0
Special Feature |

Image of the Month—Diagnosis FREE

[+] Author Affiliations

Section Editor: E. Bredenberg Carl, MD

More Author Information
Arch Surg. 2009;144(11):1088. doi:10.1001/archsurg.2009.187-b.
Text Size: A A A
Published online

Computed tomography showed concentric bowel wall thickening with inflammatory changes from the midileum to the proximal transverse colon and patent major mesenteric vessels. Colonoscopy showed severe ulcerating inflammation of the distal ileum and proximal colon. A diagnosis of inflammatory bowel disease was made and conservative management was instituted. Failure to respond led to diagnostic laparotomy. This revealed an abruptly narrowed 60-cm segment of distal ileum confluent with the ascending and transverse colon, showing a thickened, woody appearance with nodularity and fibrin deposition on the serosa (Figure 2). The major mesenteric arteries were pulsatile. Resection with a primary ileocolic anastomosis was performed. Histological analysis showed mural ischemia and necrosis of the distal ileum and colon with organization and regeneration of the mucosa. Arterioles showed mild medial hypertrophy. Arterial or venous occlusion was not evident. Thrombophilia and vasculitis screen results were negative. A diagnosis of nonocclusive ischemia of distal ileum and proximal colon was made.

Place holder to copy figure label and caption
Figure 2.

Operative photograph.

Graphic Jump Location

Ischemic colitis1has a prognosis more favorable than that of its small-bowel counterpart.2It is typically a disease of elderly persons and can broadly be divided into arterial or venous and occlusive or nonocclusive types. Arterial-occlusive etiology includes luminal thrombosis on a background of mesenteric atherosclerosis with embolic disease from atrial fibrillation or following subendocardial myocardial infarction.3,4Other causes of occlusion include vasculitis, radiation end-arteritis, complications of abdominal aortic aneurysm, aortic dissection, hypercoagulable states, and strangulation of the mesentery.3,4Venous occlusion usually occurs with mesenteric venous thrombosis, strangulation, or severe venous stasis.3Transmural infarction inevitably occurs in occlusive ischemia. A sharp transition point is seen in arterial occlusion while a vaguer penumbra is seen with venous etiology.2Nonocclusive causes include hemodynamic shock, vascular spasm, venous congestion, and luminal distention.24The degree of hypoperfusion, length of segment affected, severity, and sequelae are variable and dependent on the severity, rapidity, and duration of the insult, resolution, chronicity, collateral circulation, comorbidities, and overall organ function.2,3Damage resulting from nonocclusive ischemia may be classified as mucosal, mural, or transmural.2,3Presentation typically involves sudden-onset colicky abdominal pain, vomiting, distention, and bloody diarrhea. Signs range from mild tenderness to generalized guarding and shock in the event of perforation and frank peritonitis.

Occlusive infarction has a 90% mortality, whereas nonocclusive disease carries a 10% mortality. In a study involving 150 patients with nonocclusive ischemia, 45% had reversible disease, 13% had ischemic stricture, and 19% had gangrene or perforation.3Nonocclusive ischemia is seen in cardiogenic, hemorrhagic, or septic shock and can be precipitated by drugs including cocaine, amphetamines, and vasopressors such as noradrenaline and digitalis. It usually affects the watershed territory of colonic perfusion at the splenic flexure and the distal sigmoid colorectal interface.3In mural ischemia, sequelae range from complete resolution to chronic ulceration and stricture formation. With transmural ischemia, infarction with perforation, peritonitis, and shock usually occur.2,3

The definitive diagnosis is usually made on the basis of macroscopic findings and is confirmed by histological analysis from colonoscopy or laparotomy, including an angiogram in conjunction with the sequence of events leading to the presentation.

Return to Quiz Case.

Correspondence:Dinesh N. Ratnapala, MB, ChB, Department of Surgery, Redcliffe Hospital, Locked Bag 1, Redcliffe, Queensland 4020, Australia (dineshbrisbane@yahoo.com).

Accepted for Publication:January 2, 2009.

Author Contributions:Study concept and design: Ratnapala and Lambrianides. Acquisition of data: Ratnapala. Analysis and interpretation of data: Ratnapala, Lisle, Munn, and Lambrianides. Drafting of the manuscript: Ratnapala and Lambrianides. Critical revision of the manuscript for important intellectual content: Ratnapala, Lisle, Munn, and Lambrianides.

Financial Disclosure:None reported.

Marston  APheils  MTThomas  MLMorson  BC Ischaemic colitis. Gut 1966;7 (1) 1- 15
PubMed
Bailey  RWBulkley  GBHamilton  SRMorris  JBSmith  GW Pathogenesis of nonocclusive ischemic colitis. Ann Surg 1986;203 (6) 590- 599
PubMed
Khan  ANMacDonald  SChandramohan  MBarker  C Colitis, ischemic. http://emedicine.medscape.com/article/366808-overview. Accessed March 6, 2008
Sreenarasimhaiah  J Diagnosis and management of intestinal ischaemic disorders. BMJ 2003;326 (7403) 1372- 1376

Figures

Place holder to copy figure label and caption
Figure 2.

Operative photograph.

Graphic Jump Location

Tables

References

Marston  APheils  MTThomas  MLMorson  BC Ischaemic colitis. Gut 1966;7 (1) 1- 15
PubMed
Bailey  RWBulkley  GBHamilton  SRMorris  JBSmith  GW Pathogenesis of nonocclusive ischemic colitis. Ann Surg 1986;203 (6) 590- 599
PubMed
Khan  ANMacDonald  SChandramohan  MBarker  C Colitis, ischemic. http://emedicine.medscape.com/article/366808-overview. Accessed March 6, 2008
Sreenarasimhaiah  J Diagnosis and management of intestinal ischaemic disorders. BMJ 2003;326 (7403) 1372- 1376

Correspondence

CME
Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).
Submit a Comment

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

See Also...
Articles Related By Topic
Related Topics
PubMed Articles