Ischemic bowel disease

Lecture 11, 12

Vascular disorders

Vascular disorders• Ischemic Bowel Disease• Angiodysplasia• Hemorrhoids

DefinitionIschemic bowel disease results from

inadequate flow of oxygenated blood to the intestines.

• The extent of ischemic bowel disease can range

from mild to severe based on the amount of damage from lack of oxygenated blood.

• Ischemic lesions may be restricted to the

•Small intestine mesenteric ischemia

•Large intestine ischemic colitis or

•Both enterocolitis

Blood Supply• The majority of the GI tract is supplied by the

celiac, superior mesenteric, and inferior mesenteric arteries.

• As they approach the intestinal wall the superior

and inferior mesenteric arteries ramify into the mesenteric arcades.

• Interconnections between arcades, as well as collateral supplies from the proximal celiac and distal pudendal and iliac circulations, make it possible for the small intestine and colon to tolerate slowly progressive loss of the blood supply from one artery.

• In contrast, acute compromise of any major vessel can lead to infarction of several meters of intestine.

Levels of infarction• Transmural infarction involving all layers of the gut.

• Mural infarction– mucosa & submucosa

• Mucosal infarction- mucosa

Mural-Of Wall

• Transmural infarction is caused by acute occlusion of a major mesenteric artery.

• Mural or mucosal infarction more often results from either physiologic hypoperfusion or more localized anatomic defects and may be

acute or chronic.

Predisposing conditions1. Arterial thrombosis2. Arterial embolism Occlusive

3. Venous thrombosis- less frequent

cause

4. Nonoclusive ischemia5. Miscellaneous

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Arterial thrombosis• Severe atherosclerosis• Systemic vasculitis• Dissecting aneurism An aneurysm in which the wall of an artery rips (dissects) longitudinally

• Angiographic procedures• Aortic reconstructive surgery• Surgical accidents• Hypercoagulable states• Oral contraceptives

Arterial embolism• Cardiac vegetation An abnormal growth of tissue around a valve, composed of blood platelets, bacteria, and a protein involved in clotting.

• Angiographic procedures• Aortic atheroembolism

Venous thrombosis• Hypercoagulable states induced, for example, by oral contraceptive or antithrombin III deficiency,

• intraperitoneal sepsis, • the postoperative state, • vascular invasive neoplasm (particularly hepatocellular carcinoma),

• cirrhosis, • abdomina trauma.

Nonoclusive ischemia• Cardiac failure• Shock• Dehydration• Vasoconstrictive drugs

Miscellaneous• Radiation injury• Volvulus• Stricture• Internal & external herniation

Causes • Ischemic bowel disease occurs when an artery that

supplies blood becomes blocked or narrowed. There are several possible causes of ischemic bowel disease, including:

• Blockage in the arteries due to a tumor or blood clot

• Narrowing of the arteries supplying blood to the bowel from atherosclerosis

• Obstruction in the colon (large intestine)

Risk Factors • Advanced age• Shock induced by conditions such as blood

stream infection and blood loss• Recent heart attack• Sustained abnormal heart beat• Congestive heart failure• Peripheral vascular disease• Coronary artery bypass surgery or other vascular

surgeries

• Colon cancer• Certain medications that cause arteries to narrow• Diabetes• Hemodialysis• Sickle cell disease• Dehydration• Pregnancy

Pathophysiology

• Arterial sources v.s. venous sources: proximately 9:1. Similarly, arterial occlusive disease occurs more frequently than nonocclusive disease approximately 9:1

• The SMA and IMA, and their branches, are more frequently than the celiac artery.

Pathophysiology (a. source)

Acute: 1.atheromatous plaque with intimal calcifications 2.embolic from cardiac disease 3. abdominal aortic aneurysms with dissection into

SMA 4. hypoperfusion secondary to hypovolemic shock or

low-flow cardiac failure.

Pathophysiology (a. source)

Chronic : 1.atherosclerosis 2.fibromuscular dysplasia 3.vasculitis.

Both occlusive and nonocclusive subtypes can occur .

Pathophysiology (v. source)

• are less frequently.• In these cases, bowel ischemia results from

decreased mesenteric outflow of deoxygenated blood rather than from decreased perfusion of oxygen-rich blood

• Mortality rates generally are low. • SMV is involved more often than the IMV.

3.Nonocclusive mesenteric ischemia

– more frequently in older patients than other forms and often already in an ICU setting .

– Symptoms typically develop over several days, and may have had a prodrome of malaise and vague abdominal discomfort.

– When infarction occurs, increased pain associated with vomiting,hypotensive and tachycardic, with loose bloody stool.

4.Mesenteric venous thrombosis in a much younger patient population than other types .

– acute or subacute abdominal pain involvement of the small intestine rather than the colon.

– The symptoms are frequently less dramatic. 27% have symptoms for >30 d.

– Many patients have a history of the risk factors for hypercoagulability. include oral contraceptive use, deep vein thrombosis (DVT), liver disease, tumor, or portocaval surgery.

PathogenesisIntestinal responses to ischemia occur in two

phases.

I. The initial hypoxic injury occurs at the onset of vascular compromise. While some damage occurs during this phase, the epithelial cells lining the intestine are relatively resistant to transient hypoxia.

II. The second phase, reperfusion injury, is initiated by restoration of the blood supply and it is at this time that the greatest damage occurs.

In severe cases this may trigger

multiorgan failure. While the underlying mechanisms of reperfusion injury are incompletely understood, they involve free radical production, neutrophil infiltration, and release of inflammatory mediators, such as complement proteins and TNF.

• Activation of intracellular signaling molecules and transcription factors, including hypoxia-inducible factor 1 (HIF-1) and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that

controls the transcription of DNA) also contribute to intestinal ischemia-reperfusion injury

• The severity of vascular compromise, • the time frame during which it develops, and• the vessels affected

are the major variables in ischemic bowel disease.

• Two aspects of intestinal vascular anatomy also contribute to the distribution of ischemic damage.

1. Intestinal segments at the end of their respective arterial supplies are particularly susceptible to ischemia.

Tail enders

• These watershed zones include the

splenic flexure, where the superior and inferior mesenteric arterial circulations terminate, and, to a lesser extent,

• the sigmoid colon and rectum where inferior mesenteric, pudendal, and iliac arterial

circulations end.

• Generalized hypotension or hypoxemia can therefore cause localized injury, and ischemic disease should be considered in the differential diagnosis of focal colitis of the

splenic flexure or

• rectosigmoid colon.

2. Intestinal capillaries run alongside the glands,

from crypt to surface.

•This allows oxygenated blood to supply crypts but

leaves the surface epithelium vulnerable to ischemic injury.

• This anatomy protects the crypts, which contain the epithelial stem cells that are necessary to repopulate the surface.

• Thus, surface epithelial atrophy, or even necrosis and sloughing, with normal or hyperproliferative crypts

is a morphologic signature of ischemic intestinal disease.

Morphology Transmural Intestinal Infarction- may involve a short or long segment, depending on

the particular vessel affected and the patency of the anastomotic supply. Whether the occlusion is

arterial or venous, the infarction always has a

dark red hemorrhagic appearance (Red Infarction).

• The ischemic injury usually begins in the mucosa and extends outwards; within 18 to 24 hours.

• There is a thin, fibrinous exudate over the serosa.

• With arterial occlusion the demarcation from adjacent normal bowel is fairly sharply defined, but

• with venous occlusion the margins are less distinct.

• Affected foci may or may not be visible from the serosal surface, because by definition the ischemia does not affect the entire thickness of the bowel.

• When the bowel is opened, hemorrhagic edematous thickening of the mucosa, sometimes with superficial ulcerations, is seen.

EHNEHistologic features are those of acute

injury:Edema, hemorrhage, and outright necrosis ofthe affected tissue layers.Inflammation develops at the margins of the

lesions, and an inflammatory fibrin-containing exudate (pseudomembrane), usually secondary to bacterial superinfection, may coat the affected mucosa.

• Alternatively, Chronic vascular insufficiency may produce a

chronic inflammatory and ulcerative condition, mimicking idiopathic inflammatory bowel disease.

•Lecture 12

Morphology –Transmural infarction

• Histologically, the changes are typical of ischemic damage with

• marked edema, • interstitial hemorrhage, • necrosis and sloughing of the mucosa. • Within 24 hours intestinal bacteria produce

outright gangrene and sometimes perforation of the bowel.

Mural & mucosal infarctions- are recognised by multifocal lesions interspersed

with spared areas. Their location depends in part on the extent of preexisting atherosclerotic narrowing of

the arterial supply; lesions can be scattered over large regions of the

small or large intestines.

Patchy lesions (Necrosis)

Symptoms• Cramping and abdominal pain• Bloody stools• Frequent urge to defecate• Diarrhea• Nausea or vomiting• Abdominal distension

Ischemia bowel

• acute or chronic.• arterial or venous• occlusive or nonocclusive.

Acute transmural infarction

typically presents with sudden, severe abdominal paintenderness (more sudden with mesenteric embolism),

sometimes accompanied by nausea, vomiting, bloody diarrhea, or grossly melanotic stool.

Patients may progress to shock and vascular collapse within hours as a result of blood loss. Peristaltic sounds diminish or disappear, and muscular spasm creates

board-like

rigidity of the abdominal wall.

Because these physical signs overlap with those of other abdominal emergencies, including

acute appendicitis, perforated ulcer, and acute cholecystitis,

the diagnosis of intestinal necrosis may be

delayed or missed, with disastrous consequences.

As the mucosal barrier breaks down, bacteria enter the circulation and

sepsis can develop;

mortality may exceed 50%.

The overall progression of ischemic enteritis depends on the underlying

cause and severity of injury.

• The mortality rate with infarction of

the bowel approaches 90%, largely because

the window of time between onset of symptoms and perforation caused by gangrene is so small.

Mucosal and mural infarctions by themselves may not be fatal. However, these may progress to more extensive infarction

if the vascular supply is not restored by correction of the

insult

or, in chronic disease, by development of adequate

collateral supplies.

• The diagnosis of nonocclusive ischemic enteritis and colitis can be particularly difficult because there may be a confusing array of

nonspecific abdominal symptoms, including

intermittent bloody diarrhea and

• intestinal pseudo-obstruction.

,

Chronic ischemia may masquerade as

inflammatory bowel disease, with episodes of

bloody diarrhea interspersed with periods of healing.

Diagnosis• X-ray of abdomen• CT Scan or MRI of the abdomen• Colonoscopy—a procedure where a long

flexible tube is inserted through the rectum to inspect the colon and rectum.

• Angiography—an x-ray test used to view the arteries supplying the bowel

Differential

Appendicitis Trauma

Pseudomembranous colitis Adenocarcinoma Diverticulitis Crohn Disease

Necrotizing Enterocolitis Pneumatosis Intestinalis

Typhlitis Ulcerative Colitis

Treatment Supportive Care • Bowel rest and intravenous fluids are given in mild

cases without significant progressed damage to the bowel.

• Antibiotics • Antibiotics are administered to minimize infection,

which can quickly complicate an ischemic bowel.• Surgery • In more severe cases, surgery is required to remove

the ischemic colon.

Complications• Bowel necrosis (requiring bowel resection)

• Septic shock• Death

• Patients in whom the diagnosis is missed until infarction occurs have a mortality rate of 90%. Even with good treatment, up to 50-80% of patients die.

• Survivors of extensive bowel resection face lifelong disability.

Prevention• Stay well hydrated.• Reduce your risk of cardiovascular disease

through regular exercise and a balanced diet low in fat and calories.

• Consume plenty of fresh fruits, vegetables, and fiber, which may reduce your risk of colon cancer.

Major Causes of

Intestinal Obstruction

Major Causes of Intestinal Obstruction

Mechanical Obstruction:

• Hernias• Adhesions• Intussuception• Volvulus 80%

Intestinal obstruction. The four major causes of intestinal obstruction are (1) herniation of a segment in the umbilical or inguinal regions, (2) adhesion between

loops of intestine, (3) volvulus, and (4) intussusception.

Other less frequent conditions

• Tumors & Infarction 10-15 %• Inflammatory strictures• Obstructive gall stones, fecaliths, foreign bodies

• Congenital Strictures, atresias• Congenital bands• Meconium in cystic fibrosis• Imperforate anus