Colonic perforation in collagenous colitis: an unusual complication

Collagenous colitis is generally regarded as a benign disease with few serious complications. We report two women with collagenous colitis who presented with colonic perforation, one spontaneously and one 7 days after a barium enema, and a review of the literature. Including the present cases, 13 patients with collagenous colitis and colonic perforation have been reported, in two patients spontaneously and in 11 patients after a colonoscopy or barium enema. All were operated on except one patient who recovered after medical treatment. The pathogenesis of this complication is unknown. We propose that there might be a connection between mucosal tears and colonic perforation in collagenous colitis.     

Colonic complications in renal transplant recipients

Complications involving the colon occurred in 28 of 325 patients who received renal transplants. Pseudomembranous colitis, the most common complication, affected 15 patients, two of whom required surgery. Three instances of diverticulitis were complicated by free perforation in two cases, and by colovesical fistula in one. Appendicitis occurred in two cases. The other complications were hemorrhage (from diverticulosis or angiodysplasia), nonspecific colitis, and ischemic colitis. Spontaneous colonic perforation did not occur. Two thirds of the colonic complications occurred within 30 days after transplantation. All cases of colon perforation, however, occurred later than one month after transplantation. It is concluded that pseudomembranous colitis is the most common colonic complication in renal transplant recipients, that it usually occurs early, and that it carries a good prognosis. Colonic perforations occurred later in this series and were treated successfully. All cases of ischemic colitis were part of terminal multiorgan system failure.     

Colonic mucosal tears in collagenous colitis

In general, the colonic mucosa is macroscopically normal in collagenous colitis, although minor, non-specific abnormalities may be found. Significant endoscopic abnormalities, "mucosal tears" representing longitudinal mucosal lacerations, have been reported in a few patients with collagenous colitis. We report the cases of three women with collagenous colitis and mucosal tears detected at the index colonoscopy in order to illustrate the endoscopic characteristics and review the literature. Including the present cases, a total of 12 patients with mucosal tears and collagenous colitis have been reported. In 10 patients, the mucosal lacerations involved the ascending or the transverse colon. Three of the 12 patients had a colonic perforation immediately after the colonoscopy. The colonoscopist should be aware that the risk of perforation is likely to be increased when mucosal tears are present.     

Colonic mucosal tears in collagenous colitis

In general, the colonic mucosa is macroscopically normal in collagenous colitis, although minor, non-specific abnormalities may be found. Significant endoscopic abnormalities, “mucosal tears” representing longitudinal mucosal lacerations, have been reported in a few patients with collagenous colitis. We report the cases of three women with collagenous colitis and mucosal tears detected at the index colonoscopy in order to illustrate the endoscopic characteristics and review the literature. Including the present cases, a total of 12 patients with mucosal tears and collagenous colitis have been reported. In 10 patients, the mucosal lacerations involved the ascending or the transverse colon. Three of the 12 patients had a colonic perforation immediately after the colonoscopy. The colonoscopist should be aware that the risk of perforation is likely to be increased when mucosal tears are present.     

Perforation of the colon in unsuspected amebic colitis: Report of two cases

Two cases of amebic colitis that resulted in perforation of the colon, an ominous complication, are presented. The first was diagnosed preoperatively as acute ulcerative colitis with toxic megacolon, and the second as peritonitis complicating acute cholecystitis. In both instances the correct diagnosis was made after operation. The first patient recovered after colectomy and antiamebic therapy, but the second patient died in the early postoperative period, in septic shock. Amebic colitis occurs infrequently in the United States, and the diagnosis is rarely considered. In most cases an initial diagnosis of ulcerative or granulomatous colitis is made and the true diagnosis is recognized only after operation for colonic perforation or hepatic abscess. It is suggested that amebic colitis should be considered more frequently in cases of patients who have diarrhea. Stool examination for ova and parasites is often negative in amebic colitis. The IHA is usually positive in emebiasis, and should be performed early in casesof patients who have bloody diarrhea or other clinical symptons when amebiasis is suspected. Rectal biopsy is also a useful diagnostic approach, but failed to reveal amebae in one of our cases. Finally, it is suggested that operation be performed urgently when fulminating amebic colitis is not reversed by antiamebic therapy, when peritonitis occurs even with antiamebic treatment in progess, and for colonic perforation or toxic megacolon even when antiamebic therapy has not been indicated.     

Non-steroidal anti-inflammatory drug-induced colitis

Non-steroidal anti-inflammatory drugs (NSAIDs) may adversely affect the colon, either by causing a non-specific colitis or by exacerbating a preexisting colonic disease. Patients with NSAID-induced colitis present with bloody diarrhoea, weight loss, iron deficiency anaemia and sometimes abdominal pain. Colonoscopy may be normal or may show inflammation, ulceration or diaphragm-like stricture. Histology often concludes to nonspecific colitis. NSAIDs may cause perforation or bleeding of colonic diverticula, may cause relapse to inflammatory bowel disease and may exacerbate bleeding of colonic angiodysplasia. Pathogenesis of NSAID-induced colitis is still controversial. Local and/or systemic effects of NSAIDs on mucosal cells might lead to an increased intestinal permeability, which is a prerequisite for colitis. Treatment of NSAID-induced colitis should be to discontinue the drug, or at least, to reduce the dose as much as possible. Sulphasalazine and Metronidazole have been successfully used in few studies. Surgery is often indicated in case of life threatening complications or untractable symptoms.     

Listeria monocytogenes in the Colon in a Case of Fulminant Ulcerative Colitis

A case of ulcerative colitis in which the presence of Listeria monocytogenes was confirmed in the resected colon with polymerase chain reaction and subsequent Southern blot analysis and immunohistochemistry using antibody against Listeria is presented. The patient developed ulcerative colitis at the age of 59 years. Prednisolone, 50 mg/day, was given for severe ulcerative colitis. Later the disease became fulminating, indicating colectomy 4 months after the onset. Multiple sealed colonic perforations were observed. Numerous L. monocytogenes were found at the site of perforation, in fissures, and in cracks in the submucosa. This case indicates the possibility that L. monocytogenes contributes to the exacerbation of colitis to fulminating and colonic perforation.     

Colonic malacoplakia and ulcerative colitis: report of a case

Malacoplakia is a form of chronic granulomatous inflammatory reaction that rarely affects the digestive tract and has exceptionally been reported in association with ulcerative colitis. We report a new case in a 58-year-old woman suffering from ulcerative colitis. As colitis worsened, the patient received systemic steroid therapy but symptoms did not improve. As colonic perforation was suspected, a sub-total colectomy was performed. Histopathological study revealed a diffuse infiltration of the colonic mucosa by sheets of large macrophages with eosinophilic granular cytoplasm and characteristic cytoplasmic inclusions (Michaelis-Gutmann bodies) together with active and chronic lesions of ulcerative colitis. Malacoplakia gradually disappeared under antibiotics and did not recur whereas ulcerative colitis remained active. In our case, as in three similar published cases associated with ulcerative colitis or Crohn's disease, malacoplakia was probably triggered by steroid therapy and was not clinically suspected. This particular and potentially severe inflammation must be recognized and treated in order to prevent worsening of the associated bowel disease.     

Spontaneous Rupture of the Spleen

Crohn's disease is associated with many local complications. Spontaneous rupture of the spleen secondary to Crohn's colitis with a fistulous tract into the adjacent fixed spleen has never been reported in the literature. A case report and a brief review of spontaneous splenic rupture and colonic perforation in Crohn's disease is presented.     

Fulminant amebic colitis in an HIV-infected homosexual man

We present a case of fulminant amebic colitis in a human immunodeficiency virus (HIV)-infected homosexual man. The patient developed colonic perforation over a short time despite empirical therapy with metronidazole, and underwent right hemicolectomy. Amebic colitis was pathologically diagnosed by identifying invasive trophozoites of Entamoeba in a surgical specimen. Amebic colitis is one of the important differential diagnoses of acute abdomen in HIV-infected patients and/or homosexual men, especially in East Asia. Although fulminant amebic colitis is a rare manifestation of amebiasis, early diagnosis and treatment are thought to be important to improve the outcome of this highly fatal complication.     

Acute cytomegalovirus colitis presenting during primary HIV infection: an unusual case of an immune reconstitution inflammatory syndrome.

Severe ulcerous cytomegalovirus pancolitis developed during primary human immunodeficiency virus (HIV) infection in a patient who underwent early combination antiretroviral treatment. This massive inflammatory process led to acute colon perforation. Serological testing demonstrated cytomegalovirus reactivation. Severe immunosuppression caused by primary HIV infection resulted in cytomegalovirus colitis, and initiation of early combination antiretroviral therapy triggered an immune reconstitution inflammatory syndrome potentially leading to colonic perforation.     

Toxic megacolon: the knee-elbow position relieves bowel distension.

Toxic megacolon complicating inflammatory or infective colitis carries a high morbidity and mortality and surgical intervention is necessary in up to 80% of cases. Perforation complicates toxic megacolon in about 35% of cases. After perforation, the death rate nears 50%. Gaseous distension of the bowel causes considerable discomfort to the patient and increases transmural pressure. The latter is thought to cause a reduction in blood flow and may predispose to perforation. The use of instruments for colonic aspiration is discouraged, because of the high risk of perforation. The successful use of the knee-elbow position to relieve bowel distension in two patients with toxic megacolon is described.     

Diagnosis and management of ischemic colitis

The clinical presentation and outcome of ischemic colitis has a wide spectrum. Impaired perfusion of blood to the bowel from a variety of causes is the underlying pathophysiology. The presence of diarrhea, abdominal pain, and mild lower gastrointestinal bleeding should prompt consideration of ischemic colitis as a cause. Although many laboratory tests and radiographic images may suggest the diagnosis, endoscopic visualization of colonic mucosa with histologic analysis of biopsies is the gold standard for identification of colonic ischemia. Most cases are transient and resolve without any complications. Medical therapy for chronic ischemia has been anecdotally proven but not carefully studied. Complications of ischemic colitis can include bowel perforation, peritonitis, persistent bleeding, protein-losing colopathy, and symptomatic intestinal strictures. Thus, surgical resection of the affected segment should be considered early to minimize adverse outcomes. This review describes the etiology, pathophysiology, clinical features, diagnostic approach, and management of ischemic colitis.     

Intestinal complications of thrombotic microangiopathy in the adult. 4 cases and review of the literature

We report four cases of adult thrombotic microangiopathy associating diarrhea with severe ischemic colitis. In one case, the intestinal complications was severe and diffuse ischemic colitis, in two cases an inaugural colonic perforation requiring colectomy and in the last case a massive mesenteric infarct. In three cases, histologic examination showed vessel occlusion with microthrombi. Despite treatment with plasma exchange and plasma infusion, death ensued in two cases. Principally described in childhood thrombotic microangiopathy, intestinal complications occur exceptionally in adult thrombotic microangiopathy and are associated with a poor prognosis. Inaugural ischemic colitis revealing an adult thrombotic microangiopathy is also uncommon and thrombotic microangiopathy could be evoked in all patients presenting acute ischemic colitis.     

Colonoscopic perforations

Since its introduction into clinical medicine, flexible fiberoptic colonoscopy has had a great impact on diagnosis and management of diseases of the colon and rectum. There are three mechanisms responsible for colonoscopic perforation: specifically, mechanical perforation directly from the colonoscope or a biopsy forceps, barotrauma from overzealous air insufflation, and, finally, perforations that occur during therapeutic procedures. Perforation of the colon, which requires surgical intervention more frequently than bleeding, occurs in less than 1 percent of patients undergoing diagnostic colonoscopy and may be seen in up to 3 percent of patients undergoing therapeutic procedures such as polyp removal, dilation of strictures, or laser ablative procedures. Management of colonic perforation secondary to colonoscopy remains a controversial issue in that it can be effectively managed by operative and nonoperative measures. If a perforation does occur, signs and symptoms that the patient will experience will be related to both the size and site of the perforation, adequacy of the bowel preparation, amount of peritoneal soilage, underlying colonic pathology (where a thin walled colon from colitis or ischemia, for example, may result in a larger perforation than a healthy colon), and, finally, overall clinical condition of the patient. Radiology often establishes diagnosis. Plain films of the abdomen and an upright chest x-ray may reveal extravasated air confined to the bowel wall, free intraperitoneal air, retroperitoneal air, subcutaneous emphysema, or even a pneumothorax. A localized perforation may demonstrate lack of pneumoperitoneum. Some surgeons recommend surgery for all colonoscopic perforations; however, there does appear to be a role for conservative management in a select group of patients such as those with silent asymptomatic perforations and those with localized peritonitis without signs of sepsis that continue to improve clinically with conservative management. Finally, conservative management works well in those patients with postpolypectomy coagulation syndrome. Surgery is most definitely indicated in the presence of a large perforation demonstrated either colonoscopically or radiographically and in the setting of generalized peritonitis or ongoing sepsis. The presence of concomitant pathology at time of colonoscopic perforation such as a large sessile polyp likely to be a carcinoma, unremitting colitis, or perforation proximal to a nearly obstructing distal colonic lesion may force immediate surgery. Finally, in the patient who deteriorates with conservative management, one should proceed to surgery.     

Complications of collagenous colitis

Microscopic forms of colitis have been described, including collagenous colitis. This disorder generally has an apparently benign clinical course. However, a number of gastric and intestinal complications, possibly coincidental, may develop with collagenous colitis. Distinctive inflammatory disorders of the gastric mucosa have been described, including lymphocytic gastritis and collagenous gastritis. Celiac disease and collagenous sprue （or collagenous enteritis） may occur. Colonic ulceration has been associated with use of nonsteroidal anti-inflammatory drugs, while other forms of inflammatory bowel disease, including ulcerative colitis and Crohn＇s disease, may evolve from coUagenous colitis. Submucosal ＂dissection＂, colonic fractures or mucosal tears and perforation from air insufflation during colonoscopy may occur and has been hypothesized to be due to compromise of the colonic wall from submucosal collagen deposition. Similar changes may result from increased intraluminal pressure during barium enema contrast studies. Finally, malignant disorders have also been reported, including carcinoma and lymphoproliferative disease.     

Intravenous cyclosporine in attacks of ulcerative colitis

The present study reports the results of intravenous cyclosporine in 32 patients with refractory and/or severe attacks of ulcerative colitis (UC). Twenty of 32 patients responded to intravenous cyclosporine; cyclosporine was clinically effective and improved colonic lesions. However, one colonic perforation and one postoperative death were observed in two patients with severe endoscopic colitis who had failed to reach clinical remission with high-dose corticosteroids and cyclosporine. Moreover, after a median follow-up of 190 days, only one-third of the patients avoided colectomy. No predictive factor of response to cyclosporine was identified. This study confirms that cyclosporine is effective in severe UC but suggests that its use could be associated with serious complications in patients with severe lesions who had failed to settle with corticosteroids and cyclosporine.     

Isolated colonic ulcers: Diagnosis and management

Isolated ulcers of the large intestine are not associated with an underlying colitis and may be an incidental finding on screening colonoscopy or present with abdominal pain, hematochezia, chronic gastrointestinal bleeding, and rarely, perforation. A common cause of isolated colonic ulcers is the use of nonsteroidal anti-inflammatory drugs (NSAIDs), with ulcers in the cecum and right colon. Isolated rectal ulcers are caused by ischemia, solitary rectal ulcer syndrome (SRUS), radiation, or fecal impaction. Stercoral ulceration and nonspecific ulcers of the colon are rare but can cause colonic perforation. Infectious causes include tuberculosis and amebiasis. Histology is important to rule out malignancy but is not helpful for diagnosis except in SRUS and certain infections. The approach to isolated colonic ulceration includes biopsy of the ulcer and surrounding tissue, cessation of any NSAIDs, management of constipation, and recognition of the patient with SRUS. Inflammatory bowel disease should be ruled out in appropriate patients.     

PNEUMOMEDIASTINUM DURING RELAPSE OF ULCERATIVE COLITIS

Pneumomediastinum can be caused by gas dissecting along fascial tissue planes into the mediastinum from remote locations, including the retroperitoneum. One potential source of retroperitoneal gas is the colon. We present the third reported case of pneumomediastinum (plus pneumothorax and subeutaneous emphysema) without free intraperitoneal gas developing during an attack of ulcerative colitis. Because there was no colonic perforation noted at colectomy, the extracolonic gas was presumed to originate from a microscopic or partial thickness perforation of the colon. GI perforation must be considered not only in patients who have free intraperitoneal gas but also in those who present with symptoms, signs, or studies consistent with retroperitoneal gas, such as subcutaneous emphysema, pneumomediastinum, or pneumothorax.     

Ischaemic colitis and colorectal cancer: some problems and pitfalls

Four cases out of 204 new cases of colorectal carcinoma seen in a 24 month period were proven to have concomitant proximal ischaemic colitis. Ischaemic colitis associated with obstructing carcinoma of the colorectum may present dramatically with gangrene or colonic perforation if the acute vascular insufficiency is severe. Less severe degrees of ischaemic insult must be recognised intra-operatively as the incorporation of ischaemic colon in a colonic anastomosis may result in an anastomotic leak. Two other patients with ischaemic colitis were wrongly diagnosed as colorectal carcinoma on colonoscopy. Endoscopic features of ischaemic colitis may mimic colonic carcinoma and endoscopic biopsy is essential where any doubt exist as to the possibility of ischaemic colitis so that unnecessary surgery may be avoided.

---

Résumé 4 cas parmi 204 nouveaux cas de cancers colorectaux vus dans une période de 24 mois, montraient une colite ischémique proximale concomitante. La colite ischémique associée avec un cancer colorectal ischémique, peut se présenter dramatiquement avec gangrene et perforation colique si l'insuffisance vasculaire aigue est sévère. Les lésions moins sévères d'ischémie doivent être reconnues au cours de l'intervention car une anastomose colique sur un colon ischémique peut provoquer un lâchage anastomotique. Deux autres patients avec des colites ischémiques furent faussement diagnostiqués comme cancer colorectal à la coloscopie. Les aspects endoscopiques de la colite ischémique peuvent simuler le cancer colique et les biopsies endoscopiques sont essentielles si le moindre doute existe quant à la possibilité de colite ischémique afin qu'une chirurgie inutile soit évitée.