Ischemic Colitis: A Clinical Case and Concise Review
William K. Chan, MD Candidate 2013 [1]
Nancy Fu, BSc. (Pharm), MD [2]
Majid Alsahafi, MD [2]
Eric M. Yoshida, MD, MHSc, FRCPC (University of Toronto 8T6) [2]
[1] Department of Medicine, University of Toronto
[2] Division of Gastroenterology, University of British Columbia
Corresponding Author:
William K. Chan
University of Toronto, Faculty of Medicine
1 King’s College Circle, Toronto, ON M5S 1A8
Email: williamk.chan@utoronto.ca
1
ABSTRACT
A previously healthy 64-year-old lady presented with hematochezia, syncope, and
abdominal discomfort. Colonoscopy revealed findings consistent with segmental ischemic
colitis, which resolved with supportive therapy. Herein we review the case and discuss the
pathophysiology, diagnosis, and management of ischemic colitis.
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CASE PRESENTATION
A 64-year-old lady with hypothyroidism and celiac disease presented with a one
week history of malaise and abdominal discomfort. On the day of her admission, she had
two syncopal episodes accompanied by hematochezia and melena stools. She denied
nausea, vomiting, hematemesis, diarrhea, or weight loss. She had no recent travel or
antibiotic and NSAID use. She is an ex-smoker and consumes two glasses of wine four
times a week. She had no family history of autoimmune disease, inflammatory bowel
disease, or gastrointestinal malignancy. On examination, she was afebrile. She had an
orthostatic drop and left lower quadrant abdominal tenderness
Laboratory investigations revealed anemia with a hemoglobin of 117 g/L. She had
no previous history of iron-deficiency anemia. Her other bloodwork were normal including
complete blood counts, coagulation profile, creatinine and liver enzymes. Although her CRP
was elevated at 117 mg/L (normal <3.1), an autoimmune screen including anti-neutrophil
cytoplasmic antibody (ANCA), anti-nuclear antibody (ANA), and double-stranded DNA
were all negative. Stool cultures and C. difficile toxin were also negative.
An esophagogastroduodenoscopy performed two days into her admission only
demonstrated a small hiatus hernia. Gastric biopsies showed mild inactive chronic gastritis
with no evidence of H. pylori infection. Her colonoscopy, however, revealed a 25 cm
segment of edematous and friable mucosa with loss of vascular margins at the splenic
flexure (Figure 1). There was also significant diverticulosis. Colonic biopsy showed
pseudomembranous luminal inflammatory exudate, crypt atrophy, and laminal propria
fibrosis suspicious for ischemic versus pseudomembranous colitis.
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After these procedures, the patient was started on a 7 day course of antibiotics that
included ciprofloxacin 500 mg BID and metronidazole 500 mg BID for a diagnosis of acute
ischemic colitis.
Follow up abdominal and pelvic computed tomographic (CT) scan with IV contrast
showed scattered diverticulosis involving the descending and sigmoid colon with no bowel
wall thickening or intestinal pneumatosis. Midline arterial vessels enhanced normally with
no radiological features of bowel ischemia.
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DISCUSSION
Epidemiology:
Ischemic colitis is the most common manifestation of ischemic injury to the lower
gastrointestinal tract (1). Although it is commonly seen in the elderly between ages 70-79
years, it can occur in almost any age group. Atypical cases have been reported in young
healthy endurance runners who would otherwise have no classical risk factors of
hypertension, cerebrocardiovascular disease, or a past history of abdominal surgery (2–4).
Women are 1.48 times more likely than men to be affected, and the disease is more
common in patients with Irritable Bowel Syndrome (5). Although infrequent at baseline
(44 cases per 100,000 person-years), the incidence of ischemic colitis is rising. Moreover,
most cases of ischemic colitis likely go undetected because of its short and mild clinical
course. Clinical suspicion is often low for this disease as the clinical presentation of
ischemic colitis can be very heterogeneous (6).
Clinical Presentation:
Like our patient, those with ischemic colitis typically present with sudden left lower
quadrant pain, diarrhea, and bloody stools. Hematochezia and bleeding per rectum are
worrisome complaints in patients with a broad differential diagnosis, and medical trainees
from all levels need to properly assess and identify patients at risk for developing ischemic
colitis. The disease may manifest across a wide spectrum of injury including reversible
colopathy, transient colitis, chronic colitis, stricture, gangrene, and fulminant colitis (1).
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Although most cases of ischemic colitis resolve quickly, a few situations warrant
special attention and consideration for potentially more lethal complications. Isolated
right-sided ischemic colitis may reflect super mesenteric arterial disease with an associated
mortality rate as high as 50% (6,7). Early identification is crucial especially in elderly
patients to prevent complications and to distinguish it from colorectal carcinoma, which
can present similarly (8). Both can also occur concurrently as increased intracolonic
pressure proximal to a colonic lesion can decrease blood flow and cause ischemia. It is
necessary to assess for tissue ischemia because it can affect the integrity of a surgical
anastomosis post resection of an obstructing lesion.
Pathophysiology:
Ischemic colitis can result from modifications in the systemic circulation or
anatomic and functional changes to the local mesenteric vasculature. Elderly patients are at
higher risk because of multiple co-morbidities and more degenerative changes in the
vascular bed. The colon is particularly sensitive to low-flow states because the middle colic
and inferior mesenteric arteries create a watershed area that correspond to the splenic
flexure (Griffith’s point) and recto-sigmoid (Sudeck’s point) segments of the large bowel
(1). The rectum is relatively spared because of its collateral blood supply. Our patient’s
ischemic inflammatory changes were in the left colon in the region of the classic watershed
areas.
Etiology:
Of the cases of ischemic colitis that have a specific identifiable cause, most can be
separated into the categories of thrombophilia and medications (Table 1). Thrombophilia
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usually affects younger patients and those with recurrent colonic ischemia. The most
common inherited forms are activated protein C (APC) resistance and factor V Leiden
deficiency, while the most common acquired disorder is antiphospholipid antibody.
Medications that cause ischemic colitis work primarily through mechanisms of
vasoconstriction, allergic vasculitis, unmasking underlying thrombophilia, and severe
constipation (1). Cocaine is especially concerning among younger patients because it is
associated with a higher mortality from septic shock (9). Importantly, infectious agents that
include E. coli 0157:H7 and CMV (in immunocompromised patients) can produce a
histologic appearance that resembles ischemic colitis although their etiology remains
infectious inflammation.
Diagnosis:
Abdominal CT scan can support clinical suspicion, identify complications of ischemic
colitis, and help rule out colon cancer in up to 75% of cases (8). However, definitive
diagnosis of ischemic colitis is made by direct visualization of the bowel with biopsies to
confirm pathology. Colonoscopy must be performed carefully so as not to overdistend the
colon because high intaluminal pressures obstruct intestinal blood flow and can worsen
existing ischemic damage (1). Features that suggest ischemic colitis on colonoscopy include
a segmental distribution of disease, rectal sparing, and hemorrhagic nodules, which
represent bleeding into the mucosa and submucosa. The “colon single-stripe sign” is a
single line of erythema with erosions and ulcerations oriented along the longitudinal axis of
the colon (10). This finding corresponds to a 75% histopathologic yield and signifies a
milder course of disease than does a circumferential ulcer (10). Circumferential ulcers are
7
associated with higher rates of abdominal pain, higher baseline rates of CRP, and longer
periods of hospitalization (11). Infarction and ghost cells on pathology are pathognomonic
for ischemic colitis (12).
Histopathologic findings also give clues about the severity of injury. Mucosal and
submucosal hemorrhage and edema with or without partial necrosis and ulceration of the
mucosa indicate mild injury (1). Iron-laden macrophages, submucosal fibrosis, and
pseudomembranes suggest more severe injury and were present in our patient. Although
these findings are also found in C. difficile colitis (13), our patient tested negative for this
disease. Ultimately, she may be at risk of developing a stricture because her colonic lamina
propria showed early signs of fibrotic replacement.
Despite the diagnostic capabilities of colonoscopy, ischemia must be captured at the
right time in order for a definitive diagnosis to be made. It is recommended to perform this
procedure within 48 hours of symptom onset because the mucosal and submucosal surface
can normalize quickly in most cases.
When making a diagnosis of ischemic colitis, it is important to rule out other
possible diagnoses including infectious colitis, inflammatory bowel disease, diverticulitis,
diverticular colitis, and colon carcinoma. The work up should include stool cultures, ova,
and parasites and C. difficile toxin. C. difficile rarely causes bloody stools, but it should be
suspected in hospitalized patients with recent antibiotic use, high total white blood cell
counts, and thickening of the colon on CT scan. Increased serum lactate, LDH, elevated
white blood cell counts, and metabolic acidosis indicate advanced tissue damage or
infarction. Endoscopic features of diverticular colitis range from submucosal hemorrhages
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(peridiverticular red spots referred to as “Fawaz spots”) to chronic active inflammation
resembling inflammatory bowel disease that spares the rectum and terminal ileum.
Treatment:
In the absence of infarction or perforation, the treatment for ischemic colitis is
mainly supportive. Bowel rest and intravenous fluids are standard therapy. Surgery is
reserved for those who have failed medical treatment, have persistent symptoms, or have
sustained complications (i.e. infarction, hemorrhage, strictures, or fulminant colitis).
Intraperitoneal fluid on CT scan, absence of bleeding per rectum suggesting right-sided
ischemic colitis, and renal dysfunction indicate more severe disease and are predictive of
surgical intervention (14,15).
Role of Antibiotics:
Antibiotics are thought to protect against bacterial translocation from the loss of
mucosal integrity. Some experimental studies demonstrate that they reduce the extent and
severity of bowel damage (16,17). However, it is difficult to conduct therapeutic trials
because the prognosis of this disease is good in most cases and large patient sample sizes
are required to show just a modest effect. Some current guidelines recommend empiric
broad-spectrum antibiotics for moderate to severe cases of ischemic colitis. However, a
recent systematic review on this issue found a lack of evidence-based trials to support
antibiotic treatment (18).
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Prognosis
In over >50% of cases , symptoms of ischemic colitis resolve within 48 hours of
conservative measures. However, the colon can take up to two weeks or more to fully heal.
Symptoms that persist longer than two weeks are associated with a poor outcome with a
higher number of complications and irreversible disease. These patients are immediate
candidates for surgical bowel resection.
BACK TO THE CASE:
Three days into her admission, the patient’s symptoms were resolving and she had
no evidence of residual gastrointestinal bleeding. Her hemoglobin returned to baseline
(128 g/L) and she was discharged home uneventfully with outpatient gastroenterology
follow up.
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Redan JA, Rush BF Jr, Lysz TW, Smith S, Machiedo GW. Organ distribution of gutderived bacteria caused by bowel manipulation or ischemia. Am. J. Surg. 1990
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12
Figure 1:
Figure 1A: normal vascular pattern of
mucosa (unaffected section)
Figure 1B: pale, edematous colonic
mucosa with absent vascular pattern and
overlying white exudate in a
segmental distribution.
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Figure 1C: complete loss of vascular
pattern, friable mucosa as indicated by
erythema, edema and granularity
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Table 1: Causes of Ischemic Colitis
Causes of Ischemic Colitis
Thrombophilia
Medications
Mechanical Obstruction
Small Vessel Disease
Other

Inherited: APC resistance, Factor V Leiden deficiency

Acquired: antiphospholipid antibody

Cocaine

Digoxin

Pseudoephedrine

Amphetamines

Sumatriptan

Alosetron

Colon cancer

Fecal impaction

Diabetes, hypertension, hypercholesterolemia

Vasculitis

Long-distance running, extreme physical exertion
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