ABDOMINAL VASCULAR

EMERGENCIES
(MVO)
BY
Dr. Abd-El-Aal Ali Saleem
Assistant Professor of General Surgery
Faculty of Medicine – Sohag
University
Intestinal ischaemia
I-Acute intestinal ischaemia
Acute ischaemia of the intestine is a very serious surgical
emergency that is highly fatal. A large segment of intestine is
commonly affected, where there is evident occlusion of one or more
of the mesenteric vessels. It is usually the superior mesenteric artery
or vein that is occluded. On the other hand, ischemia may be focal
and affects a segmental branch and not the main vascular trunk thus,
it well compromise only a limited segment of the bowel that is
supplied by the occluded small branch.

(A)Acute Mesenteric Vascular Occlusion

It is commonly the superior mesenteric artery or vein that is
occluded, either by embolism or thrombosis.
Aetiology

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1. Mesenteric arterial embolism (50% of cases): The emboli
usually arise from the heart. The source may be:
a. Atrial fibrillation with a left atrial clot.
b. Mural thrombus after myocardial infarction affecting
the left ventricle.
c. Infective endocarditis.
d. Detached atheromatous plaque from aortic aneurysm.
The embolus usually lodges within few centimeters of the
mouth of the superior mesenteric artery, sparing the middle
colic and a few of the upper jejunal branches.
2. Mesenteric arterial thrombosis (25% of cases): The
condition complicates cases with mesenteric atherosclerosis.
Patients usually give history of chronic pain suggestive of
intestinal angina. The extent of ischaemia is more than with
embolism as the block is at the mouth of the superior
mesenteric artery sparing none of its branches.
3. Non-occlusive intestinal ischaemia (20% of cases):
In low cardiac output states, splanchnic vasoconstriction
occurs which leads to intestinal ischaemia. Low cardiac
output states include: arrhythmias, MI, hypothermia,
vasopressor drugs and major sepsis.
4. Mesenteric venous thrombosis (5% of cases):. The
condition is sometimes idiopathic or may be associated with
the following disorders:
a. Portal hypertension.
b. Intra-abdominal sepsis.
c. Hypercoagulable states.
d. Intake of contraceptive pills.

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 e. Sickle cell disease.

Pathology
Damage to the intestine occurs from the ischaemia, and from the re-
establishment of intestinal perfusion, the so called "reperfusion
injury".
Ischaemic damage:
1. The most sensitive layer to ischaemia is the mucosa. Within
three hours of complete vascular block it sloughs, ulcerates and
bleeds in the lumen. Bacteria can get access to the blood stream
through the damaged mucosal barrier.
2. Within sex hours the whole thickness of the intestinal wall is
affected and exudes serosanguinous fluid in the peritoneum.
The patient may lose a substantial amount of blood.
3. The intestine develops hemorrhagic infarction which rapidly
progresses to gangrene and soon perforates producing
peritonitis.
4. The gangrenous bowel segment loses peristalsis and, thus, acts
as an obstruction to the flow of intestinal contents. The
proximal intestine becomes distended with fluid and gas. With
the development of peritonitis, paralytic ileus sets in producing
more generalized distension.

Reperfuslon damage: The return of blood flow, either

spontaneously or by surgery results in the release of oxygen
radicals that damage the cell membrane which aggravate the
preexisting ischemic insult.

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Clinical features
Severe acute abdominal pain is the main symptom. pain
responds neither to narcotics nor to nasogastric aspiration.
There is a variable degree of vomiting, diarrhea and bleeding
per rectum.
In the early stage there are little physical signs to match the
severity of pain. Later with the development of hypovolaemia
from blood loss, and peritonitis from perforation, the patient
may become shocked with abdominal tenderness, rigidity and
distension.
Differential diagnosis
Acute pancreatitis: The common features are severe pain,
vomiting, minimal local signs in the early phase, and shock.
The distinction is important as the management of acute
pancreatitis is essentially conservative, while that of acute
mesenteric vascular occlusion is urgent surgery.
Strangulation Intestinal obstruction.
Aortic dissection.
Acute cholecystits.
Investigations
Unfortunately there is no specific or sensitive test to prove the
diagnosis. The most useful aid is to bear the condition in mind,
particularly in the atherosclerotic or the patient with cardiac
arrhythmia.
Laboratory findings usually show nonspecific findings:
a. Marked leukocytosis.
b. Metabolic acidosis.
c. High serum amylase in half the patients, but is not as high

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 as in acute pancreatitis.
d. The hematocrit value is usually elevated, but it may be
reduced in case of massive blood loss.
Plain X-ray of the abdomen may show air-fluid levels in the
proximal intestine. Intestinal necrosis may show lately as
intramural gas (pneumatosis intestinalis) or gas in the portal
venous system or free intraperitoneal gas.
CT mesenteric angiography can show:
a. Vascular occlusion (both arterial and venous).
b. Mural thickening, decreased enhancement, and
pneumatosis.
c. Mesenteric thickening, oedema and stranding.
Treatment
The prognosis is ominous (mortality rate may reach 70%) due
To:
1- The diagnosis is often delayed.
2- The extent of infarcted bowel is substantial.
3- The outcome of vascular reconstruction is poor.
Urgent management before intestinal gangrene, peritonitis and
systemic sepsis occur, is the key to survival.
Resuscitation by:
1. Restoration of blood volume by blood and crystalloid
infusion.
2. Correction of electrolytes and acid base imbalances.
3. Parenteral antibiotics.
4. Nasogastric decompression by a Ryle's tube.
Specific management:
1. Laparotomy to resect gangrenous intestine: Primary

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 anastomosis is better avoided in cases of:
a. Peritonitis with friable tissues.
b. Doubtful viability of the remaining intestine.
c. Patients with bad general condition.
In such cases the two bowel ends are brought out to the surface
and the effluent is collected from the proximal end using an
ileostomy bag. Bowel anastomosis is postponed until the general
and local conditions improve.
2. Restore arterial blood flow: In cases with reversible
ischaemia. Revascularization is achived by:
a. In case of embolism: Laparotomy and embolectomy (via the
ileocolic artery). Rarely, in early cases (in the absence of
peritonitis), catheter-directed thrombolysis may be tried.
b. In case of acute thrombosis: Laparotomy and bypass surgery.
Thrombectomy is not attempted as it is usually followed by
reocclusion as it occurs usually on top of atherosclerosis.
c. In case of non-occlusive ischemia: Correction of the state of
low cardiac output and local infusion of vasodilators via
selective catheterization.
3. Mesenteric venous thrombosis: Start full anticoagulation. If
the patient did not show clinical improvement or bowel
infarction is suspected, exploratory laparotomy is done. The
diagnosis is settled at operation by the presence of marked
oedema and congestion of the bowel and mesentery.
Gangrenous intestine is resected and the patient is given
postoperative heparin, and is discharged home under oral
anticoagulant therapy for at least three months to prevent
recurrence.
4. A second-look operation after 24 hours: Is advised by to
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 check the viability of the intestine in the following condtions:
a. Patients who receive primary anastomosis.
b. Patients with borderline viability of the bowel after
revascularization.
Prognosis
Mesenteric venous thrombosis has a mortality rate of 30%,
while that of arterial occlusion is about 45-65%. Embolism has
a slightly better prognosis than arterial thrombosis.
Up to 70% of the small intestine can be resected leaving at least
two meters, without major nutritional consequences. Patients
who have resection of longer segments develop the "short
bowel syndrome" whose main feature is malabsorption. Many
months are needed for the intestine to accommodate by
increasing its absorptive surface. Patients are initially fed on
total parenteral nutrition for a few months, and later oral intake
is gradually introduced, reducing the amount of parenteral
feeding, until ultimately the patient can depend totally on
normal oral feeding. In selected cases, consideration may be
given to small bowel transplantation.

(B) Focal Intestinal Ischaemia

Ischaemia of a short segment of the intestine may be caused by:
- Vascular problems as embolism, arterial thrombosis, venous
thrombosis, arteritis and trauma.
- Mechanical obstruction with strangulation as strangulated
hernia, adhesions, and volvulus.
Focal ischaemia may affect the small or large intestine. Ischaemic
colitis is one type that deserves a special attention.

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Ischaernlc colitis
Patients are usually 50-70 years old
Etiology
o 90% of cases of ischaernlc colitis are induced by non-
occlusive injury due to shock with splanchnic vasospasm,
especialy with the use of vasopressor drugs.
o Less commonly: Ischaernlc colitis may be due to
embolism, thrombosis, atherosclerosis and following
ligation of inferior mesenteric vessels during aortic
surgery.
Pathology
The splenic flexure is the most commonly affected area. The
consequences of ischemia are:
• Mild cases: Only affecting the mucosa will be followed by
complete resolution.
• Moderate cases: Affecting the muscularis will be followed
by stricture.
• Severe cases: Affecting full thicknes of colonic wall will
be followed by infarction, gangrene, perfoeation, and
peritonitis.
Clinical picture
The patient complains of acute abdominal pain (60%),
hematochezia (60%) and diarrhea (90%).
Investigations
a. Barium enema may show " Finger-printing" due to oedematous
mucosal folds.
b. CECT: Can show mural thickening, diminished enhancement,
pneumatosis and vascular occlusion.

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c. Colonoscopy (gold standard): can confirm the diagnosis,
determine the severity and exclude other causes of colitis. The
ischemic mucosa will show oedema, friability, hemorrhage,
ulceration and may be covered with grayish membrane.
Treatment
a. Supportive by intravenous fluids, bowel rest and antibiotics.
b. Surgery is required in 20% of cases for gangrene or stricture
formation. Usually resection of the affected segment is done.

II-Chronic intestinal ischaemia

Chronic intestinal ischaemia is caused by narrowing of the
superior mesenteric artery, and sometimes the coeliac artery. The
disease affects elderly patients who are likely to have atherosclerosis
of other vessels.
Aetiology
1. Atherosclerosis is the main cause. The intima is thickened
at the mouth of the superior mesenteric artery causing
narrowing.
2. Rarely the coeliac axis is compressed by the median arcuate
ligament of the diaphragm.
Clinical features
The main symptom is postprandial abdominal pain, which
starts 15~30 minutes after a meal, and lasts for about an hour.
This pain is called "abdominal angina".
The patient is usually afraid to eat and therefore loses
weight.
An upper abdominal bruit is heard in the majority of patients.
A clinical search is made to find out atherosclerotic

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 narrowing of other arteries.
Investigations
Investigations are needed to:
1. Ultrasound and upper GI endoscopy to exclude other causes
of chronic abdominal pain.
2. Confirm the narrowing of vessels. Aortography is
diagnostic, particularly its lateral view which delineates the
narrowing of the origin of the artery, as well as the presence
of collateral circulation.
3. CT angiography is non-invasive and provides a 3D image
with colour coding. It delineates the pathological details of
the lesion (site, degree of narrowing and extent).
Treatment
Atherosclerosis is surgically treated either by:
a. Endarterectomy (coring out the thickened intima).
b. Bypass of the narrow segment by a synthetic graft wiich
connects the aorta to the superior mesenteric artery stem
below the narrow segment.
c. Endovascular treatment (balloon dilatation or stenting).
Median arcuate ligament compression is treated by division
of the ligament.

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