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Intramural duodenal hematoma in acute pancreatitis
AJG – September, Suppl., 2002
After transfusion of 3 units of packer cells, upper endoscopy (EGD) and colonoscopy were carried out. Results: At EGD we found a fundal 3 cm submucosal ulcerated neoplasm, with neovascularization, biopsies were taken. Colonoscopy showed an essentially identical submucosal 1 cm ulcerated lesion at the hepatic flexure. There were no other bleeding lesions identified. Biopsies were taken. Histology showed evidence of a metastatic Merkel cell cancer, with positive immunoperoxidase staining for enolase, chomogranin, and synaptophysin. The patient was subsequently transferred to hospice. A search of the literature revealed only 2 cases of gastro– duodenal metastasis from Merkel cell tumor in the past 12 years, and no reported cases of colon metastasis. Conclusions: Gastroenterologists need to become aware that Merkel cells tumors are rare, but metastasize aggresively. These tumors, similarly to melanoma, can metastasize to the upper or lower GI tract and cause bleeding and anemia.
461 CHOLANGIO–CARCINOMA ASSOCIATED WITH CLONORCHIS SINENSIS INFECTION: AN UNUSUAL CAUSE OF BILIARY TRACT MALIGNANCY Nooman Gilani, M.D. and Mordechai Rabinovitz, M.D.*. Gastroenterology/Hepatology and Nutrition, University of Pittsburgh Medical Center, Pittsburgh, PA. Case Report: A 35 y old Laotian man was referred to us because of jaundice. Three months prior he experienced RUQ pain accompanied by dark urine, anorexia and wt. loss.Two weeks before admission developed jaundice and abnl LFTs. CT/US revealed biliary dilatation. He never had jaundice/exposure to hepatitis neither was on meds.P/E showed jaundice, tender hepatomegaly and ascites. Lytes, Hb, coags, amylase/lip were nl, TB 3.3, ALP 630, GTP 816, AST109, ALT134, ALB 3.7,WBC 7.2 (P:58,L: 27,M:8,E:6). An ERCP showed a mid CBD stricture with prox. dilation and multiple bilobar filling defects from which thick brownish material was aspirated. A stent did not improve jaundice. Chronic liver disease w/u was negative. CEA was 51, CA 19 –9 markedly elevated at 319870 with nl AFP. BD brushings and bile aspirate showed C. sinensis ova alongwith malignant cells. No adult parasites were seen. Ascitic fluid had malignant cells similar to the bile aspirate, stools negative for OP. Repeat CT showed liver mets, large LNs & nodular omentum. Chest CT showed B/L mets. Given poor prognosis he opted for hospice. Discussion: Cholangio–CA accounts for 10 –15 % of prim. hepato– biliary cancer. Although most cases remain idiopathic, risk factors include PSC, fibrocystic disease of the biliary tree, biliary adenomas/papillomatosis and pseudopyloric metaplasia & rarely has been linked to cirrhosis, viral hepatitis, hepatoliths, typhoid infection, recurrent cholangitis, exposure to thorotrast and infestation with liver flukes. Most of these factors cause Ch. inflammation and injury to the ductal epithelium which might trigger the development of neoplasia.The sequence of events appears to be; Ch. inflamm, epithelial proliferation & desquamation, free radical formation, DNA damage, mutations, hyperplasia, adenomatous proliferation and neoplasia. Conclusion: Clonorchiasis is a parasitic infection of the hepato– biliary tree. In the US up to 26 % of the East Asian immigrants have an active infection. Chronic infection can cause cholecystitis, obstructive jaundice, cholangitis, hepatic abscesses and pancreatitis. Cholangio–CA is a rare but most dreadful complication of longstanding infection with this parasite. Maintaining a high level of suspicion in the appropriate setting and early recognition of the infection is imperative to prevent complications, as treatment with praziquantel (75 mg/kg in three divided doses x 1 day) could be curative.
Abstracts
S153
462 INTRAMURAL DUODENAL HEMATOMA IN ACUTE PANCREATITIS Frederick A. Boghossian, M.D. and Ioannis Giannikopoulos, M.D., FACG*. Division of Gastroenterology, LAC–King/Drew Mecical Center, Los Angeles, CA. Background: Intramural duodenal hematoma (IDH) is an unusual clinical entity caused mainly by blunt abdominal trauma or in patients with coagulation disorders, after endoscopic injections or duodenal biopsies. Few cases of IDH due to acute pancreatitis have been reported. We present a case of IDH as a local complication in a patient with acute pancreatitis successfully resolved with medical management. Case Report: A 30 –year– old man with history of heavy alcohol drinking admitted with moderate diffuse upper abdominal pain, nausea and hematemesis for 3 days. On physical exam he was overweight, alert, but agitated, tachycardic, but normotensive. His abdomen was soft with moderate epigastric tenderness, hypoactive bowel sounds but without rebound or rigidity. Pertinent lab Results: Serum amylase ⫽ 1,334 U/L, Lipase⫽ 1,420 U/L, Ca⫹⫹ ⫽ 8.2 mg/dl; WBC ⫽ 23,500; Hgb ⫽ 14.3 g/dl; Hct ⫽ 39.9%; Platelets ⫽ 253,000; P.T. – 12.9 sec; PTT ⫽ 24.1 sec, and INR ⫽ 1.3. EGD: revealed Grade 2 esophagitis, diffuse erosive gastritis, and in duodenum a large spherical, bluish, hyperemic friable mass lesion starting at the apex of the bulb, down to the third portion, causing near complete obstruction. EUS with radial probe revealed intramural lesion similar to hematoma. C–T scan showed enlarged pancreas, peripancreatic fluid and a mass (hematoma) within the duodenal wall. CT– guided aspiration was not performed as he was stable. He remained hospitalized for 3 weeks, on analgesics, antibiotics (Imipenem) and TPN, clinically improved, tolerating feedings well upon discharge. Repeated C–T scan showed resolving hematoma and UGI series revealed no obstruction. On outpatient clinic follow– ups he is doing well. Conclusion: IDH is an unusual local complication of acute pancreatitis, successfully resolving with conservative medical management, avoiding surgical intervention with related morbidity and mortality. 463 COLONIC VARICES: AN UNUSUAL PRESENTATION OF SUPERIOR MESENTERIC VEIN THROMBOSIS Anand Madan, M.D., Jenad Hussam, M.D., Niti Madan, M.D. and Anil Minocha, M.D., FACG*. Division of Gastroenterology, Southern Illinois University School of Medicinee, Springfield, IL and Division of Digestive Diseases, University of Mississippi, Jackson, MS. Purpose: A 20 –year– old white male, National Guard by profession, presented as an outpatient with intermittent episodes of black tarry stools of 4 weeks duration. This was associated with generalized weakness and tiredness. He denied any nausea, vomiting, abdominal pain, weight loss or change in bowel habits. Past medical and surgical history were unremarkable. He denied taking any medications. He did not smoke or drink alcohol. Physical exam was unremarkable. Lab data revealed hemoglobin 9.5 mg%, Iron 19, TIBC 473 and ferritin 3. EGD was unremarkable. Colonoscopy showed minimal dilated, torturous veins in ascending colon of unclear significance. There were no ulcers seen. Other work– up including Meckel’s scan and enteroclysis was normal. Patient was started on Iron replacement therapy. Mesenteric angiogram was performed which revealed occlusion of superior mesenteric vein (SMV) with multiple collateral vessels. One month later, patient was admitted with episodes of dark red stools. His hemoglobin on admission was 6.2 mg%. Repeat colonoscopy revealed markedly dilated varicose veins in ascending colon. There were no stigmata of active bleeding. EGD done at the same time showed varicosities in distal duodenum with oozing. These were injected with sodium morrhuate with good hemostasis. There were no esophageal or gastric varices. CT abdomen demonstrated splenomegaly and SMV thrombosis with colonic, duodenal and jejunal varices. There were no mass lesions. Hypercoagulable work– up revealed elevated Factor VIIIc levels. Patient was placed on warfarin anticoagulation.
After transfusion of 3 units of packer cells, upper endoscopy (EGD) and colonoscopy were carried out. Results: At EGD we found a fundal 3 cm submucosal ulcerated neoplasm, with neovascularization, biopsies were taken. Colonoscopy showed an essentially identical submucosal 1 cm ulcerated lesion at the hepatic flexure. There were no other bleeding lesions identified. Biopsies were taken. Histology showed evidence of a metastatic Merkel cell cancer, with positive immunoperoxidase staining for enolase, chomogranin, and synaptophysin. The patient was subsequently transferred to hospice. A search of the literature revealed only 2 cases of gastro– duodenal metastasis from Merkel cell tumor in the past 12 years, and no reported cases of colon metastasis. Conclusions: Gastroenterologists need to become aware that Merkel cells tumors are rare, but metastasize aggresively. These tumors, similarly to melanoma, can metastasize to the upper or lower GI tract and cause bleeding and anemia.
461 CHOLANGIO–CARCINOMA ASSOCIATED WITH CLONORCHIS SINENSIS INFECTION: AN UNUSUAL CAUSE OF BILIARY TRACT MALIGNANCY Nooman Gilani, M.D. and Mordechai Rabinovitz, M.D.*. Gastroenterology/Hepatology and Nutrition, University of Pittsburgh Medical Center, Pittsburgh, PA. Case Report: A 35 y old Laotian man was referred to us because of jaundice. Three months prior he experienced RUQ pain accompanied by dark urine, anorexia and wt. loss.Two weeks before admission developed jaundice and abnl LFTs. CT/US revealed biliary dilatation. He never had jaundice/exposure to hepatitis neither was on meds.P/E showed jaundice, tender hepatomegaly and ascites. Lytes, Hb, coags, amylase/lip were nl, TB 3.3, ALP 630, GTP 816, AST109, ALT134, ALB 3.7,WBC 7.2 (P:58,L: 27,M:8,E:6). An ERCP showed a mid CBD stricture with prox. dilation and multiple bilobar filling defects from which thick brownish material was aspirated. A stent did not improve jaundice. Chronic liver disease w/u was negative. CEA was 51, CA 19 –9 markedly elevated at 319870 with nl AFP. BD brushings and bile aspirate showed C. sinensis ova alongwith malignant cells. No adult parasites were seen. Ascitic fluid had malignant cells similar to the bile aspirate, stools negative for OP. Repeat CT showed liver mets, large LNs & nodular omentum. Chest CT showed B/L mets. Given poor prognosis he opted for hospice. Discussion: Cholangio–CA accounts for 10 –15 % of prim. hepato– biliary cancer. Although most cases remain idiopathic, risk factors include PSC, fibrocystic disease of the biliary tree, biliary adenomas/papillomatosis and pseudopyloric metaplasia & rarely has been linked to cirrhosis, viral hepatitis, hepatoliths, typhoid infection, recurrent cholangitis, exposure to thorotrast and infestation with liver flukes. Most of these factors cause Ch. inflammation and injury to the ductal epithelium which might trigger the development of neoplasia.The sequence of events appears to be; Ch. inflamm, epithelial proliferation & desquamation, free radical formation, DNA damage, mutations, hyperplasia, adenomatous proliferation and neoplasia. Conclusion: Clonorchiasis is a parasitic infection of the hepato– biliary tree. In the US up to 26 % of the East Asian immigrants have an active infection. Chronic infection can cause cholecystitis, obstructive jaundice, cholangitis, hepatic abscesses and pancreatitis. Cholangio–CA is a rare but most dreadful complication of longstanding infection with this parasite. Maintaining a high level of suspicion in the appropriate setting and early recognition of the infection is imperative to prevent complications, as treatment with praziquantel (75 mg/kg in three divided doses x 1 day) could be curative.
Abstracts
S153
462 INTRAMURAL DUODENAL HEMATOMA IN ACUTE PANCREATITIS Frederick A. Boghossian, M.D. and Ioannis Giannikopoulos, M.D., FACG*. Division of Gastroenterology, LAC–King/Drew Mecical Center, Los Angeles, CA. Background: Intramural duodenal hematoma (IDH) is an unusual clinical entity caused mainly by blunt abdominal trauma or in patients with coagulation disorders, after endoscopic injections or duodenal biopsies. Few cases of IDH due to acute pancreatitis have been reported. We present a case of IDH as a local complication in a patient with acute pancreatitis successfully resolved with medical management. Case Report: A 30 –year– old man with history of heavy alcohol drinking admitted with moderate diffuse upper abdominal pain, nausea and hematemesis for 3 days. On physical exam he was overweight, alert, but agitated, tachycardic, but normotensive. His abdomen was soft with moderate epigastric tenderness, hypoactive bowel sounds but without rebound or rigidity. Pertinent lab Results: Serum amylase ⫽ 1,334 U/L, Lipase⫽ 1,420 U/L, Ca⫹⫹ ⫽ 8.2 mg/dl; WBC ⫽ 23,500; Hgb ⫽ 14.3 g/dl; Hct ⫽ 39.9%; Platelets ⫽ 253,000; P.T. – 12.9 sec; PTT ⫽ 24.1 sec, and INR ⫽ 1.3. EGD: revealed Grade 2 esophagitis, diffuse erosive gastritis, and in duodenum a large spherical, bluish, hyperemic friable mass lesion starting at the apex of the bulb, down to the third portion, causing near complete obstruction. EUS with radial probe revealed intramural lesion similar to hematoma. C–T scan showed enlarged pancreas, peripancreatic fluid and a mass (hematoma) within the duodenal wall. CT– guided aspiration was not performed as he was stable. He remained hospitalized for 3 weeks, on analgesics, antibiotics (Imipenem) and TPN, clinically improved, tolerating feedings well upon discharge. Repeated C–T scan showed resolving hematoma and UGI series revealed no obstruction. On outpatient clinic follow– ups he is doing well. Conclusion: IDH is an unusual local complication of acute pancreatitis, successfully resolving with conservative medical management, avoiding surgical intervention with related morbidity and mortality. 463 COLONIC VARICES: AN UNUSUAL PRESENTATION OF SUPERIOR MESENTERIC VEIN THROMBOSIS Anand Madan, M.D., Jenad Hussam, M.D., Niti Madan, M.D. and Anil Minocha, M.D., FACG*. Division of Gastroenterology, Southern Illinois University School of Medicinee, Springfield, IL and Division of Digestive Diseases, University of Mississippi, Jackson, MS. Purpose: A 20 –year– old white male, National Guard by profession, presented as an outpatient with intermittent episodes of black tarry stools of 4 weeks duration. This was associated with generalized weakness and tiredness. He denied any nausea, vomiting, abdominal pain, weight loss or change in bowel habits. Past medical and surgical history were unremarkable. He denied taking any medications. He did not smoke or drink alcohol. Physical exam was unremarkable. Lab data revealed hemoglobin 9.5 mg%, Iron 19, TIBC 473 and ferritin 3. EGD was unremarkable. Colonoscopy showed minimal dilated, torturous veins in ascending colon of unclear significance. There were no ulcers seen. Other work– up including Meckel’s scan and enteroclysis was normal. Patient was started on Iron replacement therapy. Mesenteric angiogram was performed which revealed occlusion of superior mesenteric vein (SMV) with multiple collateral vessels. One month later, patient was admitted with episodes of dark red stools. His hemoglobin on admission was 6.2 mg%. Repeat colonoscopy revealed markedly dilated varicose veins in ascending colon. There were no stigmata of active bleeding. EGD done at the same time showed varicosities in distal duodenum with oozing. These were injected with sodium morrhuate with good hemostasis. There were no esophageal or gastric varices. CT abdomen demonstrated splenomegaly and SMV thrombosis with colonic, duodenal and jejunal varices. There were no mass lesions. Hypercoagulable work– up revealed elevated Factor VIIIc levels. Patient was placed on warfarin anticoagulation.