- Case report
- Open Access
- Open Peer Review
Phlegmonous colitis: another source of sepsis in cirrhotic patients?
© Holzer et al; licensee BioMed Central Ltd. 2009
- Received: 30 July 2009
- Accepted: 15 December 2009
- Published: 15 December 2009
The clinical relevance of phlegmonous colitis (PC), a rare autopsy finding in cirrhotic patients, is poorly documented. We postulated that PC might be a source of sepsis in patients with portal hypertensive colopathy (PHC).
We report three cirrhotic patients who were admitted with abdominal sepsis and who illustrate, to various degrees, the clinico-pathological sequence of colonic alterations associated with portal hypertension. Two cirrhotic patients with PHC developed gram-negative bacteraemia and quickly responded to intravenous antibiotics. Another cirrhotic patient underwent emergency colectomy for PC, and subsequently died from multiple organ failure. Histological alterations in the operative specimen included: a) mucosal ulcerations; b) disseminated micro-abscesses in the submucosa; and c) a severe vasculopathy leading to complete obliteration of submucosal blood vessels.
These data suggest that cirrhotic patients with PHC may progress towards PC, which, in turn, may be the cause for life-threatening sepsis.
- Portal Hypertension
- Cirrhotic Patient
- Spontaneous Bacterial Peritonitis
Portal hypertension diffusely affects the gastrointestinal tract, and the colon is no exception; however, portal hypertensive colopathy (PHC), which was initially described in the 1990s, is a poorly defined entity . Colonic alterations associated with liver cirrhosis include a combination of vascular ectasias, mucosal oedema, rectal varices, and hyperemia [2, 3]. It is estimated that vascular ectasias and rectal varices are present in up to 50% of cirrhotic patients; yet, the risk of clinically significant colonic bleeding in these patients was inferior to 6% in a prospective study with a 2-year follow-up period . Thus, despite the fact that colonic lesions are frequent in cirrhotic patients, and that the fundamental pathologic change is a vasculopathy, these hemodynamic alterations are probably not associated with significant risk of lower gastro intestinal (GI) bleeding.
Phlegmonous colitis (PC) was first recognized in 1975 as a source of bacteraemia in patients with end-stage liver disease . In 2009, PC remains almost exclusively an autopsy finding, and was actually detected post-mortem in 2.5% of patients with cirrhosis: thirteen autopsy cases showed some or all of the following clinico-pathologic characteristics: (1) preferential involvement of the cecum; (2) phlegmonous changes in the submucosa; and (3) bacterial infection [6, 7]. These results suggest that PC is a severe and specific complication of portal hypertension. We postulated that, in parallel with aggravating portal hypertension, PHC could progress towards PC and sepsis. We report herein three patients, who illustrate this sequence of events.
All three patients were admitted in our institution for abdominal pain and underwent a CT-scan evaluation, which demonstrated a colonic inflammation. We report herein the three patients in increasing order of septic complications. Additional file 1: Table S1 summarizes the results of various microbiologic analyses performed in these three patients.
Cirrhotic patients are particularly susceptible to bacterial infections and the origin of these microorganisms (most commonly Escherichia Coli, Enterococcus faecalis, Proteus mirabilis and Pseudomonas aeruginosa) is often the lower digestive tract. Most clinicians would concur that: 1) the colon is the source of bacteraemia in cases 1 and 2; and 2) bacterial translocation due to increased intestinal permeability is the most likely physiopathology mechanism involved. However, bacterial translocation has been mostly documented in small animals , and is actually rare in Child A (3%) and B (8%) patients. In summary, both patients developed abdominal pain and bacteraemia; blood cultures were positive for enteric microorganisms, the colon (predominantly on the right side) was abnormal with radiologic evidence of severe oedema or inflammation of the colon and no other possible source of sepsis was found (Additional file 1).
We hypothesized that PHC may progress towards PC. The latter condition, which requires a biopsy or a surgical specimen is rarely (if ever) documented ante mortem. Another fatal case of phlegmonous colitis has been recently reported in a cirrhotic patient receiving a combination of interferon and ribavirin for hepatitis C . We suspect that this entity goes often unrecognized, because the patients' poor condition precludes any surgical intervention. Interestingly, in case 3, the only positive culture was the presence of bacteria in ascites, and it is likely that, in the absence of an operative specimen, the final diagnosis would have been spontaneous bacterial peritonitis (SBP) due to intestinal translocation. We consider that this patient had infected ascites indeed, but bacterial peritonitis in that case was secondary to phlegmonous colitis.
The data presented here suggest that in some cirrhotic patients with portal hypertensive colopathy, phlegmonous colitis could be the origin of sepsis. The underlying mechanism is a worsening of vasculopathy leading to complete obliteration of submucosal blood vessels. Mucosal erosions secondarily appear and are responsible for disseminated micro-abscesses formation in the submucosa, which constitutes the probable source of gram-negative sepsis. PC and PHC are closely related as suggested by the fact that both conditions share similar histological features: specifically, vascular alterations described in PHC (dilated venules and vascular ectasias in the submucosa) are present in PC. By contrast, mucosal ulcerations and the presence of microabscesses are dominant features of PC, which are absent in PHC. In conclusion, the three cases presented herein suggest that portal hypertensive colopathy could sometimes progress towards phlegmonous colitis. Whilst portal hypertension-induced vascular changes are initially similar throughout the GI tract, the clinical manifestations are eventually dominated by bleeding for the upper GI, and sepsis for the colon.
PHC: portal hypertensive colopathy; GI: gastro intestinal; PC: phlegmonous colitis.
Consent forms signed by the patients' relatives are submitted separately
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- The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-230X/9/94/prepub
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