surgery and administration of anesthesia.

Nursing Care Objectives

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The objectives of nursing management are;

 Provide a safe and conducive environment for rapid recovery from the disease process

 Help to relieve discomfort and pain

 Prevent occurrence of complications.

Environment

 The patient with acute abdomen is nursed in a surgical ward preferable in a side ward/or in an acute
bay, for easy observations and away from routine ward traffic to ensure maximum rest and comfort.

 The ward should be cleaned every day by thorough dump dusting, mopping and drying all the wet
surfaces. These measures prevent cross infection, provide a comfortable and soothing environment.

 It should be well ventilated for easy circulation of air.

 All emergency equipment such as emergency trolley, Oxygen machine suction machine etc should be
within reach for easy management of emergencies

 It should have adequate light for easy observations.

Position

The patient is nursed in a position he finds more comfortable, preferably lying on the unaffected side. As
he may be restricted by treatment regimes, such as immobilization, he should ensure frequent turnings
{at least 2 hourly} to promote circulation and prevent development of pressure sores.

Psychological care

 The patient may be apprehensive about the out come of the disease process and the possibility of
long term treatment or immobilization.

 His self concept is usually altered because of a number of uncertainties.

 Quickly help the patient resolve the anxieties in readiness for surgery

 Explain to the patient the disease process, its eventful outcomes without alarming the patient. Focus
on the positive outcomes but avoid giving false hopes.

 Patient should understand the need for urgent surgery /intervention.

 Ensure you obtain an informed consent

 Involve the significant others in the care of the patient as home care will be inevitable.

Rest and activity

The patient should understand the rationale for the activity restrictions.

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The joints above and below the affected part should be gently placed through a range of motions.

The nurse encourages full range of ADLs within the physical limitations to promote the general well
being.

Pain relief

There may be need to immobilize the patient or the affected part is usually immobilized in a split to
decrease pain and muscle spasm.

The nurse monitors the neuromuscular status of the affected extremity.

The wounds are usually very painful thus they should be handled with care and gentleness.

Elevation reduces swelling and the associated discomfort while the pain can be controlled prescribed
analgesia.

Observations

 Vital signs of temperature and pulse rate, blood pressure and respirations are taken every 15 minutes
to monitor the condition or disease process.

 Monitoring of the neuromuscular function is cardinal to ensure that ischemia is not developing.

 The general well being of the patient is frequently assessed,

 his reaction to pain,

 his nutritional status,

 Compliance to the treatment regimes such as immobilization and generally his reaction to
hospitalization.

 Any hemorrhages or bleeding are noted and recorded

Wound Care/Hygiene.

Daily wound care with the prescribed antiseptic solution should be done. This helps to halt the infective
process. Sterile equipment and material should be used each time dressings are done.

 Ensure all drainage tubes are patent and follow the Doctors orders to remove or change them.

 Patient is taken through the process of wound care so that they would be able to manage the
wounds at home

 Patient is also encouraged to assume personal hygiene measures such as general body hygiene oral
care, nail care and hair care.

 The clothes worn should be clean

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 And linen where patient is lying should be frequently changed.

Medications

Patient may be put on long term antibiotic therapy,

 Thus adherence to the therapeutic regime will be critical to avoid resistance developing.

 The nurse monitors the patient for super infection as a result of long term use of antibiotics. These
could be vaginal candidiasis, oral candidiasis or foul smelling stools

Patient teaching /IEC

 Patient’s relatives must learn and recognize the importance of adhering to therapeutic regimes,

 Preventing falls and other injuries.

 Patient may need to know how to manage IV at home

 Identification of additional painful sites should be reported

 Report any elevation in temperature

Complications of acute abdomen

 Infection as a result of

 Hemorrhage as a result of

 Intestinal obstruction following intuccesption or Volvulus

 Peritonitis due overflow of infected contents in the abdomen

 Aneamia due excessive loss of blood/bleeding

 Gangrene due to blood flow obstruction

 Hypovolaemic Shock due to hemorrhage

 Neurogenic shock due to pain

DISODERS OF THE RECTUM AND ANAL CANAL

Hemorrhoid

DEF: These are verivosities in the superior or inferior hemorrhoidal venous plexus resulting from
increased intravenous pressure in the hemorrhoidal plexus characterised by intermitent rectal bleeding
after defecation.

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  Hemorrhoids are normal vascular structures in the anal canal which help with stool
control.
 They become pathological or known as piles when swollen or inflamed. In their
physiological state they act as cushions composed of arterio-venous channels and connective
tissue that aid the passage of stool.
 The symptoms of pathological hemorrhoids depend on the type present. Internal
hemorrhoids usually present with painless rectal bleeding while external hemorrhoids present
with pain in the area of the anus.
 Recommended treatment consists of increasing fiber intake, oral fluids to maintain
hydration, NSAID analgesics, sitz baths, and rest.
 Surgery is reserved for those who fail to improve following these measures.

Causes

 A number of factors may lead to the formations of hemorrhoids;

 Hemorrhoids probably results from increased intravenous pressure in the hemorrhoidal
plexus.

- Predisposing factors

i. irregular bowel habits (constipation or diarrhea) straining or stool due to constipation or

diarrhoea
ii. Coughing, sneezing or vomiting
iii. Excessive exercise
iv. nutrition (low-fiber diet),
v. increased intra-abdominal pressure (prolonged straining or sitting),
vi. Pregnancy - during pregnancy, pressure from the fetus on the abdomen and hormonal
changes cause the hemorrhoidal vessels to enlarge.
vii. Delivery also leads to increased intra-abdominal pressures.
viii. genetics,
ix. absence of valves within the hemorrhoidal veins,
x. Aging – due to loss of muscle tone
xi. Conditions such as Heart failure, heaptic diseases (cirrhosis, amoebic abscess, hepatitis)
xii. Alcoholism
xiii. Ano-rectal infections, rectal surgery, anal intercose, episiotomy
xiv. obesity

Classification

 There are two types of hemorrhoids, external and internal, which are differentiated via
their position with respect to the dentate line.

External

 External hemorrhoids are those that occur outside the anal verge (the distal end of the
anal canal).
 Specifically they are varicosities of the veins draining the territory of the inferior rectal
arteries, which are branches of the internal pudendal artery.
 They are sometimes painful, and often accompanied by swelling and irritation.
 Itching, although often thought to be a symptom of external hemorrhoids, is more
commonly due to skin irritation.
 External hemorrhoids are prone to thrombosis: if the vein ruptures and/or a blood clot
develops, the hemorrhoid becomes a thrombosed hemorrhoid.

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Internal

 Internal hemorrhoids are those that occur inside the rectum. Specifically they are
varicosities of veins draining the territory of branches of the superior rectal arteries.
 As this area lacks pain receptors, internal hemorrhoids are usually not painful and most
people are not aware that they have them.
 Internal hemorrhoids, however, may bleed when irritated.
 Untreated internal hemorrhoids can lead to two severe forms of hemorrhoids:
i. prolapsed
ii. Strangulated hemorrhoids.
- Prolapsed hemorrhoids are internal hemorrhoids that are so distended that they are
pushed outside the anus.
- If the anal sphincter muscle goes into spasm and traps a prolapsed hemorrhoid outside the
anal opening, the supply of blood is cut off, and the hemorrhoid becomes a strangulated
hemorrhoid.

Internal hemorrhoids can be further graded by the degree of prolapse.

 Grade I: No prolapse.
 Grade II: Prolapse upon defecation but spontaneously reduce.
 Grade III: Prolapse upon defecation and must be manually reduced.
 Grade IV: Prolapsed and cannot be manually reduced.

Signs and symptoms

 Hemorrhoids usually present with;

- Anal itching resulting from poor anal hygiene
- rectal pain,
- Rectal bleeding with a vague feeling of anal discomfort when bleeding occurs
- Pruritis and mucus discharge
- Large subcateneous lump in the anal area in case of thrombus
- Anal tenderness
 External hemorrhoids are painful
 Internal hemorrhoids usually are not painful unless they become thrombosed or necrotic.
 Most common symptom of internal hemorrhoids is bright red blood covering the stool, a
condition known as hematochezia, on toilet paper, or in the toilet bowl. They may protrude
through the anus.
 Symptoms of external hemorrhoids include painful swelling or lump around the anus.

Pathophysiology

- Hemorrhoid cushions are a part of normal human anatomy and only become a
pathological disease when they experience abnormal changes.
- There are three cushions present in the normal anal canal.
- They are important for continence contributing to at rest 15–20% of anal closure pressure
and act to protect the anal sphincter muscles during the passage of stool.

Prevention

- The best way to prevent hemorrhoids is to keep stools soft so they pass easily, thus
decreasing pressure and straining,
- to empty bowels as soon as possible after the urge occurs.
- Exercise, including walking, and increased fiber in the diet help reduce constipation and
straining by producing stools that are softer and easier to pass.
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 - Spending less time attempting to defecate and avoiding reading while on the toilet have
been recommended.

Diagnosis

 A visual examination of the anus and surrounding area may be able to diagnose external
or prolapsed hemorrhoids.
 A rectal exam may be performed to detect possible rectal tumors, polyps, an enlarged
prostate, or abscesses. This examination may not be possible without appropriate sedation due to
pain although most internal hemorrhoids do not present with pain.
 Visual confirmation of internal hemorrhoids is via anoscopy or procotscopy. This device
is basically a hollow tube with a light attached at one end that allows one to see the internal
hemorrhoids, as well as possible polyps in the rectum.
 Endoscopic image of internal hemorrhoids seen on retroflexion of the flexible
sigmoidoscope at the ano-rectal junction.

Treatments

Aims

 Combant swelling and congestion

 Regulate bowel habits
 Reduce pain

Conservative treatment typically consists of;

- Increasing dietary fiber, oral fluids to maintain hydration, defecation

- Stool softeners to help prevent straining during
- Non-steroidal anti-inflammatory drugs (NSAID)s,
- sitz baths,
- rest
- Increased fiber intake has been shown to improve outcomes and may be achieved by
dietary alterations or the consumption of fiber supplements.
- Local anaethetic agents (lotion, cream or suppositories)
- Astringents or Cold compresses may be applied followed by warm sitz baths or thermal
packs.
- Steroids (Hydrocotisone) to relieve itching or inflamation
- Manual reduction in case of prolapsed internal hemorrhoids
- A sclerosing solution may be injected to induce scar formation and decrease prolapse

Procedures

 Rubber band ligation is a procedure in which elastic bands are applied onto an internal hemorrhoid at
least 1 cm above the dentate line to cut off its blood supply.
 Within 5–7 days, the withered hemorrhoid falls off. If the band is placed too close to the dentate line
intense pain results immediately afterwards.
 Sclerotherapy involves the injection of a sclerosing agent (such as phenol) into the hemorrhoid. This
causes the vein walls to collapse and the hemorrhoids to shrivel up.
 A number of cautery methods have been shown to be effective for hemorrhoids. This can be done
using electrocautery, infrared radiation or cryosurgery.

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 - A number of surgical techniques may be used if conservative medical management fails.
All are associated with some degree of complications including urinary retention, due to the close
proximity to the rectum of the nerves that supply the bladder, bleeding, infection, and anal
strictures.

 Hemorrhoidectomy is a surgical excision of the hemorrhoid used primary only in severe cases. [3] It is
associated with significant post operative pain and usually requires 2–4 weeks for recovery.[3]
 Doppler guided transanal hemorrhoidal dearterialization is a minimally invasive treatment using an
ultrasound Doppler to accurately locate the arterial blood inflow. These arteries are then “tied off” and the
prolapsed tissue is sutured back to its normal position. It has a slightly higher recurrence rate however has
less complications compared to a hemorrhoidectomy. [3]
 Stapled hemorrhoidectomy is a procedure that involves resection of soft tissue proximal to the dentate
line, disrupting the blood flow to the hemorrhoids. It is generally less painful than complete removal of
hemorrhoids and was associated with faster healing compare to a hemorrhoidectomy.

Complications

- Local infection or thrombosis

- Severe or recurrentbleeding
- Anaemia

Pruritus ani

Pruritus ani (also known as anusitis or "the swamps") is the irritation of the skin at the exit of the
rectum, known as the anus, causing the desire to scratch.

- The intensity of anal itching increases from moisture, pressure, and rubbing caused by
clothing and sitting.
- At worst, anal itching causes intolerable discomfort that often is accompanied by burning
and soreness.

Causes

Anal itching can be caused by irritating chemicals in the foods consumed, such as are found in:

 Spices, hot sauces, and peppers

 Coffee, tea
 Carbonated beverages
 Milk products
 Tomatoes and tomato products, such as ketchup
 White bread

The irritation can also be caused by;

- anal perspiration,
- frequent liquid stools,
- diarrhea,
- residual stool deposits,
- The escape of small amounts of stool as a result of incontinence or flatulence.
- Yeast infection or Candidiasis.

Predisposing factors
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 - Some diseases increase the possibility of yeast infections, such as diabetes mellitus or
HIV infection.
- Treatment with antibiotics can lead to a yeast infection and irritation of the anus.
- Psoriasis also can irritate the anus.
- Abnormal passageways (fistulas) from the small intestine or colon to the skin
surrounding the anus can form as a result of disease (such as Crohn's disease), and these fistulas
bring irritating fluids to the anal area.
- Other problems that can cause anal itching include pinworms, hemorrhoids, tears of the
anal skin (fissures), and skin tags (abnormal local growth of anal skin).

Treatment

Aims

- Relieving the burning and soreness.

- To clean and dry the anus thoroughly and avoid leaving soap in the anal area.

- Cleaning efforts should include gentle showering without direct rubbing or irritation of
the skin with either the washcloth or towel.
- After bowel movements, moist pads should be used for cleaning the anus instead of toilet
paper.
- Scratching the affected area is to be resisted, as it only aggravates the problem and can
lead to bleeding from the anal area.
- A gauze pad, folded in half and placed between the buttocks so that it contacts the
perianal area, is effective at wicking away the moisture that causes irritation.
- Ointments, creams, and gels--when used around the anus--should be applied as a thin
covering. When applied to the anal canal, these products should be inserted with a finger or a
"pile pipe."

Pruritus ani is often exacerbated by watery stools. To bulk them up and improve regularity, daily
spoonfuls of a "bowel recipe" consisting of 1 part unprocessed wheat bran, 1 part applesauce, and 1 part
prune juice can help, even better than commercially produced fiber supplements.

Local anesthetics

- Local anesthetics temporarily relieve pain, burning, and itching by numbing the nerve
endings.
- Local anesthetics include:

 Benzocaine 5% to 20%
 Relief, Procto Foam Non-steroid, Tronothane Hydrochloride
 Tetracaine 0.5% to 5.0%

Vasoconstrictors

- Vasoconstrictors are chemicals that resemble epinephrine, a naturally occurring chemical.

Applied to the anus, vasoconstrictors make the blood vessels become smaller, which may reduce
swelling.
- They also may reduce pain and itching due to their mild anesthetic effect.
- Vasoconstrictors applied to the perianal area--unlike vasoconstrictors that are taken orally
or by injection--have a low likelihood of causing serious side effects, such as high blood pressure,
nervousness, tremor, sleeplessness, and aggravation of diabetes or hyperthyroidism.
Vasoconstrictors include:

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 Ephedrine sulfate 0.1% to 1.25%
 Epinephrine 0.005% to 0.01%
 Phenylephrine 0.25% (Medicone Suppository, Preparation H, Rectacaine)

Protectants

- Protectants prevent irritation of the perianal area by forming a physical barrier on the skin
that prevents contact of the irritated skin with aggravating liquid or stool from the rectum.
- This barrier reduces irritation, itching, pain, and burning.
- Protectants include:

 Aluminum hydroxide gel

 Cocoa butter
 Glycerin
 Kaolin
 Lanolin
 Mineral oil (Balneol)
 Petroleum jelly
 Starch
 Zinc oxide or calamine (which contains zinc oxide) in concentrations of up to 25%
 Cod liver oil or shark liver oil if the amount of vitamin A is 10,000 USP units/day.

Astringents

- Astringents cause coagulation (clumping) of proteins in the cells of the perianal skin or
the lining of the anal canal.
- This action promotes dryness of the skin, which in turn helps relieve burning, itching, and
pain. Astringents include:

 Calamine 5% to 25%
 Zinc oxide 5% to 25% (Calmol 4, Nupercainal, Tronolane)
 Witch_hazel_(astringent) 10% to 50% (Fleet Medicated, Tucks, Witch Hazel Hemorrhoidal Pads)

Antiseptics

- Antiseptics inhibit the growth of bacteria and other organisms.

Examples of antiseptics include:

 Boric acid
 Hydrastis
 Phenol
 Benzalkonium chloride
 Cetylpyridinium chloride
 Benzethonium chloride
 Resorcinol

Keratolytics

- Keratolytics are chemicals that cause the outer layers of skin or other tissues to
disintegrate.
- The rationale for their use is that the disintegration allows medications that are applied to
the anus and perianal area to penetrate into the deeper tissues.
- The two approved keratolytics used are:
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 Aluminum chlorhydroxy allantoinate (alcloxa) 0.2% to 2.0%
 Resorcinol 1% to 3%

Analgesics

Analgesic products, like anesthetic products, relieve pain, itching, and burning by depressing receptors on
pain nerves. Examples include:

 Menthol 0.1% to 1.0% (greater than 1.0% is not recommended)

 Camphor 0.1% to 3% (greater than 3% is not recommended)
 Juniper tar 1% to 5%

Corticosteroids

- Corticosteroids reduce inflammation and can relieve itching, but their chronic use can
cause permanent damage to the skin.
 The OTC medication Lotrimin cream mixed with hydrocortisone 1% cream can be
applied daily.
- A mild alpha-hydroxyacid cream can help, as can plain petroleum jelly applied each day
to the anal area

 Methylpred 4mg (methylprednisolone tapered dose pack) has shown remission of symptoms in some
cases.

Complications

Anal fissure

DEF: An anal fissure is a crack or tear or laceration in the skin lining the anal canal that extends to the
circular muscle resulting from passege of hard stool that streaches the anal canal characterized by bright
red anal bleeding on the toilet paper, sometimes in the toilet, pain after defecation.

Causes

 Most anal fissures are caused by stretching of the anal mucosa beyond its capability.

 The most common cause of non-healing is spasming of the internal anal sphincter muscle which
results in impaired blood supply to the anal mucosa.

- The result is a non-healing ulcer, which may become infected by fecal bacteria.

 In adults, fissures may be caused by;

- constipation,

- the passing of large, hard stools,

- prolonged diarrhea and spasm

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- Rough anal sex.

 In older adults, anal fissures may be caused by;

- Decreased blood flow to the area.

Predisposing factors

 Anal fissures are also common in;

- Women after childbirth due to strening on the perineum during child birth or strictures caused by scar
tissue.

- Persons with Crohn's disease.

- Anal tuberclosis

- Anal cancer

- Proctitis

- Trauma

Signs and symptoms

- Tearing, cutting or burning pain immediately after bowel movement

- Blood on the under clothes or tissue paper

- Dysuria

- Pruritis

- Urinary frequency or urine retension

- Painful anal sphyncter spasms that results from ulceration of ‘sentinile pile’ (swelling at the lower end
of the fissure.

Diagnosis

- Anoscopy – showing longtudinal tears will help to confirm the diagnosis

- Sigmoidoscopy – to rule out inflamatory bowel disease

- Barrium enema -

Prevention

For adults, the following may help prevent anal fissure:

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 Avoiding straining when defecating. This includes treating and preventing constipation by eating food
rich in dietary fiber, drinking enough water, occasional use of a stool softener, and avoiding constipating
agents such as caffeine. Similarly, prompt treatment of diarrhea may reduce anal strain.
 Careful anal hygiene after defecation, including using soft toilet paper and/or cleaning with water.
 In cases of pre-existing or suspected fissure, use of a lubricating ointment (e.g. hemorrhoid
ointments) can be helpful.

 In infants,

- Frequent diaper change can prevent anal fissure.

- As constipation can be a cause, making sure the infant is drinking enough fluids (i.e. breastmilk,
proper ratios when mixing formulas).

- In infants, once an anal fissure has occurred, addressing underlying causes is usually enough to ensure
healing occurs.

Treatment

Aims

- Provide local pain relief with analgesics

- Prevent futher tearing by sotening stools

 Non-surgical treatment is recommended as first-line treatment of acute and chronic anal fissures.
Customary treatments include;

- Warm sitz baths,

- Topical anesthetics,

- high-fiber diet

- Stool softeners.

 Surgical treatment, under general anaesthesia, was either;

- Anal stretch (Lord's operation)

- Lateral sphincterotomy where the internal anal sphincter muscle is incised.

- Both operations aim to decrease sphincter spasming and thereby restore normal blood supply to the
anal mucosa.

- Surgical operations involve a general anaesthetic and can be painful postoperatively.

- Anal stretch is also associated with anal incontinence in a small proportion of cases and thus
sphincterotomy is the operation of choice.

- Injecting botulinum toxin into the anal sphincter to relax the sphincter and promote fissure healing.

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Drugs

- Branded preparations are now available of topical nitroglycerine ointment

- Topical nifedipine 0.3% with lidocaine 1.5% ointment

- Diltiazem 2%

- A common side effect drawback of nitroglycerine ointment is headache, caused by systemic

absorption of the drug, which limits patient acceptability.

Surgical procedures

Potential complications include;

- General risks from anesthesia,

- Infection

- Anal leakage (fecal incontinence).

 Surgical procedures include sphincterotomy and dilation.

Lateral internal sphincterotomy

- Lateral internal sphincterotomy (LIS) is the surgical procedure of choice for anal fissures due to its
simplicity and its high success rate.

- In this procedure the internal anal sphincter is partially divided in order to reduce spasming and thus
improve the blood supply to the perianal area.

- This improvement in the blood supply helps to heal the fissure, and the weakening of the sphincter is
also believed to reduce the potential for recurrence.

- LIS does, however, have a number of potential side effects including problems with incision site
healing and incontinence to flatus and faeces

Anal dilation (or dilatation)

- Anal dilatation or stretching of the anal canal (Lord's operation) has fallen out of favour in recent
years, primarily due to the perceived unacceptably high incidence of fecal incontinence.

- In addition, anal stretching can increase the rate of flatus incontinence.

Complications

- Abscess

- Fistula

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 - Spticaemia

- Haemorrhage

- Chronic fissure

- Scar tissue that may humper normal bowel evacuation

Anal fistula

An anal fistula, or fistula-in-ano, is an abnormal connection between the epithelialised surface of the anal
canal and (usually) the perianal skin.

-Anal fistulae originate from the anal glands, which are located between the two layers of the anal
sphincters and which drain into the anal canal.
-If the outlet of these glands becomes blocked, an abscess can form which can eventually point to the skin
surface. The tract formed by this process is the fistula.
-Abscesses can recur if the fistula seals over, allowing the accumulation of pus. It then points to the
surface again, and the process repeats.
 Anal fistulas per se do not generally harm, but can be very painful, and can be irritating because of the
pus-drain (it is also possible for formed stools to be passed through the fistula); additionally, recurrent
abscesses may lead to significant short term morbidity from pain, and create a nidus for systemic
spread of infection.

Symptoms

Anal fistulae can present with many different symptoms:

 Pain
 Discharge - either bloody or purulent
 Pruritus ani - itching
 Systemic symptoms if abscess becomes infected

Diagnosis

Diagnosis is by examination, either in an outpatient setting or under anaesthesia (referred to as EUA -

Examination under Anaesthesia). The examination can be an anoscopy.

Possible findings:

 The opening of the fistula onto the skin may be seen

 The area may be painful on examination
 There may be redness
 An area of induration may be felt - thickening due to chronic infection
 A discharge may be seen
 It may be possible to explore the fistula using a fistula probe (a narrow instrument) and in this way it
may be possible to find both openings of the fistula

Treatment

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Surgery is considered essential in the decompression of acute abscesses; repair of the fistula itself is
considered an elective procedure which many patients elect to undertake due to the discomfort and
inconvenience associated with a draining tract.

There are several stages to treating an anal fistula:

Definitive treatment of a fistula aims to stop it recurring. Treatment depends on where the fistula lies, and
which parts of the anal sphincter it crosses.

 There are several options:

 Doing nothing - a drainage seton can be left in place long-term to prevent problems. This is the safest
option although it does not definitively cure the fistula.

 Lay-open of fistula-in-ano - this option involves an operation to cut the fistula open. Once the fistula
has been laid open it will be packed on a daily basis for a short period of time to ensure that the wound
heals from the inside out. This option leaves behind a scar, and depending on the position of the fistula in
relation to the sphincter muscle, can cause problems with incontinence. This option is not suitable for
fistulas that cross the entire anal sphincter.

 Cutting seton - if the fistula is in a high position and it passes through a significant portion of the
sphincter muscle, a cutting seton may be used. This involves inserting a thin tube through the fistula tract
and tieing the ends together outside of the body. The seton is tightened over time, gradually cutting
through the sphincter muscle and healing as it goes. This option minimizes scarring but can cause
incontinence in a small number of cases, mainly of flatus. Once the fistula tract is in a low enough
position it may be laid open to speed up the process, or the seton can remain in place until the fistula is
completely cured.

 Seton stitch- a length of suture material looped through the fistula which keeps it open and allows pus
to drain out. In this situation, the seton is referred to as a draining seton.The stitch is placed close to the
ano- rectal ring – encourages healing and makes further surgery easy.

 Fistulotomy - till anorectal ring

 Colostomy - to allow healing

 Fibrin glue injection is a method explored in recent years, with variable success. It involves injecting
the fistula with a biodegradable glue which should, in theory, close the fistula from the inside out, and let
it heal naturally. This method is perhaps best tried before all others since, if successful, it avoids the risk
of incontinence, and creates minimal stress for the patient.
 Fistula plug involves plugging the fistula with a device made from small intestinal submucosa. The
fistula plug is positioned from the inside of the anus with suture. Small intestinal submucosa stimulates
the body to close the fistula from the inside out. According to some sources, the success rate with this
method is as high as 80%. As opposed to the staged operations, which may require multiple
hospitalizations, the fistula plug procedure requires hospitalization for only about 24 hours. Currently,
there are two different anal fistula plugs cleared by the FDA for treating ano-rectal fistulas in the United
States. This treatment option does not carry any risk of bowel incontinence.
 Endorectal advancement flap is a procedure in which the internal opening of the fistula is identified
and a flap of mucosal tissue is cut around the opening. The flap is lifted to expose the fistula, which is
then cleaned and the internal opening is sewn shut. After cutting the end of the flap on which the internal
opening was, the flap is pulled down over the sewn internal opening and sutured in place. The external
opening is cleaned and sutured. Success rates are variable and high recurrence rates are directly related to
previous attempts to correct the fistula.

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Infection

 Some patients will have active infection when they present with a fistula, and this requires clearing up
before definitive treatment can be decided.
 Antibiotics can be used as with other infections, but the best way of healing infection is to prevent the
buildup of pus in the fistula, which leads to abscess formation.
 This can be done with a Seton - a length of suture material looped through the fistula which keeps it
open and allows pus to drain out.
 In this situation, the Seton is referred to as a draining Seton.

Anorectal abscess

DEF:

Anorectal abscess (also known as an anal/rectal abscess, perianal/perirectal abscess, or) is collection of
pus adjacent to the anus arises from an infection at one of the anal crypts of Morgagni which leads to
inflammation and abscess formation.

Cause

Abscesses are caused by;

- a high density infection of (usually) common bacteria which collect in one place or another for
any variety of reasons. Anal abscesses, without treatment, are likely to spread and affect other
parts of the body, particularly the groin and rectal lumen. All abscesses can progress to serious
generalized infections requiring lengthy hospitalizations if not treated.

- Bacteria common in the digestive system, such as E. coli.

- While this still continues often to be the case, there has recently been an uptick in the causative
organism being staphylococcus, as well as the difficult to treat community-acquired methicillin-
resistant S. aureus.

- Because of the increasing appearance of more exotic bacteria in anal abscesses, microbiological
examination will always be performed on the surgical exudate to determine the proper course
of any antibiotic treatment.

- Infection of submucosal hematoma, scerosed haemorrhoids or anal fissures

- Truma resulting from abrasions, hard stool, fish bone

- Obstruction of the gland in the anal area

- Extension of the cryptitis

- Infection in the apocrine gland or folliculitis in the perianal region

- Systemic infections such as ulcerative colitis and Crohn’s disease

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Classification

- There are four types of anorectal abscesses; perianal, ischiorectal, intersphincteric, and
supralevator.

Signs and symptoms

- Pain in the perianal area is the most common symptom of an anorectal abscess. The pain may
be dull, aching, or throbbing. It is worst when the person sits down and right before a bowel
movement.

- constipation,

- drainage from the rectum,

- fever and chills,

- A palpable mass near the anus.

Diagnostic approach

- Medical history and physical exam.

- Imaging studies which can help determine the diagnosis in cases of a deep non-palpable
perirectal abscess include:

- Pelvic CT scan,

- MRI

- Trans-rectal ultrasound.

Treatment

Anal abscesses, unfortunately, cannot be treated by a simple course of antibiotics or other medications.
Even small abscesses will need the attention of a surgeon immediately. Treatment is possible in an
emergency room under local anesthesia, but it is highly preferred to be formally admitted to a hospital
and to have the surgery performed in an operating room under general anesthesia.

- A fairly small but deep incision is performed close to the root of the abscess.

- The surgeon will allow the abscess to drain its exudate and attempt to discover any other
related lesions in the area.

- A portion of the exudate is sent for microbiological analysis to determine the type of infecting
bacteria.

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 - The incision is not closed (stitched), as the damaged tissues must heal from the inside toward
the skin over a period of time.

- 'Sitz baths‘whereby a small basin (which usually fits over a toilet) is filled with warm water (and
possibly, salts) and the affected area is soaked for a period of time.

- antibiotic therapy,

- Analgesics for pain management

Complications

- Connecting the rectum to the skin

- Anao-recto fistula

- Perineal cellulitis

- Scar tissue formation

- Anal strictures

- Peritonitis

- Systemic infection.

DISORDERS OF THE CARDIOVASCULAR SYSTEM

Gas gangrene

Gas gangrene (also known as "Clostridial myonecrosis"[1]:269, and "Myonecrosis"[2]) is a bacterial

infection that produces gas tissues in gangrene. It is a deadly form of gangrene usually caused by
Clostridium perfringens bacteria. It is a medical emergency.

Myonecrosis is a condition of necrotic damage, specific to muscle tissue. It is often seen in infections
with Clostridium perfringens or any of myriad soil-borne anaerobic bacteria. Bacteria cause myonecrosis
via specific exotoxins. These microorganisms are opportunistic and, in general, enter the body via
significant skin breakage. In wartime, in particular, the unhygienic conditions and frequent gross injuries
meant that gangrenous infection of soil-borne bacteria was particularly prevalent. Indeed, mankind has
long suffered the ill-effects of gangrenous infections throughout history.

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Other causes of myonecrosis include envenomation by snakes of the Bothrops genus (family Viperidae),
ischemic necrosis, caused by vascular blockage (e.g., diabetes type II), tumours that block or hoard blood
supply, and disseminated intravascular coagulation (DIC) or other thromboses.

Features

Gas gangrene can cause myonecrosis, gas production, and sepsis. Progression to toxemia and shock is
often very rapid.

Pathophysiology

Gas gangrene is caused by exotoxin-producing Clostridial species (most often Clostridium perfringens,
and C. novyi[3] but less commonly C. septicum[4] or C. ramnosum[5]), which are mostly found in soil but
also found as normal gut flora, and other anaerobes (e.g. Bacteroides and anaerobic streptococci). The
exotoxin is commonly found in C. perfringens type A strain and is known as alpha toxin. These
environmental bacteria may enter the muscle through a wound and go on to proliferate in necrotic tissue
and secrete powerful toxins. These toxins destroy nearby tissue, generating gas at the same time.

Other organisms may rarely cause gas gangrene (for example, Klebsiella pneumoniae in the context of
diabetes).[6]

A gas composition of 5.9% hydrogen, 3.4% carbon dioxide, 74.5% nitrogen and 16.1% oxygen was
reported in one clinical case.[7]

Myonecrosis differs slightly from other types of necrosis. While the underlying causes are almost
identical, the type of affected tissue (in particular, muscle tissue) is significantly more important for the
patient's general health. Superficial necrosis is unsightly, and can lead to unattractive scarring but
otherwise does not affect the patient's likelihood of survival or physical capability to the same extent.
However, massive myonecrosis will likely result in the loss of movement of the entire region. If the
necrotic damage is allowed to continue throughout an affected limb then often that entire limb is lost
permanently.

It is often difficult to identify the extent of muscle damage, as C. perfringens may be at work in deeper
fascial layers below the skin. Unlike other anaerobic infections, discharge in these infections is often not
purulent (filled with pus). Instead, the discharge is often described as "sweetly putrid" or "dishwater pus"
because it is much thinner than normal pus. This is due to the lysis of neutrophils, a type of white blood
cell, caused by the lecithinases and other toxins released by Clostridia.

Soil-borne anaerobes are particularly well adapted to surviving harsh conditions. Often, there is a scarcity
of nutrition and the presence of numerous other species competing for resources. Changes in pH and
temperature are often significant also. Competing bacteria often also possess the ability to create
exotoxins that assist them in competing with other microbes in their natural environment. When such
bacteria are able to enter a living host, they encounter a vast supply of nutrients, warm conditions, and an
abundance of water. This enables the microbes to rapidly proliferate, far in excess of the immune system's
capability to defend, as prokaryotic bacteria possess a far greater capacity for multiplication than the
host's immune system. The combination of bacterial load and ability to multiply is the basis for the
microbes' ability to cause massive infection. Alongside such rapid proliferation is a corresponding mass-
production of exotoxin that causes severe damage to local tissue in the host. One such exotoxin is
produced by C. perfringens and is responsible for the disease manifestations. This exotoxin is known as
alpha toxin.[8]

Massive infection, gross injury, and depletion of the host's immune capability result in system-wide
sepsis. This is partly due to the burden on the immune system, its corresponding release of inflammatory
cytokines, and the distribution of bacterial toxins. Massive infection is likely to result in death from a

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combination of system-wide septic shock and the unintentionally damaging effects of the immune
response. In animals, disability and distress caused by all of these factors markedly increases the chance
of predation.

Treatment

Treatment is usually debridement and excision with amputation necessary in many cases. Antibiotics
alone are not effective because they do not penetrate ischaemic muscles enough to be effective. However,
penicillin is given as an adjuvant treatment to surgery. In addition to surgery and antibiotics, hyperbaric
oxygen therapy (HBOT) is used and acts to inhibit the growth of and kill the anaerobic C. perfringens.[9]
[10]

Any significantly massive infection is a medical emergency. In cases of gangrene, the infection is so
severe by the time that a diagnosis is made that countering the bacterial load is impossible even with the
strongest available antibiotics, for example, gentamicin and vancomycin. There are two major reasons for
this: Current antibiotics prevent only replication of bacteria, and the production of toxins continues in pre-
existing bacteria. Also, the extent of injury caused by the infection may leave the muscle tissues so
damaged that the body will never be able to replace the lost structures (including vasculature).

Other treatment options include hyperbaric oxygen and the use of anti-toxins. Anti-toxins are no longer
available because they pose a great risk for eliciting allergic reactions.

Often, when circumstances are particularly dire, the only available cure is amputation, which physically
removes the source of infection.

Peripheral vascular disease

Peripheral vascular disease (PVD), commonly referred to as peripheral arterial disease (PAD) or
peripheral artery occlusive disease (PAOD), refers to the obstruction of large arteries not within the
coronary, aortic arch vasculature, or brain. PVD can result from atherosclerosis, inflammatory processes
leading to stenosis, an embolism, or thrombus formation. It causes either acute or chronic ischemia (lack
of blood supply). Often PAD is a term used to refer to atherosclerotic blockages found in the lower
extremity.[1]

PVD also includes a subset of diseases classified as microvascular diseases resulting from episodal
narrowing of the arteries (Raynaud's phenomenon), or widening thereof (erythromelalgia), i.e. vascular
spasms.

Classification

Peripheral artery occlusive disease is commonly divided in the Fontaine stages, introduced by René
Fontaine in 1954 for ischemia:[2][3]

1. mild pain when walking (claudication), incomplete blood vessel obstruction;

2. severe pain when walking relatively shorter distances (intermittent claudication), pain triggered by
walking "after a distance of >150 m in stage IIa and after <150 m in stage II-b";
3. pain while resting (rest pain), mostly in the feet, increasing when the limb is raised;
4. biological tissue loss (gangrene) and difficulty walking.

A more recent classification by Rutherford consists of three grades and six categories: [3]

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1. Mild claudication
2. Moderate claudication
3. Severe claudication
4. Ischemic pain at rest
5. Minor tissue loss
6. Major tissue loss

Symptoms

About 20% of patients with mild PAD may be asymptomatic; other symptoms include: [1]

 Claudication - pain, weakness, numbness, or cramping in muscles due to decreased blood flow
 Sores, wounds, or ulcers that heal slowly or not at all
 Noticeable change in color (blueness or paleness) or temperature (coolness) when compared to the
other limb
 Diminished hair and nail growth on affected limb and digits.

Causes

Risk factors contributing to PAD are the same as those for atherosclerosis:[1]

 Smoking - tobacco use in any form is the single most important modifiable cause of PVD
internationally. Smokers have up to a tenfold increase in relative risk for PVD in a dose-related effect.
[citation needed]
Exposure to second-hand smoke from environmental exposure has also been shown to
promote changes in blood vessel lining (endothelium) which is a precursor to atherosclerosis.
 Diabetes mellitus - causes between two and four times increased risk of PVD by causing endothelial
and smooth muscle cell dysfunction in peripheral arteries. [citation needed] Diabetics account for up to 70% of
nontraumatic amputations performed, and a known diabetic who smokes runs an approximately 30%
risk of amputation within 5 years.[citation needed]
 Dyslipidemia (high low density lipoprotein [LDL] cholesterol, low high density lipoprotein [HDL]
cholesterol) - elevation of total cholesterol, LDL cholesterol, and triglyceride levels each have been
correlated with accelerated PAD. Correction of dyslipidemia by diet and/or medication is associated with
a major improvement in short-term rates of heart attack and stroke. [citation needed] This benefit is gained
even though current evidence does not demonstrate a major reversal of peripheral and/or coronary
atherosclerosis.[citation needed]
 Hypertension - elevated blood pressure is correlated with an increase in the risk of developing PAD,
as well as in associated coronary and cerebrovascular events (heart attack and stroke).
 Risk of PAD also increases in individuals who are over the age of 50, male, obese, or with a family
history of vascular disease, heart attack, or stroke.
 Other risk factors which are being studied include levels of various inflammatory mediators such as C-
reactive protein, homocysteine.

Diagnosis

Upon suspicion of PVD, the first-line study is the ankle brachial pressure index (ABPI/ABI). When the
blood pressure readings in the ankles is lower than that in the arms, blockages in the arteries which
provide blood from the heart to the ankle are suspected. An ABI ratio less than 0.9 is consistent with
PVD; values of ABI below 0.8 indicate moderate disease and below 0.4 imply severe ischemic disease.[1]

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It is possible for conditions which stiffen the vessel walls (such as calcifications that occur in the setting
of chronic diabetes) to produce false negatives usually, but not always, indicated by abnormally high
ABIs (> 1.3). Such results and suspicions merit further investigation and higher level studies. [citation needed]

If ABIs are abnormal the next step is generally a lower limb doppler ultrasound examination to look at
site and extent of atherosclerosis. Other imaging can be performed by angiography,[1] where a catheter
is inserted into the common femoral artery and selectively guided to the artery in question. While
injecting a radiodense contrast agent an X-ray is taken. Any flow limiting stenoses found in the x-ray can
be identified and treated by atherectomy, angioplasty or stenting.

Modern multislice computerized tomography (CT) scanners provide direct imaging of the arterial system
as an alternative to angiography. CT provides complete evaluation of the aorta and lower limb arteries
without the need for an angiogram's arterial injection of contrast agent.

Treatment

Dependent on the severity of the disease, the following steps can be taken: [4]

 Smoking cessation (cigarettes promote PVD and are a risk factor for cardiovascular disease).
 Management of diabetes.
 Management of hypertension.
 Management of cholesterol, and medication with antiplatelet drugs. Medication with aspirin,
clopidogrel and statins, which reduce clot formation and cholesterol levels, respectively, can help with
disease progression and address the other cardiovascular risks that the patient is likely to have.
 Regular exercise for those with claudication helps open up alternative small vessels (collateral flow)
and the limitation in walking often improves. Treadmill exercise (35 to 50 minutes, 3 to 4 times per
week[1]) has been reviewed as another treatment with a number of positive outcomes including
reduction in cardiovascular events and improved quality of life.
 Cilostazol[5] or pentoxifylline treatment to relieve symptoms of claudication. [1]

Treatment with other drugs or vitamins are unsupported by clinical evidence, "but trials evaluating the
effect of folate and vitamin B-12 on hyperhomocysteinaemia, a putative vascular risk factor, are near
completion".[4]

After a trial of the best medical treatment outline above, if symptoms remain unnacceptable, patients
may be referred to a vascular or endovascular surgeon; however, "No convincing evidence supports the
use of percutaneous balloon angioplasty or stenting in patients with intermittent claudication". [4]

 Angioplasty (PTA or percutaneous transluminal angioplasty) can be done on solitary lesions in large
arteries, such as the femoral artery, but angioplasty may not have sustained benefits. [6][7]
 Plaque excision, in which the plaque is scraped off of the inside of the vessel wall.
 Occasionally, bypass grafting is needed to circumvent a seriously stenosed area of the arterial
vasculature. Generally, the saphenous vein is used, although artificial (Gore-Tex) material is often used
for large tracts when the veins are of lesser quality.
 Rarely, sympathectomy is used - removing the nerves that make arteries contract, effectively leading
to vasodilatation.
 When gangrene of toes has set in, amputation is often a last resort to stop infected dying tissues
from causing septicemia.
 Arterial thrombosis or embolism has a dismal prognosis, but is occasionally treated successfully with
thrombolysis.

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Guidelines

Several different guideline standards have been developed, including:

 TASC II Guidelines[3]

 ACC/AHA Guidelines[8]

Prognosis

Individuals with PAD have an "exceptionally elevated risk for cardiovascular events and the majority will
eventually die of a cardiac or cerebrovascular etiology"; [9] prognosis is correlated with the severity of the
PAD as measured by the Ankle brachial pressure index (ABPI).[9] Large-vessel PAD increases mortality
from cardiovascular disease significantly. PAD carries a greater than "20% risk of a coronary event in 10
years".[9]

There is a low risk that an individual with claudication will develop severe ischemia and require
amputation, but the risk of death from coronary events is three to four times higher than matched
controls without claudication.[4] Of patients with intermittent claudication, only "7% will undergo lower
extremity bypass surgery, 4% major amputations, and 16% worsening claudication", but stroke and
heart attack events are elevated, and the "5-year mortality rate is estimated to be 30% (versus 10% in
controls)".[9]

Epidemiology

The prevalence of peripheral vascular disease in the general population is 12–14%, affecting up to 20%
of those over 70;[9] 70%–80% of affected individuals are asymptomatic; only a minority ever require
revascularisation or amputation. Peripheral vascular disease affects 1 in 3 diabetics over the age of 50.

In the USA peripheral arterial disease affects 12–20 percent of Americans age 65 and older.
Approximately 10 million Americans have PVD. Despite its prevalence and cardiovascular risk
implications, only 25 percent of PAD patients are undergoing treatment.

The incidence of symptomatic PVD increases with age, from about 0.3% per year for men aged 40–55
years to about 1% per year for men aged over 75 years. The prevalence of PVD varies considerably
depending on how PAD is defined, and the age of the population being studied. Diagnosis is critical, as
people with PAD have a four to five times higher risk of heart attack or stroke.

The Diabetes Control and Complications Trial and U.K. Prospective Diabetes Study trials in people with
type 1 and type 2 diabetes, respectively, demonstrated that glycemic control is more strongly associated
with microvascular disease than macrovascular disease. It may be that pathologic changes occurring in
small vessels are more sensitive to chronically elevated glucose levels than is atherosclerosis occurring in
larger arteries.[10]

DISORDERS OF THE RESPIRATORY SYSTEM

CHEST INJURIES

OBJECTIVES

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At the end of the discussion students should be able to

 Mention the different types of chest trauma

 Discuss the management of chest trauma
 Mention the complications associated with chest trauma

Def: This is trauma that occurs to the chest cavity involving the chest and surrounding structures.

It may be classified as either blunt or penetrating.

Blunt trauma results form sudden compression or positive pressure inflicted on the chest wall. Most
motor vehicle injuries /crashes from steering wheel falls etc result in blunt injuries. Although blunt chest
injuries are more common, it is often difficulty to identify the extent of the damage because the
symptoms are vague or may be generalized. In addition patients may not seek immediate medical
attention which could complicate the condition

Penetrating injuries result when an object penetrates the chest wall most of them resulting from
gunshot wounds or stabs

Injuries to the chest are often life threatening and result in one or more of the following pathological
mechanisms;

 Hypoxemia from disruption of the airway

 Injury to the lungs parenchyma, rib cage and respiratory musculature,
 Massive hemorrhage,
 Fluid loss from the great vessels,
 Cardiac failure and/Respiratory
 Haemo-thorax

Pnuemo-thorax.

CLASSIFICATION

Chest trauma may be classified as blunt or penetrating

Blunt chest trauma results from sudden compression or positive pressure inflicted to the chest wall.

Causes of blunt trauma

 Motor vehicle crashes

 Falls
 Bicycle crashes

Although Blunt trauma is common, it is often difficult to identify the extent of damage because the
symptoms may be generalized and vague. In addition patients may not seek immediate medical
attention which may complicate the problem.

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Penetrating injuries occurs when a foreign body penetrates the chest wall. Most common causes of
chest wall injuries include gunshot wounds and stabbing wounds.

CLINICAL MANIFESTATION

Injuries to the chest wall are often life threatening. They often result in one or more of the following

 Hypoxemia from disruption of airway, injury to the lungs, rib cage and respiratory
musculature.
 Hypovolaemia from massive fluid loss
 Massive hemorrhage collared lung and pneumothorax
 Haemothorax
 Cardiac failure

Diagnosis

Physical examination includes

 inspection of the airway, thorax and neck veins

 Check for chest bruising, lacerations and petechiae
 Assess the chest for symmetrical movement, breath sounds, open chest wounds
 Entrance or exit wounds,
 subcutaneous emphysema

MEDICAL MANAGEMENT

The objectives of medical management are to evaluate to evaluate the patient’s condition and too
initiate aggressive resuscitation.

A clear airway is immediately established and oxygen support given in some cases

Fluid volume is be reestablished by insertion of an IV access as the potential for massive fluid and blood
loss is high.

The principals of care mainly focus on management of a patient with post operative thoracic surgery.

TYPES OF CHEST INJURIES

 Sternal and Rib fractures

Rib fractures are the most common type of chest injuries and occur in about 60% of patients admitted
with blunt trauma.

Most rib fractures are minor and are treated conservatively. Fractures of the first three are rare but can
result in high mortality because they are associated with laceration of the subclavian vein/artery. The
fractures of the lower ribs are associated with injuries to the spleen and liver which could be lacerated
by fragmented sections of the rib.

CLINICAL MANIFESTATION

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  Anterior chest pains
 Overlying tendencies
 Ecchymosis
 Creptus
 Swelling
 Potential of chest wall deformity

MANAGEMENT

This is directed at controlling pain, avoiding excessive activity and treating any associated injuries.

 THE FRAIL CHEST

This is when three or more adjacent ribs are fractured at two or more sites resulting in free floating of a
segment. It may also be a combination of fracture of the ribs and the sternum

This often a complication of blunt chest trauma

It causes the chest wall to loss stability and there is subsequent respiratory impairment and usually
severe respiratory distress.

During respiration, as the chest expands the detached part of the rib segment {flail segment} moves in a
paradoxical manner in that it is pulled inwards during inspiration and thus reducing the amount of air
that can be drawn into the lungs. The chest moves outwards on expiration because of increased
intrathoracic pressure which is more than the atmospheric pressure. This paradoxical movement results
in increased dead space, a reduction in alveolar ventilation and decreased compliance.

This will lead to retained airway secretions and actectalsis frequently occurs .The chest develops
hypoxeama and respiratory acidosis as a result of retention of co2.

Hypotension inadequate tissue perfusion and metabolic acidosis often follow with decreased cardiac
output

MANAGEMENT

Like rib fractures, management is often supportive, ensuring adequate ventilation, clearing secretions
from the lungs and controlling pain. The specific management will depend on the degree of respiratory
dysfunction.

If only a small segment is involved then the airway is made clear by proper positioning, coughing
exercises, deep breathing exercise and suctioning to aid in the expansion of the lung and to relieve pain.

Management also comprises a serial chest x-ray, arterial blood gas analysis, pulse oximetry and bedside
pulmonary monitoring.

Pain management is key in the successful treatment.

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PNUEMOTHORAX

DEF: Pneumothorax occurs when the parietal and visceral pleura is breached and the pleural space is
exposed to atmospheric positive pressure.

Under normal circumstances the pleural space has a negative os subatmospheric pressure compared to
the atmospheric pressure. This is the pressure that is required to make the lung inflation.when the space
is breached air enters the pleural space and the lungs or portion of the lungs will collapse.

Thus pneumothorax is collection of air in the pleural space.

Pneumothorax may be open or closed. Closed pneumothorax associated external wound, most common
being a spontaneous or simple pneumothorax

TYPES OF PNUEMOTHORAX

 SIMPLE PNUEMOTHORAX

 TENSION PNEUMOTHORAX

 TRAUMATIC PNEUMOTHORAX

SIMPLE NPNEUMOTHRAX

Def: A simple pneumothorax also called spontaneous pneumothorax occurs when air enters the pleural
space through a breach of either the parietal or visceral pleura

It is caused by rapture of a bleb on the visceral space and is mostly seen in underweight male cigarette
smokers.

Other causes of closed pneumothorax are

 Injury to the lungs in mechanical ventilation

 Injury during insertion of a subclavian catheter

 Perforation of the esophagus

 Injury to the lungs due to rib fractures

 Ruptured blebs or bullae in a patient with COPD{Chronic obs pul disease}

OPEN PNEUMOTHORAX

Occurs when air enters the thorax through an opening in the chest wall. Such as may occur in a stab
wound or gunshot.

If it is a direct result of trauma it will be referred to as traumatic pneumothorax

TRAUMATIC PNEUMOTHORAX

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This occurs when air escapes from a laceration in the lung itself and enters the pleural space. It can
occur with a blunt trauma i.e. rib fracture or penetrating injury i.e. gun shot stab wound invasive
thoracic procedures.

Tension pneumothorax is a rapid accumulation of air in the plural space causing a severely high
intrapleural pressure with resultant tension on the heart and great blood vessels. it may occur as result
of open or closed pneumothorax.

Air is drawn in the chest from a lacerated wall or small lung. The air that enters is trapped and cannot be
expelled during expiration. In effect it becomes a one way valve and with each breadth, tension
develops{positive pressure}This causes the lungs to collapse and the heart and blood vessels and the
trachea to shift towards the unaffected side of the chest {medial Sternal Shift} This causes both the
respiratory and circulatory function to be compromised. Cardiac output will be decreased and there will
be impairment of the peripheral circulation.

Tension pneumothorax is a medical emergency with both the circulatory and respiratory system being
involved

Patient will present with air hunger agitation, increasing hypoxemia, central cyanosis, hypotension and
tachycardia

CARDIAC TAMPONADE

This is compression of the heart as a result of fluid within the pericardial space. Can be caused by blunt
or penetrating trauma to the chest.

SUBCUTENOUES EMPHYSEMA

This collection of air under the skin following chest injury. The air may pass to distant places from the
chest and when palpated will produce crackling sounds or sensation.

Haemothorax is accumulation of blood in the pleural cavity. It is frequently found in association with
open pneumothorax in which case it will be called heamo-pneumothorax.

Causes include chest trauma, lung malignancy and pleural embolism.

Chylothorax is lymphatic fluid in the pleural space. This may be caused by a leak in thoracic duct

CHEST DRAINAGE

This is the removal of air and/or fluids from the pleural space.

INDICATIONS

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 LOBECTOMY

Definition

 A lobectomy is the surgical removal of one lobe of the lungs, usually to remove a lung cancer.

 A bilobectomy is the removal of two lobes,

 pneumonectomy is the removal of an entire lung.

Indications of Lobectomy

 Lobectomy is usually used for the treatment of non-small cell lung cancers, especially if caught early
enough that they have not spread very far.

Lobectomy is a major operative procedure, and there are risks involved. These, along with the benefits
and the method of the procedure, should be discussed in detail with a surgeon before the operation takes
place.  

As shown in the diagram above, the lungs are actually made up of several sub-sections known as 'lobes'.
Lobes are big areas of lung tissue divided by lines or 'fissures'. The right lung has three lobes, called the
superior (meaning top), inferior (meaning bottom) and middle lobes. The left lung only has two lobes, the
superior and inferior, partially because there is less room due to the presence of the heart in the left side of
the chest. In a lobectomy, the surgeon will try and remove only one of these lobes, allowing the rest to
remain functional. Removal of two lobes of the lung is called a 'bilobectomy' and removal of an entire
lung is called a pneumonectomy.

A lobectomy is usually used for treatment of non-small cell lung cancers (NSCLC), especially those that
are caught early. The amount of lung that needs to be removed to prevent the spread of these tumours is
affected by the location of the tumour as well as whether or not there are any 'hilar lymph nodes' (that lie

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between the lobes) involved. Whether the surgeon decides to remove one lobe, two lobes or an entire lung
will depend on the site of the tumour, the size of the tumour as well as the presence of any lymph nodes
that appear to have tumour cells in them. If there are hilar nodes involved then a pneumonectomy may be
necessary. Decisions may also depend on the general state of a person's health, as a healthier patient may
be able to cope with surgery better than someone who is very unwell.

Lobectomy is not suitable therapy for all lung cancers. For example if the cancer was caught very, early
when it is small and has not spread, and if the patient is too weak to get through a lobectomy, then
removal of an even smaller section of lung called a 'segment' may be used. The type of cancer is also
important in deciding whether lobectomy is a suitable treatment or not. Lobectomy may not be as
appropriate for the treatment of small-cell cancers, as they require far more aggressive treatment.
Advanced lung cancers that have spread to other parts of the body may not be suitable candidates for
lobectomy either, as there may not be sufficient benefit from it. However for some patients, especially
those with isolated metastases (areas of spread) in their brain or adrenal glands, surgery may still have
some benefit.

Pre op care

 Before a lobectomy details about the procedure, the benefits, and the risks should all have been
explained to the patient.

 If the patient has any questions regarding the operation he should feel free to ask

as the more the patient knows then the less worried he will be regarding the surgery.

INVESTIGATIONS

Several investigations have to be done to examine both the lesion itself as well as general health.

 An X-ray and CT Scan of the chest will help to assess the size, location and operability of the lesion.

 An ECG to assess the function of the heart will give the doctor a good idea of how the heart will cope
with the strain of the operation and the suitability of a lobectomy.

 Lung Function Tests will give the doctor an idea about how well the rest of the lung is working.
Cardiac arrhythmias: the heart beats irregularly and stops pumping blood as efficiently

COMPLICATIONS

 Bleeding
 Infection
 Bronchopleural fistulae: a connection forms between the lung and the surrounding area leading to air
leakage
 Respiratory Insufficiency: if the rest of the lung cannot compensate for the loss of the lobe
 Pulmonary Embolism: a blood clot can lodge in the vessels of the lung, causing an area to lose blood
supply
 Deep Vein Thrombosis: lying in bed for long periods after surgery can cause blood to pool in the veins
of the legs and clot, causing a DVT

Pulmonary contusion

A pulmonary contusion (or lung contusion) is a contusion (bruise) of the lung, caused by chest trauma.

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As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue. The excess fluid
interferes with gas exchange, potentially leading to inadequate oxygen levels (hypoxia). Unlike
pulmonary laceration, another type of lung injury, pulmonary contusion does not involve a cut or tear of
the lung tissue.

A pulmonary contusion is usually caused directly by blunt trauma but can also result from explosion
injuries or a shock wave associated with penetrating trauma. With the use of explosives during World
Wars I and II, pulmonary contusion resulting from blasts gained recognition. In the 1960s its occurrence
in civilians began to receive wider recognition, in which cases it is usually caused by traffic accidents.
The use of seat belts and airbags reduces the risk to vehicle occupants.

Diagnosis is made by studying the cause of the injury, physical examination and chest radiography.
Typical signs and symptoms include direct effects of the physical trauma, such as chest pain and
coughing up blood, as well as signs that the body is not receiving enough oxygen, such as cyanosis. The
contusion frequently heals on its own with supportive care. Often nothing more than supplemental oxygen
and close monitoring is needed; however, intensive care may be required. For example, if breathing is
severely compromised, mechanical ventilation may be necessary. Fluid replacement may be required to
ensure adequate blood volume, but fluids are given carefully since fluid overload can worsen pulmonary
edema, which may be lethal.

The severity ranges from mild to deadly—small contusions may have little or no impact on the patient's
health—yet pulmonary contusion is the most common type of potentially lethal chest trauma. It occurs in
30–75% of severe chest injuries. With an estimated mortality rate of 14–40%, pulmonary contusion plays
a key role in determining whether an individual will die or suffer serious ill effects as the result of trauma.
Pulmonary contusion is usually accompanied by other injuries. Although associated injuries are often the
cause of death, pulmonary contusion is thought to cause death directly in a quarter to half of cases.
Children are at especially high risk for the injury because the relative flexibility of their bones prevents
the chest wall from absorbing force from an impact, causing it to be transmitted instead to the lung.
Pulmonary contusion is associated with complications including pneumonia and acute respiratory distress
syndrome, and it can cause long-term respiratory disability.

Classification

The alveoli

Pulmonary contusion and laceration are injuries to the lung tissue. Pulmonary laceration, in which lung
tissue is torn or cut, differs from pulmonary contusion in that the former involves disruption of the
macroscopic architecture of the lung, while the latter does not. When lacerations fill with blood, the result
is pulmonary hematoma, a collection of blood within the lung tissue. Contusion involves hemorrhage in
the alveoli (tiny air-filled sacs responsible for absorbing oxygen), but a hematoma is a discrete clot of
blood not interspersed with lung tissue. A collapsed lung can result when the pleural cavity (the space
outside the lung) accumulates blood (hemothorax) or air (pneumothorax) or both (hemo-pneumothorax).
These conditions do not inherently involve damage to the lung tissue itself, but they may be associated
with it. Injuries to the chest wall are also distinct from but may be associated with lung injuries. Chest
wall injuries include rib fractures and flail chest, in which multiple ribs are broken so that a segment of
the ribcage is detached from the rest of the chest wall and moves independently.

Signs and symptoms

Presentation may be subtle; people with mild contusion may have no symptoms at all. However,
pulmonary contusion is frequently associated with signs (objective indications) and symptoms (subjective
states), including those indicative of the lung injury itself and of accompanying injuries. Because gas
exchange is impaired, signs of low blood oxygen saturation, such as low concentrations of oxygen in
arterial blood gas and cyanosis (bluish color of the skin and mucous membranes) are commonly

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associated. Dyspnea (painful breathing or difficulty breathing) is commonly seen, and tolerance for
exercise may be lowered. Rapid breathing and a rapid heart rate are other signs. With more severe
contusions, breath sounds heard through a stethoscope may be decreased, or rales (an abnormal crackling
sound in the chest accompanying breathing) may be present. People with severe contusions may have
bronchorrhea (the production of watery sputum). Wheezing and coughing are other signs. Coughing up
blood or bloody sputum is present in up to half of cases.[12]Cardiac output (the volume of blood pumped
by the heart) may be reduced,[11] and hypotension (low blood pressure) is frequently present.[6] The area of
the chest wall near the contusion may be tender or painful due to associated chest wall injury.

Signs and symptoms take time to develop, and as many as half of cases are asymptomatic at the initial
presentation. The more severe the injury, the more quickly symptoms become apparent. In severe cases,
symptoms may occur as quickly as three or four hours after the trauma. Hypoxemia (low oxygen
concentration in the arterial blood) typically becomes progressively worse over 24–48 hours after injury.
In general, pulmonary contusion tends to worsen slowly over a few days, but it may also cause rapid
deterioration or death if untreated.

Causes

Motor vehicle accidents are the most common cause of pulmonary contusion.

Pulmonary contusion, which occurs in 25–35% of all blunt chest trauma, is usually caused by the rapid
deceleration that results when the moving chest strikes a fixed object. About 70% of cases result from
motor vehicle collisions, most often when the chest strikes the inside of the car. Falls, assaults, and sports
injuries are other causes. Pulmonary contusion can also be caused by explosions; the organs most
vulnerable to blast injuries are those that contain gas, such as the lungs. Blast lung is severe pulmonary
contusion, bleeding, or edema with damage to alveoli and blood vessels, or a combination of these. This
is the primary cause of death among people who initially survive an explosion.

In addition to blunt trauma, penetrating trauma can cause pulmonary contusion. Contusion resulting from
penetration by a rapidly moving projectile usually surrounds the path along which the projectile traveled
through the tissue. The pressure wave forces tissue out of the way, creating a temporary cavity; the tissue
readily moves back into place, but it is hurt. Pulmonary contusions that accompany gun and knife wounds
are not usually severe enough to have a major effect on outcome; penetrating trauma causes less
widespread lung damage than does blunt trauma. An exception is shotgun wounds, which can seriously
damage large areas of lung tissue through a blast injury mechanism.

Mechanism

The physical processes behind pulmonary contusion are poorly understood. However, it is known that
lung tissue can be crushed when the chest wall bends inward on impact. Three other possible mechanisms
have been suggested: the inertial effect, the spalling effect, and the implosion effect.

 In the inertial effect, the lighter alveolar tissue is sheared from the heavier hilar structures, an effect
similar to diffuse axonal injury in head injury. It results from the fact that different tissues have different
densities, and therefore different rates of acceleration or deceleration.
 In the spalling effect, lung tissue bursts or is sheared where a shock wave meets the lung tissue, at
interfaces between gas and liquid. The alveolar walls form such a gas-liquid interface with the air in the
alveoli. The spalling effect occurs in areas with large differences in density; particles of the denser tissue
are spalled (thrown) into the less dense particles.
 The implosion effect occurs when a pressure wave passes through a tissue containing bubbles of gas:
the bubbles first implode, then rebound and expand beyond their original volume. The air bubbles cause
many tiny explosions, resulting in tissue damage;[28] the overexpansion of gas bubbles stretches and tears
alveoli. This effect is thought to occur microscopically when the pressure in the airways increases
sharply.

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Contusion usually occurs on the lung directly under the site of impact, but, as with traumatic brain injury,
a contrecoup contusion may occur at the site opposite the impact as well. A blow to the front of the chest
may cause contusion on the back of the lungs because a shock wave travels through the chest and hits the
curved back of the chest wall; this reflects the energy onto the back of the lungs, concentrating it. (A
similar mechanism may occur at the front of the lungs when the back is struck.)

The amount of energy transferred to the lung is determined in a large part by the compliance (flexibility)
of the chest wall. Children's chests are more flexible because their ribs are more elastic and there is less
ossification of their intercostal cartilage. Therefore, their chest walls bend, absorbing less of the force and
transmitting more of it to the underlying organs. An adult's more bony chest wall absorbs more of the
force itself rather than transmitting it. Thus children commonly get pulmonary contusions without
fractures overlying them, while elderly people are more likely to suffer fractures than contusions. One
study found that pulmonary contusions were accompanied by fractures 62% of the time in children and
80% of the time in adults.

Pathophysiology

Normally, oxygen and carbon dioxide diffuse across the capillary and alveolar membranes and the
interstitial space (top). Fluid impairs this diffusion, resulting in less oxygenated blood (bottom).

Pulmonary contusion results in bleeding and fluid leakage into lung tissue, which can become stiffened
and lose its normal elasticity. The water content of the lung increases over the first 72 hours after injury,
potentially leading to frank pulmonary edema in more serious cases.[19] As a result of these and other
pathological processes, pulmonary contusion progresses over time and can cause hypoxia (insufficient
oxygen).

Bleeding and edema

In contusions, torn capillaries leak fluid into the tissues around them. The membrane between alveoli and
capillaries is torn; damage to this capillary–alveolar membrane and small blood vessels causes blood and
fluids to leak into the alveoli and the interstitial space (the space surrounding cells) of the lung. With
more severe trauma, there is a greater amount of edema, bleeding, and tearing of the alveoli. Pulmonary
contusion is characterized by micro hemorrhages (tiny bleeds) that occur when the alveoli are
traumatically separated from airway structures and blood vessels. Blood initially collects in the interstitial
space, and then edema occurs by an hour or two after injury. An area of bleeding in the contused lung is
commonly surrounded by an area of edema. In normal gas exchange, carbon dioxidediffuses across the
endothelium of the capillaries, the interstitial space, and across the alveolar epithelium; oxygen diffuses in
the other direction. Fluid accumulation interferes with gas exchange, and can cause the alveoli to fill with
proteins and collapse due to edema and bleeding. The larger the area of the injury, the more severe
respiratory compromise will be.

Consolidation and collapse

Pulmonary contusion can cause parts of the lung to consolidate, alveoli to collapse, and atelectasis (partial
or total lung collapse) to occur. Consolidation occurs when the parts of the lung that are normally filled
with air fill with material from the pathological condition, such as blood. Over a period of hours after the
injury, the alveoli in the injured area thicken and may become consolidated. A decrease in the amount of
surfactant produced also contributes to the collapse and consolidation of alveoli; [15] inactivation of
surfactant increases their surface tension. Reduced production of surfactant can also occur in surrounding
tissue that was not originally injured.

Inflammation of the lungs, which can result when components of blood enter the tissue due to contusion,
can also cause parts of the lung to collapse. Macrophages, neutrophils, and other inflammatory cells and

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blood components can enter the lung tissue and release factors that lead to inflammation, increasing the
likelihood of respiratory failure. In response to inflammation, excess mucus is produced, potentially
plugging parts of the lung and leading to their collapse. Even when only one side of the chest is injured,
inflammation may also affect the other lung. Uninjured lung tissue may develop edema, thickening of the
septa of the alveoli, and other changes.[37] If this inflammation is severe enough, it can lead to dysfunction
of the lungs like that seen in acute respiratory distress syndrome.

Ventilation/perfusion mismatch

Normally, the ratio of ventilation to perfusion is about one-to-one; the volume of air entering the alveoli
(ventilation) is about equal to that of blood in the capillaries around them (perfusion). This ratio is
reduced in pulmonary contusion; fluid-filled alveoli cannot fill with air, oxygen does not fully saturate the
hemoglobin, and the blood leaves the lung without being fully oxygenated. Insufficient inflation of the
lungs, which can result from inadequate mechanical ventilation or an associated injury such as flail chest,
can also contribute to the ventilation/perfusion mismatch. As the mismatch between ventilation and
perfusion grows, blood oxygen saturation is reduced. Pulmonary hypoxic vasoconstriction, in which
blood vessels near the hypoxic alveoli constrict (narrow their diameter) in response to the lowered oxygen
levels, can occur in pulmonary contusion. The vascular resistance increases in the contused part of the
lung, leading to a decrease in the amount of blood that flows into it, directing blood to better-ventilated
areas. Although reducing blood flow to the unventilated alveoli is a way to compensate for the fact that
blood passing unventilated alveoli is not oxygenated, the oxygenation of the blood remains lower than
normal. If it is severe enough, the hypoxemia resulting from fluid in the alveoli cannot be corrected just
by giving supplemental oxygen; this problem is the cause of a large portion of the fatalities that result
from trauma.

Diagnosis

To diagnose pulmonary contusion, health professionals use clues from a physical examination,
information about the event that caused the injury, and radiography. Laboratory findings may also be
used; for example, arterial blood gasses may show insufficient oxygen and excessive carbon dioxide even
in someone receiving supplemental oxygen. However, blood gas levels may show no abnormality early in
the course of pulmonary contusion.

X-ray

A chest X-ray showing right sided pulmonary contusion associated with rib fractures and subcutaneous
emphysema

Chest X-ray is the most common method used for diagnosis,[36] and may be used to confirm a diagnosis
already made using clinical signs.[19] Consolidated areas appear white on an X-ray film. [41] Contusion is
not typically restricted by the anatomical boundaries of the lobes or segments of the lung. [26][42][43] The X-
ray appearance of pulmonary contusion is similar to that of aspiration,[31] and the presence of hemothorax
or pneumothorax may obscure the contusion on a radiograph.[24] Signs of contusion that progress after
48 hours post-injury are likely to be actually due to aspiration, pneumonia, or ARDS. [10]

Although chest radiography is an important part of the diagnosis, it is often not sensitive enough to detect
the condition early after the injury.[34] In a third of cases, pulmonary contusion is not visible on the first
chest radiograph performed.[7] It takes an average of six hours for the characteristic white regions to show
up on a chest X-ray, and the contusion may not become apparent for 48 hours.[7][26][42] When a pulmonary
contusion is apparent in an X-ray, it suggests that the trauma to the chest was severe and that a CT scan
might reveal other injuries that were missed with X-ray. [2]

Computed tomography

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A chest CT scan revealing pulmonary contusions, pneumothorax, and pseudocysts

Computed tomography (CT scanning) is a more sensitive test for pulmonary contusion, [6][32] and it can
identify abdominal, chest, or other injuries that accompany the contusion. [37] In one study, chest X-ray
detected pulmonary contusions in 16.3% of people with serious blunt trauma, while CT detected them in
31.2% of the same people.[44] Unlike X-ray, CT scanning can detect the contusion almost immediately
after the injury.[42] However, in both X-ray and CT a contusion may become more visible over the first
24–48 hours after trauma as bleeding and edema into lung tissues progress. [45] CT scanning also helps
determine the size of a contusion, which is useful in determining whether a patient needs mechanical
ventilation; a larger volume of contused lung on CT scan is associated with an increased likelihood that
ventilation will be needed.[42] CT scans also help differentiate between contusion and pulmonary
hematoma, which may be difficult to tell apart otherwise. [46] However, pulmonary contusions that are
visible on CT but not chest X-ray are usually not severe enough to affect outcome or treatment. [36]

Ultrasound

An ultrasound image showing early pulmonary contusion, at this moment not visible on radiography.
Interstitial syndromes are expressed with the vertical white lines, the "B-lines". [47]

Pulmonary ultrasound, performed at the bedside or on the accident scene, is being explored as a diagnosis
for pulmonary contusion. Its use is still not widespread, being limited to facilities which are comfortable
with its use for other applications, like pneumothorax, airway management, and hemothorax. Accuracy
has been found to be comparable to CT scanning.[48]

Prevention

Prevention of pulmonary contusion is similar to that of other chest trauma. Airbags in combination with
seat belts can protect vehicle occupants by preventing the chest from striking the interior of the vehicle
during a collision, and by distributing forces involved in the crash more evenly across the body. [6]
However, in rare cases, an airbag causes pulmonary contusion in a person who is not properly positioned
when it deploys.[49] Child restraints such as carseats protect children in vehicle collisions from pulmonary
contusion.[50] Equipment exists for use in some sports to prevent chest and lung injury; for example, in
softball the catcher is equipped with a chest protector. [51] Athletes who do not wear such equipment, such
as basketball players, can be trained to protect their chests from impacts. [51] Protective garments can also
prevent pulmonary contusion in explosions.[52] Although traditional body armor made from rigid plates or
other heavy materials protects from projectiles generated by a blast, it does not protect against pulmonary
contusion, because it does not prevent the blast's shock wave from being transferred to the lung. [52] Special
body armor has been designed for military personnel at high risk for blast injuries; these garments can
prevent a shock wave from being propagated across the chest wall to the lung, and thus protect wearers
from blast lung injuries.[52] These garments alternate layers of materials with high and low acoustic
impedance (the product of a material's density and a wave's velocity through it) in order to "decouple" the
blast wave, preventing its propagation into the tissues. [52]

Treatment

No treatment is known to speed the healing of a pulmonary contusion; the main care is supportive. [38]
Attempts are made to discover injuries accompanying the contusion, [19] to prevent additional injury, and to
provide supportive care while waiting for the contusion to heal. [38] Monitoring, including keeping track of
fluid balance, respiratory function, and oxygen saturation using pulse oximetry is also required as the
patient's condition may progressively worsen.[53] Monitoring for complications such as pneumonia and
acute respiratory distress syndrome is of critical importance. [54] Treatment aims to prevent respiratory
failure and to ensure adequate blood oxygenation.[15][22] Supplemental oxygen can be given and it may be
warmed and humidified.[40] When the contusion does not respond to other treatments, extracorporeal

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membranous oxygenation may be used, pumping blood from the body into a machine that oxygenates it
and removes carbon dioxide prior to pumping it back in.[55]

Ventilation

Mechanical ventilation may be required if pulmonary contusion causes inadequate oxygenation.

Positive pressure ventilation, in which air is forced into the lungs, is needed when oxygenation is
significantly impaired. Noninvasive positive pressure ventilation including continuous positive airway
pressure (CPAP) and bi-level positive airway pressure (BiPAP), may be used to improve oxygenation and
treat atelectasis.[38] In both, air is blown into the airways at a prescribed pressure via a mask fitted tightly
to the face; in BiPAP the pressure changes between inhalation and exhalation, while in CPAP the pressure
is the same during both.[38] Noninvasive ventilation has advantages over invasive methods because it does
not carry the risk of infection that intubation does, and it allows normal coughing, swallowing, and
speech.[38] However, the technique may cause complications; it may force air into the stomach or cause
aspiration of stomach contents, especially when level of consciousness is decreased.[4]

People with signs of inadequate respiration or oxygenation may need to be intubated[7] and mechanically
ventilated.[12] Mechanical ventilation aims to reduce pulmonary edema and increase oxygenation. [26]
Ventilation can reopen collapsed alveoli, but it is harmful for them to be repeatedly opened, and positive
pressure ventilation can also damage the lung by overinflating it. [56] Intubation is normally reserved for
when respiratory problems occur,[7] but most significant contusions do require intubation, and it may be
done early in anticipation of this need.[4] People with pulmonary contusion who are especially likely to
need ventilation include those with prior severe lung disease or kidney problems; the elderly; those with a
lowered level of consciousness; those with low blood oxygen or high carbon dioxide levels; and those
who are going to be operated on and need anesthesia.[40]

Pulmonary contusion or its complications such as acute respiratory distress syndrome may cause lungs to
lose compliance (stiffen), so higher pressures may be needed to give normal amounts of air [4] and
oxygenate the blood adequately.[32]Positive end-expiratory pressure (PEEP), which delivers air at a given
pressure at the end of the expiratory cycle, can reduce edema and keep alveoli from collapsing. [13] PEEP is
considered necessary with mechanical ventilation; however, if the pressure is too great it can expand the
size of the contusion[16] and injure the lung.[38] When the compliance of the injured lung differs
significantly from that of the uninjured one, the lungs can be ventilated independently with two
ventilators in order to deliver air at different pressures; this helps avoid injury from overinflation while
providing adequate ventilation.[57]

Fluid therapy

The administration of fluid therapy in individuals with pulmonary contusion is controversial. [40] Excessive
fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage
from injured capillaries (pulmonary edema), which are more permeable than normal. [30][42] However, low
blood volume (hypovolemia) resulting from insufficient fluid has an even worse impact, potentially
causing hypovolemic shock; for people who have lost large amounts of blood, fluid resuscitation is
necessary.[40] A lot of the evidence supporting the idea that fluids should be withheld from people with
pulmonary contusion came from animal studies, not clinical trials with humans; human studies have had
conflicting findings on whether fluid resuscitation worsens the condition. [19] For people who do require
large amounts of intravenous fluid, a catheter may be placed in the pulmonary artery to measure the
pressure within it.[6] Measuring pulmonary artery pressure allows the clinician to give enough fluids to
prevent shock without exacerbating edema.[58]Diuretics, drugs that increase urine output to reduce
excessive fluid in the system, can be used when fluid overload does occur. [59]Furosemide, a diuretic used
in the treatment of pulmonary contusion, also relaxes the smooth muscle in the veins of the lungs, thereby
decreasing pulmonary venous resistance and reducing the pressure in the pulmonary capillaries. [42]

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Supportive care

Retaining secretions in the airways can worsen hypoxia [60] and lead to infections.[4] Thus, an important
part of treatment is pulmonary toilet, the use of suction, deep breathing, coughing, and other methods to
remove material such as mucus and blood from the airways. [7]Chest physical therapy makes use of
techniques such as breathing exercises, stimulation of coughing, suctioning, percussion, movement,
vibration, and drainage to rid the lungs of secretions, increase oxygenation, and expand collapsed parts of
the lungs.[61] People with pulmonary contusion, especially those who do not respond well to other
treatments, may be positioned with the uninjured lung lower than the injured one to improve oxygenation.
[42]
Inadequate pulmonary toilet can result in pneumonia. [39] People who do develop infections are given
antibiotics.[16] No studies have yet shown a benefit of using antibiotics as a preventative measure before
infection occurs, although some doctors do recommend prophylactic antibiotic use even without scientific
evidence of its benefit.[13] However, this can cause the development of antibiotic resistant strains of
bacteria, so giving antibiotics without a clear need is normally discouraged. [19] For people who are at
especially high risk of developing infections, the sputum can be cultured to test for the presence of
infection-causing bacteria; when they are present, antibiotics are used. [26]

Pain control is another means to facilitate the elimination of secretions. A chest wall injury can make
coughing painful, increasing the likelihood that secretions will accumulate in the airways. [62] Chest
injuries also contribute to hypoventilation (inadequate breathing) because the chest wall movement
involved in breathing adequately is painful.[62][63] Insufficient expansion of the chest may lead to
atelectasis, further reducing oxygenation of the blood.[34]Analgesics (pain medications) can be given to
reduce pain.[12] Injection of anesthetics into nerves in the chest wall, called nerve blockade, is another
approach to pain management; this does not depress respiration the way some pain medications can. [30]

Prognosis

This CT scan, taken 22 days after pulmonary contusion with major chest trauma, shows that the contusion
has completely resolved.[64]

Pulmonary contusion usually resolves itself without causing permanent complications; however it may
also have long-term ill effects on respiratory function. Most contusions resolve in five to seven days after
the injury. Signs detectable by radiography are usually gone within 10 days after the injury—when they
are not, other conditions, such as pneumonia, are the likely cause. Chronic lung disease correlates with
the size of the contusion and can interfere with an individual's ability to return to work. Fibrosis of the
lungs can occur, resulting in dyspnea (shortness of breath), low blood oxygenation, and reduced
functional residual capacity for as long as six years after the injury. As late as four years post-injury,
decreased functional residual capacity has been found in most pulmonary contusion patients studied.
During the six months after pulmonary contusion, up to 90% of people suffer difficulty breathing. In
some cases, dyspnea persists for an indefinite period. Contusion can also permanently reduce the
compliance of the lungs.

Complications

A chest X-ray showing acute respiratory distress syndrome

Pulmonary contusion can result in respiratory failure—about half of such cases occur within a few hours
of the initial trauma. Other severe complications, including infections and acute respiratory distress
syndrome (ARDS) occur in up to half of cases. Elderly people and those who have heart, lung, or kidney
disease prior to the injury are more likely to stay longer in hospital and have complications from the
injury. Complications occur in 55% of people with heart or lung disease and 13% of those without. [36] Of
people with pulmonary contusion alone, 17% develop ARDS, while 78% of people with at least two
additional injuries develop the condition.[6] A larger contusion is associated with an increased risk. In one

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study, 82% of people with 20% or more of the lung volume affected developed ARDS, while only 22% of
people with less than 20% did so.[7]

Pneumonia, another potential complication, develops in as many as 20% of people with pulmonary
contusion.[13] Contused lungs are less able to remove bacteria than uninjured lungs, predisposing them to
infection.[67] Intubation and mechanical ventilation further increase the risk of developing pneumonia; the
tube is passed through the nose or mouth into the airways, potentially tracking bacteria from the mouth or
sinuses into them.[38] Also, intubation prevents coughing, which would clear bacteria-laden secretions
from the airways, and secretions pool near the tube's cuff and allow bacteria to grow. [38] The sooner the
endotracheal tube is removed, the lower the risk of pneumonia, but if it is removed too early and has to be
put back in, the risk of pneumonia rises.[38] People who are at risk for pulmonary aspiration (e.g. those
with lowered level of consciousness due to head injuries) are especially likely to get pneumonia. [38] As
with ARDS, the chances of developing pneumonia increase with the size of the contusion. [7] Children and
adults have been found to have similar rates of complication with pneumonia and ARDS. [30]

Associated injuries

Severe pulmonary contusion with pneumothorax and hemothorax following severe chest trauma

A large amount of force is required to cause pulmonary contusion; a person injured with such force is
likely to have other types of injuries as well, [22] and pulmonary contusion can be used to gauge the
severity of trauma.[24] Up to three quarters of cases are accompanied by other chest injuries, [38] the most
common of these being hemothorax and pneumothorax. [36] Flail chest is usually associated with
pulmonary contusion,[26][42] and the contusion, rather than the chest wall injury, is often the main cause of
respiratory failure in people with these injuries. [69] Other indications of thoracic trauma may be associated,
including fracture of the sternum and bruising of the chest wall.[63] Over half of fractures of the scapula
are associated with pulmonary contusion.[26] The contusion is frequently found underlying fracture sites. [34]
When accompanied by a fracture, it is usually concentrated into a specific location—the contusion is
more diffuse when there is no fracture.[30][42]Pulmonary lacerations may result from the same blunt or
penetrating forces that cause pulmonary contusion. [6] Lacerations can result in pulmonary hematomas;
these are reported to develop in 4–11% of pulmonary contusions. [6]

Epidemiology

Pulmonary contusion is found in 30–75% of severe cases of chest injury, making it the most common
serious injury to occur in association with thoracic trauma.[6] Of people who have multiple injuries with an
injury severity score of over 15, pulmonary contusion occurs in about 17%.[19] It is difficult to determine
the death rate (mortality) because pulmonary contusion rarely occurs by itself. [16] Usually, deaths of
people with pulmonary contusion result from other injuries, commonly traumatic brain injury. [23] It is
controversial whether pulmonary contusion with flail chest is a major factor in mortality on its own or
whether it merely contributes to mortality in people with multiple injuries. [70] The mortality rate of
pulmonary contusion is estimated to range from 14–40%, depending on the severity of the contusion itself
and on associated injuries.[11] When the contusions are small, they do not normally increase the chance of
death or poor outcome for people with blunt chest trauma; however, these chances increase with the size
of the contusion.[36] One study found that 35% of people with multiple significant injuries including
pulmonary contusion die.[16] In another study, 11% of people with pulmonary contusion alone died, while
the number rose to 22% in those with additional injuries. [6] An accompanying flail chest increases the
morbidity and mortality to more than twice that of pulmonary contusion alone. [42] Pulmonary contusion is
thought to be the direct cause of death in a quarter to a half of people with polytrauma who die.[59]

Pulmonary contusion is the most common cause of death among vehicle occupants involved in accidents,
[71]
and it is thought to contribute significantly in about a quarter of deaths resulting from vehicle
collisions.[24] As vehicle use has increased, so has the number of auto accidents, and with it the number of
chest injuries.[38] However an increase in the number of airbags installed in modern cars may be

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decreasing the incidence of pulmonary contusion. [6] Use of child restraint systems has brought the
approximate incidence of pulmonary contusion in children in vehicle accidents from 22% to 10%. [50]

Since their chest walls are more flexible, children are more vulnerable to pulmonary contusion than adults
are,[22] and it is more common in children than in adults for that reason. [29] Children in forceful impacts
suffer twice as many pulmonary contusions as adults with similar injury mechanisms, yet have
proportionately fewer rib fractures.[13] Pulmonary contusion has been found in 53% of children with
significant chest injuries (those requiring hospitalization). [72] The rates of certain types of injury
mechanisms differ between children and adults; for example, children are more often hit by cars when
they are pedestrians.[30] Differences in the bodies of children and adults also lead to different
manifestations of pulmonary contusion and associated injuries; for example, children have less body
mass, so the same force is more likely to lead to trauma to multiple body systems. [30] Some differences in
children's physiology might be advantageous (for example they are less likely to have other medical
conditions), and thus they have been predicted to have a better outcome. [73] However, despite these
differences, children with pulmonary contusion have similar mortality rates to adults.

Pulmonary laceration

A pulmonary laceration is a chest injury in which lung tissue is torn or cut.[1] An injury that is
potentially more serious than pulmonary contusion, pulmonary laceration involves disruption of the
architecture of the lung,[2] while pulmonary contusion does not.[3] Pulmonary laceration is commonly
caused by penetrating trauma but may also result from forces involved in blunt trauma such as shear
stress. A cavity filled with blood, air, or both can form.[2] The injury is diagnosed when collections of air
or fluid are found on a CT scan of the chest. Surgery may be required to stitch the laceration, to drain
blood, or even to remove injured parts of the lung. The injury commonly heals quickly with few problems
if it is given proper treatment; however it may be associated with scarring of the lung or other
complications.

Causes

Pulmonary laceration is a common result of penetrating trauma but may also be caused by blunt trauma;
broken ribs may perforate the lung, or the tissue may be torn due to shearing forces[4] that result from
different rates of acceleration or deceleration of different tissues of the lung. [5] Violent compression of the
chest can cause lacerations by rupturing or shearing the lung tissue. [6] Pulmonary laceration may result
from blunt and penetrating forces that occur in the same injury and may be associated with pulmonary
contusion.[7][8] Lacerations of the lung tissue can also occur by compression of the alveoli against the ribs
or spine.[6] As with contusions, pulmonary lacerations usually occur near solid structures in the chest such
as ribs.[2] Pulmonary laceration is suspected when rib fractures are present. [9]

Classification

In 1988, a group led by R.B. Wagner divided pulmonary lacerations into four types based on the manner
in which the person was injured and indications found on a CT scan.[10] In type 1 lacerations, which occur
in the mid lung area, the air-filled lung bursts as a result of sudden compression of the chest. [10] Also
called compression-rupture lacerations, type 1 are the most common type and usually occur in a central
location of the lung.[1] They tend to be large, ranging in size from 2–8 cm.[11] The shearing stress in type 2
results when the lower chest is suddenly compressed and the lower lung is suddenly moved across the
vertebral bodies.[10][11] Type 2, also called compression-shear,[1] tends to occur near the spine and have an
elongated shape.[11] Type 2 lacerations usually occur in younger people with more flexible chests. [5] Type
3, which are caused by punctures from fractured ribs, occur in the area near the chest wall underlying the
broken rib.[10] Also called rib penetration lacerations, type 3 lacerations tend to be small [1] and
accompanied by pneumothorax.[10] Commonly, more than one type 3 laceration will occur. [11] Type 4, also
called adhesion tears,[1] occur in cases where a pleuropulmonary adhesion had formed prior to the injury,

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in which the chest wall is suddenly fractured or pushed inwards. [11] They occur in the subpleural area and
result from shearing forces at sites of transpleural adhesion. [5]

Pathophysiology

A CT scan of a pneumothorax, a chest injury that may accompany pulmonary laceration

A pulmonary laceration can cause air to leak out of the lacerated lung [12] and into the pleural space, if the
laceration goes through to it.[8] Pulmonary laceration invariably results in pneumothorax (due to torn
airways), hemothorax (due to torn blood vessels), or a hemopneumothorax (with both blood and air in the
chest cavity).[13] Unlike hemothoraces that occur due to pulmonary contusion, those due to lung laceration
may be large and long lasting.[14] However, the lungs do not usually bleed very much because the blood
vessels involved are small and the pressure within them is low. [4] Therefore, pneumothorax is usually
more of a problem than hemothorax.[8] A pneumothorax may form or be turned into a tension
pneumothorax by mechanical ventilation, which may force air out of the tear in the lung. [14]

The laceration may also close up by itself, which can cause it to trap blood and potentially form a cyst or
hematoma.[8] Because the lung is elastic, the tear forms a round cyst called a traumatic air cyst that may
be filled with air, blood, or both and that usually shrinks over a period of weeks or months. [15] Lacerations
that are filled with air are called pneumatoceles, and those that are filled with blood are called pulmonary
hematomas.[16] In some cases, both pneumatoceles and hematomas exist in the same injured lung. [14] A
pneumatocele can become enlarged, for example when the patient is mechanically ventilated or has acute
respiratory distress syndrome, in which case it may not go away for months.[14] Pulmonary hematomas
take longer to heal than simple pneumatoceles and commonly leave the lungs scarred. [16]

Over time, the walls of lung lacerations tend to grow thicker due to edema and bleeding at the edges. [1]

Diagnosis

A chest X-ray of a right sided pulmonary contusion associated with flail chest and subcutaneous
emphysema. Contusion may mask pulmonary laceration on chest X-ray.

Pulmonary laceration may not be visible using chest X-ray because an associated pulmonary contusion or
hemorrhage may mask it.[1][9] As the lung contusion clears (usually within two to four days), lacerations
begin to become visible on chest X-ray.[3]CT scanning is more sensitive and better at detecting pulmonary
laceration than X-rays are,[1][4][14][17] and often reveals multiple lacerations in cases where chest X-ray
showed only a contusion.[14] Before CT scanning was widely available, pulmonary laceration was
considered unusual because it was not common to find with X-ray alone. [14] On a CT scan, pulmonary
lacerations show up in a contused area of the lung, [9] typically appearing as cavities filled with air or
fluid[18] that usually have a round or ovoid shape due to the lung's elasticity. [6]

Hematomas appear on chest radiographs as smooth masses that are round or ovoid in shape. [1] Like
lacerations, hematomas may initially be hidden on X-ray by lung contusions, but they become more
apparent as the contusion begins to heal.[1]Pneumatoceles have a similar shape to that of hematomas but
have thin, smooth walls.[19] Lacerations may be filled completely with blood, completely with air, or
partially with both.[6] Lacerations filled with both blood and air display a distinctive air-fluid level. [6] A
single laceration may occur by itself, or many may be present, creating an appearance like Swiss cheese
in the radiography of the lung.[6]

Pulmonary laceration is usually accompanied by hemoptysis (coughing up blood or of blood-stained

sputum).[14]

Thoracoscopy may be used in both diagnosis and treatment of pulmonary laceration. [8]

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A healing laceration may resemble a pulmonary nodule on radiographs, but unlike pulmonary nodules,
lacerations decrease in size over time on radiographs. [6]

Treatment

As with other chest injuries such as pulmonary contusion, hemothorax, and pneumothorax, pulmonary
laceration can often be treated with just supplemental oxygen, ventilation, and drainage of fluids from the
chest cavity.[20] A thoracostomy tube can be used to remove blood and air from the chest cavity. [21] About
5% of cases require surgery, called thoracotomy.[13] Thoracotomy is especially likely to be needed if a
lung fails to re-expand; if pneumothorax, bleeding, or coughing up blood persist; or in order to remove
clotted blood from a hemothorax.[13] Surgical treatment includes suturing,[13] stapling, oversewing, and
wedging out of the laceration.[8] Occasionally, surgeons must perform a lobectomy, in which a lobe of the
lung is removed, or a pneumonectomy, in which an entire lung is removed.[13]

Prognosis

Full recovery is common with proper treatment. [20] Pulmonary laceration usually heals quickly after a
chest tube is inserted and is usually not associated with major long-term problems. [8] Pulmonary
lacerations usually heal within three to five weeks, [14] and lacerations filled with air will commonly heal
within one to three weeks but on occasion take longer. [1] However, the injury often takes weeks or months
to heal, and the lung may be scarred.[2] Small pulmonary lacerations frequently heal by themselves if
material is removed from the pleural space, but surgery may be required for larger lacerations that do not
heal properly or that bleed.[21]

Complications

Complications are not common but include infection, pulmonary abscess, and bronchopleural fistula (a
fistula between the pleural space and the bronchial tree).[6] A bronchopleural fistula results when there is a
communication between the laceration, a bronchiole, and the pleura; it can cause air to leak into the
pleural space despite the placement of a chest tube. [6] The laceration can also enlarge, as may occur when
the injury creates a valve that allows air to enter the laceration, progressively expanding it. [6] One
complication, air embolism, in which air enters the bloodstream, is potentially fatal, especially when it
occurs on the left side of the heart.[4] Air can enter the circulatory system through a damaged vein in the
injured chest and can travel to any organ; it is especially deadly in the heart or brain. [4]Positive pressure
ventilation can cause pulmonary embolism by forcing air out of injured lungs and into blood vessels. [4]

Pneumothorax

Pneumothorax is a medical condition and potential emergency wherein air or gas is present in the pleural
cavity (chest). It may occur spontaneously both in people with chronic lung conditions and those with no
other health problems, but many pneumothoraces occur after physical trauma to the chest, blast injury, or
as a complication of medical treatment. In the past, creating a pneumothorax was used as a treatment for
various lung disorders, such as tuberculosis; this has now been abandoned.

The symptoms of a pneumothorax are determined by the size of the air leak and the speed by which it
occurs; they may include chest pain and shortness of breath in most cases, and fainting and rarely cardiac
arrest in severe cases ("tension pneumothorax"). The diagnosis can be made by physical examination in
severe cases but usually requires a chest X-ray in milder forms.

Small pneumothoraces typically resolve by themselves and require no treatment. In larger

pneumothoraces or when there are severe symptoms, the air may be aspirated with a syringe, or a one-
way chest tube is inserted to allow the air to escape. Occasionally, surgical measures are required,
especially if tube drainage is unsuccessful.

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Signs and symptoms

Pneumothorax presents mainly as a sudden shortness of breath, dry coughs, cyanosis (turning blue) and
pain felt in the chest, back and/or arms. In penetrating chest wounds, the sound of air flowing through the
puncture hole may indicate pneumothorax, hence the term "sucking" chest wound. The flopping sound of
a punctured lung is also occasionally heard. Subcutaneous emphysema is another symptom.

If untreated, hypoxia may lead to hypercapnia, respiratory acidosis, and loss of consciousness. In a
tension pneumothorax, shifting of the mediastinum away from the site of the injury can obstruct the
superior and inferior vena cava resulting in reduced venous return. This in turn decreases cardiac preload
and cardiac output.

Spontaneous pneumothorax has been reported in young people with a marfanoid habitus. The reason for
this association, while unknown, is hypothesized to be the presence of subtle abnormalities in connective
tissue, though not necessarily in elastin per se. Most spontaneous pneumothorax result from "blebs",
expanded alveoli just under the superficial surface of the lung, that rupture allowing the escape of air into
the pleural cavity.

Pneumothorax can also occur as part of medical procedures, such as the insertion of a central venous
catheter into the subclavian vein. Other causes include mechanical ventilation, endotracheal intubation,
laparoscopic surgery, emphysema and less commonly other lung diseases bacterial or viral (pneumonia),
metastatic tumors especially sarcomas, lymphangioleiomyomatosis, eosinophilic granuloma, cystic
fibrosis, alpha1-antitrypsin deficiency, spontaneous or traumatic esophageal rupture, Pneumocystis carinii
pneumonia, lung abscess, and asthma[1].

Cause

CT scan of the chest showing a pneumothorax on the patient's left side (right side on the image). A chest
tube is in place (small black mark on the right side of the image), the air-filled pleural cavity (black) and
ribs (white) can be seen. The heart can be seen in the center.

It most commonly arises:

 Spontaneously (more commonly in tall slim young males and in Marfan syndrome)
 Following a penetrating chest wound
 Following barotrauma to the lungs[2][3]

It may also be due to:

 Chronic lung pathologies including emphysema, asthma

 Acute infections
 Chronic infections, such as tuberculosis
 Lung damage caused by cystic fibrosis
 Lung Cancer
 Rare diseases that are unique to women such as Catamenial pneumothorax (due to endometriosis in the
chest cavity) and lymphangioleiomyomatosis (LAM).

Pneumothoraces are divided into tension and non-tension pneumathoraces. A tension pneumothorax is a
medical emergency as air accumulates in the pleural space with each breath. The increase in intrathoracic
pressure results in massive shifts of the mediastinum away from the affected lung compressing
intrathoracic vessels. A non-tension pneumothorax by contrast is of lesser concern because there is no
ongoing accumulation of air and hence no increasing pressure on the organs within the chest.

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The accumulation of blood in the thoracic cavity (hemothorax) exacerbates the problem, creating a
hemopneumothorax.

Spontaneous pneumothorax

Spontaneous Pneumothorax can be classified as primary spontaneous pneumothorax and secondary

spontaneous pneumothorax. In primary spontaneous pneumothorax, it is usually characterized by a
rupture of a bleb in the lung while secondary spontaneous pneumothorax mostly occurs due to chronic
obstructive pulmonary disease (COPD).

Primary

A primary spontaneous pneumothorax may occur without either trauma to the chest or any kind of blast
injury. This type of pneumothorax is caused when a bleb (an imperfection in the lining of the lung) bursts
causing the lung to deflate. The lung is reinflated by the surgical insertion of a chest tube. A minority of
patients will suffer a second instance. In this case, thoracic surgeons often recommend
thorascopicpleurodesis to improve the contact between the lung and the pleura. If multiple and/or bilateral
occurrences continue, surgeons may opt for a far more invasive bullectomy and pleurectomy to
permanently adhere the lung to the interior of the rib cage with scar tissue, making collapse of that lung
physically impossible. Primary spontaneous pneumothorax is most common in tall, thin men between 17
and 40 years of age, without any history of lung disease. Though less common, it also occurs in women,
usually of the same age and body type. The tendency for primary spontaneous pneumothorax sufferers to
be tall and thin is not due to weight, diet or lifestyle, but because the genetic predisposition toward those
traits often coincides with a genetic predisposition toward high volume lungs with large, burstable blebs.
A small portion of primary spontaneous pneumothoraxes occur in persons outside the typical range of age
and body type.

Secondary

In secondary spontaneous pneumothorax, a known lung disease is the cause of the collapse [4]. The most
common cause is chronic obstructive pulmonary disease (COPD) with emphysematous bullae. However,
there are several other diseases that may also lead to spontaneous pneumothorax:

 Tuberculosis
 Pneumonia
 Asthma
 Cystic fibrosis
 Lung cancer
 Interstitial lung disease
 Marfan syndrome
 Lymphangioleiomyomatosis (LAM)

Differential diagnosis

When presented with this clinical picture, other possible causes include:

 Acute Myocardial Infarction: presents with shortness of breath and chest pain, though MI chest pain is
characteristically crushing, central and radiating to the jaw, left arm or stomach. Whilst not a lung
condition, patients having an MI often happen to also have lung disease.
 Emphysema: here, delicate functional lung tissue is lost and replaced with air spaces, giving shortness
of breath, and decreased air entry and increased resonance on examination. However, it is usually a
chronic condition, and signs are diffuse (not localised as in pneumothorax).

Careful history taking and examination and a chest X-ray will allow accurate diagnosis.

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Pathophysiology

Mechanics of a sucking chest wound. A. Air enters the chest through the opening in the chest wall during
inspiration (a). The lung collapses on the affected side (b), air passes out of affected bronchus. Air enters
the bronchus from the collapsed lung (c) and passes to the intact lung. The mediastinum shifts toward the
uninvolved side (d), and hemothorax occurs (e). B. During expiration, air escapes through the wound (a).
The collapsed lung expands (b). Air passes from the uninvolved side to the lung on involved side and out
the trachea (c). The mediastinum shifts to the involved side (d), and hemothorax occurs (e).

The lungs are located inside the chest cavity, which is a hollow space. Air is drawn into the lungs by the
diaphragm (a powerful abdominalmuscle). The pleural cavity is the region between the chest wall and the
lungs. If air enters the pleural cavity, either from the outside (open pneumothorax) or from the lung
(closed pneumothorax), the lung collapses and it becomes mechanically impossible for the injured person
to breathe, even with an open airway. If a piece of tissue forms a one-way valve that allows air to enter
the pleural cavity from the lung but not to escape, overpressure can build up with every breath; this is
known as tension pneumothorax. It may lead to severe shortness of breath as well as circulatory collapse,
both life-threatening conditions. This condition requires urgent intervention.

Diagnosis

The absence of audible breath sounds through a stethoscope can indicate that the lung is not unfolded in
the pleural cavity. This accompanied by hyperresonance (higher pitched sounds than normal) to
percussion of the chest wall is suggestive of the diagnosis. The "coin test" may be positive. Two coins
when tapped on the affected side, produce a tinkling resonant sound which is audible on auscultation. [6]

If the signs and symptoms are doubtful, an X-ray of the chest can be performed, but in severe hypoxia, or
evidence of tension pneumothorax emergency treatment has to be administered first. An x-ray can
illustrate the collapse of the lung as extra black space, indicating the presence of air, will be seen in the x-
ray around the lung. The lung shrivels up away from the affected side and the mediastinum (trachea and
other components) will shift towards the unaffected side.[7]

In a supine chest X-ray the deep sulcus sign is diagnostic[8], which is characterized by a low lateral
costophrenic angle on the affected side.[9] In layperson's terms, the place where rib and diaphragm meet
appears lower on an X-ray with a deep sulcus sign and suggests the diagnosis of pneumothorax.

In Neonates the use of a transilluminator to suspected area will help visualize the air as radiating rings
from light source out.

More recently, ultrasound has been shown to be more sensitive than anteroposterior x-ray for detection of
pneumothorax. This is important in the initial evaluation of these patients, when the posteroanterior and
lateral x-ray studies may not be obtainable due to the patient's clinical condition. [10]

Management

Chest wound

Penetrating wounds (also known as 'sucking chest wounds') require immediate coverage with an
occlusive dressing, field dressing, or pressure bandage made air-tight with petroleum jelly or clean plastic
sheeting. The sterile inside of a plastic bandage packaging is good for this purpose; however in an
emergency situation any airtight material, even the cellophane of a cigarette pack, can be used. A small
opening, known as a flutter valve, may be left open so the air can escape while the lung reinflates. Any
patient with a penetrating chest wound must be closely watched at all times and may develop a tension
pneumothorax or other immediately life-threatening respiratory emergency at any moment. They cannot
be left alone.

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Blast injury or tension

If the air in the pleural cavity is due to a tear in the lung tissue (in the case of a blast injury or tension
pneumothorax), it needs to be released. A thin needle can be used for this purpose, to relieve the pressure
and allow the lung to reinflate.

Pre-hospital care

Many paramedics can perform needle thoracocentesis to relieve intrathoracic pressure. Intubation may be
required, even of a conscious patient, if the situation deteriorates. Advanced medical care and immediate
evacuation are strongly indicated.

An untreated pneumothorax is an absolute contraindication of evacuation or transportation by flight.

Small pneumothoraces

Small pneumothoraces are often managed conservatively as they will resolve on their own. [11] Simple
observation is sufficient for asymptomatic patients with a minimal pneumothorax, that is, less than 15-
20% of normal lung volume or 2-3 cm from apex to cupola. [12] Close follow-up with repeat observations
via chest X-rays is indicated to exclude any expansion, and oxygen is administered. [13]

Pneumothoraces which are too small to require tube thoracostomy and too large to leave untreated, may
be aspirated with a small catheter.

Larger pneumothoraces

Large pneumothoraces may require tube thoracostomy, also known as chest tube placement. If a thorough
anesthetizing of the parietal pleura and the intercostal muscles is performed, the only major pain
experienced should be either the injury that caused the pneumothorax or the re-expanding of the lung.
Proper anesthetizing will come about by the following procedure: the needle should be inserted into the
chest cavity and a negative pressure created in the syringe. While air bubbles rise into the syringe, the
needle should be slowly pulled out of the cavity until the bubbles cease. The tip of the syringe that
contains the anesthetic is now in the intercostal muscles just next to the parietal pleura. A proper and
sizable injection should ensue (5 to 10 ml). This will allow the patient to be fairly comfortable despite a
hemostat or finger being inserted into the chest cavity. A tube is then inserted through the chest wall into
the pleural space and air is extracted using a simple one way valve or vacuum and a water valve device.
This allows the lung to re-expand within the chest cavity. The rate of re-expansion will vary widely. It is
important not to connect the chest tube to suction right away, as rapid expansion may lead to pulmonary
edema. The pneumothorax is followed up with repeated X-rays. If the pneumothorax has resolved and
there is no further air leak, the chest tube is removed. If, during the time that the tube is still in the chest,
the lung manages to sustain the re-expansion, but once suction is turned off, the lung collapses, a
Heimlich valve may be used. This flutter valve allows air and fluid in the pleural cavity to escape the
pleura into a drainage bag while not letting any air or fluid back in. This method was developed by the
military in order to get soldiers with lung injuries stable and out of the battlefield faster. It is a rarely used
medical device in the treatment of patients these days, but may be used in order to allow the patient to
leave the hospital.

It is critical that the chest tube be managed in such a way that it does not become kinked or occluded with
clot or other fibrinous material. Chest tube clogging can result in build up of air in the pleural space. At
the very least, this will lead to a recurrent pneumothorax. In the worse case, the patient can have a tension
pneumothorax if the air builds up under pressure and impairs venous return to the heart. This can be fatal.
The tubes have a tendency to form clot from blood and other fibrinous material that can occlude them. To
keep them open they must be stripped, milked or even replaced if they totally occlude. Smaller tubes are
less traumatic, but more prone to clogging, although this can also occur with larger tubes. One sign the

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chest tube is clogged is subcutaneous emphysema. Another is a loss of respiratory variation in the fluid
level at the water seal valve in the drainage canister.

In the situation that the chest tube is not sufficient in healing of the lung (for example, a continued air leak
despite chest tube drainage), or if CT scans show the presence of large "bullae" on the surface of the lung,
thoracoscopic surgery, or video assisted thorascopic surgery (VATS), may be done in order to staple the
leak shut and to irritate the pleura to promote adhesions between the lung and pleura (pleurodesis). Two
or three small incisions are made in the side of the chest and back, one for a small camera and the other
(s) for tools used to seal the lung and abrade or remove the pleura. When finished the wound is covered
with a steri-strip and bandaged up.

In case of penetrating wounds, these require attention, but generally only after the airway has been
secured and a chest drain inserted. Supportive therapy may include mechanical ventilation.

Surgery

Recurrent pneumothorax may require further corrective and/or preventive measures such as pleurodesis.
If the pneumothorax is the result of ruptured bullae, then bullectomy (the removal or stapling of bullae or
other faults in the lung) is preferred. Chemical pleurodesis is the injection of a chemical irritant that
triggers an inflammatory reaction, leading to adhesion of the visceral pleura, which is in contact with the
lung, to the parietal pleura. Substances used for pleurodesis include talc, blood, tetracycline and
bleomycin. Mechanical pleurodesis is done by abrading the pleura and does not use chemicals. The
surgeon "roughens" up the inside chest wall ("parietal pleura") so the lung attaches to the wall with scar
tissue. This can also include a partial "parietal" pleurectomy, which is the removal of the "parietal"
pleura; "parietal" pleura is the serous membrane lining the inner surface of the thoracic cage and facing
the "visceral" pleura, which lies all over the lung surface. Both operations can be performed using
keyhole surgery (VATS) to minimise discomfort to the patient. Sometimes pneumothorax occurs
bilaterally in sequence or, more rarely, simultaneously; that is often associated to bilateral apical blebs
and obviously requires bilateral treatment. [14][15]

Hemothorax

A hemothorax (or haemothorax) is a condition that results from blood accumulating in the pleural
cavity.

Cause and presentation

Its cause is usually traumatic, from a blunt or penetrating injury to the thorax, resulting in a rupture of the
serous membrane either lining the thorax or covering the lungs. This rupture allows blood to spill into the
pleural space, equalizing the pressures between it and the lungs. Blood loss may be massive in people
with these conditions, as each side of the thorax can hold 30–40% of a person's blood volume. Even
minor injury to the chest wall can lead to significant hemothorax. [1]

Prognosis

If left untreated, the condition can progress to a point where the blood accumulation begins to put
pressure on the mediastinum and the trachea, effectively limiting the amount that the heart's ventricles are
able to fill. The condition can cause the trachea to deviate, or move, toward the unaffected side.

Signs and symptoms

 Tachypnea
 Dyspnea
 Cyanosis

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 Decreased or absent breath sounds on affected side
 Tracheal deviation to unaffected side
 Dull resonance on percussion
 Unequal chest rise
 Tachycardia
 Hypotension
 Pale, cool, clammy skin
 Possibly subcutaneous emphysema
 Narrowing pulse pressure

Management

A hemothorax is managed by removing the source of bleeding and by draining the blood already in the
thoracic cavity. Blood in the cavity can be removed by inserting a drain (chest tube) in a procedure called
a tube thoracostomy. Usually the lung will expand and the bleeding will stop after a chest tube is inserted.
The blood in the chest can thicken as the clotting cascade is activated when the blood leaves the blood
vessels and is activated by the pleural surface, injured lung or chest wall, or contact with the chest tube.
As the blood thickens, it can clot in the pleural space (leading to a retained hemothorax) or within the
chest tube, leading to chest tube clogging or occlusion. Chest tube clogging or occlusion can lead to
worse outcomes as it prevents adequate drainage of the pleural space, contributing to the problem of
retained hemothorax. In this case, patients can be hypoxic, short of breath, or in some cases, the retained
hemothorax can become infected (empyema). Therefore adequately functioning chest tubes are essential
in the setting of a hemothorax treated with a chest tube. To attempt to minimize the potential for clogging,
the surgeons will often place more than one tube, or large diameter tubes. Maintaining an adequately
functioning chest tube is an active process, usually for the nurses, that often requires tapping the tubes,
milking the tubes, or stripping the tubes to minimize potential for clogging in the tube in the setting of a
hemothorax. When these efforts fail a new chest tube must be placed, or the patient must be taken to the
operating room by a surgeon to open the chest and remove the blood clot, and re insert adequately
functioning chest tubes.

Thrombolytic agents have been used to break up clot in tubes or when the clot becomes organized in the
pleural space, however this is risky as it can lead to increased bleeding and the need for reoperation. [2]
Therefore, ideally, the tubes maintain their function so that the blood cannot clot in the chest or the tube.

In some cases bleeding continues and surgery is necessary to stop the source of bleeding. For example, if
the cause is rupture of the aorta in high energy trauma, the intervention by a thoracic surgeon is
mandatory.

 Cardiac tamponade
 Hemopneumothorax
 Pleural effusion
 Pneumothorax
 Tension pneumothorax
 Pulmonary contusion

Hemopneumothorax

Hemopneumothorax, or haemopneumothorax, is a medical term describing the combination of two

conditions: pneumothorax, or air in the chest cavity, and hemothorax (also called hæmothorax), or blood
in the chest cavity.

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A haemothorax, pneumothorax or both can occur if the chest wall is punctured. To understand the
ramifications of this it is important to have an understanding of the role of the pleural space. The pleural
space is located anatomically between the visceral membrane, which is firmly attached to the lungs, and
the parietal membrane which is firmly attached to the chest wall (aka ribcage and intercostal muscles,
muscles between the ribs). The pleural space contains pleural fluid. This fluid holds the two membranes
together by surface tension, much as a drop of water between two sheets of glass prevents them from
separating. Because of this, when the intercostal muscles move the ribcage outward, the lungs are pulled
out as well, dropping the pressure in the lungs and pulling air into the bronchi, when we 'breathe in'. The
pleural space is maintained in a constant state of negative pressure (in comparison to atmospheric
pressure).

If the chest wall, and thus the pleural space, is punctured, blood, air or both can enter the pleural space.
Air/blood rushes into the space in order to equalise the pressure with that of the atmosphere. As a result
the fluid is disrupted and the two membranes no longer adhere to each other. When the rib cage moves
out, it no longer pulls the lungs with it. Thus the lungs cannot expand, the pressure in the lungs never
drops and no air is pulled into the bronchi. Respiration is not possible. The affected lung, which has a
great deal of elastic tissue, shrivels in what is referred to as a collapsed lung.

Treatment

Treatment for this condition is the same as for hemothorax and pneumothorax independently: by tube
thoracostomy, the insertion of a chest drain through an incision made between the ribs, into the intercostal
space. A chest tube must be inserted to drain blood and air from the pleural space so it can return to a
state of negative pressure and function normally.

Commonly, surgery is needed to close off whatever injuries caused the blood and air to enter the cavity
(e.g. stabbing, broken ribs).

Lung cancer

Lung cancer is a disease which consists of uncontrolled cell growth in tissues of the lung (especially the
epithelial cells) which may result from smoking or exposure to carcinogens characterized by persistent
cough, haemoptysis and dyspnea.

- This growth may lead to metastasis, which is the invasion of adjacent tissue and infiltration beyond
the lungs.
- The vast majority of primary lung cancers are carcinomas of the lung, derived from epithelial cells.

Causes

 The main causes of any cancer include carcinogens (such as those in tobacco smoke), ionizing
radiation, and viral infection.
- This exposure causes cumulative changes to the DNA in the tissue lining the bronchi of the lungs (the
bronchial epithelium). As more tissue becomes damaged, eventually a cancer develops.
- The occurrence of lung cancer in nonsmokers, is often attributed to a combination of genetic factors,
radon gas, asbestos, and air pollution including secondhand smoke.

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 Smoking

 Smoking, particularly of cigarettes, is by far the main contributor to lung cancer. Cigarette smoke
contains over 60 known carcinogens, including radioisotopes from the radon decay sequence,
nitrosamine, and benzopyrene.
 Additionally, nicotine appears to depress the immune response to malignant growths in exposed tissue
 Passive smoking—the inhalation of smoke from another's smoking—is a cause of lung cancer in
nonsmokers

Radon gas

 Radon is a colorless and odorless gas generated by the breakdown of radioactive radium, which in turn
is the decay product of uranium, found in the Earth's crust.
 The radiation decay products ionize genetic material, causing mutations that sometimes turn
cancerous.
 Radon exposure is the second major cause of lung cancer in the general population, after smoking

Asbestos

 Asbestos can cause a variety of lung diseases, including lung cancer.

 There is a synergistic effect between tobacco smoking and asbestos in the formation of lung cancer.

Viruses

 Implicated viruses include human papillomavirus, JC virus, simian virus 40 (SV40), BK virus, and
cytomegalovirus.
 These viruses may affect the cell cycle and inhibit apoptosis, allowing uncontrolled cell division.

Particulate matter

 If the concentration of particles in the air increases by only 1%, the risk of developing a lung cancer
increases by 14%.
 Further, it has been established that particle size matters, as ultrafine particles penetrate further into the
lungs.

Classifications/Types of lung cancer

i. Small cell lung carcinoma

ii. Non-small cell lung carcinoma.
- Non-small cell lung carcinoma (NSCLC) is sometimes treated with surgery,

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- Small cell lung carcinoma (SCLC) usually responds better to chemotherapy and radiation.

i. Non-small cell lung carcinoma (NSCLC)

 The non-small cell lung carcinomas are grouped together because their prognosis and management are
similar. There are three main sub-types:
i. squamous cell lung carcinoma
ii. adenocarcinoma
iii. Large cell lung carcinoma.
 Squamous cell lung carcinoma - accounts for 25% of non small cell lung carcinoma and usually starts
near a central bronchus.
- A hollow cavity and associated necrosis are commonly found at the center of the tumor.
- Well-differentiated squamous cell lung cancers often grow more slowly than other cancer types.
 Adenocarcinoma - accounts for 40% of non-small cell lung cancers. It usually originates in peripheral
lung tissue.
- Most cases of adenocarcinoma are associated with smoking; however, among people who have never
smoked ("never-smokers"), adenocarcinoma is the most common form of lung cancer.
- A subtype of adenocarcinoma, the bronchioloalveolar carcinoma, is more common in female never-
smokers, and may have different responses to treatment.
 Large cells lung carcinoma -

ii. Small cell lung carcinoma (SCLC)

 Small cell lung carcinoma is less common. It was formerly referred to as "oat cell" carcinoma.
- Most cases arise in the larger airways (primary and secondary bronchi) and grow rapidly, becoming
quite large.
- The small cells contain dense neurosecretory granules (vesicles containing neuroendocrine
hormones), which give this tumor an endocrine/paraneoplastic syndrome association.
- While initially more sensitive to chemotherapy and radiation, it is often metastatic at presentation, and
ultimately carries a worse prognosis.
- Small cell lung cancers have long been dichotomously staged into limited and extensive stage disease.
This type of lung cancer is strongly associated with smoking.
 Other types
- Alveolar cell carcinoma – originates in the air sac (alveolar) of the lungs
- Can be a single growth but develops in more than one area of the lungs

Secondary cancers
 The lung is a common place for metastasis of tumors from other parts of the body. Secondary cancers
are classified by the site of origin; e.g., breast cancer that has spread to the lung is called breast cancer.
 Metastases often have a characteristic round appearance on chest radiograph. Solitary round lung
nodules are not infrequently of an uncertain etiology and may prompt a lung biopsy.
 In children, the majority of lung cancers are secondary.
 Primary lung cancers themselves most commonly metastasize to the adrenal glands, liver, brain, and
bone.

Staging

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- Lung cancer staging is an assessment of the degree of spread of the cancer from its original source. It
is an important factor affecting the prognosis and potential treatment of lung cancer.
- Non-small cell lung carcinoma is staged from IA ("one A"; best prognosis) to IV ("four"; worst
prognosis).
- Small cell lung carcinoma is classified as limited stage if it is confined to one half of the chest and
within the scope of a single radiotherapy field; otherwise, it is extensive stage.

Staging according to (tumor, node, metastasis) TNM system

 Primary tumors
- TX – primary tumor can be assessed or malignant tumor cells detected in sputum or bronchial or
bronchial washing but undetected by x-ray or bronchoscopy
- TO – no evidence of primary tumor
- Tis – tumor in situ
- T1 – tumor 3cm or less in greatest dimension, surrounded by normal lung or visceral pleural; no
bronchoscopic evidence of cancer closer to the center of the body than the lobar bronchus
- T2 – tumor longer than 3cm; or one that involves the main bronchus and is 2cm or more from the
carina, or one that invades the visceral pleural; or one that is accompanied by atelectasis or obstructive
pneumonitis that extends to the hilar region but does not involve the entire lung
- T3 – tumor of any size that extends to the neighboring structure such as the chest wall, the diaphragm,
or mediastinal pleural; or tumor in the main bronchus that does not involve but is less than 2cm from the
carina; or tumor that is accompanied by atelectasis or obstructive pneumonitis of the entire lung
- T4 – tumor of any size that invades the mediastinum, heart, great vessels, trachea, esophagus, vertebral
body or carina; or tumor with malignant pleural effusion.
 Regional lymph nodes
- NX – regional lymph nodes can’t be assessed
- NO – no detectable metastasis to lymph nodes
- N1 – metastasis to the ipsilateral peribronchial or hilar lymph nodes or both
- N2 – metastasis to the ipsilateral mediastinal and the subcarina lymph nodes or both
- N3 – metastasis to the contralateral mediastinal or hilar lymph nodes, the ipsilateral or the contralateral
scalene, or the subclavicular lymph nodes

Distant metastasis

- MX – distant metastasis can’t be assessed

- MO – no evidence of distant metastasis
- M1 – distant metastasis

STARGING CATEGORY

- Lung cancer progressed from mild to severe and can be staged as follows:
Occult carcinoma – TX, NO, MO
Stage 0 – Tis, NO, MO
Stage I – T1, NO, MO; T2, N1, MO
Stage II – T1, N1, MO; T2, NO, MO
Stage IIIA – T1, N1, MO;T2, N2, MO;T3, NO, MO; T3, N1, MO; T3, N2, MO
Stage IIIB – any T, N3, MO; T4, any N, MO
Stage IV – any T, any N, M1

Signs and symptoms

Symptoms that suggest lung cancer include:

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 dyspnea (shortness of breath) – due to tumor occluding the air way
 hemoptysis (coughing up blood)
 chronic coughing or change in regular coughing pattern – induced by tumor stimulating nerve endings
 wheezing
 chest pain or pain in the abdomen
 cachexia (weight loss),
 fatigue,
 loss of appetite
 dysphonia (hoarse voice) - resulting from tumor pressing on the laryngeal nerve
 clubbing of the fingernails (uncommon)
 Dysphagia (difficulty swallowing).
 If the cancer grows in the airway, it may obstruct airflow, causing breathing difficulties.

- This can lead to accumulation of secretions behind the blockage, predisposing the patient to
pneumonia.
- Many lung cancers have a rich blood supply. The surface of the cancer may be fragile, leading to
bleeding from the cancer into the airway. This blood may subsequently be coughed up.

Pathogenesis

 Similar to many other cancers, lung cancer is initiated by activation of oncogenes or inactivation of
tumor suppressor genes.
 Oncogenes are genes that are believed to make people more susceptible to cancer.
 Proto-oncogenes are believed to turn into oncogenes when exposed to particular carcinogens.
 Mutations in the K-ras proto-oncogene are responsible for 10–30% of lung adenocarcinomas.
 The epidermal growth factor receptor (EGFR) regulates cell proliferation, apoptosis, angiogenesis,
and tumor invasion.
 Mutations and amplification of EGFR are common in non-small cell lung cancer and provide the basis
for treatment with EGFR-inhibitors.
 Her2/neu is affected less frequently.
 Chromosomal damage can lead to loss of heterozygosity. This can cause inactivation of tumor
suppressor genes.
 Damage to chromosomes 3p, 5q, 13q, and 17p are particularly common in small cell lung carcinoma.
The p53 tumor suppressor gene, located on chromosome 17p, is affected in 60-75% of cases.
 Other genes that are often mutated or amplified are c-MET, NKX2-1, LKB1, PIK3CA, and BRAF.
 Several genetic polymorphisms are associated with lung cancer. These include polymorphisms in
genes coding for interleukin-1, cytochrome P450, apoptosis promoters such as caspase-8, and DNA repair
molecules such as XRCC1.
 People with these polymorphisms are more likely to develop lung cancer after exposure to
carcinogens.

Diagnosis

 History -
 Physical examinations -
 chest radiograph - may reveal an obvious mass, widening of the mediastinum (suggestive of spread to
lymph nodes there), atelectasis (collapse), consolidation (pneumonia), or pleural effusion.
 Computed tomography (CT scan) - to identify the tumor type
 biopsy – bronchoscopy or CT-guided biopsy
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 Bronchoscopy - to identify the tumor type
 Sputum cytological examination - may help in the early detection of lung cancer.
 Needle biopsy of the lungs
 Thoracentesis – allow chemical and cytological examination of the pleural fluid

Prevention

 Industrial and domestic carcinogens should be identified and banned

 Eliminating tobacco smoking is a primary goal in the prevention of lung cancer, and smoking
cessation is an important preventive tool in this process.
 Policy interventions to decrease passive smoking in public areas such as restaurants and workplaces

Treatment

 Treatment and prognosis depend upon the histological type of cancer, the stage (degree of spread), and
the patient's performance status.
 Possible treatments include
 surgery,
 chemotherapy,
 Radiotherapy.

Surgery

- Gross appearance of the cut surface of a pneumonectomy specimen containing a lung cancer, here a
squamous cell carcinoma (the whitish tumor near the bronchi).
- If investigations confirm lung cancer, CT scan and often positron emission tomography (PET) are used
to determine whether the disease is localized and amenable to surgery or whether it has spread to the
point where it cannot be cured surgically.
- Blood tests and spirometry (lung function testing) are also necessary to assess whether the patient is
well enough to be operated on. If spirometry reveals poor respiratory reserve (often due to chronic
obstructive pulmonary disease), surgery may be contraindicated.
- Surgery is usually only an option in non-small cell lung carcinoma limited to one lung, up to stage
IIIA. This is assessed with medical imaging (computed tomography, positron emission tomography). A
sufficient preoperative respiratory reserve must be present to allow adequate lung function after the tissue
is removed.
- Procedures include (i) wedge resection (removal of part of a lobe), (ii) segmentectomy (removal of an
anatomic division of a particular lobe of the lung), (iii) lobectomy (one lobe), (iv) bilobectomy (two
lobes), or (v) pneumonectomy (whole lung).
- In patients with adequate respiratory reserve, lobectomy is the preferred option, as this minimizes the
chance of local recurrence.
- If the patient does not have enough functional lung for this, wedge resection may be performed.
Radioactive iodine brachytherapy at the margins of wedge excision may reduce recurrence to that of
lobectomy.
- Video-assisted thoracoscopic surgery and VATS lobectomy have allowed for minimally invasive
approaches to lung cancer surgery that may have the advantages of quicker recovery, shorter hospital stay
and diminished hospital costs.

Chemotherapy

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- The combination regimen depends on the tumor type. Small cell lung carcinoma, even if relatively
early stage is treated primarily with chemotherapy and radiation as surgery has no demonstrable influence
on survival.
- In small cell lung carcinoma, cisplatin and etoposide are most commonly used. Combinations with
carboplatin, gemcitabine, paclitaxel, vinorelbine, topotecan, and irinotecan are also used.
- In extensive-stage small-cell lung cancer celecoxib may have a role.
- Primary chemotherapy is also given in metastatic non-small cell lung carcinoma. Advanced non-small
cell lung carcinoma is often treated with cisplatin or carboplatin, in combination with gemcitabine,
paclitaxel, docetaxel, etoposide, or vinorelbine. Bevacizumab improves results in non-squamous cancers
treated with paclitaxel and carboplatin in patients less than 70 years old who have reasonable general
performance status. Bronchoalveolar carcinoma is a subtype of non-small cell lung carcinoma that may
respond to gefitinib and erlotinib.
- Testing for the molecular genetic subtype of non-small cell lung cancer may be of assistance in
selecting the most appropriate initial therapy e.g. mutation of the epidermal growth factor receptor gene
may predict whether initial treatment with a specific inhibitor or with chemotherapy is more
advantageous.
- Maintenance therapy in advanced non-small cell lung cancer refers to continuing treatment after an
initial response to therapy. Switch maintenance changes to different medications than the initial therapy
and can use pemetrexed, erlotinib, and docetaxel, although pemetrexed is only used in non-squamous
NSCLC.

Adjuvant chemotherapy for NSCLC

- Adjuvant chemotherapy refers to the use of chemotherapy after surgery to improve the outcome.
- During surgery, samples are taken from the lymph nodes. If these samples contain cancer, the patient
has stage II or III disease. In this situation, adjuvant chemotherapy may improve survival by up to 15%.
- Standard practice has often been to offer platinum-based chemotherapy (including either cisplatin or
carboplatin).
- However, the benefit of platinum-based adjuvant chemotherapy was confined to patients who had
tumors with low ERCC1 (excision repair cross-complementing 1) activity.

Radiotherapy

- Radiotherapy is often given together with chemotherapy, and may be used with curative intent in
patients with non-small cell lung carcinoma who are not eligible for surgery.
- This form of high intensity radiotherapy is called radical radiotherapy. A refinement of this technique
is continuous hyper fractionated accelerated radiotherapy (CHART), in which a high dose of radiotherapy
is given in a short time period.
- For small cell lung carcinoma cases that are potentially curable, chest radiation is often recommended
in addition to chemotherapy.
- For both non-small cell lung carcinoma and small cell lung carcinoma patients, smaller doses of
radiation to the chest may be used for symptom control (palliative radiotherapy).
- Unlike other treatments, it is possible to deliver palliative radiotherapy without confirming the
histological diagnosis of lung cancer.
- Brachytherapy (localized radiotherapy) may be given directly inside the airway when cancer affects a
short section of bronchus. It is used when inoperable lung cancer causes blockage of a large airway.
- Patients with limited stage small cell lung carcinoma are usually given prophylactic cranial irradiation
(PCI). This is a type of radiotherapy to the brain, used to reduce the risk of metastasis.
- Recent improvements in targeting and imaging have led to the development of extra cranial
stereotactic radiation in the treatment of early-stage lung cancer. In this form of radiation therapy, very
high doses are delivered in a small number of sessions using stereotactic targeting techniques. Its use is
primarily in patients who are not surgical candidates due to medical comorbidities.
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Interventional radiology

- Radiofrequency ablation should currently be considered an investigational technique in the treatment

of bronchogenic carcinoma. It is done by inserting a small heat probe into the tumor to kill the tumor
cells.

Lung abscess

Lung abscess is necrosis of the pulmonary tissue and formation of cavities containing necrotic debris or
fluid caused by microbial infection (inhalation or aspiration of anaerobic bacteria) characterized by
productive cough, fever and chest pains.

 This pus-filled cavity is often caused by aspiration, which may occur during altered consciousness.
Alcoholism is the most common condition predisposing to lung abscesses.
 Lung abscess is considered primary when it results from existing lung parenchyma process and is
termed secondary when it complicates another process e.g. vascular emboli or follows rupture of extra-
pulmonary abscess into lung.

Causes

Conditions contributing to lung abscess

 Aspiration of oropharyngeal or gastric secretion

 Septic emboli
 Necrotizing pneumonia
 Vasculitis: Wegener's granulomatosis
 Necrotizing tumors: due to neoplasms across all age groups, higher in older people primary
squamous carcinoma of the lung is the commonest.
 Alcoholism
 Drug addicts
 Lowered immunity
 Neurological conditions such as stroke
 Unconsciousness
 Anesthesia
 Patients receiving NGT feeding

Organisms

 Anaerobic bacteria: Peptostreptococcus, Bacteroides, Fusobacterium species,

 Microaerophilic streptococcus : Streptococcus milleri
 Aerobic bacteria: Staphylococcus, Klebsiella, Haemophilus, Pseudomonas, Nocardia, Escherichia coli,
Streptococcus, Mycobacteria
 Fungi: Candida, Aspergillus
 Parasites: Entamoeba histolytica,

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Signs and symptoms

Onset of symptoms is often gradual, but in necrotizing staphylococcal or gram-negative bacillary

pneumonias patients can be acutely ill.

 Cough - can be productive with foul smelling purulent sputum with blood (hemoptysis)
 fever with shivering
 night sweats (Diaphoresis)
 chest pain,
 shortness of breath,
 lethargy
 finger clubbing
 Dental decay is common especially in alcoholics and children.
 On examination of chest there will be features of consolidation such as localized dullness on
percussion, bronchial, decreased, crackles and avernous breath sound
 Dyspnea
 Anorexia
 Weight loss
 Headache

Diagnosis

 Pathology image of a lung abscess.

 Chest X-ray and other imaging studies – reveals localized infiltrates with clear air spaces containing
fluid
 Laboratory studies

 FBC - Raised inflammatory markers (high WBCs, ESR, CRP)

 Examination of sputum is important in any pulmonary infections and here often reveals mixed flora.
 Blood and sputum for culture and gram stain to detect the causative organism
 (Percutaneous aspiration of the abscess) Transtracheal or Transbronchial (via bronchoscopy)
aspirates for cultured.
 Fiber optic bronchoscopy is often performed to exclude obstructive lesion; it also helps in bronchial
drainage of pus.
 CT scan to differentiate the type of lesion

Management

 Broad spectrum antibiotic to cover mixed flora is the mainstay of treatment.

 Pulmonary physiotherapy and postural drainage are also important.
 Surgical procedures are required in selective patients for drainage or pulmonary resection or
lobectomy.
 Analgesics to relive pain
 Oxygen therapy

Complications

 spread of infection to other lung segments

 bronchiectasis
 empyema
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 bacteraemia/septicemia
 metastatic infection such as brain abscess
 Massive hemorrhage
 Respiratory failure

Prevention

 Appropriate antibiotic therapy before tooth extraction in patients with infection

 Adequate dental/oral hygiene
 Adequate antimicrobial therapy for patients with pneumonia

Information, Education and Communication

 Teach the patient and relatives how to do chest physiotherapy to promote removal of secretions
 Teach patient deep breathing and coughing exercises
 Encourage patient to maintain good oral hygiene
 Advice patient to follow a nutritious high calorie and protein diet, low in fat and salt
 Instruct patient to take plenty of fluids to help loosen secretions.

Emphysema

Def: This is a slow progressive disease of the respiratory system leading to destruction of the alveoli, enlargement of
the distal air spaces and a breakdown of alveolar walls.

 Or Emphysema is a long-term, progressive disease of the lungs that primarily causes shortness of
breath.

 The term means swelling and comes from the Greek emhysan meaning inflate, itself composed of en
meaning in and physa meaning breath, blast.
 Emphysema is called an obstructive lung disease because the destruction of lung tissue around
smaller sacs, called alveoli, makes these air sacs unable to hold their functional shape upon exhalation. It
is often caused by smoking.

CLASSFICATION

Emphysema can be classified into primary and secondary. However, it is more commonly classified by
location.

Emphysema can be subdivided into panacinary and centroacinary (or panacinar and centriacinar, or
centrilobular and panlobular).

 Panacinar (or panlobular) emphysema: The entire respiratory acinus, from respiratory bronchiole to
alveoli, is expanded. Occurs more commonly in the lower lobes, especially basal segments, and anterior
margins of the lungs.[2]
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 Centriacinar (or centrilobular) emphysema: The respiratory bronchiole (proximal and central part of
the acinus) is expanded. The distal acinus or alveoli are unchanged. Occurs more commonly in the upper
lobes.

TYPES

 Congenital lobar emphysema

 CLE results in overexpansion of a pulmonary lobe and resultant compression of the remaining lobes
of the ipsilateral lung, and possibly also the contralateral lung. There is bronchial narrowing because of
weakened or absent bronchial cartilage.[4]
 There may be congenital extrinsic compression, commonly by an abnormally large pulmonary artery.
This causes malformation of bronchial cartilage, making them soft and collapsible. [4]
 CLE is potentially reversible, yet possibly life-threatening, causing respiratory distress in the neonate.

Causes

 Smoking of cigarettes.
 alpha 1-antitrypsin deficiency
 Some types of emphysema are considered a normal part of aging and are found in the elderly whose
lungs have deteriorated due to age.

 At about 20 years of age, people stop developing new alveoli tissue.

 In the years following the cessation of the development of new alveoli, lung tissue can start to
deteriorate.
 This is a normal, natural part of aging in healthy people. Alveoli will die, the amount of lung capillaries
will decline and the elastin of the lungs will begin to break down causing a loss of pulmonary elasticity.
 As people age, they will also lose strength and mass in their chest muscles causing these muscles to
become weaker.
 In addition, bones can start to deteriorate and a person’s posture can change.

 Other causes of emphysema can be anything that causes the body to be unable to inhibit proteolytic
enzymes in the lung.

 This could be exposure to air pollution, second hand smoke or other chemicals and toxins.

PREDISPOSING FACTORS

 Cigarette smoking
 Air pollution
 Allergy
 Auto-immunity
 Infection
 Genetic pre-disposition
 Aging

SIGNS AND SYMPTOMS

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 Shortness of breath on exertion - show in on set and steadily progressive.
 Chronic cough - which may be minimal except if there is respiratory infection .The cough may not be productive.
 Weakness - due to inadequate oxygen in the blood which is needed for metabolism.
 Weight loss - due to hypoxia.
 Increased respiratory muscle effort and respiratory acidosis.
 Wheezing sounds - due to the presents of secretions in the airway.
 Anxiety - due to reduced oxygen content in the blood.
 Feet and ankles may swell.
 Patient may develop a barrel chest in which the distance from the chest to the back is more pronounced due to
trapped air within the lungs.
 Depression.
 Sleep problems.
 Tachypnea when they try to extend their expiration.
 Breathing is difficult (dyspnea) and the patient must use accessory muscles to help them breathe.
 The patient can have an increase of the antero-posterior diameter of their chest which is sometimes
referred as "barrel chest."
 The patient is often seen leaning forward with arms extended or leaning on something to help them
breathe.
 When lung auscultation and chest percussion is done there is a hyper-resonant sound that is heard.
 cyanosis,
 Lowered oxygen levels and increased carbon dioxide levels.

Pathophysiology

 Pathology of lung showing centri-lobular emphysema characteristic of smoking. Close up of fixed; cut
surface shows multiple cavities lined by heavy black carbon deposits.

 In normal breathing, air is drawn in through the bronchi and into the alveoli, which are tiny sacs
surrounded by capillaries. Alveoli absorb oxygen and then transfer it into the blood. When toxicants,
such as cigarette smoke, are breathed into the lungs, the harmful particles become trapped in the
alveoli, causing a localized inflammatory response.
 Chemicals released during the inflammatory response (e.g., elastase) can eventually cause the
alveolar septum to disintegrate. This condition, known as septal rupture, leads to significant
deformation of the lung architecture. The large cavities left by the septal degeneration are known as
bullae (single - bulla). These deformations result in a large decrease of alveoli surface area used for gas
exchange. This results in a decreased Transfer Factor of the Lung for Carbon Monoxide (TLCO).
 To accommodate the decreased surface area, thoracic cage expansion (barrel chest) and diaphragm
contraction (flattening) take place. Expiration increasingly depends on the thoracic cage and abdominal
muscle action, particularly in the end expiratory phase. Due to decreased ventilation, the ability to
exude carbon dioxide is significantly impaired. In the more serious cases, oxygen uptake is also impaired.
 As the alveoli continue to break down, hyperventilation is unable to compensate for the progressively
shrinking surface area, and the body is not able to maintain high enough oxygen levels in the blood. The
body's last resort is vaso-constricting appropriate vessels. This leads to pulmonary hypertension, which
places increased strain on the right side of the heart, the side responsible for pumping deoxygenated
blood to the lungs. The heart muscle thickens in order to pump more blood. This condition is often
accompanied by the appearance of jugular venous distension. Eventually, as the heart continues to fail,
it becomes larger and blood backs up in the liver.
 Patients with alpha 1-antitrypsin deficiency (A1AD) are more likely to suffer from emphysema. A1AT
inhibits inflammatory enzymes (such as elastase) from destroying the alveolar tissue. Most A1AD
patients do not develop clinically significant emphysema, but smoking and severely decreased A1AT
levels can cause emphysema at a young age. The type of emphysema caused by A1AD is known as

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panacinar emphysema (involving the entire acinus) as opposed to centrilobular emphysema, which is
caused by smoking.
 Panacinar emphysema typically affects the lower lungs, while centrilobular emphysema affects the
upper lungs. Smokers with A1AD are at the greatest risk for emphysema
 While A1AD provides some insight into the pathogenesis of the disease, hereditary A1AT deficiency
only accounts for a small proportion of the disease.
 Studies for the better part of the past century have focused mainly upon the putative role of
leukocyte elastase (also neutrophil elastase), a serine protease found in neutrophils, as a primary
contributor to the connective tissue damage seen in the disease.
 This hypothesis, a result of the observation that neutrophil elastase is the primary substrate for A1AT,
and A1AT is the primary inhibitor of neutrophil elastase, together have been known as the "protease-
antiprotease" theory, implicating neutrophils as an important mediator of the disease. However, more
recent studies have brought into light the possibility that one of the many other numerous proteases,
especially matrix metalloproteases might be equally or more relevant than neutrophil elastase in the
development of non-hereditary emphysema.

INVESTIGATIONS

 Clinical assessment of the patient

 History of cough, exertion dyspnoea, wheezing, smoking, exposure to dust, fumes and gases.
 Pulmonary functions test (e.g. spirometry); will reveal abnormalities.
 Arterial blood gas analysis.
 Apha 1 antrysin assay –used to indentify person at risk.
 Sputum for cultural and sensitivity and also microscopy.
 X-ray radiography may aid in the diagnosis.
 A DLCO test may be used to differentiate Emphysema from other types of Obstructive disorders such
as Chronic Bronchitis and Asthma. DLCO is a test that measures the ability of gases to diffuse across the
alveolar-capillary membrane. A DLCO will be decreased in Emphysema whereas it will be normal or
increased in Asthma and Chronic Bronchitis.

MANAGEMENT

OBJECTIVES

 To improve the quality of life

 To reduce the progress of the disease.

TREATMENT

 Administer prescribed bronchodilators to relieve bronchial mucosal edema. Avoid excessive use of broncho –
dilator.
 Auscultation the chest after administration of aerosol broncho-dilators to assess improvement of air entry.
 Give corticosteroids as the ant- inflammatory effect helps to relieve airway obstruction.
 Offer oxygen therapy to prevent hypoxemia thus minimizing carbon dioxide in he blood as there is poor exchange
of gases.
 Give prescribed antibiotics.

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 If patient is an able to cough, bronchoscopic remove of secretions may be done.
 Endotracheal intubation or tracheotomy may be done permit more effective suctioning of secretions and to
provide ventilation assistance.
 Under water seal drainage.

Prognosis and treatment

 Stop smoking and avoid all exposure to cigarette smoke and lung irritants.
 Pulmonary rehabilitation can be very helpful to optimize the patient's quality of life and teach the
patient how to actively manage his or her care.
 Treat patient with other conditions such as gastric reflux and allergies to improve lung function.
 supporting the breathing with:

- anticholinergics,
- bronchodilators,
- steroid medication (inhaled or oral),
- effective body positioning (High Fowlers),
- supplemental oxygen

 Lung volume reduction surgery (LVRS) to improve the quality of life

 Surgical transplantation also requires the patient to take an anti-rejection drug regimen which
suppresses the immune system, and can lead to microbial infection of the patient.

NURSING CARE

1. ENVIRONMENT

Nurse patient in a well ventilated room and it should be dust free.

2. POSITION

 -Sitting position upright forward leaning forward on a cardiac table will be help

3. OBSERVATIONS

 -Observe the general condition of the patient.

 -Check the vital sig ns i.e. temperature pulse, respiration and blood pressure frequent to monitor progress of the
patient.
 -Observe patient for dyspnoea, cyanosis pallor

4. HYGIENE

 Offer daily baths and oral hygiene

 Change soiled linen and ensure that he has a sputum mug which should be decontaminated before disposing of
the sputum

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 Depending on the condition of the patient, a urinary or bed may be offered to Mr. Gondwe.
NUTRITION

 Encourage the patient to take small frequent meals high in proteins, with snacks in between meals
 Give supplemental oxygen while patient is eating to relieve dyspoea
 Encourage a lot of fluids to liquefy secretions.

PHSIOTHERAPY

 Utilize techniques of breathing strength the diaphragm muscles of respiration.

 Use pursed- lip breathing at intervals and period of dyspnoea to control rate and depth of respiration and improve
respiratory muscle co-ordination.
 Apply relaxation exercises to reduce stress, tension and anxiety

PSYCHOLOGICAL CARE

The consent shortness of breath and fatigue make the patient irritable, anxious and depressed.

 Show positive and interested approach to the patient

 Be a good listener
 Allow patient to express his feelings

ELIMINATION

 Offer bed pen and urinal or take the patient to toilet depending on the condition of the patient.

Breast cancer

DEF: Breast cancer (malignant breast neoplasm) is a malignant cancer originating from breast tissue,
most commonly from the inner lining of milk ducts or the lobules that supply the ducts with milk
resulting from hormonal, genetic or environmental events characterized by painless lump or mass in the
breast and thickening of breast tissue.

 Cancers originating from ducts are known as ductal carcinomas; those originating from lobules are
known as lobular carcinomas.

Cause

The cause is not known.

Risk factors

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 The primary epidemiologic and risk factors that have been identified are;
- Sex – more common in women than men
- Age – women over the age of 45 years and pre-menopausal
- Lack of childbearing or breastfeeding – women who have never been pregnant before
-First pregnancy after the age of 35 years
- Higher hormone levels – longer exposure to estrogen helps the cancer cells to grow.
- Race – more common in blacks
-Economic status – more commonly associated to women of low social economic status
-Hereditary syndromes – 1st degree family history of breast cancer
-Genetic factors – (changes in mutation in normal genes) usually increase the risk slightly or moderately;
the exception is women and men who are carriers of BRCA1 or BRCA2 mutations. These people have a
very high lifetime risk for breast and ovarian cancer, depending on the portion of the proteins where the
mutation occurs.
-Diet high - fat diet
-other behaviors such as alcohol intake,
-obesity –
-prolonged menstrual cycle
-early menses (before 12 years) or late menopause (after age of 55 years)
-environmental factors such as tobacco use
-radiation,
-endocrine disruptors
-Women who are taking or have taken contraceptives
-Endometrial or ovarian cancer
-Pre-existing fibrocystic disease
-Women taking Diethylstilbestrol to prevent miscarriage

Demographic and medical risk factors

 Personal history of breast cancer: A woman who had breast cancer in one breast has an increased risk
of getting cancer in her other breast.
 Family history: A woman's risk of breast cancer is higher if her mother, sister, or daughter had breast
cancer. The risk is higher if her family member got breast cancer before age 40.
 Certain breast changes: Atypical hyperplasia and lobular carcinoma in situ found in benign breast
conditions such as fibrocystic breast changes are correlated with an increased breast cancer risk.

Classification

 Breast cancers can be classified by different schemata. Every aspect influences treatment response and
prognosis. Description of a breast cancer would optimally include multiple classification aspects, as well
as other findings, such as signs found on physical exam. Classification aspects include stage (TNM),
pathology, grade, receptor status, and the presence or absence of genes as determined by DNA testing:

 Stage.

 The TNM classification for breast cancer is based on the size of the tumor (T), whether or not the
tumor has spread to the lymph nodes (N) in the armpits, and whether the tumor has metastasized (M) (i.e.
spread to a more distant part of the body). Larger size, nodal spread, and metastasis have a larger stage
number and a worse prognosis.
The main stages are:
- Stage 0 - is a pre-malignant disease or marker (sometimes called DCIS: Ductal Carcinoma in Situ) .
- Stages 1–3 - are defined as 'early' cancer and potentially curable.
- Stage 4 - is defined as 'advanced' and/or 'metastatic' cancer and incurable.

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  Histopathology.

 Breast cancer is usually, but not always, primarily classified by its histological appearance. Most
breast cancers are' derived from the epithelium lining the ducts or lobules, and are classified as mammary
ductal carcinoma. Carcinoma in situ is proliferation of cancer cells within the epithelial tissue without
invasion of the surrounding tissue. In contrast, invasive carcinoma invades the surrounding tissue.
-Adenocarcinoma (ductal) – cancer arising from the epithelium
-Intraductal – cancer developing inside the duct
-Infiltrating – occurring in the breast’s parenchyma tissue
-Inflammatory (rare) – growing rapidly and causing overlying skin to become edematous, inflamed and
indurate.
-Lobular carcinoma in situ – involving the lobes of the glandular tissue
-Medullar or circumscribed – enlarged tumor with rapid growth rate

 Grade (Bloom-Richardson grade).

 When cells become differentiated, they take different shapes and forms to function as part of an organ.
Cancerous cells lose that differentiation. In cancer grading, tumor cells are generally classified as well
differentiated (low grade), moderately differentiated (intermediate grade), and poorly differentiated (high
grade). Poorly differentiated cancers have a worse prognosis.

 Receptor status.

 Cells have receptors on their surface and in their cytoplasm and nucleus. Chemical messengers such as
hormones bind to receptors, and this causes changes in the cell. Breast cancer cells may or may not have
three important receptors: estrogen receptor (ER), progesterone receptor (PR), and HER2/neu. Cells with
none of these receptors are called basal-like or triple negative. ER+ cancer cells depend on estrogen for
their growth, so they can be treated with drugs to block estrogen effects (e.g. tamoxifen), and generally
have a better prognosis.
Generally, HER2+ had a worse prognosis, however HER2+ cancer cells respond to drugs such as the
monoclonal antibody, trastuzumab, (in combination with conventional chemotherapy) and this has
improved the prognosis significantly.

 DNA microarrays have compared normal cells to breast cancer cells and found differences in hundreds
of genes, but the significance of most of those differences is unknown.

50% - upper
outer quadrant

15% upper inner

quadrant

18% nipple

6% lower inner
quadrant 11% lower outer
quadrant

Signs and symptoms

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 The first noticeable symptom of breast cancer is typically a painless lump that feels different from the
rest of the breast tissue. The earliest breast cancers are detected by a mammogram. Lumps found in lymph
nodes located in the armpits can also indicate breast cancer.
 changes in breast size or shape,
 Skin changes such as dimpling, orange-peel texture to the skin referred to as peau d'orange.
 nipple inversion (nipple retraction)
 Spontaneous single-nipple discharge (clear, blood or milky nipple discharge).
 Pain ("mastodynia") is an unreliable tool in determining the presence or absence of breast cancer, but
may be indicative of other breast health issues.
 When breast cancer cells invade the dermal lymphatic - small lymph vessels in the skin of the breast -
its presentation can resemble skin inflammation and thus is known as inflammatory breast cancer (IBC).
 Symptoms of inflammatory breast cancer include;
 pain,
 swelling due to obstructed lymph circulation in the dermal layer
 warmth and redness throughout the breast,
 arm edema
 thickening of the breast tissue and non tender, painless fixed lesions with irregular borders
 scaly skin around the nipple
 supra-clavicular and auxiliary nodes may be disclosed lumps or enlargement
 Another reported symptom complex of breast cancer is Paget's disease of the breast. This syndrome
presents as eczematoid skin changes such as redness and mild flaking of the nipple skin. As Paget's
advances, symptoms may include tingling, itching, increased sensitivity, burning, and pain. There may
also be discharge from the nipple.
 Ulcerating and fungating lesions

Pathophysiology

Breast cancer, like other cancers, occurs because of an interaction between the environment and a
defective gene. Normal cells divide as many times as needed and stop. They attach to other cells and stay
in place in tissues. Cells become cancerous when mutations destroy their ability to stop dividing, to attach
to other cells and to stay where they belong. When cells divide, their DNA is normally copied with many
mistakes. Error-correcting proteins fix those mistakes. The mutations known to cause cancer, such as p53,
BRCA1 and BRCA2, occur in the error-correcting mechanisms. These mutations are either inherited or
acquired after birth. Presumably, they allow the other mutations, which allow uncontrolled division, lack
of attachment, and metastasis to distant organs. [36][51] Normal cells will commit cell suicide (apoptosis)
when they are no longer needed. Until then, they are protected from cell suicide by several protein
clusters and pathways. One of the protective pathways is the PI3K/AKT pathway; another is the
RAS/MEK/ERK pathway. Sometimes the genes along these protective pathways are mutated in a way
that turns them permanently "on", rendering the cell incapable of committing suicide when it is no longer
needed. This is one of the steps that cause cancer in combination with other mutations. Normally, the
PTEN protein turns off the PI3K/AKT pathway when the cell is ready for cell suicide. In some breast
cancers, the gene for the PTEN protein is mutated, so the PI3K/AKT pathway is stuck in the "on"
position, and the cancer cell does not commit suicide. [52]

 Mutations that can lead to breast cancer have been experimentally linked to:
- Estrogen exposure.
-Failure of immune surveillance, the removal of malignant cells throughout one's life by the immune
system.
-Abnormal growth factor signaling in the interaction between stromal cells and epithelial cells can
facilitate malignant cell growth.

Diagnosis

 ‘Triple test’ of clinical breast examination (breast examination by a trained medical practitioner),

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 Mammography - can indicate an approximate likelihood that a lump is cancer, and may also identify
any other lesions
 Fine needle aspiration cytology - may be done using local anesthetic if required, involves attempting to
extract a small portion of fluid from the lump.
-Clear fluid makes the lump highly unlikely to be cancerous, but bloody fluid may be sent off for
inspection under a microscope for cancerous cells
 Core biopsy - where a section of the breast lump is removed,
 Excisional biopsy - where the entire lump is removed.
 Vacuum-assisted breast biopsy (VAB) - may help diagnose breast cancer among patients with a
mammographically detected breast in women.
 Ultrasound
 Magnetic resonance imaging.
 A clinical or self breast exam involves feeling the breast for lumps or other abnormalities.
Mammographic screening for breast cancer uses x-rays to examine the breast for any uncharacteristic
masses or lumps.

Treatment
 Breast cancer is usually treated with surgery and then possibly with chemotherapy or radiation, or
both.
 Hormone positive cancers are treated with long term hormone blocking therapy.
 Treatments are given with increasing aggressiveness according to the prognosis and risk of recurrence.
-Stage 1 cancers (and DCIS) have an excellent prognosis and are generally treated with lumpectomy and
sometimes radiation.
-The aggressive HER2+ cancers should be treated with the trastuzumab (Herceptin) regime but
chemotherapy is otherwise uncommon.

-Stage 2 and 3 cancers with a progressively poorer prognosis and greater risk of recurrence are generally
treated with surgery (lumpectomy or mastectomy with or without lymph node removal), chemotherapy
(plus trastuzumab for HER2+ cancers) and sometimes radiation (particularly following large cancers,
multiple positive nodes or lumpectomy).

-Stage 4, metastatic cancer, (i.e. spread to distant sites) is not curable and is managed by various
combinations of all treatments from surgery, radiation, chemotherapy and targeted therapies. However,
stage 4 breast cancer management has been very disappointing, with only a 6 month increase in median
survival following these treatments. But there is still about 8 percent of living.

Medications

 Drugs used after and in addition to surgery are called adjuvant therapy.
 Chemotherapy prior to surgery is called neo-adjuvant therapy.
 There are currently 3 main groups of medications used for adjuvant breast cancer treatment:

 Hormone Blocking Therapy

 Chemotherapy
 Monoclonal Antibodies

-One or all of these groups can be used.

 Hormone Blocking Therapy: - Some breast cancers require estrogen to continue growing.
-They can be identified by the presence of estrogen receptors (ER+) and progesterone receptors (PR+) on
their surface (sometimes referred to together as hormone receptors).

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-These ER+ cancers can be treated with drugs that either block the receptors, e.g. tamoxifen, or
alternatively block the production of estrogen with an aromatase inhibitor, e.g. anastrozole (Arimidex)
or letrozole (Femara).
-Aromatase inhibitors, however, are only suitable for post-menopausal patients.

 Chemotherapy: - Predominately used for stage 2-4 disease, being particularly beneficial in estrogen
receptor-negative (ER-) disease. They are given in combinations, usually for 3–6 months.

-One of the most common treatments is cyclophosphamide plus doxorubicin (Adriamycin), known as
AC; these drugs damage DNA in the cancer, but also in fast-growing normal cells where they cause
serious side effects.
-Damage to the heart muscle is the most dangerous complication of doxorubicin. Sometimes a taxane
drug, such as docetaxel, is added, and the regime is then known as CAT; taxane attacks the microtubules
in cancer cells.
-Another common treatment, which produces equivalent results, is cyclophosphamide, methotrexate, and
fluorouracil (CMF).
-Chemotherapy can literally refer to any drug, but it is usually used to refer to traditional non-hormone
treatments for cancer.

 Monoclonal antibodies: A relatively recent development in HER2+ breast cancer treatment.

-Approximately 15-20 percent of breast cancers have an amplification of the HER2/neu gene or over-
expression of its protein product.
- This receptor is normally stimulated by a growth factor which causes the cell to divide; in the absence of
the growth factor, the cell will normally stop growing.
-Over-expression of this receptor in breast cancer is associated with increased disease recurrence and
worse prognosis.
-Trastuzumab (Herceptin), a monoclonal antibody to HER2, has improved the 5 year disease free
survival of stage 1–3 HER2+ breast cancers to about 87% (overall survival 95%).
-Trastuzumab, however, is expensive, and approx 2% of patients suffer significant heart damage; it is
otherwise well tolerated, with far milder side effects than conventional chemotherapy.
- Other monoclonal antibodies are also undergoing clinical trials.
-Aspirin may reduce mortality from breast cancer??????

Breast Cancer Medication Side Effects

 While breast cancer medications can reduce the size of tumors, eliminate cancer cells left behind after
surgery, and help prevent recurrences of the disease, they can also cause unwanted side effects.
 Patients in advanced stages might find it is difficult for their bodies to tolerate some of these side
effects.
 Those taking breast cancer medications might experience nausea, weight loss, vomiting, hot flashes,
vaginal dryness, and incontinence.
 Some breast cancer medications also increase the risks of developing other diseases. The drug
tamoxifen, for instance, increases a woman's risk of getting cataracts, uterine cancer, and blood clots that
can result in stroke.

Radiation

 Radiotherapy is given after surgery to the region of the tumor bed, to destroy microscopic tumors that
may have escaped surgery.
 It may also have a beneficial effect on tumor microenvironment.
 Radiation therapy can be delivered as external beam radiotherapy or as brachytherapy (internal
radiotherapy).

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 Conventionally radiotherapy is given after the operation for breast cancer. Radiation can also be given,
arguably more efficiently, at the time of operation on the breast cancer- intraoperatively.)

CHOLECYSTITIS

Cholecystitis or a gall bladder attack is inflammation of the gall bladder.

Causes and pathology

Cholecystitis is often caused by cholelithiasis (the presence of choleliths, or gallstones, in the

gallbladder), with choleliths most commonly blocking the cystic duct directly. This leads to inspissation
(thickening) of bile, bile stasis, and secondary infection by gut organisms, predominantly E. coli and
Bacteroides species.

The gallbladder's wall becomes inflamed. Extreme cases may result in necrosis and rupture. Inflammation
often spreads to its outer covering, thus irritating surrounding structures such as the diaphragm and bowel.

Less commonly, in debilitated and trauma patients, the gallbladder may become inflamed and infected in
the absence of cholelithiasis, and is known as acute acalculous cholecystitis.

Stones in the gallbladder may cause obstruction and the accompanying acute attack. The patient might
develop a chronic, low-level inflammation which leads to a chronic cholecystitis, where the gallbladder is
fibrotic and calcified.

Symptoms

Cholecystitis usually presents as a pain in the right upper quadrant. This is usually a constant, severe pain.
The pain may be felt to 'refer' to the right flank or right scapular region at first.

This may also present with the above mentioned pain after eating greasy or fatty foods such as pastries,
pies and fried foods.

This is usually accompanied by a low grade fever, diarrhea, vomiting and nausea.

More severe symptoms such as high fever, shock and jaundice indicate the development of complications
such as abscess formation, perforation or ascending cholangitis. Another complication, gallstone ileus,
occurs if the gallbladder perforates and forms a fistula with the nearby small bowel, leading to symptoms
of intestinal obstruction.

Chronic cholecystitis manifests with non-specific symptoms such as nausea, vague abdominal pain,
belching, and diarrhea.

Diagnosis

Cholecystitis is usually diagnosed by a history of the above symptoms, as well examination findings:

 fever (usually low grade in uncomplicated cases)

 tender right upper quadrant +/- Murphy's sign
 Ortner's sign - tenderness when hand taps the edge of right costal arch.
 Georgievskiy-Myussi's sign (phrenic nerve sign) - pain when press between edges of
sternocleidomastoid muscle.[1]

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Subsequent laboratory and imaging tests are used to confirm the diagnosis and exclude other possible
causes.

Ultrasound can assist in the differential.[2][3]

Differential diagnosis

Acute cholecystitis

 This should be suspected whenever there is acute right upper quadrant or epigastric pain.
o Other possible causes include:
 Perforated peptic ulcer
 Acute peptic ulcer exacerbation
 Amoebic liver abscess
 Acute amoebic liver colitis
 Acute pancreatitis
 Acute intestinal obstruction
 Renal colic
 Acute retrocolic appendicitis

Chronic cholecystitis

The symptoms of chronic cholecystitis are non-specific, thus chronic cholecystitis may be mistaken for
other common disorders:

 Peptic ulcer
 Hiatus hernia
 Colitis
 Functional bowel syndrome

It is defined pathologically by the columnar epithelium has reached down the muscular layer.

Quick Differential

 Biliary colic - Caused by obstruction of the cystic duct. It is associated with sharp and constant
epigastric pain in the absence of fever and usually there is a negative Murphy's sign. Liver function tests
are within normal limits since the obstruction does not necessarily cause blockage in the common
hepatic duct, thereby allowing normal bile excretion from the liver. An ultrasound scan is used to
visualise the gallbladder and associated ducts, and also to determine the size and precise position of the
obstruction.
 Cholecystitis - Caused by blockage of the cystic duct with surrounding inflammation, usually due to
infection. Typically, the pain is initially 'colicky' (intermittent), and becomes constant and severe, mostly
in the right upper quadrant. Infectious agents that cause cholecystitis include E. coli, Klebsiella,
Pseudomonas, B. fragilis and Enterococcus. Murphy's sign is positive, particularly because of increased
irritation of the gallbladder lining, and similarly this pain radiates (spreads) to the shoulder, flank or in a
band like pattern around the lower abdomen. Laboratory tests frequently show raised hepatocellular
liver enzymes (AST, ALT) with a high white cell count (WBC). Ultrasound is used to visualise the
gallbladder and ducts.
 Choledocholithiasis - This refers to blockage of the common bile duct where a gallstone has left the
gallbladder or has formed in the common bile duct (primary cholelithiasis). As with other biliary tree
obstructions it is usually associated with 'colicky' pain, and because there is direct obstruction of biliary

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output, obstructive jaundice. Liver function tests will therefore show increased serum bilirubin, with
high conjugated bilirubin. Liver enzymes will also be raised, predominately GGT and ALP, which are
associated with biliary epithelium. The diagnosis is made using endoscopic retrograde
cholangiopancreatography (ERCP), or the nuclear alternative (MRCP). One of the more serious
complications of choledocholithiasis is acute pancreatitis, which may result in significant permanent
pancreatic damage and brittle diabetes.
 Cholangitis - An infection of entire biliary tract, and may also be known as 'ascending cholangitis',
which refers to the presence of pathogens that typically inhabit more distal regions of the bowel [4]

Cholangitis is a medical emergency as it may be life threatening and patients can rapidly succumb to
acute liver failure or bacterial sepsis. The classical sign of cholangitis is Charcot's triad, which is right
upper quadrant pain, fever and jaundice. Liver function tests will likely show increases across all enzymes
(AST, ALT, ALP, GGT) with raised bilirubin. As with choledocholithiasis, diagnosis is confirmed using
cholangiopancreatography.

It is worth noting that bile is an extremely favourable growth medium for bacteria, and infections in this
space develop rapidly and may become quite severe.

Investigations

Blood

Laboratory values may be notable for an elevated alkaline phosphatase, possibly an elevated bilirubin
(although this may indicate choledocholithiasis), and possibly an elevation of the WBC count. CRP (C-
reactive protein) is often elevated. The degree of elevation of these laboratory values may depend on the
degree of inflammation of the gallbladder. Patients with acute cholecystitis are much more likely to
manifest abnormal laboratory values, while in chronic cholecystitis the laboratory values are frequently
normal.

Radiology

Sonography is a sensitive and specific modality for diagnosis of acute cholecystitis; adjusted sensitivity
and specificity for diagnosis of acute cholecystitis are 88% and 80%, respectively. The 2 major diagnostic
criteria are cholelithiasis and sonographic Murphy's sign. Minor criteria include gallbladder wall
thickening greater than 3mm, pericholecystic fluid, and gallbladder dilatation.

The reported sensitivity and specificity of CT scan findings are in the range of 90-95%. CT is more
sensitive than ultrasonography in the depiction of pericholecystic inflammatory response and in localizing
pericholecystic abscesses, pericholecystic gas, and calculi outside the lumen of the gallbladder. CT cannot
see noncalcified gallbladder calculi, and cannot assess for a Murphy's sign.

Hepatobiliary scintigraphy with technetium-99m DISIDA (bilirubin) analog is also sensitive and accurate
for diagnosis of chronic and acute cholecystitis. It can also assess the ability of the gall bladder to expel
bile (gall bladder ejection fraction), and low gall bladder ejection fraction has been linked to chronic
cholecystitis. However, since most patients with right upper quadrant pain do not have cholecystitis,
primary evaluation is usually accomplished with a modality that can diagnose other causes, as well.

Therapy

X-Ray during laparoscopic cholecystectomy

For most patients, in most centres, the definitive treatment is surgical removal of the gallbladder.
Supportive measures are instituted in the meantime and to prepare the patient for surgery. These measures

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include fluid resuscitation and antibiotics. Antibiotic regimens usually consist of a broad spectrum
antibiotic such as piperacillin-tazobactam (Zosyn), ampicillin-sulbactam (Unasyn), ticarcillin-clavulanate
(Timentin), or a cephalosporin (e.g.ceftriaxone) and an antibacterial with good coverage (fluoroquinolone
such as ciprofloxacin) and anaerobic bacteria coverage, such as metronidazole. For penicillin allergic
patients, aztreonam and clindamycin may be used.cis

Gallbladder removal, cholecystectomy, can be accomplished via open surgery or a laparoscopic

procedure. Laparoscopic procedures can have less morbidity and a shorter recovery stay. Open
procedures are usually done if complications have developed or the patient has had prior surgery to the
area, making laparoscopic surgery technically difficult. A laparoscopic procedure may also be 'converted'
to an open procedure during the operation if the surgeon feels that further attempts at laparoscopic
removal might harm the patient. Open procedure may also be done if the surgeon does not know how to
perform a laparoscopic cholecystectomy.

In cases of severe inflammation, shock, or if the patient has higher risk for general anesthesia (required
for cholecystectomy), the managing physician may elect to have an interventional radiologist insert a
percutaneous drainage catheter into the gallbladder ('percutaneous cholecystostomy tube') and treat the
patient with antibiotics until the acute inflammation resolves. The patient may later warrant
cholecystectomy if their condition improves.

Complications of cholecystitis

 Perforation or rupture
 Ascending cholangitis
 Rokitansky-Aschoff sinuses

Complications of cholecystectomy

 bile leak ("biloma")

 bile duct injury (about 5-7 out of 1000 operations. Open and laparoscopic surgeries have essentially
equal rate of injuries, but the recent trend is towards fewer injuries with laparoscopy. It may be that the
open cases often result because the gallbladder is too difficult or risky to remove with laparoscopy)
 abscess
 wound infection
 bleeding (liver surface and cystic artery are most common sites)
 hernia
 organ injury (intestine and liver are at highest risk, especially if the gallbladder has become
adherent/scarred to other organs due to inflammation (e.g. transverse colon)
 deep vein thrombosis/pulmonary embolism (unusual- risk can be decreased through use of
sequential compression devices on legs during surgery)
 fatty acid and fat-soluble vitamin malabsorption

Gall bladder perforation

Gall bladder perforation (GBP) is a rare but life-threatening complication of acute cholecystitis. The early
diagnosis and treatment of GBP are crucial to decrease patient morbidity and mortality.

Approaches to this complication will vary based on the condition of an individual patient, the evaluation
of the treating surgeon or physician, and the facilities' capability. Perforation can happen at the neck from
pressure necrosis due to the impacted calculus, or at the fundus. It can result in a local abscess, or
perforation into the general peritoneal cavity. If the bile is infected, diffuse peritonitis may occur readily
and rapidly and may result in death.

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A retrospective study looked at 332 patients who received medical and/or surgical treatment with the
diagnosis of acute cholecystitis. Patients were treated with analgesics and antibiotics within the first 36
hours after admission (with a mean of 9 hours), and proceeded to surgery for a cholecystectomy. Two
patients died and 6 patients had further complications. The morbidity and mortality rates were 37.5% and
12.5%, respectively in the present study. The authors of this study suggests that early diagnosis and
emergency surgical treatment of gallbladder perforation are of crucial importance. [5]

State three factors responsible for formation of cholesterol gall stones.

 Cholesterol super saturation of bile
 This can occur as a result of excess cholesterol secretion into bile due to an increase of enzyme
activities.
 Crystallization- Promoting factors within bile
 A number of lipoproteins have reported to be putative crystallizing factors.
 Motility of the gall bladder
 Gall bladder stasis leads to cholesterol crystallization.

Five clinical features of Acute Cholecystitis ( 15 marks)

 Colic pain that starts suddenly and persists for 1-4 hours.
 Aching pain with sensation of pressure in the epigastric region.
 Nausea and vomiting.
 Low –grade fever.
 Jaundice (Saver obstructive)
 Right upper Quadrant guarding
 Inability to take deep inspiration when examining finger are pressing below the hepatic margin.

POST OPERATIVE CARE IN THE FIRST 48 HOURS

OBJECTIVES

 To return the physiological function back to normal as early as possible.

 To promote wound healing.

ENVIRONMENT

 Ensure post- operative equipment and tray is available for immediate access in case of the need for
resuscitation.
 The room should be well ventilated and clean to ensure a soothing environment and to prevent cross
infection
POSITION

 Place the patient in low – fowler’s one side to allow easy flow of secretion, so as to prevent choking
and maintain patient airway for effective breathing.
 This position will also promote easy observation of the position.
 Assist in regular change of position to encourage circulation of blood

OBSERVATION

 Vital sign observation- Blood Pressure, Pulse, respiration and temperature, initially done at ¼ hourly,
½ hourly, 1 hourly, 2 hourly then 4 hourly if the general condition proves to be improving progressively.
 Observe the wound for bleeding if it is evident, apply pressure.
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 Low blood pressure may indicate internal bleeding – inform the surgeon.
 Observe the tubing’s for patency especially the T tube

INTRAVENOUS INFUSION

 Ensure that the IV line is running well.

 Infuse as per Doctors orders
 Observe for fluid overload and stop drip if face looks puffy with breathing difficulties.
 Record intake and out on the fluid balance chart.

PHYSIOLOGICAL CARE

 Explain to the patient to the patient the nature of the disease process to ally anxiety.
 Explain to her the treatment regime and expectations regarding the care.
 Reinforce on knowledge of the possible outcome of the surgery.

DRUG ADMINISTRATION AND PAIN RELIEF.

 Give medications as ordered, such as prophylactic antibiotic and analgesics such as pethedine to
relieve pain.
 Observe relieving pain and any drug reactions

NUTRITION

 Patient is kept nil orally on zero day until bowl sound are head, flatus is passed and this is usually by
the 5th day post operatively and prevents paralytic ileus
 Ideally, the surgeon will order when to start sips of water. During this time, nutrition is by IV fluids up
to 2nd day post operative.
 The patient then progresses to free fluids the following day, soft food and then full diet according to
surgeon orders.
 Low fat diet is given because there is hardly bile to fats cholecystectomy as there is bile leakage in the
few days post operative give food rich in proteins and vitamins for wound healing.
 Asses for nausea and vomiting and administer antiemetic.
 Encourage a lot of fluid intake to replace discharged and leaking bile from the T-tube.
 Test food tolerance by clamping the T-tube when indicated.
Note this part is specific and you need as many points as you can

BOWEL ELIMINATION

 Patient should begin to open bowels soon after beginning to take normal diet above two days.

CARE OF NASO GASTRIC TUBE:

 Mrs.Chanda will have a naso gastric tube, to relieve the complication of vomiting bile.
 Aspirations must be done in the 1st 24 hours.
 Care of the tube and nostrils as well as oral care must be done.
 Measure inspects and records the aspirate all these measures help to keep the\tube patent

CARE OF DRAINAGE TUBES

 Care and observation of the drainage tube in the sub hepatic pouch be done recode the drainage.
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 The purpose of the tube is to drain the oozing blood from the liver bed and leaking bile.
 It is also useful for revealing internal reactionary hemorrhage.
 It also helps to reveal reactionary hemorrhage.
 It is removed after 48 hours.
 Note this part is specific and you need as many points as you can

T-TUBE FROM COMMON BILE DUCT

 Un clamp the tube immediately the patient is put on her bed.

 Measure and record the bile draining into a bag, specifying colour and amount at least every 2 hours.
 Administer replacement fluids if indicated.
 Clamp the Tube when indicated.
 Report any increase or decrease of drainage.
 Maintain patency of the tube.
 The tube may be removed on the 7 th-10th day meaning it will be in situ in the 1 st 48 hours post
operatively.

WOUND CARE

 Maintain a dry and intact dressing, usually drains that is working is left in situ.
 If wound is bleeding apply pressure.
 First dressing is removed by the surgeon.
 There after the wound is cleaned aseptically. Inspect for any swelling, discharging and gasping.
 Maintain skin integrity by adequate hydration, remove the soiled dressing around the T tube and
replace with the clean sterile one.

CATHETER CARE

 Aseptic catheter toilet to be done to prevent urinary infection.

 Observe urine for colour, sediments and amount. Record findings.

EXERCISES AND EARLY AMBULATION

 Breathing and coughing then exercises to prevent hypostatic pneumonia at regular intervals such as
1-2 hourly.
 Passive exercises the actively to prevent deep vein thrombosis.
 Promote early ambulation to prevent respiratory leg and renal complications.
 Assist the patient to sit up in bed and to sit in chair when the doctor has ordered ambulatory
exercises.
 Note this part is specific and you need as many points as you can

OTHER ASPECTS OF GENARAL CARE

 Bed baths to remove dirty on the body and maintain general hygiene
 Two hourly turnings to prevent pressure sore formation
 Hair care to improve hygiene self care image
 Nail care to improve hygiene and prevent infection
 Pressure area care to prevent pressure formation
 Oral toilet to improve oral hygiene and enhance appetite

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HEALTH EDUCATION

 Low fat diet as there is little or no bile to help in the digestion

 To encourage weight loss as reduces the amount of fats to be deposited in the body
 Encourage rest.
 Care of the healing wound.

possible complications following cholecystectomy and how they can be prevented

 Pulmonary Embolism
o Give analgesics and anticoagulants as well as early ambulation coupled with breathing exercises.
 Hemorrhage and leakage of bile
o From the gall bladder bed which may accumulate to cause abdominal distension and peritonitis. It is
necessary to ensure patency of sub hepatic drainage tube.
 Renal failure and liver failure
o In jaundiced patients, renal failure and liver failure may occur. This is prevented by post-operative
administration of IV fluids with osmotic diuretic during surgery.
 Recurrences
o Recurrence stones in the common bile duct. Endoscopic division of the splinter of oddi will help
prevent this.
 Backache
o Backache by use of bridge on the operation table. Avoid its use in early patients.

Cholecystectomy

Cholecystectomy (pronounced /ˌkɒləsɪsˈtɛktəmi/, plural: cholecystectomies) is the surgical removal

of the gallbladder. It is the most common method for treating symptomatic gallstones. Surgical options
include the standard procedure, called laparoscopic cholecystectomy, and an older more invasive
procedure, called open cholecystectomy.

Open surgery

A traditional open cholecystectomy is a major abdominal surgery in which the surgeon removes the
gallbladder through a 5-7 inch incision. Patients usually remain in the hospital overnight and may require
several additional weeks to recover at home.

Laparoscopic surgery

Laparoscopic cholecystectomy has now replaced open cholecystectomy as the first-choice of treatment
for gallstones and inflammation of the gallbladder unless there are contraindications to the laparoscopic
approach. Sometimes, a laparoscopic cholecystectomy will be converted to an open cholecystectomy for
technical reasons or safety.

A US Navy general surgeon and an operating room nurse discuss proper procedures while performing a
laparoscopic cholecystectomy surgery.

Laparoscopic cholecystectomy requires several small incisions in the abdomen to allow the insertion of
operating ports, small cylindrical tubes approximately 5-10 mm in diameter, through which surgical
instruments and a video camera are placed into the abdominal cavity. The camera illuminates the surgical

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field and sends a magnified image from inside the body to a video monitor, giving the surgeon a close-up
view of the organs and tissues. The surgeon watches the monitor and performs the operation by
manipulating the surgical instruments through the operating ports.

To begin the operation, the patient is anesthetized and placed in the supine position on the operating table.
A scalpel is used to make a small incision at the umbilicus. Using either a Veress needle or Hasson
technique the abdominal cavity is entered. The surgeon inflates the abdominal cavity with carbon dioxide
to create a working space. The camera is placed through the umbilical port and the abdominal cavity is
inspected. Additional ports are placed inferior to the ribs at the epigastric, midclavicular, and anterior
axillary positions. The gallbladder fundus is identified, grasped, and retracted superiorly. With a second
grasper, the gallbladder infundibulum is retracted laterally to expose and open Calot's Triangle (the area
bound by the inferior border of the liver, cystic duct, and common hepatic duct). The triangle is gently
dissected to clear the peritoneal covering and obtain a view of the underlying structures. The cystic duct
and the cystic artery are identified, clipped with tiny titanium clips and cut. Then the gallbladder is
dissected away from the liver bed and removed through one of the ports. This type of surgery requires
meticulous surgical skill, but in straightforward cases can be done in about an hour.

Recently, this procedure is performed through a single incision in the patient's umbilicus. This advanced
technique is called Laparoendoscopic Single Site Surgery or "LESS".

Procedural Risks and Complications

Laparoscopic cholecystectomy does not require the abdominal muscles to be cut, resulting in less pain,
quicker healing, improved cosmetic results, and fewer complications such as infection and adhesions.
Most patients can be discharged on the same or following day as the surgery, and most patients can return
to any type of occupation in about a week.

An uncommon but potentially serious complication is injury to the common bile duct, which connects the
gallbladder and liver. An injured bile duct can leak bile and cause a painful and potentially dangerous
infection. Many cases of minor injury to the common bile duct can be managed non-surgically. Major
injury to the bile duct, however, is a very serious problem and may require corrective surgery. This
surgery should be performed by an experienced biliary surgeon. [1]

Abdominal peritoneal adhesions, gangrenous gallbladders, and other problems that obscure vision are
discovered during about 5% of laparoscopic surgeries, forcing surgeons to switch to the standard
cholecystectomy for safe removal of the gallbladder. Adhesions and gangrene, of course, can be quite
serious, but converting to open surgery does not equate to a complication.

A Consensus Development Conference panel, convened by the National Institutes of Health in September
1992, endorsed laparoscopic cholecystectomy as a safe and effective surgical treatment for gallbladder
removal, equal in efficacy to the traditional open surgery. The panel noted, however, that laparoscopic
cholecystectomy should be performed only by experienced surgeons and only on patients who have
symptoms of gallstones.

In addition, the panel noted that the outcome of laparoscopic cholecystectomy is greatly influenced by the
training, experience, skill, and judgment of the surgeon performing the procedure. Therefore, the panel
recommended that strict guidelines be developed for training and granting credentials in laparoscopic
surgery, determining competence, and monitoring quality. According to the panel, efforts should continue
toward developing a noninvasive approach to gallstone treatment that will not only eliminate existing
stones, but also prevent their formation or recurrence.

One common complication of cholecystectomy is inadvertent injury to an anomalous bile duct known as
Ducts of Luschka, occurring in 33% of the population. It is non-problematic until the gall bladder is
removed, and the tiny supravesicular ducts may be incompletely cauterized or remain unobserved, leading

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to biliary leak post operatively. The patient will develop biliary peritonitis within 5 to 7 days following
surgery, and will require a temporary biliary stent. It is important that the clinician recognize the
possibility of bile peritonitis early and confirm diagnosis via HIDA scan to lower morbidity rate.
Aggressive pain management and antibiotic therapy should be initiated as soon as diagnosed.

Biopsy

After removal, the gall bladder should be sent for biopsy . (pathological examination) to confirm the
diagnosis and look for an incidental cancer. If cancer is present, a reoperation to remove part of the liver
and lymph nodes will be required in most cases. [2]

Long-Term Prognosis

A minority of the population, from 5% to 40%, develop a condition called postcholecystectomy

syndrome, or PCS.[3] Symptoms can include gastrointestinal distress and persistent pain in the upper right
abdomen.

As many as twenty percent of patients develop chronic diarrhea. The cause is unclear, but is presumed to
involve the disturbance to the bile system. Most cases clear up within weeks, though in rare cases the
condition may last for many years. It can be controlled with drugs.

BENIGN PROSTATIC HYPERTROPHY

Benign prostatic hyperplasia (BPH) also known as benign prostatic hypertrophy (technically a
misnomer), benign enlargement of the prostate (BEP), and adenofibromyomatous hyperplasia, refers
to the increase in size of the prostate in elderly men.

To be accurate, the process is one of hyperplasia rather than hypertrophy, but the nomenclature is often
interchangeable, even amongst urologists.[1] It is characterized by hyperplasia of prostatic stromal and
epithelial cells, resulting in the formation of large, fairly discrete nodules in the periurethral region of the
prostate. When sufficiently large, the nodules compress the urethral canal to cause partial, or sometimes
virtually complete, obstruction of the urethra, which interferes the normal flow of urine. It leads to
symptoms of urinary hesitancy, frequent urination, dysuria (painful urination), increased risk of urinary
tract infections, and urinary retention. Although prostate specific antigen levels may be elevated in these
patients because of increased organ volume and inflammation due to urinary tract infections, BPH is not
considered to be a premalignant lesion.

Adenomatous prostatic growth is believed to begin at approximately age 30 years. An estimated 50% of
men have histologic evidence of BPH by age 50 years and 75% by age 80 years. In 40-50% of these
patients, BPH becomes clinically significant.[2]

Signs and symptoms

Benign prostatic hyperplasia symptoms are classified as storage or voiding.

Storage symptoms include urinary frequency, urgency (compelling need to void that cannot be deferred),
urgency incontinence, and voiding at night (nocturia).

Voiding symptoms include weak urinary stream, hesitancy (needing to wait for the stream to begin),
intermittency (when the stream starts and stops intermittently), straining to void, and dribbling. Pain and

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dysuria are usually not present. These storage and voiding symptoms are evaluated using the International
Prostate Symptom Score (IPSS) questionnaire, designed to assess the severity of BPH. [3]

BPH can be a progressive disease, especially if left untreated. Incomplete voiding results in stasis of
bacteria in the bladder residue and an increased risk of urinary tract infection. Urinary bladder stones are
formed from the crystallization of salts in the residual urine. Urinary retention, termed acute or chronic, is
another form of progression. Acute urinary retention is the inability to void, while in chronic urinary
retention the residual urinary volume gradually increases, and the bladder distends. Some patients that
suffer from chronic urinary retention may eventually progress to renal failure, a condition termed
obstructive uropathy.

Cause

A study published in 2008 in the journal of andrology "Andrologia" [4] reports on a newly discovered
venous route by which free (active) testosterone reaches the prostate in extremely high concentrations,
promoting the accelerated proliferation of prostate cells, leading to the gland's enlargement. The study
suggests that BPH is caused by malfunction of the valves in the internal Spermatic veins manifesting as
varicocele, a phenomenon which has been shown to increase rapidly with age, [5][6] roughly equal to the
10% per year increasing prevalence of BPH. The 6- to 8-fold elevated hydrostatic pressure then leads to
retrograde venous drainage, allowing free communication with the prostatic circulation. Having measured
a concentration of free testosterone of some 130-fold above serum level in the internal spermatic vein (the
testes being the main source and the blood being undiluted in systemic circulation), the authors conclude
that the elevated venous pressure causes hypertrophy and exposure to high concentrations of free
testosterone causes hyperplasia in the prostate. The study also proposes a treatment method (Gat–Goren
Technique) similar to that used in treating varicocele, which restores normal pressure in the venous
drainage system, effectively reducing the volume of the prostate and clinical manifestation of BPH.

Androgens (testosterone and related hormones) are considered to play a permissive role in BPH by most
experts. This means that androgens have to be present for BPH to occur, but do not necessarily directly
cause the condition. This is supported by the fact that castrated boys do not develop BPH when they age.
On the other hand, administering exogenous testosterone is not associated with a significant increase in
the risk of BPH symptoms.[citation needed] Dihydrotestosterone (DHT), a metabolite of testosterone, is a critical
mediator of prostatic growth. DHT is synthesized in the prostate from circulating testosterone by the
action of the enzyme 5α-reductase, type 2. This enzyme is localized principally in the stromal cells;
hence, those cells are the main site for the synthesis of DHT.

DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby
epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the
transcription of growth factors that are mitogenic to the epithelial and stromal cells. DHT is 10 times
more potent than testosterone because it dissociates from the androgen receptor more slowly. The
importance of DHT in causing nodular hyperplasia is supported by clinical observations in which an
inhibitor of 5α-reductase is given to men with this condition. Therapy with 5α-reductase inhibitor
markedly reduces the DHT content of the prostate and, in turn, reduces prostate volume and, in many
cases, BPH symptoms.[citation needed]

Testosterone promotes prostate cell proliferation, [7] but relatively low levels of serum testosterone are
found in patients with BPH.[8][9] One small study has shown that that medical castration lowers the serum
and prostate hormone levels unevenly, having less effect on testosterone and dihydrotestosterone levels in
the prostate.[10]

While there is some evidence that estrogen may play a role in the etiology of BPH, this effect appears to
be mediated mainly through local conversion of estrogen to androgens in the prostate tissue rather than a
direct effect of estrogen itself.[11] In canine in vivo studies castration, which significantly reduced
androgen levels but left estrogen levels unchanged, caused significant atrophy of the prostate. [12] Studies

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looking for a correlation between prostatic hyperplasia and serum estrogen levels in humans have
generally shown none.[9][13]

On a microscopic level, BPH can be seen in the vast majority of men as they age, in particular over the
age of 70 years, around the world. However, rates of clinically significant, symptomatic BPH vary
dramatically depending on lifestyle. Men that lead a western lifestyle have a much higher incidence of
symptomatic BPH than men that lead a traditional or rural lifestyle. This is confirmed by research in
China showing that men in rural areas have very low rates of clinical BPH, while men living in cities
adopting a western lifestyle have a skyrocketing incidence of this condition, though it is still below rates
seen in the West.

Much work remains to be done to completely clarify the causes of BPH.

Diagnosis

Micrograph showing nodular hyperplasia (left off center) of the prostate from a transurethral resection
of the prostate (TURP). H&E stain.

Microscopic examination of different types of prostate tissues (stained with immunohistochemical

techniques): A. Normal (non-neoplastic) prostatic tissue (NNT). B. Benign prostatic hyperplasia. C. High-
grade prostatic intraepithelial neoplasia (PIN). D. Prostatic adenocarcinoma (PCA).

Prostate with a large median lobe bulging upwards. A metal instrument is placed in the urethra (which
passes through the prostate). This specimen was almost 7 centimeters long with a volume of about 60
cubic centimetres on transrectal ultrasound and was removed during a Hryntschak procedure or
transvesical prostatectomy (removal of the prostate through the bladder) for benign prostatic
hyperplasia.

Rectal examination (palpation of the prostate through the rectum) may reveal a markedly enlarged
prostate, usually affecting the middle lobe.

Often, blood tests are performed to rule out prostatic malignancy: Elevated prostate specific antigen
(PSA) levels needs further investigations such as reinterpretation of PSA results, in terms of PSA density
and PSA free percentage, rectal examination and transrectal ultrasonography. These combined measures
can provide early cancer detection.

Ultrasound examination of the testicles, prostate, and kidneys is often performed, again to rule out
malignancy and hydronephrosis.

Screening and diagnostic procedures for BPH are similar to those used for prostate cancer. Some signs to
look for include:[14]

 Weak urinary stream

 Prolonged emptying of the bladder
 Abdominal straining
 Hesitancy
 Irregular need to urinate
 Incomplete bladder emptying
 Post-urination dribble
 Irritation during urination
 Frequent urination
 Nocturia (need to urinate during the night)
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 Urgency
 Incontinence (involuntary leakage of urine)
 Bladder pain
 Dysuria (painful urination)
 Problems in ejaculation

Lifestyle

Patients should decrease fluid intake before bedtime, moderate the consumption of alcohol and caffeine-
containing products, and follow timed voiding schedules.

Medications

The two main medications for management of BPH are alpha blockers and 5α-reductase inhibitors.

 Alpha blockers (technically α1-adrenergic receptor antagonists) are the most common choice for
initial therapy in the USA[15][16] and Europe.[17] Alpha blockers used for BPH include doxazosin,[18]
terazosin, alfuzosin,[19][20] tamsulosin, and silodosin. All five are equally effective but have slightly
different side effect profiles. [21] The older drugs phenoxybenzamine and prazosin are not recommended.
[22]
Alpha blockers relax smooth muscle in the prostate and the bladder neck, thus decreasing the
blockage of urine flow. Common side effects of alpha blockers include orthostatic hypotension,
ejaculation changes, nasal congestion, and weakness.[citation needed]

 The 5α-reductase inhibitors finasteride[23] and dutasteride[24] are another treatment option. These
medications inhibit 5a-reductase, which in turn inhibits production of DHT, a hormone responsible for
enlarging the prostate. Effects may take longer to appear than alpha blockers, but they persist for many
years.[25] When used together with alpha blockers, a reduction of BPH progression to acute urinary
retention and surgery has been noted in patients with larger prostates. [26] Side effects include decreased
libido and ejaculatory or erectile dysfunction.[23]

Antimuscarinics such as tolterodine may also be used, especially in combination with alpha blockers. [27]
They act by decreasing acetylcholine effects on the smooth muscle of the bladder, thus helping control
symptoms of an overactive bladder.[citation needed]

Sildenafil citrate shows some symptomatic relief, suggesting a possible common etiology with erectile
dysfunction.[28]

Herbal remedies

People often seek herbal remedies for BPH.[29] Several are approved in European countries, but none in
the USA. Saw palmetto extract from Serenoa repens is one of the most extensively studied. It showed
promise in early studies,[30] though later trials of higher methodological quality indicated no difference
from placebo.[31][32][33]

Other herbal medicines that have research support in systematic reviews include beta-Sitosterol[34] from
Hypoxis rooperi (African star grass) and pygeum (extracted from the bark of Prunus africana),[35] while
there is less substantial support for the efficacy of pumpkin seed (Cucurbita pepo) and stinging nettle
(Urtica dioica) root.[36] There is weak evidence that pollen extracts frp, rye grass (Secale cereale) may
also correlate with modest symptomatic relief. [37]

Minimally invasive therapies

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The European Urology Review[38] published in 2009 that two Israeli doctors, Yigal Gat and Menahem
Goren, who discovered the main reason for the gland's enlargement, have also developed the Gat-Goren
nonsurgical method for BPH.[39] Using an interventional radiological technique that reduces prostate
volume and reverses BPH symptoms, the treatment, known as super-selective intra-prostatic androgen
deprivation (SPAD) therapy, involves a percutaneus venography and sclerotherapy of the internal
spermatic vein network, including associated venous bypasses and retroperitoneal collaterals. The
European Urology Review also declared that using the Gat Goren nonsurgical method results in
decreased prostate volume, which leads to significantly decreased nocturia, improved urine stream, and
also improves emptying of the urinary bladder, since the reduction in prostate volume increases the
diameter of the prostatic portion of the urethra and therefore may also prevent urinary retention.

While medication is often prescribed as the first treatment option, there are many patients who do not
achieve success with this line of treatment. Those patients may not achieve sustained improvement in
symptoms or they may stop taking the medication because of side-effects. [40] There are options for
treatment in a urologist's office before proceeding to surgery. The two most common types of office-
based therapies are Transurethral microwave thermotherapy (TUMT) and Transurethral Needle Ablation
(TUNA). Both of these procedures rely on delivering enough energy to create sufficient heat to cause cell
death (necrosis) in the prostate. The goal of the therapies is to cause enough necrosis so that, when the
dead tissue is reabsorbed by the body, the prostate shrinks, relieving the obstruction of the urethra. These
procedures are typically performed with local anesthesia, and the patient returns home the same day.
Some urologists have studied and published long-term data on the outcomes of these procedures, with
data out to five years. The most recent American Urological Association (AUA) Guidelines for the
Treatment of BPH in 2003 lists minimally invasive therapies including TUMT and TUNA as acceptable
alternatives for certain patients with BPH. [41]

Transuretheral microwave therapy (TUMT) was originally approved by the FDA in 1996, with the first
generation system by EDAP Technomed. Since 1996, other companies have received FDA approval for
TUMT devices, including Urologix, Dornier, Thermatrix, Celsion, and Prostalund. Multiple clinical
studies have been published on TUMT. The general principle underlying all the devices is that a
microwave antenna that resides in a urethral catheter is placed in the intraprostatic area of the urethra. The
catheter is connected to a control box outside of the patient's body and is energized to emit microwave
radiation into the prostate to heat the tissue and cause necrosis. It is a one-time treatment that takes
approximately 30 minutes to 1 hour, depending on the system used. It takes approximately 4 to 6 weeks
for the damaged tissue to be reabsorbed into the patient's body. Some of the devices incorporate
circulating coolant through the treatment area with the intent of preserving the urethra while the
microwave energy heats the prostatic tissue surrounding the urethra.

Transuretheral needle ablation (TUNA) operates with a different type of energy, radio frequency (RF)
energy, but is designed along the same premise as TUMT devices, that the heat the device generates will
cause necrosis of the prostatic tissue and shrink the prostate. The TUNA device is inserted into the urethra
using a rigid scope much like a cystoscope. The energy is delivered into the prostate using two needles
that emerge from the sides of the device, through the urethral wall and into the prostate. The needle-based
ablation devices are very effective at heating a localized area to a high enough temperature to cause
necrosis. The treatment is typically performed in one session, but may require multiple sticks of the
needles depending on the size of the prostate.

Surgery

If medical treatment fails, and the patient elects not to try office-based therapies or the physician
determines the patient is a better candidate for transurethral resection of prostate (TURP), surgery may
need to be performed. In general, TURP is still considered the gold standard of prostate interventions for
patients that require a procedure. This involves removing (part of) the prostate through the urethra. There
are also a number of new methods for reducing the size of an enlarged prostate, some of which have not
been around long enough to fully establish their safety or side-effects. These include various methods to

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destroy or remove part of the excess tissue while trying to avoid damaging what remains. Transurethral
electrovaporization of the prostate (TVP), laser TURP, visual laser ablation (VLAP), ethanol injection,
and others are studied as alternatives.

Newer techniques involving lasers in urology have emerged in the last 5–10 years, starting with the
VLAP technique involving the Nd:YAG laser with contact on the prostatic tissue. A similar technology
called Photoselective Vaporization of the Prostate (PVP) with the GreenLight (KTP) laser have emerged
very recently. This procedure involves a high-power 80-watt KTP laser with a 550-micrometre laser fiber
inserted into the prostate. This fiber has an internal reflection with a 70-degree deflecting angle. It is used
to vaporize the tissue to the prostatic capsule. KTP lasers target haemoglobin as the chromophore and
typically have a penetration depth of 2.0 mm (four times deeper than holmium).

Another procedure termed Holmium Laser Ablation of the Prostate (HoLAP) has also been gaining
acceptance around the world. Like KTP, the delivery device for HoLAP procedures is a 550 um
disposable side-firing fiber that directs the beam from a high-power 100-watt laser at a 70-degree angle
from the fiber axis. The holmium wavelength is 2,140 nm, which falls within the infrared portion of the
spectrum and is invisible to the naked eye. Whereas KTP relies on haemoglobin as a chromophore, water
within the target tissue is the chromophore for Holmium lasers. The penetration depth of Holmium lasers
is <0.5 mm, avoiding complications associated with tissue necrosis often found with the deeper
penetration and lower peak powers of KTP.

HoLEP, Holmium Laser Enucleation of the Prostate, is another Holmium laser procedure reported to
carry fewer risks compared with either TURP or open prostatectomy. [42] HoLEP is largely similar to the
HoLAP procedure; the main difference is that this procedure is typically performed on larger prostates.
Instead of ablating the tissue, the laser cuts a portion of the prostate, which is then cut into smaller pieces
and flushed with irrigation fluid. As with the HoLAP procedure, there is little bleeding during or after the
procedure.

PROSTATECTOMY

A prostatectomy is the surgical removal of all or part of the prostate gland. Abnormalities of the prostate,
such as a tumour, or if the gland itself becomes enlarged for any reason, can restrict the normal flow of
urine along the urethra.

There are several forms of the operation:

Transurethral resection of the prostate (TURP)

Main article: Transurethral resection of the prostate

A cystoscope [a resectoscope which has a 30 degree viewing angle, along with resectoscopy sheath &
working element] is passed up the urethra to the prostate, where the surrounding prostate tissue is excised.
This is a common operation for benign prostatic hyperplasia (BPH) and outcomes are excellent for a high
percentage of these patients (80-90%).

Conventional (monopolar) TURP

The conventional TURP method in tissue removal utilizes a wire loop with electrical current flowing in
one direction (thus monopolar) through the resectoscope to cut the tissue. A grounding ESU pad and
irrigation by a nonconducting fluid is required to prevent this current from disturbing surrounding tissues.

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This fluid (usually glycine) can cause damage to surrounding tissue after prolonged exposure, resulting in
TUR syndrome, so surgery time is limited.

Bipolar TURP

Bipolar TURP is a newer technique that uses bipolar current to remove the tissue. Bipolar TURP allows
saline irrigation and eliminates the need for an ESU grounding pad thus preventing TUR syndrome and
reducing other complications. As a result bipolar Turp is also not subject to the same surgical time
constraints of conventional TURP.

Laser prostate surgery

Another surgical method utilizes laser energy to remove tissue. With laser prostate surgery a fiber optic
cable pushed through the urethra is used to transmit lasers such as holmium-Nd:YAG high powered "red"
or potassium titanyl phosphate(KTP) to vaporize the adenoma. More recently the KTP laser has been
supplanted by a higher power laser source based on a lithium triborate crystal, though it is still commonly
referred to as a "Greenlight" or KTP procedure. The specific advantages of utilizing laser energy rather
than a traditional electrosurgical TURP is a decrease in the relative bloodloss, elimination of the risk of
TUR syndrome, the ability to treat larger glands, as well as treating patients who are actively being
treated with anti-coagulation therapy for unrelated diagnoses.

Open prostatectomy

In an open prostatectomy the prostate is accessed through an incision that allows manual manipulation
and open visualization through the incision. The most common types of open prostatectomy are radical
retropubic prostatectomy(RRP) and radical perineal prostatectomy(RPP).

Radical retropubic prostatectomy

Main article: radical retropubic prostatectomy

With RRP, an incision is made in the lower abdomen, and the prostate is removed, by going behind the
pubic bone (retropubic).

Radical perineal prostatectomy

Main article: radical perineal prostatectomy

In RPP an incision is made in the perineum, midway between the rectum and scrotum through which the
prostate is removed. This procedure has become less common due to limited access to lymph nodes and
difficulty in avoiding nerves.

Suprapubic transvesical prostatectomy

Another type of open prostatectomy is suprapubic transvesical prostatectomy (SPP) where an incision is
made in the bladder. SPP remains a common surgical treatment for BPH in Africa but has largely been
supplanted by TURP in the West for this application.[1] SPP may be indicated for use with large patients
and prostates because of the surgical time constraints associated with conventional TURP.

Laparoscopic radical prostatectomy

Main article: Laparoscopic Radical Prostatectomy

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This is a laparoscopic procedure involving four small incisions made in the abdomen used to remove the
entire prostate for treatment of prostate cancer.

Robotic-assisted laparoscopic radical prostatectomy (RALP)

Robotic instruments are inserted through several small abdominal incisions and controlled by a surgeon.
The robot gives the surgeon much more dexterity than conventional laparoscopy while offering the same
advantages over open prostatectomy including much smaller incisions, less pain, less bleeding, less risk
of infection, faster healing time, and shorter hospital stay. [2]. The cost of such procedures is higher
whereas long-term functional and oncological superiority has yet to be established. [3][4][5]

Sexual effects of prostatectomy

Surgical removal of the prostate risks reduction of the likelihood that patients will experience erections.
Nerve-sparing surgery reduces the risk that patients will experience erectile dysfunction. However, the
experience and the skill of the nerve-sparing surgeon, as well as any surgeon are critical determinants of
the likelihood of positive erectile function of the patient. [6]

Remedies to post-operative sexual dysfunction

Very few surgeons will claim that patients return to the erectile experience they had prior to surgery. The
rates of erectile recovery that surgeons often cite are qualified by the addition of Viagra to the recovery
regimen.[7]

Remedies to the problem of post-operative sexual dysfunction include: [8]

 Medications
 Intraurethral suppositories
 Penile injections
 Vacuum devices
 Penile implants

 Prostatectomy refers to the surgical removal of part of the prostate gland or the entire prostate (radical
prostatectomy).

Indications

 Benign prostate enlargement.

Path physiology of benign disease

 When men rich their mid 40s.the prostate gland begins to enlarge. This condition, benign prostatic hyperplasia
(BPH) is present in more than half of men in their 60s and as many as 90% of those over 90. Because the prostate
surrounds the urethra, the enlarging prostate narrows this passage and makes urination difficult. The bladder does
not empty complete each time a man urinates, and as a result, he must urinate with greater frequency, night and day.
In time, the bladder can overfill, and urine escapes from the urethra, resulting in incontinence. An operation called
transurethral resection of the prostate (TURP) relieves symptoms of BPH by removing the prostate tissue that is
blocking the urethra. No incision is needed. Instead a tube (retro scope) is passed through the penis to the level of
the prostate, and tissue is either removed or destroyed, so that urine can freely pass from the body

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Path Physiology of Malignant disease

 Prostate cancer is the single most common form of non –skin cancer in the United State and the most common
cancer in men over 50. Half of men over 70 and almost all men over the age of 90 have prostate cancer, and the
American Cancer Society estimates that 198000 new cases will be diagnosed in 2001. This condition does not
always require surely, In fact, many elderly men adopt a policy of watchful waiting “especially if their cancer is
growing slowly. Younger men often elect to have their prostate gland totally removed along with the cancer it
contains- an operation called radical prostatectomy. The two main types of this surgery, radical retro pubic
prostatectomy and radical pineal prostatectomy, are performed only patient whose cancer is limiting to the prostate. If
cancer has broken out of the capsule surrounding the prostate gland and spread in the area to distant sites, removing
the prostate will not prevent the remaining cancer from growing and spread throughout the body.

GENERAL SURGICAL MANAGEMENT FOR PROSTATE CANCER

PRECAUTIONS BEFORE SURGERY.

 Open (incision) prostatectomy for cancer should not be done if the cancer has spread bound the prostate, as
serious side effects may occur with the benefit of removing all the cancer. If the bladder is retaining urine, it is
necessary to insert a catheter before starting surgery. Patients should be in the best possible general condition
before radical prostatectomy. Before surgery, the bladder is inspected using instrument called a cyst scope to help
determine the best surgical technique to use and to rule out other local problems.

TYPES OF SURGERY THAT COULD BE PERFORMED

 TRANS _URETHRA RESECTON OF PROSTATE (TURP)

 This procedure does not require an abdominal incision. With the patient under either general or spinal anesthesia,
a cutting instrument or heated wire loop is inserted to remove as much prostate tissue as possible and seal blood
vessels. The excised tissue is washed into the bladder, and then flushed out at the end of the operation. A catheter is
left in the bladder for one to five days to drain urine and blood. Advanced laser technology enables surgeons to drain
urine and blood. Advanced laser technology enables surgeons to safely and affectively burn off exceed prostate
tissue blocking the bladder opening with fewer of the early and late complications associated with other forms of
prostate surgery. This procedure can be performed on an outpatient basis, but urinary symptoms do not improve until
swelling subsides several weeks after surgery.

 RADICAL RETROPUBIC PROSTATECTOMY

 This is a useful approach if the prostate is very large, or cancer is suspected. With the patient under general or
spinal anesthesia or an epididural, a horizontal incision is made in the center of the lower abdomen. Some surgeons
begin the operation by removing pelvic lymph nodes to determine whether cancer has invaded them. But recent
findings suggest that there is no need to sample them in patients whose like hood of lymph node metastases is less
than 18%. A doctor who removes the lymph nodes for examination will not continue the operation if they contain
cancer cells, because the surgery will not cure the patient. Other surgeons remove the glad before examining the
lymph nodes. A tube (catheter) inserted into the penis to drain fluid from the body is left in place for 14 - 21 days.

 Originally, this operation also removed a thin rim of bladder tissue in the area of the urethra sphincter- a muscular
structure that keeps urine from escaping from the bladder. In addition, the nerves supplying the penis often were
damaged, and many men found themselves important (unable to achieve erections) after prostatectomy. A newer
surgical method called potency-sparing radical prostatectomy preserves sexual potency in 75% of patients fewer
than 5% become incontinent following this procedure.

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 RADICAL PERINAL PROSTATECTOMY

 This procedure is just as curative as radical retro public prostatectomy but is performed less often because it does
not allow the surgical to spar the nerves associated with erection or, or because the incision is made above the
rectum and below the scrotum, to remove lymph nodes. Radical Perineal prostatectomy is sometimes used when the
cancer is limited to the prostate and there is no need spare nerves or when patient’s health might be compromised by
the longer procedure. The Perineal operation is less invasive than retro pubic prostatectomy. Some parts of the
prostate can be seen batter, and blood loss is limited. The absence of an abdominal incision allows patients to
recover more rapidly. Many urologic surgeons have not been trained to perform this procedure. Radical
prostatectomy procedure last one to four hours, with radical Perineal prostatectomy taking less time than radical retro
pubic prostatectomy. The patient remains in the hospital three to five days following surgery and can return to work in
three to five weeks.
 Ongoing research indicates that laparoscopic radical prostatectomy may be as effective as open surgery in
treatment of early- stage disease.

CRYOSURGERY

 Also called cry therapy or cry ablation, this minimally invasive procedure uses very low temperature to freeze and
destroy cancer cells in and around the prostate gland. A catheter circulates warm fluid through

HEAD INJURY

Head injury refers to trauma to the head. This may or may not include injury to the brain.[1] However, the
terms traumatic brain injury and head injury are often used interchangeably in the medical literature. [2]

The incidence (number of new cases) of head injury is 300 per 100,000 per year (0.3% of the population),
with a mortality of 25 per 100,000 in North America and 9 per 100,000 in Britain. Head trauma is a
common cause of childhood hospitalization.[citation needed]

Classification

Head injuries include both injuries to the brain and those to other parts of the head, such as the scalp and
skull.

Head injuries may be closed or open. A closed (non-missile) head injury is one in which the skull is not
broken. A penetrating head injury occurs when an object pierces the skull and breaches the dura mater.
Brain injuries may be diffuse, occurring over a wide area, or focal, located in a small, specific area.

A head injury may cause a minor headache skull fracture, which may or may not be associated with injury
to the brain. Some patients may have linear or depressed skull fractures.

If intracranial hemorrhage occurs, a hematoma within the skull can put pressure on the brain. Types of
intracranial hemorrage include subdural, subarachnoid, extradural, and intraparenchymal hematoma.
Craniotomy surgeries are used in these cases to lessen the pressure by draining off blood.

Brain injury can be at the site of impact, but can also be at the opposite side of the skull due to a
contrecoup effect (the impact to the head can cause the brain to move within the skull, causing the brain
to impact the interior of the skull opposite the head-impact).

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If the impact causes the head to move, the injury may be worsened, because the brain may ricochet inside
the skull causing additional impacts, or the brain may stay relatively still (due to inertia) but be hit by the
moving skull (both are contrecoup injuries).

Specific problems after head injury can include [citation needed]:

 Skull fracture
 Lacerations to the scalp and resulting hemorrhage of the skin
 Traumatic subdural hematoma, a bleeding below the dura mater which may develop slowly
 Traumatic extradural, or epidural hematoma, bleeding between the dura mater and the skull
 Traumatic subarachnoid hemorrhage
 Cerebral contusion, a bruise of the brain
 Concussion, a temporary loss of function due to trauma
 Dementia pugilistica, or "punch-drunk syndrome", caused by repetitive head injuries, for example in
boxing or other contact sports
 A severe injury may lead to a coma or death
 Shaken Baby Syndrome - a form of child abuse

Concussion

Over 4 million concussions are estimated to occur each year [3]

Mild concussions are associated with sequelae. Severity is measured using various concussion grading
systems.

A slightly greater injury is associated with both anterograde and retrograde amnesia (inability to
remember events before or after the injury). The amount of time that the amnesia is present correlates
with the severity of the injury. In all cases the patients develop postconcussion syndrome, which includes
memory problems, dizziness, tiredness, sickness and depression.

Cerebral concussion is the most common head injury seen in children

Intracranial hemorrhage

Types of intracranial hemorrhage are roughly grouped into intra-axial and extra-axial. The hemorrhage is
considered a focal brain injury; that is, it occurs in a localized spot rather than causing diffuse damage
over a wider area.

Intra-axial hemorrhage

Intra-axial hemorrhage is bleeding within the brain itself, or cerebral hemorrhage. This category includes
intraparenchymal hemorrhage, or bleeding within the brain tissue, and intraventricular hemorrhage,
bleeding within the brain's ventricles (particularly of premature infants). Intra-axial hemorrhages are more
dangerous and harder to treat than extra-axial bleeds. [4]

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 view • talk • edit
Extra-axial hemorrhage Hematoma Epidural Subdural
type
Extra-axial hemorrhage, bleeding that occurs
within the skull but outside of the brain tissue, Between the Between the
falls into three subtypes:
Location skull and dura and
the dura the arachnoid
 Epidural hemorrhage (extradural
hemorrhage) which occur between the dura
Middle meningeal
mater (the outermost meninx) and the skull, Involved vessel Bridging veins
artery
is caused by trauma. It may result from
laceration of an artery, most commonly the
Lucid interval Gradually increasing
middle meningeal artery. This is a very
Symptoms followed by headache and
dangerous type of injury because the bleed is
from a high-pressure system and deadly unconsciousness confusion
increases in intracranial pressure can result
Appearance on
rapidly. However , it is the least common type Lens Crescent-shaped
of meningeal bleeding and is seen in 1% to CT
3% cases of head injury .
o Patients have a loss of consciousness (LOC), then a lucid interval, then sudden deterioration
(vomiting, restlessness, LOC)
o Head CT shows lenticular (convex) deformity.
 Subdural hemorrhage results from tearing of the bridging veins in the subdural space between the
dura and arachnoid mater.
o Head CT shows crescent-shaped deformity
 Subarachnoid hemorrhage, which occur between the arachnoid and pia meningeal layers, like
intraparenchymal hemorrhage, can result either from trauma or from ruptures of aneurysms or
arteriovenous malformations. Blood is seen layering into the brain along sulci and fissures, or filling
cisterns (most often the suprasellar cistern because of the presence of the vessels of the circle of Willis
and their branchpoints within that space). The classic presentation of subarachnoid hemorrhage is the
sudden onset of a severe headache (a thunderclap headache). This can be a very dangerous entity, and
requires emergent neurosurgical evaluation, and sometimes urgent intervention.

Cerebral contusion

Cerebral contusion is bruising of the brain tissue. The majority of contusions occur in the frontal and
temporal lobes. Complications may include cerebral edema and transtentorial herniation. The goal of
treatment should be to treat the increased intracranial pressure. The prognosis is guarded.

Diffuse axonal injury

Diffuse axonal injury, or DAI, usually occurs as the result of an acceleration or deceleration motion, not
necessarily an impact. Axons are stretched and damaged when parts of the brain of differing density slide
over one another. Prognoses vary widely depending on the extent of damage.

Symptoms

Presentation varies according to the injury. Some patients with head trauma stabilize and other patients
deteriorate. A patient may present with or without neurologic deficit.

Patients with concussion may have a history of seconds to minutes unconsciousness, then normal arousal.
Disturbance of vision and equilibrium may also occur.

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Common symptoms of head injury include coma, confusion, drowsiness, personality change, seizures,
nausea and vomiting, headache and a lucid interval, during which a patient appears conscious only to
deteriorate later.[5]

Symptoms of skull fracture can include:

 leaking cerebrospinal fluid (a clear fluid drainage from nose, mouth or ear) may be and is strongly
indicative of basilar skull fracture and the tearing of sheaths surrounding the brain, which can lead to
secondary brain infection.
 visible deformity or depression in the head or face; for example a sunken eye can indicate a maxillar
fracture
 an eye that cannot move or is deviated to one side can indicate that a broken facial bone is pinching a
nerve that innervates eye muscles
 wounds or bruises on the scalp or face.
 Basilar skull fractures, those that occur at the base of the skull, are associated with Battle's sign, a
subcutaneous bleed over the mastoid, hemotympanum, and cerebrospinal fluid rhinorrhea and
otorrhea.

Because brain injuries can be life threatening, even people with apparently slight injuries, with no
noticeable signs or complaints, require close observation. The caretakers of those patients with mild
trauma who are released from the hospital are frequently advised to rouse the patient several times during
the next 12 to 24 hours to assess for worsening symptoms.

The Glasgow Coma Scale is a tool for measuring degree of unconsciousness and is thus a useful tool for
determining severity of injury. The Pediatric Glasgow Coma Scale is used in young children.

Causes

Common causes of head injury are motor vehicle traffic collisions, home and occupational accidents,
falls, and assaults. Bicycle accidents are also a cause of head injury-related death and disability,
especially among children. Wilsons disease has also been indicative of head injury. [6]

Diagnosis

The need for imaging in patients who have suffered a minor head injury is debated. A non-contrast CT of
the head should be performed immediately in all those who have suffered a moderate or severe head
injury.[7]

Management

Most head injuries are of a benign nature and require no treatment beyond analgesics and close
monitoring for potential complications such as intracranial bleeding. If the brain has been severely
damaged by trauma, neurosurgical evaluation may be useful. Treatments may involve controlling
elevated intracranial pressure. This can include sedation, paralytics, cerebrospinal fluid diversion. Second
line alternatives include decompressive craniectomy (Jagannathan et al. found a net 65% favorable
outcomes rate in pediatric patients), barbiturate coma, hypertonic saline and hypothermia. Although all of
these methods have potential benefits, there has been no randomized study that has shown unequivocal
benefit.

Prognosis

In children with uncomplicated minor head injuries the risk of intra cranial bleeding over the next year is
rare at 2 cases per 1 million.[8]

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In some cases transient neurological disturbances may occur, lasting minutes to hours. Malignant post
traumatic cerebral swelling can develop unexpectedly in stable patients after an injury, as can post
traumatic seizures. Recovery in children with neurologic deficits will vary. Children with neurologic
deficits who improve daily are more likely to recover, while those who are vegetative for months are less
likely to improve. Most patients without deficits have full recovery. However, persons who sustain head
trauma resulting in unconsciousness for an hour or more have twice the risk of developing Alzheimer's
disease later in life.[9]

Head injury may be associated with a neck injury. Bruises on the back or neck, neck pain, or pain
radiating to the arms are signs of cervical spine injury and merit spinal immobilization via application of a
cervical collar and possibly a long board.

If the neurological exam is normal this is reassuring. Reassessment is needed if there is a worsening
headache, seizure, one sided weakness, or has persistent vomiting.

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