Gastroenterology
Volume 130, Issue 3 , Page 631, March 2006

Image of the Month:

David M. Warshauer, Section Editor

  • D.R. Gaya, MD (MRCP)

      Affiliations

    • Department of Gastroenterology, Glasgow Royal Infirmary, Glasgow, Scotland
  • ,
  • A.K. Foulis, MD (FRCPath)

      Affiliations

    • Department of Pathology, Glasgow Royal Infirmary, Glasgow, Scotland
  • ,
  • A.J. Morris, MD (FRCP)

      Affiliations

    • Department of Gastroenterology, Glasgow Royal Infirmary, Glasgow, Scotland

Article Outline

 

Question: A 74-year-old man was referred for investigation of anemia. He had a past history of ischemic heart disease, chronic renal failure (secondary to renovascular disease), and an abdominal aortic aneurysm (4.8-cm wide by 7-cm long). He denied any gastroenterological symptoms.

Clinical examination revealed borderline pyrexia and bruits over the femoral, renal, and carotid arteries bilaterally. Laboratory investigations revealed hemoglobin 8 g/dL (14–17.5), mean corpuscular volume 70 fL (80–96), erythrocyte sedimentation rate 66 mm/h (<20), urea 15 mmol/L (3–7), creatinine 240 μmol/L (<120), and C-reactive protein 81 mg/L (<10). Liver function tests were normal.

Upper GI endoscopy was unremarkable, including distal duodenal biopsies. Colonoscopy revealed multiple small areas of raised focal ulceration throughout the colon (Figure A). The terminal ileum was normal both macro- and microscopically. Initially, the diagnosis was thought to be colonic Crohn’s disease. However, this was refuted on histological analysis of biopsies from the ulcerated colonic lesions. What is the diagnosis?

Look on page 1022 for the answer and see the Gastroenterology website (http://www.gastrojournal.org) for more information on submitting your favorite image to Image of the Month.

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Answer to the Image of the Month Question (page 631): Cholesterol Embolization 

Colonic biopsy (Figure B) revealed focal ulceration (thin arrow) of the colonic mucosa. Deep to this, in the submucosa, is a small arteriole cuffed by inflammatory cells (thick arrow). The biopsy specimens revealed preserved colonic crypt architecture with no features to support a diagnosis of chronic inflammatory bowel disease. In the higher-power view of the vessels deep to the ulcer (Figure C), one of several arterioles filled by cholesterol crystals in this field is arrowed. The underlying diagnosis is thus cholesterol embolization.

Cholesterol embolization complicates severe atherosclerosis and is caused by embolization of fragments from unstable atheromatous plaques. It is an under-recognized phenomenon which may mimic a systemic vasculitis. It may be spontaneous (as in this case), but recognized risk factors are intra-arterial catheterization and thrombolytic and anticoagulant administration. Patients may present with fever, raised inflammatory indices, eosinophilia, livedo reticularis, and acute renal impairment. The gastrointestinal manifestations have received little attention in the medical literature, yet it would seem that the GI tract is the third most commonly affected organ in this condition. Common clinical presentations include abdominal pain, diarrhea and GI bleeding (secondary to mucosal ulceration), but bowel infarction and even pancreatitis have been reported.1 The diagnostic test is biopsy of an affected organ which reveals pathognomonic intra-arteriolar needle-shaped clefts where cholesterol crystals have dissolved out during processing. Prevention of this syndrome involves attention to vascular risk factors. In those with clinically apparent cholesterol embolization, a highly conservative approach avoiding anticoagulation, arterial instrumentation, and vascular surgery can produce a favorable outcome.2 Hydroxy-methyl-glutaryl coenzyme A reductase inhibitors (statins) may have a role in atheromatous plaque stabilization,3 but many patients will go on to require dialysis. Although still a relatively uncommon condition, the practicing gastroenterologist should remember cholesterol embolization as one cause of raised focal ulcers at endoscopy. It is likely that this condition will become more common due to the improved secondary preventative therapies in those with atherosclerosis (leading to increased survival of such patients), coupled with the increasingly invasive endovascular interventions performed by radiologists and cardiologists.

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References 

  1. Ben-Horin S , Bardan E , Barshack I , et al.   Cholesterol crystal embolization to the digestive system (characterization of a common yet overlooked presentation of atherothromboembolism) . Am J Gastroenterol . 2003;98:1471–1479
  2. Belenfant X , Meyrier A , Jacquot C . Supportive treatment improves survival in multivisceral cholesterol crystal embolism . Am J Kidney Dis . 1999;33:840–850
  3. DiNapoli M . Benefits of statins in cerebrovascular disease . Curr Opin Ivestig Drugs . 2004;5:295–305

 For submission instructions, please see the Gastroenterology website (http://www.gastrojournal.org).

PII: S0016-5085(06)00199-5

doi:10.1053/j.gastro.2005.04.041

Gastroenterology
Volume 130, Issue 3 , Page 631, March 2006