THE ACUTE ABDOMEN and GASTROINTESTINAL HEMORRHAGE

The term acute abdomen is widely understood but is difficult to define precisely.
Typically the symptoms are of acute onset and strongly suggest an abdominal
cause.
Many of the disorders causing an “acute abdomen” are serious and potentially
life-threatening unless treated promptly.
On the other hand, simple and relatively trivial conditions such as constipation
can produce acute and severe symptoms.
Sometimes the diagnosis in acute abdomen may become apparent after a period
of observation or after special investigations.

Common causes of acute abdominal emergencies in adults

1. Bowel obstruction
Any part of the gastrointestinal tract may become obstructed and present as an
acute abdomen.
The possible causes are:
- adhesions or bands resulting from previous surgery or intraperitoneal infection.
- strangulated hernias, volvulus
- tumours: gastric carcinoma near the pylorus, colonic carcinoma, small bowel
tumours.
- inflammatory strictures: diverticular disease, Crohn’s disease.
- bolus obstruction: impacted faeces, foreign bodies, solitary gallstone,
phytobezoar (a mass of impacted vegetable matter such an orange pith).
- intussusception (a segment of bowel becoming telescoped into the segment
distal to it, usually initiated by a mass in the bowel wall which is dragged along
by peristalsis.
Obstruction leads to proximal dilatation of the bowel and disrupts peristalsis.
The presentation depends on the level of obstruction (stomach- proximal, distal-
small bowel or large bowel) and on the completeness of obstruction.
The most acute presentation is upper small bowel obstruction; this is because of
obstruction to the large volume of pancreatic and biliary secretion. In contrast,
distal large bowel obstruction is often much more chronic.
The more proximal the obstruction, the earlier the vomiting develops.
Vomiting occurs, even if nothing is taken by mouth, because saliva and other
gastrointestinal secretions continue to be produced and enter the stomach.
At least 10 l. of fluid are secreted into the gastrointestinal tract each day.
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The nature of the vomitus gives important clues to the level of obstruction.
For example, semi-digested food, eaten a day or two previously strongly
suggests gastric outlet obstruction, particularly if there is no bile present.
Copious vomiting of bile-stained fluid suggests upper small bowel
obstruction.
If vomitus is thicker and foul-smelling, a more distal obstruction is likely.
Proximal distension of the bowel causes pain.
The pain is of variable intensity, often quite mild, and usually colicky as
peristalsis tries to overcome the obstruction.
Absolute constipation (neither faeces nor flatus is passed rectally) is
pathognomonic of bowel obstruction.
If the bowel is only partially obstructed, the clinical features are less clearly
defined.
Excessive peristaltic activity is responsible for the bouts of colicky pain which
are more prominent in incomplete obstruction than in complete obstruction.
The pain is often accompanied by visible peristalsis, which is the hallmark of
incomplete obstruction.

Physical examination
Vomiting, diminished fluid intake and sequestration of fluid in the small bowel
commonly lead to dehydration.
This is manifest clinically by extreme dryness of the mouth and characteristic
loss of skin turgor and elasticity.
Gas-filled loops of bowel produce abdominal distention; the more distal the
obstruction, the greater the distention.
Episodes of visible peristalsis may be observed in thin patients in whom the
obstruction is incomplete and of long duration.
General examination may reveal signs of anemia or lymphadenopathy due to the
primary disorder.
The most striking feature on abdominal palpation is the lack of tenderness; the
exception is when strangulation has occurred.
Obstruction with tenderness must be diagnosed as strangulation, necessitating
urgent operation.
An obstructing abdominal mass may be palpable if large.
The groin must always be examined for hernias.
An obstructed femoral hernia causes minor local symptoms but instead produces
symptoms and signs of small bowel obstruction.
It is small and it is easily missed if not specifically sought.
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On percussion - hyperresonance due to the gas-filled loops.

Bowel sounds in obstruction are traditionally described as being loud and
frequent, high-piched and tinkling. In practice, obstructed bowel sounds can
sound like the gentle lapping of water against a boat. This is due to fluid slashing
about in distended, gas-filled loops of bowel.

Investigation of suspected bowel obstruction

The most useful investigation is plain abdominal X-ray; this is usually
performed in both erect and supine position. Bowel proximal to the obstruction
is distended by gas. Distally, bowel gas is absent, but some rectal gas may be
seen if a digital examination has been done.
The pattern and distribution of gas will often indicate the aproximative site of
obstruction.
Fluid levels may be seen in small bowel obstruction on an erect film.
When the radiological diameter of the cecum reaches 10-12 cm. it is considered
to be in imminent danger of rupture and therefore needs urgent operation.
In large bowel obstruction of less acute onset, a barium enema is helpful to
demonstrate the site and nature of the obstruction.

2. Adinamic bowel obstruction

Temporary disruption of normal peristaltic activity without mechanical blockage
causes adynamic bowel obstruction.
Most commonly, it arises after abdominal surgery in which the bowel has been
handled. The condition is known as ileus or paralytic ileus.
Normal postoperative ileus should not persist for more than about four days. It is
one of the reasons why fluids and solids must be introduced gradually after
abdominal surgery.
Persistent postoperative ileus is usually due to a complication of surgery such as
anastomotic leakage or intra-abdominal infection, which has local bad effects
upon the bowel wall.
Occasionally, electrolyte disturbances like hypokalaemia are responsible for
adynamic obstruction.
A form of adynamic obstruction peculiar to the large bowel is called pseudo-
obstruction, and is caused by a wide range of apparently unrelated conditions.
These include retroperitoneal inflammation or hemorrhage, prolonged
recumbency.

Physical signs are similar to those of mechanical obstruction with the exception
that bowel sounds are not of obstructed type or may be inaudible.
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Principles of management of intestinal obstruction

Once intestinal obstruction has been recognised and the approximate level of
obstruction identified, management proceeds as follows:
- oral intake is discontinued and intravenous fluids given, the volume and type of
fluid depending on the state of hydration and serum electrolyte estimations. After
prolonged vomiting, patients may be seriously depleted of fluid and electrolytes.
- if the patient is vomiting or there is marked small bowel dilatation, a naso-
gastric tube is passed and gastric contents aspirated. This will control nausea and
vomiting, removed swallowed air and reduce gaseous distention. Most
important, it will minimize the risk of inhalation of gastric contents, particularly
during induction of general anaesthesia.
- uncomplicated cases of obstruction due to adhesion will usually resolve with
conservative measures.
- large bowel obstruction due to faecal impact can be relieved by enemas or
manual removal of faeces.
- adynamic bowel obstruction in most cases eventually resolves with
conservative measures.
- operation may be required to relieve the obstruction. Provided strangulation can
be excluded and the caecum is not dangerously distended, operation can safely
be deferred for a day or two. This gives time for the patient to be stabilised and
for any other desirable investigations. During this period of conservative
management, the obstruction may well settle, particularly if caused by adhesions
from previous surgery.

3. Bowel strangulation
Strangulation occurs when a segment of bowel becomes trapped so that its lumen
becomes obstructed and its blood supply disrupted. If unrelieved this progresses
to infarction and perforation. Strangulation can occur when there is an external
hernia, when loops of bowel become trapped within the hernial sac or when there
is mass rotation of bowel (volvulus).
The closed loop of bowel becomes progressively dilated by gas from
fermentation. The combination of gas pressure and venous back-pressure inhibit
arterial inflow, causing ischaemia and then infarction.
Strangulation most commonly occurs when small bowel is cought within a
hernia (inguinal, femoral, umbilical or incisional). The bowel undergoes necrosis
and soon perforates within the hernial sac; initially this may be contained, but
generalised peritonitis usually ensues.
Clinically, the patient develops symptoms and signs of small bowel obstruction.
A newly irreducible hernia can usually be found and this is likely to be tender
and inflammed. However a strangulated femoral hernia is a trap for the unwary.
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These are often small and non-tender and will be missed unless the groins are
carefully examined.
Bowel may also become strangulated within the abdominal cavity if a loop
becomes trapped by fibrous bands or adhesions, or passes through an omental or
mesenteric defect.
Strangulation occurs if a large loop of bowel becomes twisted on its mesentery, a
condition known as volvulus.
Intraabdominal strangulation exhibits the usual symptoms and signs of bowel
obstruction but is accompanied by abdominal tenderness which is not a feature
of uncomplicated bowel obstruction.
The tenderness is probably due to distension of the closed loop. When compared
with uncomplicated obstruction, patients with strangulation are systemically
more unwell with a tachycardia and leucocytosis.

Clinical features of bowel obstruction and strangulation

Symptoms
Vomiting-time of onset and nature of the vomitus suggests the level of
obstruction.
Abdominal pain-usually colicky in character, often mild in uncomplicated
obstruction and more severe in strangulation.
Absolute constipation (no flatus or faeces passed rectally)- pathognomonic of
complete obstruction (but not present in partial obstruction).
Physical signs
Dehydration- caused by vomiting, lack of fluid intake and fluid sequestration.
Abdominal distension - due to gas-filled loops of bowel. The more distal the
obstruction, the greater the distension.
Visible peristalsis - uncommon finding, usually in a very thin patient with
prolonged distal obstruction.
Central resonance to percussion with dullness in the flanks - gas within dilated
bowel loops rising to the uppermost point in the abdomen.
Abdominal tenderness - important feature distinguishing bowel strangulation
from uncomplicated obstruction.
Abdominal bowel sounds - exaggerated, lapping, sloshing, high-pitched or
tinkling.
Bowel sounds are absent in adynamic obstruction.

Principles of management of suspected bowel strangulation

When strangulation is diagnosed, or even suspected, operation must be
performed urgently to try to prevent infarction and perforation.
Specific investigations are limited to plain abdominal X ray in which a single
dilated, gas-filled strangulated loop may be prominent.
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There are no other investigations to help diagnose bowel strangulation, which is

a clinical diagnosis.

4. Peritonitis
Peritonitis is defined as inflammation of the peritoneal cavity. This includes the
serosal covering of the bowel and mesentery, the omentum and the lining of the
abdominal cavity.
Initially, peritoneal inflammation is often localised and the affected area
contained by a wrapping of omentum, adjacent bowel and fibrous adhesions.
This may, however, be insufficient to prevent spread, resulting in generalized
peritonitis.
Sudden perforation of any viscus almost invariably leads to life-threatening
generalised peritonitis.

Localised peritonitis
Transmural inflammation of the bowel: appendicitis, Crohn’s disease,
diverticulitis or of other viscera: cholecystitis, salpingitis may progress into a
palpable inflammatory painfull intraabdominal mass.

Generalised peritonitis
1. Irritation of the peritoneum by noxious fluids: bile, stomach or small bowel
contents (due to perforation), enzyme-containing exudates of acute pancreatitis.
2. Spreading intraperitoneal infection:rupture of intra-abdominal abscess or
faecal contamination due to bowel perforation, trauma,surgical spillage or
anastomotic leak.

Localised peritonitis occurs in the vicinity of any primary intraabdominal

inflammatory process. The surrounding organs become adherent in an attempt to
avoid the spreading of the infection.
Once the parietal peritoneum becomes involved, pain becomes localised to the
affected area and is exacerbated by movement of the abdominal muscles.
The area is tender to palpation and there is contraction of the overlying
abdominal wall muscles when examination is attempted.
This sign is known as guarding.
If the palpating hand is quickly removed, the sudden movement of the
peritoneum causes intense pain which is described as rebound tenderness.
However, this test is unkind and its diagnostic value overstated.
Rebound tenderness is better elicited by gentle percussion.
Rectal examination should always be performed as anterior tenderness can be a
sign of pelvic peritonitis.
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Localised peritontis is usually accompanied by low grade fever, malaise,

tachycardia, leucocytosis.
With generalised peritonitis, the patient is seriouslly ill.
There is massive exudation of inflammatory fluid into the peritoneal cavity
causing hypovolemia.
The severity of the systemic illness depends on the cause of the peritonitis, being
most severe when there is widespread contamination by faeces,pus or infected
bile.
Peritonitis is less severe when infection is absent (peforated duodenal ulcer in its
early stages).
On examination, the abdomen is rigid and tender and bowel sounds are absent
because of peristaltic paralysis.
Rectal examination provides a means of direct palpation of the pelvic
peritoneum and will reveal anterior tenderness. This is a most important sign
which if present, is strong evidence of pelvic peritonitis.
It is unkind and unnecessary to subject a patient to abdominal X rays if a
decision has already been taken to perform an emergency laparotomy.

Principles of management of peritonitis

Local peritonitis is treated according to the diagnosis. For example, appendicitis
requires urgent appendicectomy whilst acute diverticulitis and salpingitis are
usually managed with antibiotics.
With generalised peritonitis, the patient is at the risk of death from toxaemia or
septic shock. As soon as the diagnosis is made,high doses of antibiotics are given
intravenously. With the exception of acute pancreatitis, generalised peritonitis
requires urgent laparotomy to discover the cause and to clear the contamining
material (peritoneal toilet).

5. Intra-abdominal haemorrhage
Blood may enter the abdominal cavity from a variety of sourses, including
ruptured ectopic pregnancy, leaking aortic aneurysm or blunt trauma, especially
to the liver and spleen.
Blood in the abdominal cavity causes moderate peritoneal irritation and
symptoms similar to peritonitis, but often muted.
Distinguishing between the two is usually not difficult because the history and
other symptoms and signs give enaugh clues.
Intraperitoneal bleeding may be confirmed by peritoneal lavage which involves
instillation of saline via a peritoneal cannula; retrieval of blood-stained fluid is
diagnostic.
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Treatment-when hemoperitoneum is diagnosed upon history, clinical grounds,

hematologic tests ,ultrasound of the abdomen and peritoneal lavage an urgent
laparotomy is mandatory to perform the surgical hemostasis (ruptured spleen-
splenectomy, rupture of the liver-hepatoraphy, hepatectomy, ruptured ectopic
pregnancy-salpingectomy, etc.

6. Intra-abdominal abscess
Pathophysiology and clinical features
There are two common causes of intra-abdominal abscess. The first occurs after
bowel perforation, when omentum and adjacent gut attempt to wall off the
defect.
The second is a complication of bowel surgery where has been localised faecal
contamination or an anastomotic leak.
Appendiceal perforation may cause a local abscess or one which tracks down
into the pelvis.
Diverticular disease often causes a pericolic abscess, particularly in the
rectosigmoid area or pelvis.
Less commonly,perforation of a colonic tumour results in a pericolic abscess.
Gall bladder perforation is rare and occasionally results is a right-sided
subphrenic abscess.
Finally, perforation of an ulcer in the posterior wall of the stomach may produce
a lesser sac abscess.
Clinical diagnosis
With intra-abdominal abscess, abdominal pain is usually continuous rather than
colicky and tends to increase inexorably.
Local bowel irritation may cause diarrhea or adymanic obstruction.
A swinging pyrexia is an important sign which points to the diagnosis.
The patient is otherwise relatively well, except the patient with a postoperative
abscess, where is a degree of toxemia or even septicaemia.
On physical examination, there may be a palpable abdominal inflammatory mass
which most commonly originates with appendicitis or acute diverticular disease.
Rectal examination may reveal a hot, tender mass, displacing the rectum
backwards.
Investigations
Lab. tests: leukocytosis, high ESR, secondary anaemia.
Ultrasound of the abdomen and pelvis is most useful in demonstrating the site
and size of an abscess: drainage may be possible under ultrasound control.
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CT scanning may also be useful. When an abscess is suspected but cannot be

demonstrated, radioisotope scanning, using the patient’s own white cell labelled
with indium, may be useful.

Principles of management of an intraabdominal abscess

Small abscesses may resolve without intervention but larger ones can be drained
percutaneously under ultrasound control.
With these exceptions, intra-abdominal abscesses require laparotomy to effect
drainage and deal with the sourse.

7. Perforation of an abdominal viscus

Pathophysiology and clinical features
Disease in any hollow abdominal viscus may be complicated by perforation into
the peritoneal cavity. The common sites of perforation are stomach and
duodenum (from peptic ulcer), sigmoid colon (from diverticular disease) and the
appendix (from appendicitis).
The symptoms and signs of a perforated viscus depend on the nature of its
contents, the volume of spillage and the effectiveness of the local defences.
A small perforation may be immediately walled off by omentum and nearby
bowel, but a local abscess will then develop.
In this case, symptoms and signs are often grumbling and rather non-specific.
A typical example of this is appendicitis in adults.
A small diverticular perforation without faecal spillage may cause localised
peritonitis, which may even resolve spontaneously.
At the opposite extreme, a large colonic perforation causes sudden
overwhelming faecal peritonitis, which is often fatal despite treatment.
A perforated peptic ulcer causes marked abdominal signs of peritonitis but little
systemic upset. This is because the fluid spilled is usually sterile.
Perforation is essentially a clinical diagnosis- immobile abdomen on inspection,
rigid or guarding abdomen on palpation, absent bowel sounds due to paralytic
ileus, but can usually be confirmed by the presence of free gas in the peritoneal
cavity on plain abdominal X ray.
This can usually be seen as a radiolucent line beneath one or both
hemidiaphragm on an erect chest film or on a lateral decubitus film of the
abdomen. Radiology does not always demonstrate free gas when there is a
perforation; if X ray fails to support the clinical diagnosis, action should be taken
on the clinical diagnosis.
In case of perforated appendicitis, free gas is very rarely seen.
Principles of management of perforation
Perforation is a surgical emergency.
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Most cases require urgent laparotomy to repair the defect or resect the segment
of diseased bowel. A temporary colostomy is often required in large bowel
perforations because healing may be impaired if there has been peritoneal
contamination. Occasionally,conservative management is appropriate (small
perforation of a peptic ulcer which was immediately sealed by omentum).

8. Acute bowel ischemia

Pathology and clinical features
Occlusion of the superior mesenteric artery may lead to acute midgut ischemia
(jejunum,ileum,right colon),this causes massive infarction and later,fatal
perforation.There are two distinct types of acute superior mesenteric occlusion.
The first is embolism, which originates from left atrial thrombus in atrial
fibrillation or from left ventricular wall thrombus after recent myocardial
infarction.
Secondly, thrombosis of the artery may occur. This is usually a terminal event in
gross low output cardiac failure; thrombosis takes place more readily if the
mesenteric vessels are already atherosclerotic.
Acute bowel ischemia can be a difficult diagnosis to make because of the lack of
specific clinical features and diagnostic tests.
The severity of abdominal symptoms and signs often gives no clue to the
catastrophe within.
Diagnosis depends almost on history and clinical examination.
The patient complains of excruciating abdominal pain.
There may be diffuse tenderness, abdominal distension and absent bowel sounds.
Typically, there is a disproportionate degree of cardiovascular collapse.
Diagnosis depends therefore on clinical suspicion. In the late stages, gas may
appear within the bowel wall and be visible on plain abdominal X-ray;by this
time surgery is unlikely to be successful.

Principles of management of intestinal ischaemia

If intestinal ischaemia is suspected, laparotomy must be performed urgently. It is
sometimes possible to restore the mesenteric arterial supply by embolectomy
before the bowel becomes necrotic.If the infarcted segment is not too extensive,
resection gives a chance of recovery.

Major gastrointestinal haemorrhage

Pathophysiology and clinical features

Major gastrointestinal haemorrhage presents either as vomiting of blood or
passage of frank or altered blood rectally.
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Vomited blood (haematemesis) may be fresh or partly digested. In the latter case,
it is dark in colour and may have the typical appearance of “coffee grounds”.
Haematemesis usually indicates bleeding from the oesophagus or stomach but
may indicate bleeding from the duodenum.
Blood emanating beyond the duodenum will usually be passed rectally.
The extent to which it is altered by digestion and the degree of mixing with the
stool are useful indicators of its level of origin.
Upper GI bleeding is often manifest by melena. This is the passage of loose,
black, tarry stools with a characteristic foul smell.
Causes of major GI bleeding
- chronic gastric and duodenal ulcers, acute gastric erosions and stress ulcers
- diverticular disease-fresh rectal bleeding
- oesophageal varices-hematemesis and/or melena
- Mallory-Weiss oesophageal tears-hematemesis
- colonic or small bowel angiodisplasia-fresh or altered blood per rectum
- fulminant inflammatory bowel disease-bloody diarrhea
- malignant tumours
Diagnosis is based on history, clinical examination, lab.tests, endoscopy.

Principles of management of severe GI bleeding

Any patient presenting with severe GI bleeding is at risk of death from
hypovolemic shock. The volume of blood vomited or passed per rectum is
unreliable as a measure of true blood loss because a great deal may still remain
in the gut.
It is essential during resuscitation to adjust the rate and volume of iv fluid
replacement (plasma expanders or blood) against the responses of pulse rate,
blood pressure, central venous pressure and hourly urine output.
Once the patient is stable, further details of the history can be taken, including
any relevant previous of peptic ulceration and gastric surgery, diverticular
disease or cirrhosis. Abdominal examination is usually unremarkable but general
examination may show signs of chronic liver disease suggesting possible
oesophageal varices.
Rectal examination may reveal melena stool or altered blood and this can be
helpful if the history of hematemesis is not substantiated (coffee-ground vomit
not seen by a doctor).
After the initial hemorrhage, most patients stop bleeding with conservative
management. Rebleeding might be catastrophic therefore close observation is
mandatory.
Gastroscopy should be performed as soon as practicable. If bleeding persists an
operation will be needed.
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The real value of gastroscopy is the ability to diagnose unusual sources of

bleeding, most of which present particular operative problems.
If bleeding is suspected to come from large bowel then colonoscopy is useful.
In difficult cases when the site of bleeding has not been revealed, radioisotope
scanning using the patient’s own labelled red cells or highly selective
arteriography is well worthwhile.

Treatment
- iv. fluids on two lines to correct hypovolemic shock with colloids, blood,
cristaloids.
- the arrest of bleeding (hemostasis)- medical, endoscopic, surgical.

Study questions:
1. How do you make the diagnosis of distal small bowel obstruction?
2. A 70 years old female came in Accident & Emergency, with 4 hours
history of severe colicky pain in the lower abdomen, nausea, bile-stained
vomitus and absolute constipation. On examination the abdomen is
distended, moving with respiration, visible peristalsis in the lower
abdomen, no scars from previous surgery and there is a lump in the groin
such as a tender lymphnode. There is no cough impulse, the lump is
irreducible. What do you do next?
3. What is the most important clinical sign in a generalized peritonitis?
4. A patient 45 years old, known with cirrhosis, came in Casualty with 3
hours history of repeted hemetemesis and melena, following drinking 2
glasses of alcohol. The patient looks pale, sweaty, systolic BP of 90
mm.Hg. and a PR of 110. Physical examination of the abdomen was
unremarkable but PR examination revealed melena. How do you manage
this patient?