body, most notably on the trunk and upper thighs. The rest of the physicalexam was within normal limits.Upper endoscopy showed non-erosivegastritis and multiple 2–3 mm erosions with surrounding erythema in themid and distal esophagus. A pinch biopsy of the esophageal lesions resultedin a 2 x 2 cm sloughing of the mucosa, consistent with an esophagealNikolsky’s sign. There was no bleeding. Pathology revealed a normalepithelial mucosa.Conclusion: Esophageal involvement in bullous pemphigoid is rare. Thetypical findings of sloughing epithelium and esophageal casts were notpresent in this case.We postulate that the classical endoscopic findings ofbullous pemphigoid may not always be present, even though esophagealinvolvment is suspected based on clinical presentation. The demonstrationof an esophageal Nikolsky’s sign via pinch biopsy can be used to confirmesophageal involvement in the absence of typical findings.

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SPLENIC HEMATOMA AS A COMPLICATION OFCOLONOSCOPY-A RARE CASEYashma Patel, M.D., Lakshmanasamy Somasundaram, M.D.,Anshuman Jyoti, M.D., Yatin R. Patel, M.D.,Raman M. Patel, M.D., FACG*. Lancaster, CA.

Splenic injury is an extremely rare complication of colonoscopy yet needsto be kept in mind to make a timely diagnosis. Review of the literature hasshown that approximately 27 cases have been reported. We present anothercase of splenic hematoma resulting from a routine colonoscopy. A 65year-old Caucasian female with a history of colon polyps presented for afollow up colonoscopy. The procedure went well and 2 benign polyps wereremoved from the sigmoid colon. After the procedure, in the recoveryroom, the patient had severe left sided chest pain radiating to the leftshoulder as well as pain on deep inspiration. Complete examination of thelungs and abdomen was carried out which was perfectly normal. She wastreated with IV Meperidine after which the pain subsided and she wasdischarged home on Hydrocodone plus acetaminophen. She presented tothe emergency room that evening because of similar symptoms. She did nothave abdominal pain, nausea, vomiting, fever, chills, or evidence of gas-trointestinal bleeding. The patient underwent thorough evaluation thatincluded physical examination, EKG, chest x-ray, x-ray of the left shoulderand complete blood count all of which were normal. She was advised tohave a CT scan of the abdomen but apparently she was unable to lie flat soshe refused at the time. The patient was discharged to home again onanalgesics and muscle relaxants. Two days later the patient presented foroutpatient follow-up. She was feeling fairly well, but physical exam re-vealed that there were decreased sounds at the left base and a pleural rub.There was also moderate tenderness in the left upper quadrant area. At thattime CT scan of the abdomen and pelvis were ordered and showed multiplelayered subcapsular hematoma involving the spleen. The patient was ad-mitted to the hospital and surgical evaluation was done.Because of thepersistent pain and dropping hematocrit, the patient underwent exploratorylaparotomy and splenectomy. Her postoperative course was unremarkable.Colonoscopy has become a routine and usually well-tolerated procedure inthe diagnosis of colorectal diseases. Complications of colonoscopy are rarebut can occur. The origin of this patients’ left sided pain involving thechest, shoulder, neck, and later the left upper quadrant tenderness, was dueto splenic injury. A high index of suspicion and awareness of all possiblecomplications is required in order to make a timely diagnosis and preventa possibly fatal outcome.

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ACUTE ON CHRONIC MESENTERIC ISCHEMIAYatin R. Patel, M.D., Yashma Patel, M.D.,Lakshmanasamy Somasundaram, M.D., Anshuman Jyoti, M.D.,Raman M. Patel, M.D., FACG*. High Desert Gastroenterology,Lancaster, CA.

We present a case of a patient who has chronic mesenteric ischemiaresponsible for recurrent abdominal pain, nausea, vomiting, diarrhea, andweight loss. She then had an acute ischemic episode, which led to thishospitalization and required surgery. A 74 year-old Caucasian female wasseen in my office on 4/19/99 complaining of recurrent abdominal pain,nausea, vomiting, and diarrhea for 2 weeks. She has had similar symptomsfor the past 5 years and a 25 lb. weight loss during the previous 2 years. In1998, she had presented with similar symptoms at which time she had anEGD, colonoscopy, and small bowel follow thru that were essentiallynonrevealing. On physical examination a mildly cachectic elderly womanin no apparent distress was seen. Her abdominal examination revealedtenderness in the right lower quadrant. The rest of the examination wasnormal. CBC, chemistry panel, and an ultrasound were all within normallimits. An EGD done on April 23, 1999 showed moderate erosive gastritis.At this time her symptoms had continued to worsen with several episodesof vomiting and diarrhea. On reevaluation she was found to have significanttenderness in the right lower quadrant with some guarding and bruit in themidepigastric area. WBC count was now 20,000/mm3. A CT scan showedthickening of the wall of the cecum and ascending colon. Because ofworsening of symptoms, more significant tenderness and the results of theCT scan, the patient was hospitalized for further management. The patientwas evaluated by a surgeon and underwent an abdominal aortogram and amesenteric angiogram on April 27, 1999, which showed complete obstruc-tion of the superior mesenteric artery, and 70% narrowing of the celiac axis.An attempt to do an angioplasty was unsuccessful. Subsequently on 4/30/99, she had an exploratory laparotomy and underwent a right hemicolec-tomy with revascularization of both arteries. Histopathology of a section ofthe bowel showed ischemic ulceration and edema. Post operatively she didwell. She has been followed till today and I happily report that all of herG.I. symptoms have resolved and she has gained back 30 lbs. of weight.The spectrum of ischemic bowel disease comprises of acute and chronicmesenteric ischemia and colon ischemia and includes arterial as well asvenous disorders. Mortality rates average 71% for the past 70 years.Diagnosis before intestinal infarction is the single most important factor toimprove these unfortunate results.

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AMEBIC COLITIS MIMICKING ULCERATIVE PANCOLITISDhanasekaran Ramasamy, M.D., K. Shiva Kumar, M.D.,Pratheba Chandra, M.D.*. Cleveland Clinic, Cleveland, OH; MayoClinic, Rochester, MN and Center for Digestive Diseases, Union, NJ.

Introduction: Entameba histolytica is distributed throughout the world andremains a health risk in many countries. Amebiasis is the second leadingcause of death from parasitic disease worldwide. Amebic colitis rarelypresents with contiguous mucosal inflammation mimicking ulcerative pan-colitis. We present a case of amebic pancolitis that was clinically andendoscopically indistinguishable from ulcerative colitis (UC).Case Report: A 57 year-old Indian male presented with a 2-week historyof hematochezia and rectal pain. Physical exam was unremarkable exceptfor tenderness on rectal exam. Lab studies were unremarkable except foranemia (Hb 11 gm/dl). Colonoscopy revealed mucosal friability, edema,erythema with extensive ulceration extending from the rectum to cecum.He was empirically started on mesalamine for presumed UC, pendingbiopsy results. Histology revealed moderately active acute and chronicinflammation with ulceration and Entameba trophozoites were noted onPAS staining. He was subsequently treated with metronidazole, resulting incomplete resolution of symptoms.Discussion: Although most patients infected with E. histolytica are asymp-tomatic, 4-10% develop invasive disease over a year. Common presentingsymptoms of amebic colitis are bloody diarrhea and abdominal pain.Complications are fulminant colitis, toxic megacolon, paralytic ileus, per-foration and obstructive symptoms secondary to amebomas. Invasion ofEntameba through the mucosa and into the submucosal tissues is thehallmark of amebic colitis. The pathologic spectrum encompasses mucosalthickening, discrete ulcers, diffusely inflamed and edematous mucosa, and

S215AJG – September, Suppl., 2003 Abstracts

necrosis and perforation of the intestinal wall. The diagnosis of amebiccolitis rests on the demonstration of E. histolytica in the stool or colonicmucosa. The mainstay of treatment remains metronidazole, followed by aluminal agent (paromomycin, iodoquinol, or diloxanide furoate) to eradi-cate colonization. Amebic colitis rarely presents with continuous mucosalinflammation, making it indistinguishable from UC. Since the erroneousdiagnosis of UC can lead to disastrous complications, it is imperative toexclude amebic colitis prior to undertaking steroid therapy, especially inpatients with a prior history of travel to or residence in areas endemic forE. histolytica. Our case illustrates the need for high index of suspicion inimmigrants and visitors from developing world for amebiasis in the dif-ferential diagnosis of pancolitis.

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NEW APPROACH IN THE MANAGEMENT OF PROXIMALLYMIGRATED STENT WITH AN OBSTRUCTING ANTI-REFLUXVALVESanjay Nayyar, M.D., Archana Verma, M.D., Benjamin T. Go, M.D.*,Gonzalo Pandolfi, M.D., Frida Abrahamian, M.D.,Bashar M. Attar, M.D. Cook County Hospital, Chicago, IL.

Esophageal cancers are usually diagnosed at a late stage requiring palliativetreatment. The use of self-expandable metallic stents (SEMS) have pro-duced impressive results in improving dysphagia. Even with the increasinguse of SEMS, there are still complications. The most important includeesophageal perforation, hemorrhage, stent migration and fistulization. Weare reporting a case of proximal migration of SEMS with an antirefluxvalve (ARV) causing complete occlusion and management. The patient isa 60 year-old male who was diagnosed 4 weeks prior with an unresectablesquamous carcinoma of the distal esophagus at another hospital. An esoph-ageal Z-stent with dua ARV was placed. Patient presented to our hospital2 weeks after placement with inability to handle his secretions. EGDperformed showed the stent located from 20 to 32 cm, with completeobstruction by the ARV. Attempts to remove the stent were unsuccessfuldue to siginificant inflammatory reaction at the proximal end of the stentbut distal to the UES. A needle knife sphincterotome was used to carefullycut through the ARV to allow the passage of an ERCP catheter into thestomach. The ARV was then removed by piecemeal fashion with snareelectrocautery to allow deployment of a second SEMS. The tumor extendedfrom 34 to 41 cm with the GE junction at 40 cm and was dilated with a 12mm balloon. A 14 cm Z-stent with ARV was deployed through the firststent with the proximal end at 27 cm and the distal end at 41 cm.Post-procedure gastrograffin showed ideal stent placement with passage ofcontrast into the stomach. Patient was discharged after 2 days withoutcomplications. While most stent migrations occur distally, they can rarelymigrate proximally and be complicated by the ARV. In cases where thestent cannot be removed endoscopically, removal of the ARV can be donewith a snare electrocautery to allow deployment of a second stent. Thesame technique can be utilized with a double channel scope to shorten anARV after SEMS deployment.

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GASTRIC NECROSIS: A COMPLICATION OF GASTRICBANDINGGerald Fruchter, M.D.*, Vlado Simko, M.D., Hatem Shoukeir, M.D.,Hueldine Webb, M.D., Ayse Aytaman, M.D. VA NY Harbor HCS,Brooklyn, NY.

Background: Morbid obesity is a growing health problem in the UnitedStates. Patients, who fail conservative measures at weight loss, are potentialcandidates for bariatric surgery. Current weight reduction surgery tech-niques include gastric restriction procedures, gastric bypass, and biliopan-creatic bypass. We report a rare, potentially lethal, complication of gastricbanding: gastric necrosis necessitating emergent laparotomy and gastrec-tomy.

Case Report: A 55 year-old male with history of morbid obesity presentedwith 5 days of epigastric pain, progressive dysphagia, and vomiting. He hadundergone a laparoscopic gastric banding 7 years prior with subsequentloss of 150lbs. Upon presentation, the patient was in no distress, weight187lbs with stable vital signs. Abdominal exam revealed a soft, non-distended abdomen with mild epigastric tenderness, no guarding or re-bound with a LUQ subcutaneous reservoir. The WBC was 9.2. CXR andabdominal films were unremarkable. Esophagogram showed marked con-striction at the level of the gastric band encircling the fundus with signif-icant hang-up of barium. On the second day of hospital stay, WBC rose to29.7; exam was unchanged. An abdominal CT scan was unrevealing exceptfor a left lung base infiltrate. Antibiotics were initiated. The following day,patient’s WBC rose to 35.2 with an unchanged exam. Upper endoscopyrevealed a distended proximal gastric pouch filled with coffee ground liquidand a large area of confluent ischemia covered by eschar as well as multiplesmall islands of ischemia. At surgery, there were multiple areas of necrosisin the serosal surface of the dilated fundus proximal to the strangulatingring as well as evidence of peritonitis. The stomach contained over 3 litersof sloughed gastric lining. A near total gastrectomy with roux-en-y gas-trojejunostomy was performed. Pathological exam revealed transmuralhemorrhagic necrosis of the fundus with marked thinning and impendingperforation. The patient had an uneventful post-op course.Discussion: Bariatric surgery is effective in treating morbid obesity. Forgastric banding, revision is occasionally needed to address gastric slippage,stenosis, as well as stomal obstruction. In our case, gastric banding inducedstrangulation with resultant full-thickness gastric necrosis and peritonitis.Clinicians involved in management of patients who undergo bariatricsurgery need to be aware of the potentially serious consequences inherentin this form of surgery.

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SUPRAGLOTTIC LARYNGEAL STENOSIS-A RAREEXTRAESOPHAGEAL MANIFESTATION OF GERDSailaja M. Cheruku, M.D., John O’Brien, M.D.*, Carl Malone, M.D.Southern Illinois University School of Medicine, Springfield, IL.

A 60 year-old caucasian female admitted to hospital for progressive, severeshortness of breath, over the past 2–3 weeks. She was sleeping upright ina chair secondary to orthopnea. She has no history of recent fever or acuteillness. Past medical history included chronic heart burn, hypertension andobesity. She denied tobacco, alcohol and illicit drug use. She took over thecounter antacids for heart burn. On exam, she had audible inspiratorystridor and room air oxygen saturation was 80%. An urgent transnasalfiberoptic laryngoscopy showed inability to visualize true vocal cords anda large 23 cm mass along the right aryepiglottic fold extending back toposterior commissure completely obstructing the view of her glottis. Theimpression was supraglottic mass obstructing the air way. She underwentemergency tracheostomy and direct laryngoscopic biopsy of the mass.Histology showed severe inflammation with granulation tissue and noevidence of malignancy. Laboratory evaluation of anti nuclear antibody,anti neutrophil cytoplasmic antibody and angiotensin converting enzymelevels were normal. Her sedimentation rate was 22. A CT Scan of neckshowed normal appearance of true vocal cords and severe supraglotticstenosis. In consideration of acid reflux induced ulceration, an upperendoscopy was performed, which demonstrated a hiatal hernia, normalesophagus, stomach and duodenum. She was given Pantoprazole twicedaily and discharged home to follow up as out patient, as her post operativecourse was uneventful. Ten weeks after treatment with pantoprazole, shewas evaluated with videostroboscopy and fiberoptic nasopharyngolaryn-goscopy, which demonstrated significant decrease in supraglottic swellingand inflammation. She denied any episodes of acid reflux. Despite discus-sions regarding surgery for acid reflux, the patient declined surgery. She iscurrently taking once a day pantoprazole. The Plan is to do supraglotticlaryngectomy and removal of tracheostomy tube. Common otolaryngologicmanifestations of GERD include cough, sore throat, hoarseness, laryngitis,chronic sinusitis, vocal cord nodules, globus, subglottic stenosis and rarely

S216 Abstracts AJG – Vol. 98, No. 9, Suppl., 2003