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PubMed2000

[Recurrent severe lower gastrointestinal hemorrhage. Acute recurrent diverticulum hemorrhage in the cecum].

This 83-year-old patient was admitted to the emergency room after a sudden and abundant rectal bleeding without any other abdominal symptoms. The physical examination showed normal abdominal findings. However, digital rectal examination revealed dark red blood. Upper and lower endoscopic examination did not show an active bleeding source. A diagnosis of an acute lower gastrointestinal bleeding probably originating from a diverticulum was made. The patient was dismissed two days later without any signs of further bleeding. However, the same day he was readmitted again because of acute rebleeding. Emergency colonoscopy was not conclusive because of massive hemorrhage. Angiography of the abdominal arteries was performed which showed marked active bleeding in the coecal region. Ileocoecal resection was performed and histopathological examination showed a solitary coecal diverticulum.

Aged↗
PubMed2001

[Risk factor for cerebral hemorrhage for the patient with lacunar infarction: investigation of 5 cases associated with both of symptomatic hemorrhagic and ischemic strokes].

BACKGROUND AND PURPOSE: Microangiopathy is regarded as an important cause of intracerebral hematoma(ICH) and lacunar infarction. Dot-like low intensity spots on T2-weighted echo planar image(EPI) have been regarded as hemosiderin deposit associated with microangiopathy. However, clinical significance of dot-like hemosiderin spot(dotHS) is still debated. Therefore, we analyzed the number of dotHS on EPI of symptomatic lacunar infarction associated with ICH. METHODS: To investigate how the dotHS or risk factors contributed to hemorrhagic strokes for patients with lacunar infarction, the number of dotHS and various risk factors were made a comparison between 20 cases with symptomatic lacunar infarctions(lacunar group) and 5 cases with both symptomatic lacunar infarction and symptomatic ICH(complicated group). In addition to EPI, fluid attenuated inversion recovery image, and T1- and T2-weighted MR images were performed for differential diagnosis of dot HS. RESULTS: EPI demonstrated that asymptomatic ICH was significantly more frequent in complicated group (60%) than in lacunar group(10%), and dotHS were significantly more frequent in complicated group(100%) than in lacunar group(50%). The number of dotHS of complicated group was 14.6 +/- 4.3, which was significantly larger than that of lacunar group(4.1 +/- 9.2). No significant difference between two groups were founded in other risk factors including hypertension, diabetes mellitus, hyperlipidemia, and smoking. CONCLUSION: These results suggested that dotHS was one of the risk factors for ICH for patients with symptomatic lacunar infarction, and an increasing number of dotHS was one of the predictive factors of symptomatic and/or asymptomatic ICH.

Aged↗
PubMed1990

[Detection of infectious hemorrhagic disease of domestic rabbits (rabbit viral hemorrhagic disease) in wild rabbits (Oryctolagus cuniculus)].

The occurrence of Rabbit Viral Hemorrhagic Disease of domestic rabbits in the population of wild rabbits in Germany was proven through detection of antigen (hemagglutination) in spleen and liver in one animal and through detection of specific antibody in another animal. There was no epizootic connection between the two animals (different locations). The necropsy and histopathologic findings are presented from five wild rabbits which died from RVHD.

Animals↗
PubMed1990

[Non-surgical treatment of hemorrhage caused by portal hypertension in cirrhosis: hemostatic treatment, prevention of the first hemorrhage, prevention of recurrence].

Oesophageal varices are found in two-thirds of cirrhotic patients, and they bleed by rupture in only 50% of the cases. Each bleeding episode carries a mortality risk of about 30%. Recurrences occur in 70% of survivors. Patients with cirrhosis may be considered as being at risk of haemorrhage when large varices, notably with "red signs", are discovered at endoscopy. In two-thirds of the cases, the hemorrhage from ruptured oesophageal varices has stopped by the time emergency endoscopy is performed, but its severity mainly depends on its early recurrence. Haemostatic treatments are justified only in the presence of an active haemorrhage. The best method seems to be endoscopic variceal sclerotherapy carried out in a specialized centre by a centre by a trained endoscopist. The other methods should be used only when sclerotherapy has failed. The prevention of recurrences (secondary prophylaxis) mainly rests on the eradication of varices by endoscopic sclerosis. The addition of propranolol to treatment is probably useful. The seriousness of haemorrhages due to rupture of oesophageal varices justifies primary prophylaxis in patients with large varices found at endoscopy. At present, nonselective beta-blockers constitute the best method of primary prophylaxis. In about 1 out of 5 cases, haemorrhages in cirrhotic patients are due to a different lesion, such as ruptured gastric varices or gastric disease due to portal hypertension. The treatment of haemorrhages causes by these lesions has not been clearly defined, but surgical haemostasis is sometimes indicated in case of ruptures gastric varices.

Esophageal and Gastric Varices↗
PubMed1990

[Intracranial hemorrhage during hemorrhagic disease of the newborn infant at term].

The authors report a case of intra-cerebral hematoma in a patient with hemorrhagic disease of the newborn. This hematoma had to be taped, and after that, an hydrocephalus shunted. The state of deficiency of vitamin K in the newborn should be treated systematically. The oral route is as good as the intra-muscular route for the baby.

Cerebral Hemorrhage↗
PubMedDate not supplied

Coagulopathy in hemorrhagic fever with renal syndrome (Korean hemorrhagic fever).

The pathophysiology of bleeding manifestations in hemorrhagic fever with renal syndrome (HFRS) was elucidated by serially evaluating coagulation and fibrinolytic profiles and complement alterations in patients with HFRS. In the early stage of the disease, platelet counts, platelet survival time, and platelet aggregation in vitro decreased. Prolongation of bleeding time, prothrombin time, and activated partial thromboplastin time was noted, with decreases in coagulation factors II, V, VIII, IX, and X. Levels of fibrinogen were decreased, and those of fibrinogen-fibrin degradation products in serum and urine were increased. Concentrations of plasminogen, alpha 2-plasmin inhibitor, and antithrombin III in plasma were depressed. Procoagulant activity was present in plasma. Circulating immune complexes were found, whereas serum levels of C3 were decreased. In the early stage of HFRS, thrombocytopenia, defects in platelet function, and disseminated intravascular coagulation may play central roles in the pathogenesis of bleeding manifestations. Vasculopathy and immunologic aberrations also may play a role.

Antigen-Antibody Complex↗
PubMedDate not supplied

Hemorrhagic enteritis of turkeys in California: serologic study of hemorrhagic enteritis virus antibody with an enzyme-linked immunosorbent assay.

The incidence of hemorrhagic enteritis (HE) infection in California turkeys was studied by testing 2220 turkey blood samples from 173 flocks for HE virus (HEV) antibody by the enzyme-linked immunosorbent assay (ELISA). Maternal antibody was detected at 1 day of age in all flocks tested, and it vanished after 3 weeks. Acquired HEV antibody appeared at 8 to 10 weeks, and 100% of the meat and breeder turkey flocks were positive after 11 weeks of age. HEV infection occurred earlier in the meat flocks than in the breeder flocks, and it also occurred earlier during summer than during the fall and winter months.

Animals↗
PubMed1981

Studies on immunopathogenesis in epidemic hemorrhagic fever: sequential observations on activation of the first complement component in sera from patients with epidemic hemorrhagic fever.

Sequential measurements of activation of the 1st component of complement (C1) in the sera of 29 patients hospitalized with epidemic hemorrhagic fever (EHF) were performed according to a method recently developed. These patients were treated with supportive, routine therapy, but not immunosuppressive agents. This paper describes the kinetic observations on the activation of C1 in the 29 cases. The data confirm that an apparently increased extent of activation occurred in their sera. It was found that the more severely ill the patients were, the more apparent the activation. Additionally, beginning with the 15th day of disease, the extent of C1 activation diminished in most of the moderate and severe types of patients, but not in those with moribund illness and fatal ones. On the basis of the study, it may be reasonably concluded that C1 activation was correlated well with the severity and clinical course of EHF, indicating that the classical C pathway was activated in these patients. We feel that our findings are important to an understanding and elucidation of the immunopathogenetic mechanisms of EHF.

Adolescent↗
PubMed1981

[Hemorrhage and blood replacement. 2. Hemorrhage prevention and hemostasis, volume replacement].

Reviewed are the causes of hemorrhagic shock, pathophysiology of blood loss as well as clinical signs and diagnostic measures. The problematic nature of determination and judgement of blood loss, especially at internal bleeding and during operations is pointed out. Measures for prevention and stanching of bleeding are touched. Blood, blood plasma and colloids (dextran, gelatine and hydroxyethyl starch) for volume replacement and their side effects are discussed briefly.

Blood Transfusion↗
PubMed1993

[Hemorrhage through Wirsung's duct: rare form of upper gastrointestinal hemorrhage. A case report].

The case of a 41-year-old alcoholic patient who presented with massive upper gastrointestinal bleeding is reported. The diagnosis was established rapidly by endoscopy which revealed bleeding through the papilla of Vater. Selective angiography of the superior mesenteric artery opacified the pancreatic duct as well as the duodenum. CT scan showed signs of chronic pancreatitis. Because of the recurrence of bleeding and shock, an urgent operation was necessary and a Whipple procedure was performed. Recovery was complete. The clinical presentation, the etiology, the diagnostic modalities and the treatment of this particular condition are discussed. Usually, hemorrhage through the pancreatic duct presents as repeated episodes of upper gastrointestinal bleeding with no source found at endoscopy. The presence of chronic pancreatitis or of epigastric pain during bleeding should suggest the diagnosis. Upper gastrointestinal endoscopy and angiography are the principal diagnostic tools. Definitive treatment requires surgery, and resection in most of the cases.

Adult↗
PubMed1993

[Structural protein of hemorrhagic fever renal syndrome virus in uric fusion cells in hemorrhagic fever renal syndrome].

The efoliative cells in the urine of 21 hemorrhagic fever patients with renal syndrome (HFRS) were examined with Swiss blue staining. Fusion cells were found in the urine of 18 HFRS patients. The quantity of fusion cells was closely related to the severity of patients' condition and renal damage. Specific antigen of HFRS virus (HFRSV) was found immunohistochemically in all fusion cells. Specific monoclonal antibodies (McAb) of membrane protein and nucleocapsid protein from HFRSV were used for analyzing antigen in fusion cells. The positive rate of membrane protein antigen was 72.2%. Nucleocapsid protein was not found in all fusion cells. The above results suggested that the forming of fusion cells in the urine of HFRS patients is related membrane protein of HFRSV.

Adolescent↗