Giant sigmoid diverticulum: a case report

Giant sigmoid diverticulum: a case report

S208 Abstracts and ribavirin was initiated. The combination therapy was discontinued at eight weeks because of the onset of stomatitis (positive Her...

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S208

Abstracts

and ribavirin was initiated. The combination therapy was discontinued at eight weeks because of the onset of stomatitis (positive Herpes simplex virus) and a right–sided Bell’s Palsy. MRI showed mild enhancement of the right facial nerve consistent with Bell’s Palsy. She was treated with a course of Prednisone and her symptoms markedly improved. She has since elected not to further pursue anti–viral therapy at this time. Conclusion: We report on two patients who developed Bell’s Palsy following initiation of INF and ribavirin therapy for hepatitis C. The first patient was subsequently retreated with combination therapy without recurrence of the Bell’s palsy. The second case occurred in the setting of an HSV stomatitis infection. HSV has also been reported to be associated with Bell’s Palsy. These cases serve to underscore the need for further research into the interaction of immune–system activating agents and INF. Retreatment with INF and ribavirin can be accomplished following an episode of Bell’s Palsy.

635 HISTOPLASMOSIS CAUSING DUODENAL OBSTRUCTION AS THE INITIAL PRESENTATION OF ACQUIRED IMMUNODEFICIENCY SYNDROME Arthi Sanjeevi, M.D., Richard K. Gilroy, M.B.B.S.,F.R.A.C.P.*, Hemant K. Roy, M.D.,FACG and Susan Swindells, M.D. Dept. of Internal Medicine, University of Nebraska Medical Center, Omaha, NE; Div. of Gastroenterology & Hepatology, University of Nebraska Medical Center, Omaha, NE and Div. of Infectious Diseases, University of Nebraska Medical Center, Omaha, NE. Purpose: Histoplasmosis is a systemic infection which, in immunocompromised patients, may result in intestinal obstruction. The obstructing lesions mostly involve the ileocecal region. In HIV disease, lymphoma and mycobacterial infections are also common causes of intestinal obstruction. To our knowledge, we present the first case of histoplasmosis in a HIV– infected patient causing obstruction at the third part of the duodenum. A 29 –year– old Latino male from Mexico, presented with a 4 –week history of anorexia, regurgitation, and 20 lbs weight loss. Accompanying this he had progressive fevers, chills, night sweats and diarrhea. Three days following his initial presentation he developed intractable vomiting resulting in hypokalemia and dehydration requiring hospitalization. On examination he appeared cachectic, with generalized lymphadenopathy and abdominal examination revealed an ill– defined epigastric mass. Hematology displayed anemia with marked lymphopenia (0.2x 103/cmm) and HIV serology was positive. CD4⫹ T cell count was 54/cumm and HIV–1 PCR was ⬎ 750,000 copies/ml . CT scan displayed diffuse intra–abdominal adenopathy and a markedly dilated small bowel proximal to the ligament of Treitz. Limited enteroscopy with a pediatric colonoscope revealed an irregular sub–mucosal mass obstructing the 3rd part of the duodenum. Histology showed fungal organisms consistent with histoplasma capsulatum infection without evidence of lymphoma or mycobacteria. For nutrition and venting, a gastrojejunostomy tube was placed and the patient was started on oral itraconazole suspension through the tube. One month later, the feeding tube was removed in the face of established oral tolerance and the patient was started on antiretroviral therapy. Two years after the initial hospitalization, the patient is well with no recurrence of symptoms. He remains on antiretroviral therapy and suppressive itraconazole. This case represents the first report of histoplasmosis causing duodenal obstruction in a HIV–infected patient. It underscores the importance of considering this differential diagnosis in immunocompromised patients presenting with lymphadenopathy and intestinal obstruction.

636 RIGHT COLONIC ISCHEMIA: A COMPLICATION OF COLONOSCOPY Wichit Srikureja, M.D. and Stanley Condon, M.D.*. Gastroenterology, Jerry L. Pettis Veterans Memorial Medical Center, Loma Linda, CA.

AJG – Vol. 97, No. 9, Suppl., 2002

Purpose: A 75–year– old man was admitted prior to his polyp surveillance colonoscopy for intravenous heparinization. He has had a mitral valve replacement with a St. Jude valve and has been on chronic anticoagulation therapy. Other significant medical problems included coronary artery disease with prior coronary arterial bypass graft and left ventricular ischemic dysfunction with left ventricular ejection fraction of 20% He underwent colonoscopy forty– eight hours after admission. During colonoscopy, he developed transient hypotension of 87/42 mmHg. Hypotension rapidly resolved with resuscitation with intravenous saline. A four–millimeter sessile polyp was encountered and removed in the proximal transverse colon. The procedure was completed uneventfully. Four hours after the procedure, he began to have right–sided abdominal discomfort. Initial acute abdominal series did not reveal evidence of perforation. The abdominal pain intensified over the next twelve hours. Physical examination at this time revealed exquisite tenderness of the right lower quadrant area with mild focal guarding and no rebound tenderness. A follow up acute abdominal series revealed a moderately dilated cecum and proximal ascending colon up to eight centimeter. A repeat colonoscopy was done. Patches of hemorrhagic ulcerated mucosa covered with whitish exudates with focal area of necrosis was noted in the cecum and proximal ascending colon. Isolated colonic ischemia was diagnosed based on endoscopic appearances. The patient was started on broad–spectrum intravenous antibiotics and bowel rest. He recovered fully after one week. Isolated ischemia of the cecum and proximal ascending colon is an unusual entity. Ischemic colitis occurs in the susceptible individual and is due to a reduced blood flow to the affected area of the colon. The mechanism of cecal and proximal ascending colon ischemia in the patient described is believed to be an interplay between low–flow state from the transient hypotension, underlying chronic ischemic left ventricular dysfunction, and proximal right colonic distension during colonoscopic procedure. Right lower quadrant pain, fever, and leukocytosis are usually the presenting symptoms. Management of colonic ischemia is with broad antibiotics coverage and bowel rest. If signs of peritonitis or perforation develop, surgical resection may be necessary. Isolated cecal and proximal ascending colon ischemia is a rare complication following colonoscopy. 637 GIANT SIGMOID DIVERTICULUM: A CASE REPORT Bakul Patel, M.D., Farooque Ahmed, M.D., Nalini Parikh, M.D., Joseph DePasquale, M.D.* and Robert Spira, M.D. Division of Gastroenterology, Seton Hall University School of Graduate Medical Education,South Orange,NJ; St Michael’s Medical Center, Newark, NJ. Introduction: Diverticulosis of the colon is common, Giant Colonic Diverticulum (GCD) is a rare finding that presents with different symptoms and sizes. GCD has been described radiographically and histologically, however endoscopic imaging is rare. We present the clinical, radiographic, and endoscopic findings of a GCD. Case Report: 72 year old female presents with increasing abdominal discomfort with distension, decreased appetite, and weakness. Vitals: T–97.3; P–76; R–18; BP– 80/50. Abdomen was soft, distended with mild tenderness. No guarding or rigidity and bowel sounds present. Percussion revealed a tympanic note. X–ray: large air filled structure (26cm) in the mid abdomen extending into the pelvis. No free intraperitoneal air. CT scan: large air filled structure with minimal fluid level in the mid abdomen which appears to be connected to the sigmoid colon. Cannot exclude sigmoid volvulus. Lab: WBC– 38.2; Hb–7.7; Hct–23; Plt–751; 7 Bands 21%. Differential diagnosis included Sigmoid volvulus, duplication cyst, giant diverticulum, abscess collection. Colonoscopy for decompression of possible volvulus revealed a narrowed area at recto–sigmoid region which opened into a large cavity. Lining appeared black and necrotic consistent with a possible sigmoid volvulus with vascular compromise. Exploratory lap done with left hemi– colectomy and Hartmann’s pouch done with drainage of the abdominal abscess. Intraoperative findings include loculated peritonitis and large abscess arising from a perforated diverticulum. Pathology specimens revealed fibrotic and granulation tissue lining the wall of the large cavity.

AJG – September, Suppl., 2002

Discussion: GCD is relatively rare with only 103 cases reported since the first case was reported in 1946. Case reports describe the entity in age groups ranging from 38 to 78 with sizes ranging from 6cm to 29cm. GCD commonly occurs in the sigmoid colon, involving the anti–mesenteric border, and is found in the setting of concomitant diverticular disease of the colon. The usual histology reveals dense fibrotic tissue along with a chronic inflammatory cell infiltrate in contrast to a duplication cyst where the walls would be lined with smooth muscle. Previously one other report provides an endoscopic description of the inside of a GCD as fibrotic in appearance. The management of GCD is clear and involves surgical resection of the diseased segment along with anastomosis. 638 LABETALOL–INDUCED FULMINANT HEPATIC FAILURE TREATED SUCCESSFULLY WITH LIVER TRANSPLANTATION Srinivasa Ayinala, M.D., Bradley Rubery, M.D., Maher Azzouz, M.D.* and Shirley Donelson, M.D. Division of Digestive Diseases, University of Mississippi Medical Center, Jackson, MS. Purpose: Labetalol is associated with mild reversible hepatotoxicity manifesting as aminotransferase elevation or cholestasis. Limited data is available in the literature that reports serious hepatotoxicity with high fatality rates (27%). The labetalol drug label was changed in 1988 to include the potential for serious hepatotoxicity. The outcome of previous case reports included recovery with prolonged hospitalization or death, in one case death occurred after liver transplantation. We report a case of labetalol– induced fulminant hepatic failure that was successfully treated via liver transplantation. A 51 y o hypertensive f presented with jaundice, malaise, nausea and RUQ abdominal pain. She was started on labetalol 100 mg tid and HCTZ 25 mg qd 3 months prior to presentation. Labs included ALT 1102 U/L, AST 757 U/L and T.Bili 7.0 mg/dl. Drug induced hepatitis was suspected and above medications were discontinued. Patient resumed labetalol therapy and presented one month later with jaundice, pruritis and nausea. Labs tests included prothrombin time 23 sec, AST 5753 U/L, ALT 4026 U/L, T.Bili 24 mg/dl and alfa–fetoprotein 75.6 ng/ml. Repeat viral serology and autoimmune markers were negative. Patient had persistent coagulopathy and jaundice. Liver biopsy revealed lobular hepatocyte necrosis (30 – 40%) with porto–portal and porto– central bridging necrosis, lymphocytic infiltrate, severe canalicular cholestasis with moderate regenerative changes and mild bile duct proliferation consistent with severe hepatocellular injury. After two weeks, she developed hepatic encephalopathy, ascites and renal dysfunction. Orthotopic liver transplantation was performed and her recovery was uneventful, She was in good condition at one month follow– up. We believe that this case of fulminant liver failure was due to labetalol since patient was not taking any other hepatotoxic agents and did not consume alcohol. Discussion: Labetalol induced liver failure is very rare, especially considering the common use of this drug. .The mechanism of liver injury associated with labetalol is unclear. The proposed mechanism of hepatic injury is a metabolic idiosyncratic reaction in susceptible patients. Although, an immune hypersensitivity pathology could also be considered. In conclusion Labetalol and other hepatotoxic drugs should be monitored carefully when liver injury is suspected as there is risk of fulminant hepatic failure. 639 GASTRIC ISCHEMIA FROM CHOLESTEROL CRYSTAL EMBOLIZATION: A CASE REPORT Eugene Y. Lee, M.D., Douglas F. Meyer, M.D., Charles M. Noyer, M.D., Panna S. Mahadevia, M.D. and Lawrence J. Brandt, M.D., M.A.C.G.*. Medicine, Division of Gastroenterology, Montefiore Medical Center, Bronx, NY and Pathology, Montefiore Medical Center, Bronx, NY. Intro: Cholesterol crystal embolization (CCE) has been recognized as a complication of atherosclerotic plaques. Ischemia of gastric arterioles from

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CCE, however, is uncommon due to the rich collateral circulation of the stomach; clinical manifestations of CCE–induced gastric ischemia are even more unusual. Case: We report an 80 yo male with hypertension, hypercholesterolemia, and coronary atherosclerotic disease who presented with chest pain and epigastric pain with nausea and non– bilious vomiting. Vital signs were normal. The abdomen was flat with normoactive bowel sounds, and was markedly tender in the epigastrium. There was no rebound, guarding, or abdominal masses. Stool was negative for occult blood. Lab data were significant for a hct of 37%, an elevated BUN of 22 mg/dL, and creatinine of 2.1 mg/dL. CT scan showed a thick–walled stomach with a focus of extra–luminal air in the porta hepatis. Cefoxitin 2 gm IV q8 hrs. and pantoprazole 40 mg IV q12 hrs were begun. UGI series showed a markedly narrowed gastric body and antrum with no obstruction or leakage of contrast. On EGD, purplish, thickened folds with foci of exudative, necrotic–appearing mucosa resembling malignancy were seen in the gastric body and fundus. Multiple biopsies showed extensive ulceration without malignancy. Repeat EGD three days later revealed less exudation and discoloration with EUS showing thickening of the first three layers of the wall in the gastric body and fundus. Biopsies showed gastric ischemia associated with CCE (figure EUS, path). Symptoms resolved without specific therapy.