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(Radiology. 2000;214:513-516.)
© RSNA, 2000

Gastrointestinal Imaging

Isolated Infarction of the Cecum: CT Findings in Two Patients1

A. Michael Simon, MD, Bernard A. Birnbaum, MD and Jill E. Jacobs, MD

1 From the Department of Radiology, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104. Received February 24, 1999; revision requested April 28; revision received May 25; accepted August 23. Address reprint requests to B.A.B. (e-mail: birnbaum@rad.upenn.edu).


   Abstract
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 Abstract
Introduction
 Case Reports
 Discussion
 References
 
Colonic ischemia isolated to the cecum is a rare entity. The authors evaluated two patients who underwent computed tomography (CT) because appendicitis was suspected at clinical examination. CT findings were suggestive of isolated cecal ischemia or infarction. Surgical-histopathologic findings helped confirm the presumptive CT diagnoses. Isolated cecal infarction should be included in the differential diagnosis of acute right lower quadrant pain.

Index terms: Abdomen, CT, 70.12115 • Colon, abnormalities, 752.795 • Colon, infarction, 752.799 • Colon, ischemia, 752.799


   Introduction
TOP
 Abstract
 Introduction
Case Reports
 Discussion
 References
 
Acute colonic ischemia is the most common cause of colitis in the elderly population (1). In most patients, ischemia results from either a low-flow state or small vessel disease and tends to affect the colon in segmental fashion (2). The splenic flexure and rectosigmoid portions of the colon are most commonly affected. When severe, the entire large bowel may be diseased. Isolated involvement of the right side of the colon has been reported with increasing frequency, particularly in association with shock (3,4). In contrast to segmental or diffuse colonic ischemia, focal ischemia or infarction isolated to the cecum is a rare entity (5–7).

We recently encountered two patients with isolated cecal infarction in whom computed tomographic (CT) findings were used to prospectively suggest this diagnosis. The purpose of this report is to describe the CT findings of isolated cecal infarction, which, to the best of our knowledge, have not been previously described in the radiology literature.


   Case Reports
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 Abstract
 Introduction
 Case Reports
Discussion
 References
 
Case 1
A 65-year-old woman with a history of long-standing type II diabetes mellitus and hypertension presented at our emergency department complaining of approximately 12 hours of acute, progressive right lower quadrant pain. Physical examination results were notable for exquisite tenderness at the McBurney point and a slightly elevated body temperature of 37.2°C. Laboratory data revealed peripheral leukocytosis (15,900 white blood cells per cubic millimeter). Conventional radiography of the abdomen showed no evidence of obstruction, pneumoperitoneum, or calcified appendicolith. A clinical diagnosis of acute appendicitis was postulated, and a CT study was requested for diagnostic confirmation.

The patient underwent helical CT (HiSpeed Advantage; GE Medical Systems, Milwaukee, Wis) of the abdomen and pelvis, performed after intravenous and oral administration of iothalamate meglumine (Conray 60; Mallinckrodt Medical, St Louis, Mo) and diatrizoate meglumine (Gastroview; Mallinckrodt Medical), respectively. Prospective image acquisition was performed through the right lower quadrant by using 5-mm-thick sections. Helical pitch was 1:1 with contiguous section reconstruction (no overlapping images). CT demonstrated the presence of a mobile cecum arising from the pelvis, with associated circumferential cecal wall thickening and pneumatosis coli isolated to the cecal caput (Fig 1). A presumptive CT diagnosis of cecal infarction was established.



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  		Figure 1. Transverse contrast-enhanced CT scan demonstrates mild circumferential mural thickening of the cecum (arrows) with cecal pneumatosis coli.

 
Exploratory laparotomy with ileocolic resection was performed, and histopathologic examination revealed focal necrosis, hemorrhage, and ulceration, which were limited to the cecum. The adjacent ascending colon, appendix, and terminal ileum were normal. The final histopathologic diagnosis was isolated cecal ischemia complicated by infarction. The patient's postoperative course was uneventful.

Case 2
A 67-year-old obese woman with a history of hypertension, coronary artery disease, and insulin-dependent type II diabetes mellitus presented at our emergency department complaining of nausea, diarrhea, and 24 hours of epigastric and right upper quadrant pain. Physical examination results revealed mild to moderate epigastric tenderness. Laboratory values, including white blood cell count, liver function test results, and serum amylase and lipase levels were normal. Conventional radiography of the abdomen showed no evidence of intestinal obstruction or pneumoperitoneum. A nuclear medicine cholescintigraphic study showed no evidence of cholecystitis. The patient's symptoms improved with administration of aluminum hydroxide–magnesium hydroxide compound (Maalox; Rhône-Poulenc Rorer Pharmaceuticals, Collegeville, Pa) and simethicone, and she was discharged with a presumptive diagnosis of acute gastritis.

The patient returned to the emergency department the following day complaining of new periumbilical and right lower quadrant pain, anorexia, and mild diarrhea. She now had a low-grade fever of 38°C and peripheral leukocytosis (12,400 white blood cells per cubic millimeter). Physical examination results revealed moderate right lower quadrant tenderness without peritoneal signs. Repeat conventional radiographs of the abdomen were normal. The patient underwent helical CT of the abdomen and pelvis performed with intravenous and oral administration of iohexol (Omnipaque 300; Nycomed Amersham, Princeton, NJ) and diatrizoate meglumine, respectively. Prospective image acquisition was performed through the right lower quadrant by using 5-mm-thick sections. Helical pitch was 1:1 with contiguous data reconstruction. CT demonstrated circumferential mural thickening of the cecum, with a "target sign" enhancement pattern, mild pericecal inflammatory stranding, and a normal appendix (Fig 2). A presumptive diagnosis of focal cecal ischemia or inflammation was established.



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  		Figure 2. Transverse contrast-enhanced CT scan shows moderate circumferential thickening of the cecal wall with a target sign enhancement pattern (arrow). Mild pericecal inflammatory stranding (arrowheads) also is present.

 
The patient underwent exploratory laparotomy, and a right hemicolectomy was performed after intraoperative findings were interpreted as consistent with impending perforation of a cecal carcinoma. Histopathologic examination results revealed acute ischemic changes with transmural inflammation and serositis isolated to the cecum. No cecal neoplasm was identified. The patient's postoperative course was notable only for infection of a superficial wound. She was subsequently discharged in stable condition on postoperative day 12.


   Discussion
TOP
 Abstract
 Introduction
 Case Reports
 Discussion
References
 
Colonic ischemia is an important cause of morbidity in elderly patients. The causes of colonic ischemia can be classified in terms of occlusive and nonocclusive states (8). Occlusive factors include occlusion of a large artery, small artery disease, venous occlusion, and mechanical bowel obstruction. Large artery occlusion results from embolization, thrombosis, or vessel ligation. Small artery disease typically is seen in patients with diabetes mellitus or vasculitis or in patients who have previously undergone radiation therapy. Colonic ischemia may result from high-grade obstruction produced by distal neoplasms and sigmoid volvulus. It is rarely caused by venous outflow obstruction, as seen in patients with a hypercoagulable state, pancreatitis, or portal hypertension (8). Conversely, nonocclusive colonic ischemia is believed to be due to a low-flow state (eg, cardiogenic, septic, or neurogenic shock), which causes severe mesenteric vasoconstriction as the body diverts blood flow to vital organs in an attempt to maintain adequate systemic circulation. This degree of mesenteric vasoconstriction may also be caused by medications such as digitalis (9) and catecholamines (10). It is noteworthy that the overwhelming majority of patients with colonic ischemia have no evidence of major vessel occlusion, and ischemic colitis in these individuals usually is attributed to a low-flow state, small vessel disease, or both (2).

Isolated cecal infarction is a rare entity. It has been reported to occur spontaneously and in association with chronic heart disease (5), cardiopulmonary bypass surgery (6), systemic chemotherapy (7), cholesterol embolization (11,12), and aortitis syndrome (13). It has been postulated (5,13) that isolated cecal ischemia may occur because the ileocecal region is a "watershed area," similar to the splenic flexure and rectosigmoid colon. In an attempt to understand why the cecum may be vulnerable to ischemia, it is necessary to review the blood supply to the cecum, appendix, and adjacent intestinal segments.

The ascending colon receives its blood supply from the superior mesenteric artery via the right colic artery, middle colic artery, the colic branch of the ileocolic artery, and anastomoses between these vessels (14). The terminal ileum is supplied directly from the ileal branch of the ileocolic artery and anastomoses with vessels supplying adjacent small-bowel segments. The appendicular arteries may originate from the colic branch of the ileocolic artery, the ileocolic arcade, or the anterior or posterior cecal arteries; however, they most commonly arise from the ileal branch of the ileocolic artery, which may then communicate with ileal branches of the superior mesenteric artery (5,14).

In contrast to the potential dual blood supply serving the ileum, appendix, and ascending colon, the cecum is supplied by end arteries, which may render this bowel segment more susceptible to ischemia. This is the basis for the watershed theory proposed by Rist et al (5), who attempted to explain isolated cecal necrosis in three patients with compensated chronic heart disease. The cecum is supplied by the anterior and posterior cecal arteries, which are terminal branches of the ileocolic artery (5,14). These end arteries may arise from either the ileal or colic branch of the ileocolic artery or from an inconstant arcade that may form between these vessels (Fig 3). The presence of an ileocolic vascular arcade may play an important role in the prevention of cecal ischemia because it enables anastomoses to form with adjacent intestinal segments. If the anterior and posterior cecal arteries do not originate from a vascular arcade, the cecal blood supply may be relatively deficient in comparison with that of the adjacent intestinal segments, which usually have a dual blood supply.



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  		Figure 3a. (a) Diagram illustrates the dual blood supply to the cecum. The anterior and posterior cecal arteries arise from a vascular arcade that bridges the ileal and colic branches of the ileocolic artery. In this anatomic setting, the vascular anastomosis may facilitate collateral blood flow to the cecum. (b) Diagram illustrates a single blood supply to the cecum. The anterior and posterior cecal arteries arise from the colic branch of the ileocolic artery. The absence of a vascular arcade makes the cecum more susceptible to ischemia. (Reprinted, with permission, from reference 14.)

 


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  		Figure 3b. (a) Diagram illustrates the dual blood supply to the cecum. The anterior and posterior cecal arteries arise from a vascular arcade that bridges the ileal and colic branches of the ileocolic artery. In this anatomic setting, the vascular anastomosis may facilitate collateral blood flow to the cecum. (b) Diagram illustrates a single blood supply to the cecum. The anterior and posterior cecal arteries arise from the colic branch of the ileocolic artery. The absence of a vascular arcade makes the cecum more susceptible to ischemia. (Reprinted, with permission, from reference 14.)

 
Another anatomic factor that may make the cecum vulnerable to ischemia is the length of its vasa recta end arteries. The vasa recta supplying the colon are longer on the right side of the colon than on the left and are longest in the cecum because this segment of bowel has the widest diameter of the large intestine (4). Moreover, Stewart and Rankin (15) demonstrated that the vasa recta share minimal collateral vessel flow between them. The presence of long vasa recta with poor collateral vessel flow between them may further predispose the cecum to ischemia in patients whose cecal arteries do not originate from a vascular arcade. In addition to predisposing the cecum to nonocclusive ischemia, the end artery anatomy and poor collateral vessel flow may put the cecum at risk for embolic infarction. Atheromatous emboli are a known cause of isolated cecal infarction (11,12).

Like most cases of colonic ischemia, the exact precipitating event in our two cases of isolated cecal infarction remains unclear. Because both patients had diabetes, small vessel disease may have been a contributing factor. Chronic arteriosclerotic heart disease was documented in the second patient, but there was no evidence of arrhythmia or decompensated heart failure. Weakly positive results from an antiphospholipid antibody assay were obtained in this patient, which raised the possibility that she may have had a hypercoagulable state. Histopathologic specimens in both patients showed no evidence of atheromatous embolization. Neither patient underwent preoperative angiography; therefore, we are uncertain whether they had vascular anatomic structures that may have predisposed them to watershed infarction of the cecum.

The CT findings of bowel ischemia include circumferential bowel wall thickening, thumbprinting, intramural hemorrhage, focal or diffuse bowel dilatation, mesenteric arterial thrombus, engorged mesentery, pneumatosis intestinalis, portal or mesenteric venous gas, and pneumoperitoneum (16–18). Circumferential bowel wall thickening is the most sensitive finding, but it is nonspecific. Air in the mesenteric vessels, especially when associated with intramural air, is the most specific CT sign of bowel ischemia (18).

Both of these patients demonstrated CT evidence of circumferential mural thickening of the cecum. Pneumatosis coli isolated to the cecal caput was identified in the first patient, and this was strongly suggestive of a diagnosis of cecal ischemia or infarction. Identification of cecal pneumatosis was straightforward in this patient because intramural air was present in a circumferential pattern. Recognition of right-sided pneumatosis may sometimes be difficult, because an admixture of fecal contents may occasionally produce a pseudopneumatosis appearance of the cecum and ascending colon. A mural stratification pattern consisting of a target sign in the cecum was present in the second patient. This finding is nonspecific and reflects the presence of submucosal edema in the bowel wall. In the clinical setting of acute right lower quadrant pain, the differential diagnosis for cecal wall thickening with a target sign includes cecal ischemia, cecal diverticulitis, cecal infection, neutropenic cecitis, Crohn disease, and appendicitis with secondary inflammation of the cecum.

In summary, isolated cecal infarction is a rare entity that may have multiple causes. Cecal ischemia should be included in the differential diagnosis when a patient presents with acute right lower quadrant pain, particularly if the patient is elderly or has predisposing risk factors (eg, vasculitis, small vessel disease, or a hypercoagulable state). The diagnosis is strongly suggested if CT demonstrates cecal wall thickening with isolated pneumatosis coli. Radiologists should be aware of the entity of cecal infarction because they may be the first to alert the clinician to the presence of this unusual, potentially life-threatening cause of acute right lower quadrant pain.


   Footnotes
 
Author contributions: Guarantors of integrity of entire study, A.M.S., B.A.B., J.E.J.; study concepts and design, A.M.S., B.A.B.; definition of intellectual content, B.A.B.; literature research, A.M.S.; clinical studies, A.M.S., J.E.J.; data acquisition, A.M.S., J.E.J.; data analysis, A.M.S., B.A.B., J.E.J.; manuscript preparation, A.M.S., B.A.B.; manuscript editing and review, B.A.B., J.E.J.


   References
TOP
 Abstract
 Introduction
 Case Reports
 Discussion
 References
 

  1. Boley SJ. Colonic ischemia: 25 years later. Am J Gastroenterol 1990; 85:931-934.[Medline]
  2. Wolf EL. Ischemic disease of the gut. In: Gore RJ, Levine MS, Laufer I, eds. Textbook of gastrointestinal radiology. Philadelphia, Pa: Saunders, 1994; 2694-2706.
  3. Flynn TC, Rowlands BJ, Gilliland M, Ward RE, Fischer RP. Hypotension-induced post-traumatic necrosis of the right colon. Am J Surg 1983; 146:715-718.[Medline]
  4. Landrenau RJ, Fry WJ. The right colon as target organ of nonocclusive mesenteric ischemia. Arch Surg 1990; 125:591-594.[Abstract]
  5. Rist CB, Watts JC, Lucas RJ. Isolated ischemic necrosis of the cecum in patients with chronic heart disease. Dis Colon Rectum 1984; 27:548-551.[Medline]
  6. Hargrove WC, Rosato EF, Hicks RE, Mullen JL. Cecal necrosis after open-heart operation. Ann Surg 1978; 25:71-73.
  7. Kingry RL, Hobson RW, Muir RW. Cecal necrosis and perforation with systemic chemotherapy. Am Surg 1973; 39:129-133.[Medline]
  8. Bower TC. Ischemic colitis. Surg Clin North Am 1993; 73:1037-1053.[Medline]
  9. Gazes PC, Holmes CR, Moseley V, Pratt-Thomas HR. Acute hemorrhage and necrosis of the intestines associated with digitalization. Circulation 1961; 23:358-364.[Abstract/Free Full Text]
  10. Johnson TD, Berenson MM. Methamphetamine-induced ischemic colitis. J Clin Gastroenterol 1991; 13:687-689.[Medline]
  11. Chan T, Levine MS, Park Y. Cholesterol embolization as a cause of cecal infarct mimicking carcinoma. AJR Am J Roentgenol 1988; 150:1315-1316.[Free Full Text]
  12. Carnevale NJ, Delaney HM. Cholesterol embolization to the cecum with bowel infarction. Arch Surg 1973; 106:94-96.[Medline]
  13. Yamazaki T, Shirai Y, Tada T, Sasaki M, Sakai Y, Hatakeyama K. Ischemic colitis arising in watershed areas of the colonic blood supply. Surg Today 1997; 27:460-462.[Medline]
  14. Netter FH. Atlas of human anatomy Colacino S, ed. Summit, NJ: Ciba-Geigy, 1989; plates 291-293.
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