Is ischemic colitis curable?


Need-to-Know Facts About Ischemic Colitis and Seniors

If you’re over 50, you should be aware of ischemic colitis. This condition causes part of your colon to become inflamed due to reduced blood flow to the area.

Ischemic colitis appears to be on the rise in recent decades. A small population-based study published in April 2015 in the journal Clinical Gastroenterology and Hepatology found that the rate of ischemic colitis nearly quadrupled between 1976 and 2009. This could be partly explained by increases in cardiovascular risk factors, such as coronary artery disease, that make the disease more likely.

So how does ischemic colitis happen, and what should you expect if you develop this condition?

Know the Risk Factors for Ischemic Colitis

Ischemic colitis happens when blood flow is reduced to part of your colon. According to Sumona Saha, MD, a gastroenterologist and assistant professor of medicine at the University of Wisconsin School of Medicine and Public Health in Madison, there are three main causes of reduced intestinal blood flow:

  1. A buildup of plaque in the arteries that feed the colon or the small intestine makes it more difficult for blood to flow through that area.
  2. A blood clot travels to one of the blood vessels leading to the colon. “That part of the colon will immediately have less blood flow,” Dr. Saha notes.
  3. A spasm in a blood vessel — called vasospasm — reduces blood flow to the area near where it occurs. Saha notes that certain drugs can increase the risk of this happening.

When a segment of the colon experiences a severe enough reduction in blood flow, it begins to deteriorate. This causes inflammation when blood flow returns to the area.

By the time the symptoms of ischemic colitis develop, blood flow is typically back to normal, says Lawrence J. Brandt, MD, a gastroenterologist and professor of medicine and surgery at the Albert Einstein College of Medicine in New York City. So unlike conditions in which blood flow to the small intestine is disrupted, such as acute mesenteric ischemia, ischemic colitis rarely requires that blood flow be immediately restored to the area.

Other risk factors for ischemic colitis include:

  • Cardiovascular disease
  • High blood pressure
  • Abnormal blood lipid levels
  • Diabetes
  • Certain kinds of medication, including some used to treat migraines and for hormone replacement therapy

Symptoms, Diagnosis, and Treatment of Ischemic Colitis

The most common symptoms of ischemic colitis are abdominal pain and bleeding, which can come in the form of bloody diarrhea.

According to an article published in December 2016 in The American Journal of Gastroenterology, symptoms of the condition, as well as its severity, often depend on which side of the colon it affects.

When only the right side of the colon is affected, it’s common to experience severe pain but no bleeding. And in these cases, outcomes of the condition tend to be worse, so it’s very important to be closely monitored by a physician in a hospital — especially since surgery is more likely to be necessary if you have this form of the disease.

Saha says that your doctor may diagnose you with ischemic colitis based on your symptoms, age, health history, and lab tests finding markers of inflammation in your blood. “Like everything in medicine, it’s like putting together pieces of a puzzle,” she notes.

If your main symptom is abdominal pain, Dr. Brandt says it’s likely that your doctor will order a CT scan of your abdomen prior to a colonoscopy. But if rectal bleeding is your main symptom, your doctor will most likely order a colonoscopy right away.

The recommended treatment will depend on the severity of your condition, Saha says. If your condition is mild, then you may just receive IV fluids to ensure maximum blood flow.

If the condition is more severe, in addition to being closely monitored and receiving fluids, you’ll probably be given antibiotics. That’s because when your colon is badly inflamed, bacteria from your colon can leak out into your bloodstream.

And if the condition is very severe — with significant deterioration of part of your colon — then the affected segment of your colon may need to be surgically removed. Failure to do so could lead to widespread infection in your body, known as sepsis, and could be fatal.

But most of the time, Brandt notes, people with ischemic colitis don’t get anywhere near needing surgery, and outcomes are positive. “For the most part,” he says, “it gets better by itself, and it usually doesn’t recur.”

Additional reporting by Ajai Raj

Acute ischemic colitis in elderly: medical or surgical urgency?

Seventy-two elderly patients (m:39, f:33; median age 74.8 years) affected by ischemic colitis were observed in the Surgery Unit of the University of L’Aquila from 1986 to 2008. The clinical records of the patients were reviewed retrospectively in order to asses clinical, biohumoral, endoscopic and x-ray findings predictive of the most suitable treatment. Clinical follow-up was implemented to evaluate the long-term prognosis after mean period of 6 years post treatment.

Fifty-eight percent of the ischaemic lesions involved the left colon, 23.6% the right colon, 9.7% the sigmoid colon and 8.3% involved transverse colon. Cardiovascular disease was associated in 79% of patients. Fifty-tree patients (73.6%) were treated by medical therapy only (broad spectrum antibiotics, fasting, parenteral nutrition and heparin prophylaxis) for a mean period of 7 days, with positive outcome. Nineteen patients (26.3%) underwent surgery: left (42.1%) and right hemicolectomy (15.7%), Hartmann resection (26.3%), subtotal resection (10.5%), sigmoid resection (5.4%). Urgent surgery was performed in 6 patients within 12–36 hours from admission; 13 patients underwent surgery after failure of previous medical treatment.

Bowel ischaemia has been classified into three main types:

  • Acute mesenteric ischaemia.
  • Chronic mesenteric ischaemia.
  • Ischaemic colitis (colonic ischaemia).

Acute mesenteric ischaemia

This is an umbrella term covering a number of conditions, including acute mesenteric arterial embolus and thrombus, mesenteric venous thrombus and non-occlusive mesenteric ischaemia (NOMI). They all have the features of impaired blood transfusion to the intestine, bacterial translocation (the passage of intestinal bacteria to normally sterile tissue) and systemic inflammatory response.


This is chiefly a disease of people aged over 50, although younger people with risk factors for mesenteric venous thrombosis (MVT) – eg, atrial fibrillation (AF) – can be affected. The overall incidence is 0.09-0.2% of all hospital admissions.

Predisposing factors

  • Conditions causing arterial emboli – eg, mural thrombus following myocardial infarction, auricular thrombus associated with mitral stenosis and AF, septic emboli from valvular endocarditis, fragments of proximal aortic thrombus, arterial catheterisation dislodging bits of plaque.
  • Conditions causing arterial thrombosis – atherosclerosis (most common), aortic aneurysm or dissection, arteritis, decreased cardiac output (eg, from myocardial infarction or chronic heart failure), dehydration.
  • NOMI – hypotension, vasopressive drugs, ergotamines, cocaine, digitalis.
  • MVT can be caused by:
    • Hypercoagulability disorders (eg, protein C and S deficiency).
    • Tumour causing venous compression or hypercoagulability.
    • Infection – usually intra-abdominal such as appendicitis, diverticulitis, or abscess, venous congestion from cirrhosis (portal hypertension).
    • Venous trauma from accidents or surgery, especially portocaval surgery, pancreatitis, decompression sickness.


The presentation of the various types is similar, with moderate-to-severe colicky or constant and poorly localised pain. A striking feature is that the physical findings are out of proportion to the degree of pain and, in the early stages, there may be minimal or no tenderness and no signs of peritonitis. In the later stages typical symptoms of peritonism develop, with rebound guarding and tenderness. A mass is sometimes palpable. Examination may reveal associated causes (eg, AF).


A high level of suspicion and early diagnosis with CT angiography are the key to lower mortality rates.

  • There are no specific laboratory tests. A raised white cell count and the presence of metabolic acidosis may be helpful.
  • Plain abdominal X-ray may be required to rule out other causes and may show small bowel obstruction, ileus and thickened bowel wall in the later stages. CT scan may show gas in various ectopic places such as bowel wall (pneumatosis intestinalis) or portal vein, bowel wall and/or mesenteric oedema, thumbprinting, streaking of mesentery and solid organ infarction.
  • CT angiography is the gold standard and shows arterial blockage due to emboli or thrombus. Multidetector computerised tomography (MDCT) with intravenous contrast enhancement is the specific investigation of choice.
  • Ultrasound or MRI scan may also be contributory.
  • Electrocardiogram may show atrial fibrillation or infarction.
  • Echocardiogram may be needed to show the cause of an embolism or valvular pathology.
  • Intraoperative fluorescein administration may be required to highlight those areas of bowel that need resection.

Differential diagnosis

  • Other causes of an acute abdomen.
  • Abdominal aortic aneurysm.
  • Biliary disease.
  • Chronic mesenteric ischaemia.
  • Diverticulitis.
  • Ectopic pregnancy.
  • Helicobacter pylori infection.
  • Multisystem organ failure of sepsis.
  • Myocardial infarction.
  • Pneumonia.
  • Pneumothorax.
  • Acute intermittent porphyria.
  • Testicular torsion.


Medical care

  • Initial resuscitation with intravenous fluids and oxygen should be carried out.
  • Nasogastric tube should be sited.
  • Intravenous broad-spectrum antibiotics are recommended.
  • Unless contra-indicated, intravenous unfractionated heparin is also recommended.

Surgical care

  • Prompt laparotomy should be done for patients with overt peritonitis.
  • The goals of surgery include re-establishment of the blood supply to the ischaemic bowel; resection of all non-viable regions and preservation of all viable bowel.

Endovascular revascularisation procedures may have a role with partial arterial occlusion.


Even in the best hands, the outcome is poor. If the diagnosis is missed, the mortality rate is 90%. With treatment, the mortality rate is still 50-90%. Survivors of extensive bowel surgery face considerable disability.

Chronic mesenteric ischaemia

This is a chronic atherosclerotic disease of the vessels supplying the intestine. It is also known as intestinal angina. Usually all three major mesenteric arteries are involved.

Chronic mesenteric ischaemia has a very low incidence, accounting for less than 1 in 1,000 hospital admissions for abdominal pain. Patients are typically female and between 50 and 70 years of age. They usually have other coexisting manifestations of atherosclerotic disease.

This is generally caused by factors predisposing to atherosclerosis – eg, smoking, hypertension, diabetes mellitus and hyperlipidaemia.

The presentation of the various types is similar, with moderate-to-severe colicky or constant and poorly localised pain.

The history is typically one of weight loss, postprandial pain (‘intestinal angina’) and a fear of eating. There is usually a history of cardiovascular disease such as myocardial infarction or cerebral vascular disease. Other nonspecific symptoms may include nausea, vomiting, or bowel irregularity.

Examination may show vague abdominal tenderness disproportionate to the severity of the pain, an abdominal bruit and signs of generalised cardiovascular disease.

  • Acute mesenteric ischaemia.
  • Other causes of an acute abdomen.
  • Causes of dyspepsia.
  • Diverticulitis.
  • Gastric cancer.
  • Chronic pancreatitis.
  • Chronic pyelonephritis.
  • Laboratory tests such as FBC, LFTs and U&E may reflect malnutrition or dehydration.
  • CXR should be carried out to exclude pneumonia, and cardiac scanning to exclude comorbidity.
  • Arteriography is the gold standard investigation to show the site of arterial blockage or stenosis.
  • Mesenteric duplex ultrasonography is a non-invasive method of demonstrating arterial blood flow but is more affected by extraneous factors such as obesity or respiratory movements.

Asymptomatic patients are managed conservatively, with smoking cessation and antiplatelet therapy. These patients have a five-year mortality of 40%, with the majority of deaths attributed to myocardial infarction or cardiovascular death.

Symptomatic chronic mesenteric ischaemia (CMI) is an indication for either open or endovascular revascularisation, as patients with untreated symptomatic CMI carry a five-year mortality rate that approaches 100%.

Nutrition is important in pre-operative assessment, as patients are often malnourished at the time of diagnosis; total parenteral nutrition may be necessary both pre- and postoperatively. The optimal revascularisation approach depends heavily on the anatomy and pre-operative condition of the patient. Renal failure is a common postoperative complication.

For most patients the quality of life is poor. The constant fear of abdominal pain that may occur when eating food leads to significant weight loss. The malnourished state often leads to other metabolic and endocrine problems, such as osteoporosis and easy bruising.

Ischaemic colitis

This is caused by a compromise of the blood circulation supplying the colon. Marginal branches of the middle colic (superior mesenteric territory) and left colic (inferior mesenteric territory) arteries supply the transverse and descending segments of the colon and, with an arterial and lymphatic watershed existing near to the splenic flexure, supported by an additional vascular arcade, this part of the colon is at risk. Also, blood flow may be impaired by colonic distension with ischaemic colitis occurring within the segment of intestine immediately proximal to an obstruction (stercoral ulceration) or pseudo-obstruction. Ischaemic colitis may also be caused by venous occlusion.

The incidence of ischaemic colitis has risen from 6.1 cases/100 000 person-years in 1976-80 to 22.9/100 000 in 2005-09. Many mild cases may go unreported. Because the most common cause is atheroma of the mesenteric vessels it is mainly a disease of the elderly and is rare before the age of 60. The average age for diagnosis is 70. The incidence is likely to increase with the increasing age of the population. The condition is, however, by no means unknown in younger age groups, due to non-cardiovascular causes such as cocaine abuse.

  • Thrombosis:
    • Inferior mesenteric artery thrombosis.
  • Emboli:
    • Mesenteric arterial emboli.
    • Cholesterol emboli.
  • Decreased cardiac output or arrhythmias.
  • Shock (sepsis, haemorrhage, hypovolaemia).
  • Trauma.
  • Strangulated hernia or volvulus.
  • Drugs:
    • Digitalis.
    • Oestrogens.
    • Antihypertensive drugs.
    • Cocaine and methamfetamine.
    • Vasopressin.
    • Phenylephrine.
    • Pseudoephedrine.
    • Immunosuppressive agents.
    • Psychotropic agents.
  • Surgery:
    • Cardiac bypass.
    • Aortic dissection and repair.
    • Aortoiliac reconstruction.
    • Colectomy with inferior mesenteric artery ligation.
    • Gynaecological operations.
  • Vasculitis:
    • Systemic lupus erythematosus.
    • Polyarteritis nodosa (hepatitis B, hepatitis C).
    • Thromboangiitis obliterans.
    • Rheumatoid vasculitis.
    • Sickle cell disease.
  • Disorders of coagulation:
    • Protein C deficiency.
    • Protein S deficiency.
    • Paroxysmal nocturnal haemoglobinuria.
    • Activated protein C resistance.
    • Antithrombin III deficiency.
  • Long-distance running.
  • Colonoscopy or barium enema.
  • Idiopathic.

The condition may be difficult to diagnose, with nonspecific symptoms of an ‘acute abdomen’, such as acute-onset abdominal pain. The pain is most frequently located in the left iliac fossa. Nausea and vomiting often occur and, in the later stages, loose motion containing dark blood. Marked tenderness may be found in the left iliac fossa but the presence of peritonitis suggests full thickness ischaemia, perforation, or alternative diagnosis. The acute onset of the symptoms is a useful distinguishing factor between ischaemic colitis and inflammatory or infective colitis, where abdominal pain often has a more insidious onset. Symptoms of ischaemic colitis manifest in a matter of hours and, unlike infective or inflammatory colitis, continue to worsen with systemic instability.

The diagnosis may be one of exclusion and should always be borne in mind in patients presenting with abdominal pain of indeterminate cause. In younger patients it is often associated with taking the contraceptive pill, cocaine or methamfetamine abuse, the use of pseudoephedrine, sickle cell disease and inherited coagulopathies.

  • The presence of metabolic acidosis may be a clue.
  • Colonoscopy may show blue, swollen mucosa not showing contact bleeding and sparing the rectum.
  • Plain abdominal X-ray may show abnormal segment outlined with gas. However, the findings may be nonspecific for 12-18 hours after onset.
  • Barium enema shows ‘thumb printing’ in the early phase that may last for several days. The mucosa may then return to normal or progress to ulceration with similar appearance to segmental ulcerative colitis or Crohn’s disease. It may either resolve spontaneously or progress to narrowing of the intestine +/- sacculation of the antimesenteric border.
  • Other modalities occasionally used include CT scan, MRI scan and angiography.
  • Dysentery.
  • Acute diverticular disease of the colon.
  • Acute inflammatory bowel disease.
  • Perforation of a hollow viscus or pancreatitis causing left-sided peritonitis.

Medical care

  • The ischaemia may be transient and resolve once the cause of the hypoperfusion has been alleviated. Bowel rest and supportive care are often helpful.
  • Broad-spectrum antibiotics are recommended.

Surgical care

  • If symptoms do not improve in 24-48 hours, repeat colonoscopy or imaging of the mesenteric vasculature with CT angiography is necessary to re-evaluate the severity and degree of the disease.
  • Increasing abdominal tenderness with guarding and rebound tenderness, fever, uncontrollable bleeding, and paralytic ileus indicate possible infarction of the colon (severe disease) and require urgent laparotomy and removal of the necrotic part of the colon.

This depends on the location and extent of the disease, coexistent diseases, and whether or not the patient’s condition requires emergency surgery. The severity of the IC and the overall mortality is higher in right-sided disease, but the overall mortality is about 22%.

Ischemic Colitis Causes

Doctors often can’t pinpoint the cause of ischemic colitis. But these things can raise your odds of getting it:

  • Chronic constipation . This raises pressure inside your colon and makes it hard for blood to flow. If you have irritable bowel syndrome with constipation, you may be at even more risk.
  • Hardening of the arteries (atherosclerosis). Fatty gunk can build up and clog the arteries in your intestines.
  • Very low blood pressure or flow. This causes colon arteries to tighten and send more blood to your brain. A number of health problems can cause low blood pressure. But dehydration, heart failure, large blood loss, and shock are the leading reasons.
  • A blood clot . One can form inside an artery wall or break off from somewhere else and move toward your colon. Certain health problems you get from your parents at birth can cause blood to clot too easily. Your doctor may give you tests to see if you have one of these conditions.
  • Bowel blockage. This can result from a hernia, scar tissue, or a tumor.

Surgery to repair an aortic aneurysm (a bulge in the artery) can lead to ischemic colitis. Other operations in your belly or your circulatory system can also cause problems.

The risk also goes up if you’re a long distance runner. During a marathon, blood flow may shift away from your gut to meet the oxygen needs of your leg muscles. Dehydration could play a role, too.

It’s rare, but some medications can trigger an ischemic colitis attack. These include:

  • The decongestant pseudoephedrine
  • Some migraine and heart drugs
  • Estrogen

A Low-Residue Diet for Colitis

White bread, cheese, eggs, and fruit like watermelon are just some of the foods a person with ulcerative colitis can eat on a low residue diet. (4)

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Severe flare-ups are one of the greatest challenges of living with ulcerative colitis. One option to try is a low-residue diet, designed to reduce the amount of dietary fiber and ‘residue’ — or, undigested remains of fiber and other food — that goes through your digestive system and irritates the bowel.

A low-fiber diet can help reduce your most stressful symptoms of ulcerative colitis, such as abdominal pain and cramping. While a low-residue diet isn’t intended for the long-term, it can help the bowel heal during active flare-ups of this inflammatory bowel disease (IBD).

The Advantages of a Low-Residue Diet

“One reason people with an active flare of colitis go on a low-residue diet is to reduce symptoms in addition to trying to treat them,” says David T. Rubin, MD, Joseph B. Kirsner professor of medicine and chief for the section of gastroenterology, hepatology, and nutrition at the University of Chicago Medicine. “It helps to heal the bowel by reducing the amount of indigestible or poorly digestible fibers. This will reduce trauma to the bowel and, therefore, allow the bowel to heal.”

But Dr. Rubin cautions that dietary changes won’t cure or treat ulcerative colitis — they’re used in addition to other medical treatments to help manage symptoms associated with IBD.

“Symptom management is not the same as disease control,” says Rubin. Diet alone isn’t enough to put colitis in remission.

He adds that your diet must take into account your body’s nutritional needs. Long-term use of restrictive diets, like the low-residue diet, could increase the risk of nutrient deficiencies — when you’re not getting enough of what your body needs for daily function.

What to Avoid on a Low-Residue Diet

Dietary fiber is a type of carbohydrate found in plants that cannot be readily digested by the body. Residue is the undigested remains of fiber and food that goes into the stool.

A low-residue diet limits the amount of indigestible or hard-to-digest fiber in the diet to reduce the amount of residue that enters the large intestine.

The goal of a low-residue diet for people with IBD is to limit total fiber consumption to less than 10 to 15 grams per day. Rubin urges people to work with their physician to make sure they receive the nutrition their bodies need while at the same time eliminating foods that make the bowel work more, like beans and legumes, whole grains, and most raw fruits and vegetables.

“Elimination diets don’t work,” says Rubin. “People can avoid certain foods when they are actively flaring, but not chronically. The goal is to provide a healthy and enjoyable quality of life for patients.”

Nuts, seeds, dried fruits, and other foods with hulls, like corn, also add residue to the stool and should be avoided when you’re on a low-residue diet. You’ll also want to skip fatty, spicy, and sugary foods.

What to Eat on a Low-Residue Diet

Put together low-residue meals from these groups:

Cooked vegetables You can include spinach, pumpkin, eggplant, skinless potatoes, green beans, wax beans, asparagus, beets, carrots, and yellow squash (without seeds) as long as they are thoroughly cooked or canned. You can also drink juices made from these vegetables.

Refined grains You can have white bread and dry cereals containing less than one gram of fiber per serving (such as puffed rice, corn flakes, and others) on a low-residue diet.

Dairy products Include yogurt, cottage cheese, milk, or creamy soups — set a limit of 2 cups per day — or 1.5 ounces of hard cheese.

Very ripe fruits Apricots, bananas, cantaloupe, honeydew melon, papayas, peaches, plums, watermelon, and nectarines are okay to eat on a low-residue diet. You can include juices without pulp and fruit sauces like applesauce, but avoid all other raw fruits.

Protein Choose servings of cooked meat, bacon, poultry, eggs, and smooth peanut butter. Make sure the meats are tender and not chewy — and remove all residue-producing gristle.

Before starting a low-residue diet, talk to your doctor or registered dietitian about whether you may need a supplement to meet all your vitamin and mineral requirements, both while you’re on the diet and on other days.

How can I be sure that the patient has ischemic colitis?

Ischemic colitis most commonly presents with the sudden onset of mild cramping abdominal pain and the urgent desire to defecate. The patient usually passes bright red or maroon blood per rectum with diarrhea within 24 hours of symptom onset. There is usually mild-to-moderate abdominal tenderness over the segment of bowel that is involved. In patients who have isolated ischemic colitis of the right-colon (e.g. cecum and/or ascending colon), abdominal pain may be severe and occur without obvious rectal bleeding. To diagnose ischemic colitis, use history and physical findings with appropriate imaging (e.g., Computed Tomography with oral and IV contrast) and other diagnostic tests (e.g., colonoscopy when indicated).

What history is important to obtain from the patient?

In any patient presenting with bright red blood per rectum, or lower abdominal pain, the clinician should ask about recent medication exposures (e.g., immunomodulators, constipation-inducing medications), medical co-morbidities (e.g., peripheral vascular disease, colon cancer, chronic obstructive pulmonary disease), accompanying diarrhea, tenesmus, and fever, the timing of passage of red blood per rectum, the volume of blood passed, history of similar symptoms in the past, and the acuity of onset, character, and location of the abdominal pain.

Pathognomonic or characteristic features

The characteristic features include cramping abdominal pain in the distribution of affected colon, followed by a short course of bloody diarrhea. There are no pathognomonic features of ischemic colitis.

See Table I for signs and symptoms of ischemic colitis.

Table I.n

Signs and symptoms of ischemic colitis

Less common clinical presentations

Ischemic colitis can present in various ways including reversible colopathy, transient colitis, chronic colitis, stricture and gangrene. Irreversible manifestations include chronic colitis (chronic watery or bloody diarrhea), stricture (large bowel obstruction) and gangrene (abdominal pain).

Differential diagnoses

A broad differential diagnosis is useful when diagnosing ischemic colitis because many colitides can present similarly to colon ischemia, and more than one disease process may be present. (See Table II.)

Table II.n

Differential diagnoses

What is the difference between acute mesenteric ischemia and ischemic colitis?

Acute mesenteric ischemia results from inadequate blood flow to all or part of the small intestine and may involve the right half of the colon, within the distribution of the superior mesenteric artery. The spectrum of injury in acute mesenteric ischemia ranges from transient alteration of bowel function to gangrene. Acute mesenteric ischemia commonly results from an embolus (superior mesenteric artery) or a low flow state (nonocclusive mesenteric ischemia), although a thrombus (superior mesenteric artery or superior mesenteric vein) can be the etiology as well. Patients with acute mesenteric is commonly present with an elevated white blood cell count (approximately 12,000-15,000 cells/mm3) and CT angiogram is the diagnostic modality of choice to assess for a clot in the arteries or veins, of the small bowel, and to evaluate small bowel wall thickening.

Ischemic colitis in contrast involves the colon and has a wide spectrum of presentation. Ischemic colitis occurs within the distribution of the superior mesenteric artery (right colon through transverse colon) or inferior mesenteric artery (transverse colon to the rectum).

Acute mesenteric ischemia is associated with a high mortality rate, while ischemic colitis has a generally good prognosis. Isolated-right sided ischemic colitis (IRCI) has a worse prognosis than all other patterns of involvement of ischemic colitis. Acute mesenteric ischemia can either occur with or after IRCI, an occurrence that has the worse prognosis of ischemic colitis regardless of location of colon affected.

How can I confirm the diagnosis?

What tests should be ordered first?

Blood tests and stool studies are useful first tests to assess for ischemic colitis. Blood tests should include complete blood count, basic metabolic panel and liver biochemical profile; stool studies should include culture, testing for C. difficile, and ova and parasite examination. If the patient appears acutely ill, the clinician should consider obtaining a serum lactate level, bicarbonate, sodium, lactate dehydrogenase, creatine kinase, and amylase level.

What tests should be used to confirm the initial tests?

Repeat testing, as above, is indicated to follow the patient’s condition and course.

A CT scan of the abdomen and pelvis can show a segmental colitis or complications including “free air” and pneumatosis coli, as well as thrombi in the arteries or veins. If intravenous contrast is given, the CT scan also can help determine if bowel still has blood supply and if the bowel is “dead.” If the patient is presenting with severe abdominal pain with or without rectal bleeding, they have severe right-sided pains and/or they appear acutely ill, consider a CT-angiogram for a more accurate assessment of the vascular supply to the bowel.

If the diagnosis is suspected but unclear, colonoscopy within 48 hours of presentation should be considered unless the patient has signs of acute peritonitis or evidence or irreversible ischemic damage. Colonoscopy may reveal subepithelial hemorrhage or edema or, if more than 48 hours after onset, ulcerations. Biopsies should be obtained during colonoscopy in all circumstances except gangrene.

It is important to remember that there is no ideal test for suspected colon ischemia. Any of these tests may support the diagnosis but none can provide actual confirmation, except biopsy in some circumstances. The clinician should choose a test based on the clinical scenario and the expertise of the department of radiology at his/her institution.

What tests are useful if diagnosis is still in doubt?

Although colonoscopy is the main diagnostic test today, it may not show conclusive results.

Biopsies should be obtained to characterize the disease and its segmental nature. Biopsies consistent with ischemic colitis might show subepithelial hemorrhage and edema, iron-laden macrophages, and submucosal fibrosis; only gangrene provides the diagnosis. Note that mesenteric angiography is not usually needed in patients with suspected ischemic colitis unless the patient has severe abdominal pain or is thought to have isolated involvement of just the cecum and/or ascending colon because of the coincidence or development of acute mesenteric ischemia.

A diagnostic algorithm

See Figure 1 for a diagnostic algorithm for ischemic colitis.

Figure 1.

When is it important to consult a gastroenterologist or surgeon?

It is most important to refer to a gastroenterologist and/or surgeon when patients present with an acute abdomen, the physical exam is remarkable for pain out of proportion to the exam, and the patient has blood work remarkable for an elevated lactate, lactate dehydrogenase, creatine kinase, substantial leukocytosis, or metabolic acidosis. Refer to a gastroenterologist when a patient presents with bloody diarrhea or bright red blood per rectum. Also, if the CT scan or angiogram shows an acute thrombus, embolus, or other cause of mesenteric ischemia or mesenteric venous thrombosis surgical (general, vascular), consultation should be obtained.

Which patients require hospitalization?

Patients who have severe abdominal pain, persistent bloody diarrhea, are hemodynamically unstable, or have any signs of bowel perforation or infarction should be hospitalized. All elderly patients presenting with symptoms consistent with ischemic colitis should be hospitalized and managed conservatively for 24 hours.

See Table III for a listing of laboratory, radiographic, and endoscopic tests.

Table III.n

Diagnostic tests for ischemic colitis

What other diseases, conditions, or complications should I look for in patients with ischemic colitis?

Major risk factors and diseases predisposing to ischemic colitis
  • Age >60 years

  • Female gender

  • Atherosclerosis, congestive heart failure, chronic obstructive pulmonary disease, diabetes mellitus, hypertension, irritable bowel syndrome

  • Medication use, including alosetron, amiodarone, bisacodyl, buproprion, “constipation inducing drugs” (e.g., opioids, non-opioids), danazol, digitalis, ergot, estrogens, flutamide, furosemide, glycerin enema, gold salts, immunosuppressive agents, interferon, magnesium citrate, NSAIDs (nonsteroidal anti-inflammatory drugs), paroxetine, penicillin, phenylephrine, polyethylene glycol, alproic acid, progestins, pseudoephedrine, saline laxatives, statin medications, sumatriptan, TNF-α inhibitors, vasopressin

  • Illicit drug use, including cocaine, methamphetamine, psychotropic drugs

  • Smoking

Diseases associated with ischemic colitis
  • Amyloidosis

  • Cardiac failure or arrhythmias

  • Chronic obstructive pulmonary disease

  • Hematologic coagulopathies

  • Hypertension

  • Pancreatitis

  • Peripheral vascular disease

  • Pheochromocytoma

  • Ruptured ectopic pregnancy

  • Shock

  • Sources of arterial emboli

  • Strangulated hernia

  • Vasculitis

  • Volvulus

Commonly encountered complications

There are various clinical sequelae of ischemic colitis. These include reversible colopathy (most common), transient colitis, chronic colitis, stricture, gangrene, and universal/fulminant colitis.

The initial presentation for each of these sequelae is usually the same and does not predict the clinical course of disease. The exception to this rule is disease isolated to the right-colon, which is associated with more severe disease and a worse prognosis.

Symptoms of colonic ischemia generally resolve in 48 to 72 hours with colonic healing in 1 to 2 weeks (reversible colopathy and transient colitis). Symptoms persisting for more than 2 weeks are associated with a higher incidence of gangrene, perforation, segmental ulcerating colitis, or stricture. Chronic colitis is a rare manifestation of chronic colon ischemia.

What is the right therapy for the patient with ischemic colitis?

Effective treatment options

Intravenous fluids, antibiotics, and surgical intervention are all effective treatments in the appropriate clinical setting.

Treatment options

Intravenous fluid administration is the best nondrug therapy for ischemic colitis. All patients admitted with ischemic colitis should receive intravenous fluids. This will increase circulating intravascular volume and improve bowel perfusion, thereby preventing further episodes of ischemia.

Antibiotic therapy is indicated in ill patients hospitalized with advanced ischemic colitis. Antibiotics should cover gut flora, including gram-negative rods and anaerobes.

Surgical therapy is needed in a minority of patients who present acutely with ischemic colitis. Patients requiring emergent surgical intervention include those with signs of peritonitis, massive bleeding, portal venous gas and/or pneumatosis on imaging, universal fulminant colitis, with or without megacolon and deteriorating clinical conditions. Some patients will require nonemergent surgical intervention. These include patients with continued symptoms for 2 or more weeks, persistent protein-losing colopathy, and those with recurrent sepsis because of bacteria that seed the bloodstream via the damaged colon lining (“bacterial translocation”). Patients with irreversible manifestations of colonic ischemia, including stricture formation with obstruction and chronic colitis with diarrhea and rectal bleeding, also may require surgery.

What is the most effective initial therapy?

The most effective initial therapy is intravenous fluids. This will increase circulating intravascular volume and improve bowel perfusion. Give a bolus of isotonic fluid to correct fluid depletion, followed by a maintenance infusion. If the patient has a contraindication to fluids (e.g., congestive heart failure), initiate gentle hydration and maintain a low rate. Continue intravenous fluids for 24 or 48 hours, always being mindful of fluid overload. Consider broad spectrum antibiotics in addition to fluids for patients with up to three of the following factors:

Patients with more than three of the factors listed above, should receive intravenous fluids, antimicrobials, have correction of cardiovascular abnormalities, be seen emergently by the surgical service and transferred to the intensive care unit for appropriate monitoring.

There are no randomized controlled trials of intravenous fluids or antibiotics for ischemic colitis. Recommendations are based on expert consensus.

Listing of usual initial therapeutic options, including guidelines for use, along with expected result of therapy.

With fluid administration, the patient’s bloody diarrhea should subside in 24 to 48 hours. The patient should also have improvement in cramping abdominal pain within 24 hours of intravenous fluid hydration for treatment.

The clinician should optimize medications to maximize colonic blood perfusion. Blood pressure medications should maintain the patients’ systolic blood pressure over 120 mmHg. Congestive heart failure medications should be titrated to improve forward blood flow.

If a patient is hospitalized for ischemic colitis, especially with severe or persistent symptoms, consider giving antibiotic therapy. The antibiotic therapy should treat gut flora, including gram-negative rods and anaerobes. Possible treatment regimens include fluoroquinolone or aminoglycoside or third-generation cephalosporin plus anti-anaerobe coverage. Use antibiotics for a minimum of 72 hours; if the patient does not improve after 72 hours, consider broadening the antibiotic coverage and continuing treatment.

If patients do not symptomatically improve in the first 24 to 48 hours or if they have complicated or severe disease, consider referral to a gastroenterologist.

If initial therapy with intravenous fluids and/or antibiotics fails or the patient has severe disease with an acute abdominal exam, then surgical intervention is usually indicated. Treatment failure can be defined by a lack of improvement within 48 to 72 hours of symptom onset or a worsening of symptoms during that time period.

Obtain surgical consultation in patients with peritoneal signs, massive bleeding, portal venous gas and/or pneumatosis on imaging, universal fulminant colitis with or without toxic megacolon and deteriorating clinical condition. When the patient has been diagnosed with a vascular stenosis or occlusion of the intestinal arteries, consider consulting a vascular surgeon for endovascular or other surgical treatments.

Nonemergent surgical laparotomy is indicated in patients with continued symptoms despite conservative measures after 2 to 3 weeks following onset, persistent protein losing colopathy, or in those with overall symptomatic improvement but with recurrent bouts of sepsis.

A listing of a subset of second-line therapies, including guidelines for choosing and using these salvage therapies

What is the rationale behind using antibiotic therapy?

Some authors believe that antibiotics prevent gut flora translocation because the episode of ischemia will lead to ulceration and access of the gut flora to the blood supply. Other investigators believe that antibiotics serve a different but unspecified protective mechanism and that using the medications can prevent a worse outcome (i.e., colectomy, mortality).

Studies assessing the effectiveness of antibiotics are limited and based on data using canine and mouse models. Models show less inflammation with use of antibiotics. Of note, there are no set guidelines for the type, dosage, or duration of antibiotic treatment and the information presented is based on expert recommendations.

How often is surgical management needed and what is the mortality rate?

Surgical management has been estimated to be required in up to 2% of patients admitted to the hospital with ischemic colitis. In patients who underwent surgical intervention for ischemic colitis, the mortality rate was up to 50% for those patients who had infarcted bowel at the time of surgery.

Listing of these, including any guidelines for monitoring side effects.

Side effects from antibiotic therapy

Ciprofloxacin. Rash, nausea, vomiting, diarrhea, abdominal pain, headache, increased AST/ALT, increased serum creatinine, tendon rupture, and arthropathy

Metronidazole. Headache, nausea, vomiting, diarrhea, dizziness, loss of appetite, metallic taste in the mouth, and neuropathy

Gentamicin. Nephrotoxicity, auditory and vestibular ototoxicity, gait instability, neurotoxicity

Ceftriaxone. Pain or erythema at the injection site, rash, diarrhea, eosinophilia, thrombocytosis, elevated aminotransferases (AST/ALT), and elevated blood nitrogen urea (BUN)

How should I monitor the patient with ischemic colitis?

The clinician must always consider that patients with ischemic colitis might form a stricture or develop chronic colitis. Stricture formation might present in a variety of ways including constipation, narrowing caliber of stool, or large bowel obstruction. This can be assessed with either a CT scan or barium enema. If a patient’s stricture is clinically significant surgical resection may be indicated.

Chronic colitis may present with recurrent episodes of bloody diarrhea, chronic watery diarrhea, or a protein losing colopathy. It is unclear whether there is a connection between chronic colitis associated with ischemia and inflammatory bowel disease.

Follow-up recommendations

Patients with mild episodes of ischemic colitis can usually follow up with their physician within 1 month. During patient follow-up, the clinician should ask the patient about his/her bowel habits, the presence or absence of blood in stool, and abdominal pain. Persistent diarrhea or blood in the stool might indicate another disease process. It is usually not necessary to repate colonoscopy to assess healing if the patient has no symptoms of colitis.

A CBC should be obtained to monitor for anemia. The clinician also should reaffirm the importance of adequate hydration. If a medication that the patient was chronically being treated with was stopped because of ischemic colitis, a replacement medication should be started.

Patients who required surgical intervention will require closer follow-up and evaluation. These patients should be seen within 2 weeks of discharge from the hospital.

What information should patients be told about ischemic colitis?

It is important that patients understand that ischemic colitis is a self-limited disease usually lasting 24 to 48 hours and that it is unlikely to recur.

Patients should be encouraged to drink 8 glasses (2 liters) of water daily to maintain hydration, unless otherwise contraindicated (e.g., congestive heart failure).

If the patient has hypertension and is on a blood pressure medication, the patient must closely monitor his/her blood pressure to make sure it is well controlled.

Patients should have their medication lists reviewed with them. If a medication was changed, it is important to explain to the patient why this change occurred (e.g., associated with ischemic colitis). Patients should also be provided with information about alternative medication and be treated with whatever medications the gastroenterologist and primary care doctor decide is optimal.

What’s the evidence?

Feuerstadt, P, Aroniadis, O, Brandt, LJ. “Features and Outcomes of Patients With Ischemia Isolated to the Right Side of the Colon When Accompanied or Followed by Acute Mesenteric Ischemia”. Clin Gastroenterol Hepatol. vol. 13. 2015 Nov. pp. 1962-8. (This retrospective study of 65 patients is a comparative analysis of the medical co-morbidities, diagnostic serology, imaging and outcomes of those with IRCI alone versus those with accompanying or subsequent development acute mesenteric ischemia.)

Brandt, LJ, Feuerstadt, P, Longstreth, GF, Boley, SJ. “ACG clinical guideline: Epidemiology, risk factors, patterns of presentation, diagnosis, and management of colon ischemia (CI)”. Am J Gastroenterol. 2015. pp. 110-18. (These clinical guidelines from the ACG discussing colon ischemia, published in 2015)

Brandt, LJ, Feuerstadt, P, Blaszka, M. “Anatomic patterns, patient characteristics and clinical outcomes in ischemic colitis: a study of 313 cases supported by histology”. Am J Gastroenterol. vol. 105. 2010. pp. 2245-52. (This retrospective study of 313 patients with biopsy-proven ischemic colitis and complete colonoscopic or radiologic evaluation of disease distribution provides a comparative analysis of medical comorbidities, presentations, and outcomes of ischemic colitis, based on which segments of the colon are affected.)

Longstreth, GF, Yao, JF. “Epidemiology, clinical features, high-risk factors, and outcome of acute large bowel ischemia”. Clin Gastroenterol Hepatol. vol. 7. 2009. pp. 1075-80. (This retrospective study of 401 patients with colon ischemia offers a comprehensive primary analysis of the epidemiology, high-risk features, and outcomes of a cohort of patients with ischemic colitis.)

Feuerstadt, P, Brandt, LJ. “Update on Colon ischemia: recent insights and advances”. Curr Gastroenterol Rep. 2015. pp. 17-45. (This is a review article summarizing the most recent findings and advances in the field of ischemic colitis.)

Ibrahim, CB, Aroniadis, OC, Brandt, LJ. “On the role of ischemia in the pathogenesis of IBD: a review”. Inflamm Bowel Dis. vol. 16. 2010. pp. 696-702. (This clinical review article examines the etiologic roles of macro- and microvasculature and of intestinal ischemia in the pathogenesis of inflammatory bowel disease.)

Hass, DJ, Kozuch, P, Brandt, LJ. “Pharmacologically mediated colon ischemia”. Am J Gastroenterol. vol. 102. 2007. pp. 1765-80. (This article provides a comprehensive review of pharmacologically mediated ischemic colitis, including classes of medications commonly associated with ischemic colitis and their hypothesized mechanism of action.)

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