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Results for “HEMORRHAGE, GASTROINTESTINAL”

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At least 289 records · Page 16Linked to original sources
PubMed1998

Systemic calciphylaxis associated with massive gastrointestinal hemorrhage.

A 38-year-old woman with insulin-dependent diabetes mellitus, hypertension, and end-stage renal disease developed digital ischemia, widespread cutaneous necrosis and eschar formation of both lower extremities, and extensive ulceration of the large intestine and cecum resulting in gastrointestinal hemorrhage. A mesenteric arteriogram revealed multiple stenotic areas and filling defects of the superior mesenteric artery and its tributaries, suggestive of vasculitis. A diagnosis of calciphylaxis was suspected, on antemortem skin biopsy, and was later confirmed by postmortem examination. This case further documents the relationship between calciphylaxis and significant visceral injury, and it represents, to our knowledge, the first case of calciphylaxis associated with massive gastrointestinal hemorrhage.

Adult↗
PubMedDate not supplied

[Gastrointestinal hemorrhage in neurosurgical patients].

Analysis of 445 fatal cases among which 21 were marked by profuse gastroduodenal hemorrhage showed that this complication develops in ulceration of the mucous-membrane in the upper parts of the digestive tract and occurs most frequently in affection of the hypothalamic region and brain stem. Gastrointestinal hemorrhages are caused to a certain measure by medication with massive doses of corticosteroids in the stage of tension of the general adaptation syndrome, hypoxia of the mucous membrane, azotemia, and other disorders of homeostasis. Gastrointestinal hemorrhages greatly aggravate the condition of neurosurgical patients, they are diagnosed with difficulty, and their prevention calls for a complex approach.

Adult↗
PubMed1987

[Acute massive gastrointestinal hemorrhage in jejunal diverticulosis].

Two cases which presented with acute massive lower gastrointestinal hemorrhage from jejunal diverticulosis are reported. The various clinical presentations of this rare disease are discussed. The life-threatening complication of massive bleeding is specially outlined. The cases reported in the literature resemble the Dieulafoy ulcer lesion of the stomach.

Aged↗
PubMed1992

[Massive gastrointestinal hemorrhage from a hepaticojejunostomy in pancreatogenic mesenteric vein thrombosis. Diagnosis and therapy].

Gastrointestinal hemorrhage in a patient with a biliodigestive anastomosis necessitates exclusion of a bleeding source in the region of the choledocho- or hepaticojejunal anastomosis. This cannot be achieved by endoscopic methods. The source of bleeding can sometimes, though rarely, be localised by performance of selective angiography during hemorrhage. Laparotomy with exploration of the anastomosis during such an episode is at the same time a diagnostic and a therapeutic intervention. The surgical procedure of choice is de-anastomosis, resection of the bypassed jejunal loop and formation of a hepatico-duodenostomy.

Anastomosis, Roux-en-Y↗
PubMed2004

Gastrointestinal hemorrhage: The prehospital recognition, assessment & management of patients with a GI bleed.

Gastrointestinal hemorrhage may result from an upper or a lower source. It may present in many different ways; however, prehospital management is similar regardless of cause. It's imperative to recognize that a seemingly stable GI bleed can become hemodynamically unstable at any time. The prehospital provider, therefore, should understand the pathophysiology, signs, symptoms and therapeutic interventions for patients with GI bleeds to be better prepared to manage any such emergency when it arises.

Adolescent↗
PubMed1996

Care of patients with upper gastrointestinal hemorrhage in academic medical centers: a community-based comparison.

BACKGROUND & AIMS: A common perception among purchasers is that academic medical centers are inefficient and overutilize technology; however, little empirical information exists. The aim of this study was to compare treatment and outcomes of patients with upper gastrointestinal hemorrhage admitted to major teaching hospitals and other hospitals in a large metropolitan area. METHODS: Data on 3801 consecutive eligible patients admitted to five major teaching hospitals and 25 other hospitals from 1991 to 1993 were obtained by review of medical records. Admission severity of illness was measured using validated multivariable models. RESULTS: Rates of upper endoscopy were somewhat lower among the 1004 patients discharged from fellowship hospitals, compared with the other 2797 patients (82.9% vs. 85.6%; P < 0.05), and the use of other procedures was similar. Although patients admitted to fellowship hospitals tended to have a higher severity of illness, both unadjusted (6.3 +/- 9.0 vs. 7.1 +/- 7.5 days; P < 0.01) and risk-adjusted length of stay were somewhat shorter. Mortality rates were similar between hospitals, and patients admitted to fellowship hospitals were somewhat less likely to be transfused. CONCLUSIONS: In patients with upper gastrointestinal hemorrhage, teaching hospitals do not appear to provide inefficient care or overutilize expensive treatments when compared with community facilities. These findings are noteworthy at a time when viability of academic centers and fellowship training is threatened.

Academic Medical Centers↗
PubMed1986

Ten year follow-up of gastrointestinal hemorrhage patients.

The mortality and morbidity of the 241 survivors of an acute gastrointestinal hemorrhage treated between 1958 and 1964 are reported. The major purpose of this study was to assess the subsequent risk to life and health of patients presenting with acute upper gastrointestinal bleeding. Patients without dyspepsia and with a negative single contrast barium meal study had an excellent prognosis. Life Table analysis showed that the gastric ulcer patients had a mortality not significantly different from that of the Australian population, with the higher risk of death from ulcer balanced by a lower risk of fatal vascular disease. Duodenal ulcer patients had an increased mortality attributable to a 290% increase in deaths from vascular disease, but only one of the 84 died of an ulcer complication. The association between duodenal ulcer and vascular disease has been present for decades. It is unlikely to be associated with hypertension, diabetes mellitus, diet, stress, or smoking and deserves further study.

Acute Disease↗
PubMed1992

Hyperfibrinolysis increases the risk of gastrointestinal hemorrhage in patients with advanced cirrhosis.

Sixty-one patients with different degrees of liver failure, 23 with Child-Pugh class B and 38 with Child-Pugh class C, were studied and observed for 3 yr. Coagulation index analysis showed significantly lower values of prothrombin activity, more prolonged activated partial thromboplastin time, higher bilirubin and fibrinogen degradation products values in class C patients. Among all patients, 28 had fibrinogen degradation products values greater than 10 micrograms/ml, and in these patients a hyperfibrinolytic state was confirmed by higher values of circulating plasminogen activator antigen (17.3 +/- 8.7 ng/ml vs. 5.41 +/- 1.9 ng/ml; p less than 0.0001) and activity (6.6 +/- 2.1 IU/ml vs. 1.92 +/- 1.12 IU/ml; p less than 0.0001) and significantly lower plasminogen activator inhibitor antigen (6.4 +/- 3.5 ng/ml vs. 15.8 +/- 5.6 ng/ml; p less than 0.0001) and activity (3.6 +/- 2.2 IU/ml vs. 8.5 +/- 3.9 IU/ml; p less than 0.0001). Patients with positive fibrinogen degradation products had higher serum bilirubin (6 +/- 4 mg/dl vs. 2 +/- 2 mg/dl; p less than 0.0001) and lower fibrinogen (156 +/- 52 mg/dl vs. 194 +/- 62 mg/dl; p less than 0.02) than patients without hyperfibrinolysis. During the follow-up period, 41 patients died, 22 from fatal gastrointestinal hemorrhage and 19 from liver failure. Thirty patients experienced fatal (22 patients) and nonfatal (8 patients) gastrointestinal hemorrhage. Patients with positive fibrinogen degradation products or class C had a higher risk of gastrointestinal bleeding than patients with negative fibrinogen degradation products (odds ratio = 8) or class B (odds ratio = 3.5), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1981

Spontaneous portosystemic shunt: relationship to spontaneous encephalopathy and gastrointestinal hemorrhage.

This study examined the effect of large spontaneous portosystemic shunts on the incidence of variceal hemorrhage and hepatic encephalopathy. Twenty cases of chronic liver disease with large spontaneous shunts were compared with a group of patients with liver disease and with Cruveilhier-Baumgarten (C-B) murmurs and with a control group having liver disease and absence of large shunts on angiography. Gastrointestinal hemorrhage was present in similar proportions of patients in the three groups. Hepatic encephalopathy occurred more frequently in the spontaneous shunt group and C-B murmur group. The encephalopathy was spontaneous in 12 of 14 patients with large natural shunts whereas it was precipitated by events such as gastrointestinal bleeding, diuretics, or infection in 14 of 15 of the patients with C-B murmur and five of the seven controls. Therefore, spontaneous portosystemic shunts do not protect against gastrointestinal hemorrhage and are associated with an increased risk of spontaneous hepatic encephalopathy.

Adolescent↗