Endoscopy-negative upper gastrointestinal bleeding in a patient with chronic pancreatitis.

Endoscopy-negative upper gastrointestinal bleeding in a patient with chronic pancreatitis.
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慢性胰腺炎患者内镜检查阴性上消化道出血。

DOI:
10.1016/0016-5085(92)91818-o
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发表时间:
1992
期刊:
影响因子:
29.4
通讯作者:
Grendell,JH
Grendell,JH
中科院分区:
医学1区
文献类型:
--
作者:
Forsmark,CE;Wilcox,CM;Grendell,JH

文献摘要

被引文献

相似文献

C医生Me1 Wilcox:一名54岁男性,有酒精诱导的慢性胰腺炎病史,因腹痛加重、呕血、黑便和体位性症状入院。他在入院前3个月之前一直处于正常健康状态,当时他因抗溃疡治疗的经验性试验失败后慢性上腹痛加重而接受了食管胃镜检查。内镜检查结果包括轻度食管炎和近端胃炎。当时,血红蛋白为130 g/L(13 g/dL),血清淀粉酶浓度为2.47 pkat/L(148 U/L)[正常值上限,1.83 pkat/L(110 U/L)]。为了进一步评价腹痛,进行了腹部超声检查,显示胰头中的超声结构,尺寸为5.1 X 3.8 cm,与假性囊肿相符。发现胆总管直径为1.2 cm。当时通过静脉注射造影剂进行腹部计算机断层扫描(CT)证实存在胰腺假性囊肿。此外,还观察到大量胰腺钙化。他开始接受β受体阻滞剂治疗,疼痛有所改善。入院前六周,随后的腹部超声检查显示假性囊肿的大小或外观没有变化。在决定治疗前,再观察假性囊肿6周。入院前5天,他发现上腹痛恶化,表现为痉挛和烧灼感。第二天,他发现了黑便。在接下来的3天里,他出现间歇性恶心、呕吐鲜红色血以及体位性症状,于是去了医院。在急诊室,鼻胃管抽吸物显示50 mL鲜红色血液和太妃糖渣物质,经500 mL自来水灌洗后清除。他的病史是酒精引起的慢性胰腺炎和持续3年的轻度间歇性慢性腹痛。入院前2年,经食管胃镜检查发现食管溃疡,根据内镜和组织病理学标准推测为酸消化性溃疡。2年前,他在结肠镜息肉切除术后因结肠穿孔接受了剖腹手术。家族史中无胰腺疾病。20多年来,他每天抽一包烟。虽然以前每天喝六瓶或更多的啤酒,但他现在每周喝一到三瓶啤酒。
Dr. C. Me1 Wilcox: A 54-year-old man with a history of alcohol-induced chronic pancreatitis presented to the hospita1 with worsening abdominal pain, hematemesis, melena, and postural symptoms. He was in his usual state of health until 3 months before admission, when he underwent esophagogastroduodenoscopy for an exacerbation of chronic epigastric pain after an unsuccessful empirie trial of antiulcer therapy. Endoscopic findings included mild esophagitis and proximal gastritis. At that time, the hemoglobin was 130 g/L (13 g/dL) and the serum amylase concentration was 2.47 pkat/L (148 U/L)[upper limit of normal, 1.83 pkat/L (110 U/L)]. To further evaluate the abdominal pain, abdominal ultrasonography was performed demonstrating a sonolucent structure in the head of the pancreas measuring 5.1 X 3.8 cm, compatible with a pseudocyst. The common bile duet was noted to be 1.2 cm in diameter. Abdominal computed tomography (CT) at that time with IV contrast confirmed the presence of a pancreatic pseudocyst. In addition, abundant pancreatic calcifications were noted. He was begun on H,-blocker therapy with some amelioration of pain. Six weeks before admission, a subsequent abdominal ultrasonography showed no change in the size or appearance of the pseudocyst. The pseudocyst was to be observed for another 6 weeks before deciding on therapy. Five days before admission, he noted the onset of worsening epigastric pain characterized as crampy and burning. The following day he noted the presence of black stool. Over the next 3 days, intermittent nausea and vomiting of bright red blood as wel1 as postural symptoms occurred, and he went to the hospital. In the emergency department, a nasogastric tube aspirate showed 50 mL of bright red blood and toffee-grounds material, which cleared after 500 mL of tap water lavage. He was thus admitted.His medical history was notable for alcohol-induced chronic pancreatitis and mild intermittent chronic abdominal pain of 3 years’ duration. Two years before admission, he was found to have an esophageal ulcer by esophagogastroduodenoscopy, presumed to be acid-peptic in origin by endoscopic and histopathological criteria. He underwent a laparotomy for colonic perforation after colonoscopic polypectomy 2 years previously. There was no pancreatie disease in his family history. He smoked one pack of cigarettes per day for more than 20 years. Although previously drinking six or more beers per day, he was currently consuming one to three beers per week.