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At least 19 recordsLinked to original sources
PubMed1979

[Diagnosis and treatment of cerebellar hemorrhage: comparison of hypertensive hemorrhage with hemorrhage caused by small angiomas, and CT findings (author's transl)].

In spontaneous cerebellar hemorrhage emergency surgical intervention is often life-saving. Clinical features and the operative results of hypertensive cerebellar hemorrhage (18 cases) were compared with those of hemorrhage caused by small angiomas (7 cases). Hypertensive hemorrhage occured most frequently in the seventh decades. Two thirds of the patients developed brainstem compression syndrome within a week from onset. One third remained awake or drowsy throughout their clinical course. Surgical removal of a hematoma was carried out in 13 patients with four deaths. Of note, two comatose patients regained consciousness after surgery, and were discharged with residual ataxia. Rupture of a small angioma occurred in younger patients. Their clinical course was sub-acute or chronic associated with focal cerebellar dysfunction. All seven surgically treated patients subsequently regained independent function. CT findings have been found helpful not only for diagnosis but also in defining appropriate therapy. Hematomas larger than 3 cm in diameter produced signs of rapidly progressing compression of the brainstem. Thereby, regardless of the cause of bleeding, emergency removal of a clot is indicated even in awake patients. Hematomas of 2 to 3 cm produced brainstem compression or prolonged cerebellar dysfunction, and occasionally require surgical decompression. Hematomas smaller than 2 cm can be managed conservatively, since they were absorbed spontaneously in three weeks without residual functional disturbances. However, in case of a young patient exploration should be performed for a probable "cryptic" angioma.

Adolescent↗
PubMed1978

Hemorrhagic toxins from rattlesnake (Crotalus atrox) venom. Pathogenesis of hemorrhage induced by three purified toxins.

The pathogenesis of hemorrhage induced by three purified components of rattlesnake (Crotalus atrox) venom was studied at the light and electron microscopic levels. Crude venom was fractionated by anion exchange and gel filtration in four steps. beta-Alanine acetate disk gel electrophoresis was used to demonstrate electrophoretic homogeneity. White mice were injected intramuscularly with 0.1 ml of a sublethal dose of hemorrhagic toxin. Gross examination revealed extensive hemorrhage 5 minutes after the injection of hemorrhagic toxins alpha and episilon; the same amount of hemorrhage was not present until 3 hours after the injection of hemorrhagic toxin beta. Light microscopic examination of muscel after injection of the toxins revealed areas of extensive hemorrhage in which very few intact capillaries could be found and also adjacent areas of slight hemorrhage in which capillaries were in various stages of degeneration. Necrosis of muscle cells was evident in tissue injected with hemorrhagic toxin beta. Electron microscopic examination showed that capillaries from toxin-injected muscle were in various stages of degeneration. Endothelial cells became very thin and broke down into vesicles prior to complete rupture. Gaps were formed within the cells while intercellular junctions remained intact. Plasma and erythrocytes leaked through these gaps and were observed in the endomysium. Many gaps were plugged with platelet aggregations. Collagen and the basal lamina associated with capillaries were usually disorganized or absent. The experimental injection of three purified hemorrhagic toxins induced hemorrhage by the same mechanism as does the crude venom, ie, per rhexis. In addition, one of the toxins, hemorrhagic toxin beta, causes myonecrosis.

Animals↗
PubMed1978

Hemorrhagic toxins from Western diamondback rattlesnake (Crotalus atrox) venom: isolation and characterization of five toxins and the role of zinc in hemorrhagic toxin e.

Five previously unknown hemorrhagic proteins, designated hemorrhagic toxins a,b,c,d, and e, were isolated from the venom of the western diamondback rattlesnake (Crotalus atrox). Molecular weights of hemorrhagic toxins a-e were determined to be 68 000, 24 000, 24 000, 24 000, and 25 700, respectively, by sodium dodecyl sulfate-phosphate gel electrophoresis using various polyacrylamide gel concentrations. Amino acid composition showed a total of 636, 200, 213, 214, and 219 amino acids for hemorrhagic toxins a-e, respectively. All the hemorrhagic toxins were found to lose their hemorrhagic activities with the metal chelators ethylenediaminetetraacetic acid and 1, 10-phenanthroline. All the hemorrhagic toxins were found to contain approximately 1 mol of zinc/mol of toxin, and they were all demonstrated to be proteolytic when dimethylcasein and dimethylhemoglobin were used as substrates. When zinc was removed from hemorrhagic toxin e with 1,10-phenanthroline, both both the proteolytic and hemorrhagic activities were equally inhibited. When the apohemorrhagic toxin e thus produced was incubated with zinc, the hemorrhagic and proteolytic activities were regenerated to the same extent. CD, UV, and Raman spectroscopy were used to study the structure of native hemorrhagin toxin e as well as the structural changes caused by zinc removal. From CD spectroscopy the native toxin was estimated to consist of 23% alpha helix, 6% beta structure, and 71% random-coil conformation. When over 90% of the zinc was removed, the alpha-helix content dropped from 23 to 7%.

Amino Acids↗
PubMed1977

The significance of intraocular hemorrhages due to subarachnoid hemorrhage.

A retrospective study of 320 patients with spontaneous subarachnoid hemorrhage revealed a 20.8% incidence of intraocular hemorrhages. While diagnostically helpful, intraocular hemorrhages also were prognostically significant. The overall patient mortality was 31.6%. In those with intraocular hemorrhages the mortality was 53.6% compared to 19.7% in those without intraocular hemorrhages. Fifty-eight percent with bilateral intraocular hemorrhages died versus 48% with unilateral hemorrhages. Vitreous hemorrhage, though infrequent, may be a major complication in survivors of subarachnoid hemorrhage.

Cerebrovascular Disorders↗
PubMed1975

Vitreous hemorrhage after intracranial hemorrhage.

Eight patients, aged 2 months to 55 years, developed vitreous hemorrhages as a result of subarachnoid or subdural bleeding. Subhyaloid hemorrhages were associated with, or preceded, hemorrhage into the vitreous cavity in four cases. Most vitreous hemorrhages cleared spontaneously, several months later, without major visual sequelae. In one patient, intravitreal blood persisted after 28 months. Vitreous hemorrhage can be a serious complication in patients surviving subarachnoid or subdural hemorrhages and, though uncommon, probably occurs with greater frequency than previously acknowledged. While vitrectomy may be a reasonable therapeutic approach in selected cases, in most instances vitreous hemorrhage following intracranial hemorrhage should be treated conservatively.

Adult↗
PubMed1979

[Vitreous hemorrhage as a complication of subarachnoid hemorrhage (Terson's syndrome) (author's transl)].

We represent a case of vitreous hemorrhage due to subarachnoid hemorrhage from a ruptured aneurysm of the right vertebral artery to draw attention to this complication. A 53-year-old man was admitted to our hospital because of generalized headache and reduced visual acuity of both eyes. On admission the patient was alert and there were moderate nuchal stiffness and mild symmetrical hyperreflexia in the extremities. Ophthalmological consultation revealed bilateral retinal, subhyaloid and vitreous hemorrhages. Four-vessel angiography demonstrated an aneurysm of the right vertebral artery. At operation, it became clear that the aneurysm was a dissecting one. The vertebral artery was clipped at the most proximal intracranial portion. Postoperative course was smooth and uneventful except deteriorated visual acuity. His visual acuity deteriorated continuously to hand movements 18 days after subarachnoid hemorrhage. His visual acuity, however, gradually improved without specific treatment. At the time of this writing, his visual acuity is 1.0 on both sides. Vitreous hemorrhage is a rare complication following a reptured aneurysm. Pertinent literature concerning fundal hemorrhage, especially vitreous hemorrhage, associated with subarachnoid hemorrhage suggests that it may occur as a result of sudden increase of intracranial pressure.

Eye Diseases↗
PubMed1979

Etiological relation between Korean hemorrhagic fever and epidemic hemorrhagic fever in Japan.

The first case of epidemic hemorrhagic fever in Japan was seen in Osaka in 1960. The etiologic agent of this disease has not yet been isolated, but a close etiologic relation between Korean hemorrhagic fever and epidemic hemorrhagic fever in Japan has been suspected because of similarities in the clinical and pathological pictures of the two diseases. This relation has now been confirmed serologically by demonstrating specific immunofluorescent antibodies to Korean hemorrhagic fever virus in 19 of 20 sera obtained from subjects 7 to 17 years after an acute attack of epidemic hemorrhagic fever.

Adolescent↗
PubMed1977

von Willebrand's disease and hemorrhagic telangiectasia: association of two complex disorders of hemostasis resulting in life-threatening hemorrhage.

The clinical and laboratory findings in a patient with uncontrolled gastrointestinal bleeding secondary to combined hemostatic defects (von Willebrand's disease and hemorrhagic telangiectasia) are described. Evidence for von Willebrand's disease was found in five family members, but no other affected relative was found to have hemorrhagic telangiectasia. Complete assestivity, factor VIII antigen and von Willebrand factor levels. The patient described also was evaluated for her response to transfusion utilizing these same measurements. Previous reports of the coexistence of hemostatic defects with hereditary hemorrhagic telangiectasia are reviewed. The importance of complete hemostatic evaluation of patients with mucocutaneous bleeding is stressed in light or current knowledge of the diagnostic specificity of available laboratory tests.

Blood Coagulation Tests↗
PubMed1975

[Digestive tract hemorrhages of cirrhotic patients. Relation between hepatic insufficiency and the hemorrhagic lesion].

The cause of upper gastrointestinal bleeding was studied in 85 cirrhotic patients by emergency endoscopy. In every patient, one or several lesions were observed and the site of bleeding was ascertained in 59. The two main causes were oesophago-gastric varices (46 p.cent) and acute mucosal lesions(42 p.cent). The source of bleeding appeared to be related to the degree of liver function impairment. In patients with no or moderate liver function impariment, bleeding usually originated from varices or from drug-associated mucosal erosions. Patients with severe impairment of liver function most often bled from spontaneous acute oeso-gastro-duodenal ulcerations. These ulcerations resembled what has been described in "stress" hemorrhage. Because of the relationship between liver function and the cause of hemorrhage, mortality was lower in variceal bleeders (29 p.cent) than in patients with spontaneous ulcerations (83 p.cent). In patients with severely impaired liver function, portacaval shunt was rarely indicated since hemorrhage was generally due to acute mucosal ulcerations.

Adult↗
PubMed1977

[Recurrent massive hemorrhage of the distal part of the digestive tract due to hemorrhagic hereditary telangiectasia].

Massive gastrointestinal bleeding is known to occur in patients presenting the hemorrhagic hereditary telangiectasis condition known as Rendu-Osler-Weber (ROW) disease. Bleeding is most frequent in the fourth decade. Endoscopic coagulation of upper gastrointestinal telangiectatic spots is nowadays possible even in the presence of active bleeding. In the lower digestive tract the naevi are basicallly located on the terminal ileum and the right colon; emergency coloscopic examination is difficult when active bleeding occurs. 10-15% of ROW patients present sudden life-threatening episodes of bleeding. The danger is aggravated through delayed diagnosis as well as difficulty in localizing the hemorrhagic area. Selective angiogram of the three digestive arteries is a safe and efficient method of diagnosing the nature and source of the bleeding. It should be obtained routinely, on an emergency basis, before surgery. Operation includes removal of the involved part of the digestive tract. A specimen angiogram should be obtained during the procedure, to make sure that the bleeding malformation has been removed. Laparotomy without preliminary angiogram is likely to be unsuccessful. An illustrative case is presented.

Aged↗
PubMed1979

[Central serous retinitis or chorioretinitis (retinopathy or chorioretinopathy) and central hemorrhagic chorioretinitis (juvenile disciform macular detachment; focal hemorrhagic chorioiditis, presumed histoplasmosis) (author's transl)].

There are no clinical or etiological connections between central serous and central hemorrhagic chorioretinitis, Serous chorioretinitis is seen mostly in men; full visual acuity is regained in approx. 80% of all cases. It mainly affects subjects aged between 36 and 45. Hemorrhagic chorioretinitis affects both sexes to about the same extent and causes severe impairment of visual acuity. Both forms should be regarded as genuine inflammations (chorioretinitis centralis serosa, chorioretinitis centralis hemorrhagica), not as "pathies". Whereas the hemorrhagica disease is generally thought to be caused by inflammation, the serous form also often shows signs of inflammation such as varying leakages with inflammatory depigmentation and more frequently inflammatory protein increase (exudate) with precipitation on the posterior surface of the retina/anterior surface of the pigment epithelium.

Adult↗
PubMedDate not supplied

[Role of the blood kinin system in the pathogenesis of the hemorrhagic syndrome in hemorrhagic vasculitis].

Total esterase activity of blood plasma from healthy persons was equal to 27.4 +/- 4.96 micrometer/ml/hr, activity of kallikrein--74.4 +/- 8.65 micrometer of hydrolysed substrate/hr/ml of blood plasma, inhibitory capacity of blood plasma towards kallikrein was 0.9 +/- 0.1 app. un. Total esterase activity of blood plasma, reflecting the activity of trypsin-like enzymes and kallikrein, was distinctly increased in patients with hemorrhagic vasculitis as compared with control group; content of prekallikrein and the inhibitory capacity of blood plasma towards kallikrein were decreased. In patients with severe forms of hemorrhagic vasculitis the most pronounced activation of blood kinine system was observed due to decrease in content of kallikrein and in the inhibitory capacity of blood plasma towards kallikrein.

Adolescent↗
PubMed1979

[The significance of blocked arteries in the pathogenesis of hemorrhages and of minor hemorrhagic infarctions in the human lung in fat embolism (author's transl)].

The significance of blocked arteries with regard to minor hemorrhagic infarctions in the lung in venous and systemic fat embolism is discussed. In an experiment it is proved that blood in the anastomoses between the arteria bronchialis and arteria pulmonalis (blocked arteries) contains fat emboli. It is suggested that these fat emboli may in addition be transported into an area of the lung, which is no longer functional following embolic occlusion of a branch of the arteria pulmonalis.

Bronchial Arteries↗
PubMedDate not supplied

Intracranial aneurysms and subarachnoid hemorrhage. A cooperative study. Antifibrinolytic therapy in recent onset subarachnoid hemorrhage.

In this cooperative study among 13 institutions, 502 patients were treated with antifibrinolytic medication (epsilon-aminocaproic acid or tranexamic acid) within a 14-day period following rupture of an intracranial aneurysm. Mortality at the end of 14 days was 11.6%; proved rebleed rate was 12.7%. Patients with an internal carotid or anterior cerebral aneurysm had the highest mortality and rebleed rate. Most rebleeds occurred between the sixth and eleventh days following the initial bleed. Significantly higher mortality was reported among patients with cerebral vasospasm, yet rebleed rate was no different among those patients with or without vasospasm. The same pattern was observed among patients with a mean blood pressure value above and below 110 mm Hg. We conclude that antifibrinolytic therapy provides beneficial treatment to patients with recent onset subarachnoid hemorrhage (SAH) following rupture of an intracranial aneurysm.

Age Factors↗
PubMed1977

Adrenal hemorrhage in the newborn. The phenomenon of "enclosed" hemorrhage as a cause of neonatal jaundice and later adrenal calcifications.

In an infant with unexplained hyperbilirubinemia, abdominal mass and a fall in hematocrit, an IVP with total body opacification should be considered so that the diagnosis of adrenal hemorrhage, which is almost always a benign conditions, may be made. Follow-up abdominal films at 3 months of age may further substantiate the etiology by revealing calcifications in the involved areas.

Adrenal Gland Diseases↗
PubMed1975

Factors affecting liver fat accumulation and liver hemorrhages associated with fatty liver-hemorrhagic syndrome in laying chickens.

A series of four experiments was conducted with a commercial strain of laying chickens in an attempt to experimentally produce Fatty Liver-Hemorrhagic syndrome (FLHS). Different dietary energy sources, environmental temperatures and feeding schedules were the experimental variables. Increasing the environmental temperature from 12.2 degrees C. (experiment 1) to 27.8 degrees C. (experiment 2) did not drastically alter total liver fat, 2.7 g. (experiment 1) vs. 2.9 g. (experiment 2) or the incidence of FLHS, 0.0% (experiment 1) vs. 1.0% (experiment 2). Likewise, in experiment 4, changing the environmental temperature from 22.2 degrees C. to 30.6 degrees C. or from 30.6 degrees C. to 22.2 degrees C. did not significantly (P greater than .05) alter total liver fat or liver wet weight. The greatest incidence (50%) of FLHS occurred in birds which were restricted in feed intake and exposed to an environmental temperature of 30.6 degrees C. from 32-36 weeks of age followed by ad libitum feeding at a temperature of 22.2 degrees C. from 36-40 weeks of age. These birds ate 26.8% more feed than the control birds during the ad libitum feeding period. Restricted feed schedules (experiment 3) resulted in significantly (P less than .05) lower 40 week liver wet weights and total fat when applied during the growing (14-20 weeks of age) and early lay (20-28 weeks of age) periods.

Age Factors↗