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[Duodenal varix. ½ÊÀÌÁöÀå Á¤¸Æ·ù]

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Budd chiari syndrome ȯÀÚ¿¡¼­ ¹ß°ßµÈ ½ÊÀÌÁöÀå Á¤¸Æ·ùÀÔ´Ï´Ù.

°£¾Ï ȯÀÚÀÇ ¹Ýº¹ÀûÀÎ ½ÊÀÌÁöÀå Á¤¸Æ·ù ÃâÇ÷·Î clipping¿Í histoacryl·Î ÁöÇ÷¼úÀ» ÇÏ¿´À¸³ª ÃâÇ÷ÀÌ ¹Ýº¹µÇ¾ú´ø ȯÀÚÀÔ´Ï´Ù. (F/60, 2017)

Histoacryl injectionÀ» ÇÏ¿´½À´Ï´Ù.

Fatal duodenal varix bleeding


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A 30-year-old man with a history of alcoholic cirrhosis presented with 1 week of melena and 1 day of lightheadedness. On initial presentation, the patient was tachycardic (heart rate 123 bpm); blood pressure was normal. Physical exam was remarkable for mild abdominal distension. In laboratory tests at admission, hemoglobin concentration was 5.2 g/dl, platelet count was 141, 000/¥ìl, and international normalized ratio was 1.3. Total bilirubin was slightly elevated: 1.5 mg/dl. The results of other liver-function tests were within normal limits. Esophagogastroduodenoscopy showed a large (>5 mm) varix with a nipple sign (a) in the second portion of the duodenum. Computed tomography of the abdomen showed stigmata of portal hypertension, including paraduodenal varices (b). Portal venography demonstrated dominant duodenal varices originating from the superior mesenteric vein and inferior vena cava. Portosystemic gradient was measured at 6 mm Hg. Coil embolization of the duodenal varices was successful (c). Bleeding from duodenal varices is rare but potentially fatal; the nipple sign on a varix correlates positively with recent severe bleeding and warrants urgent intervention. (Am J Gastroenterol 2017)

A 78-year-old woman presented with 500 mL hematochezia, hypotension, and a hemoglobin level of 5.4 g/dL. She had a history of right hemilobectomy of the liver and hepatojejunostomy for Klatskin tumor IIIA at other institutions 2 years before. Her medical history also included mitral regurgitation. Emergency esophagogastroduodenoscopy revealed a large, bluish, rugged mass with a smooth surface in the 3rd portion of the duodenum. A red spot was observed at the middle of the lesion (Fig. A). Contrast-enhanced CT of the abdomen revealed a brightly enhanced mass without lobulation in the same location (Fig. B, arrow). What was her diagnosis, and how would you treat the patient? Her diagnosis was duodenal varices. First, endoscopic band ligation of the varices was considered. However, the lesion was too huge to be obliterated completely. Endoscopic sclerotherapy could not be performed because of the risk of lipiodol embolization through a large-bore efferent systemic shunt from the varices. Therefore, the patient underwent angiographic embolization under fluoroscopic guidance, and the lesion was successfully obliterated. Three days after vascular intervention, follow-up endoscopy revealed slight discoloration and reduction of the varices without evidence of bleeding (Fig. C). Further regression of the varix was observed on follow-up endoscopy after 1 week (Fig. D). Finally, the duodenal varix completely disappeared 3 months after the intervention (Fig. E). (Intest Res 2017)


[Brief review]

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°æ»ó´ëÇп¡¼­ ´ëÇѼÒÈ­±â³»½Ã°æÇÐȸÁö(2008;36:292-297)¿¡ ±â°íÇÑ ±ÛÀÇ ÀϺθ¦ ¿Å±é´Ï´Ù.

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Ginsberg textbook 2005¿¡¼­ ¿Å±é´Ï´Ù.

In portal hypertension, varices can also develop in other parts of the GI tract including the anorectal region, colon, and small intestine. Portal hypertensive gastropathy, colopathy, and enteropathy are other sequelae. Primay duodenal varices are rare and are usually found incidentally at the time of endoscopy, more often in patients with extrahepatic portal vein obstruction or in cirrhotics with portal vein thrombosis. Usually the afferent vessel of the duodenal varices is the superior or inferior pancreaticoduodenal vein originating in the portal vein trunk or superior mesenteric vein. The efferent vain drains into the inferior vena cava. In a review of 169 cases of bleeding ectopic varices, 17% occurred in the duodenum, 17% in the jejunum or ileum, 14% in the colon, 8% in the rectum, and 9% in the peritoneum.



© ÀÏ¿ø³»½Ã°æ±³½Ç ¹Ù¸¥³»½Ã°æ¿¬±¸¼Ò ÀÌÁØÇà. EndoTODAY Endoscopy Learning Center. Lee Jun Haeng.