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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of fatal heat stroke, concerning a 20 year-old soldier and a 44 year-old psychiatric patient, treated with neuroleptics, are reported. The clinical picture, starting suddenly with coma and hyperthermia, was quite identical for both. Secondarily, while hyperthermia decreases and the conscience improved partially, an hemorrhagic syndrome similar to a consumption coagulopathy, acute renal insufficiency and acute hepatic failure appear. Death occurred after aggravated neurological disorders and respiratory distress. The anatomical lesions spread on all the viscera include tubular nephritis, and hepatic centro-lobular necrosis and an interstitial and alveolar oedema with hemorrhages and hyaline membranes in the lungs.
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PMID:[Heat stroke and disseminated intravascular coagulation. Apropos of 2 cases]. 21 8

The hemodynamic response to slow and rapid defibrination was sutdied in anesthetized beagle dogs, with the following results: 1. Slow defibrination was a benign procedure that had little or no effect on the hemodynamic variables studied. 2. Rapid defibrination induced statistically significant decreases in cardiac output, stroke volume, and mean aortic arterial pressure. 3. Bradycardia, a drop in mean left v"ntricular pressure, cardiac and minute work indices, an increase in pulmonary artery pressure, and a drastic rise in pulmonary and systemic vascular resistances were also observed. Although physiologically apparent, these changes were not statistically significantly different from control levels. 4. Pulmonary capillary wedge pressure, left ventricular end-disatolic pressure, arterial pH, and blood gases were not altered by rapid defibrination. 5. In view of the similarities between the hemodynamic changes observed after rapid defibrination and acute myocardial ischemia, the role of decreasing fibrinogen concentrations and blood viscosity in aucte myocardial infarction and the sudden death syndrome is questioned.
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PMID:Hemodynamic effects of slow and rapid defibrination with defibrizyme, the thrombin-like enzyme from venom of the timber rattlesnake. 23 15

Two patients developed heat stroke following jogging. Transient disturbance of cerebral function was the most dramatic clinical feature. Although haemorrhagic complications were not seen, marked changes in the haemostatic system occurred with both thrombocytopenia and a reduction of clotting factors synthesised by the liver. No evidence of disseminated intravascular coagulation was found. Heat stroke must now be added to the list of jogging hazards.
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PMID:Jogger's heat stroke. 28 29

Two patients are presented in whom cerebral angiography was complicated by bioccipital infarcts resulting in cortical blindness with persisting severe restriction of the visual field (case 1) and persisting cortical blindness (case 2). One patient (case 1) demonstrated a compensated, protracted disseminated intravascular coagulation (Table 1), which disappeared after treatment with phenprocoumon (Marcoumar). The other patient (case 2) demonstrated increasee spontaneous platelet aggregability (Table 2), which was treated sucessfully with acetylsalicylic acid (Magnyl) and dipyridamole (Persantine). We presume that the coagulation disturbances demonstrated after the angiography may be pathogenetic to the complications. We propose that patients with transient cerebral ischemia and apoplexy who are undergoing cerebral angiography should be studied with regard to coagulation before and after the cerebral angiography so that coagulation disturbances demonstrated may be treated before, or corrected after the angiography.
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PMID:Possible increased tendency to thrombosis after cerebral angiography. 45 38

A 14-year-old patient with heat stroke, disseminated intravascular coagulation, central nervous system dysfunction, and renal failure was treated, in addition to conventional therapy, with heparin sodium for seven days. Despite very poor prognostic signs on addmission, the patient survived the acute episode and ultimately progressed to a complete recovery.
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PMID:Disseminated intravascular coagulation in heat stroke. Response to heparin therapy. 80 83

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
Stroke
PMID:Coagulopathy following experimental cerebral ischemia. 84 91

Consumption coagulopathy is frequently observed in a resuscitation department. 120 cases of various etiologies are reviewed: complications of pregnancy (61 cases), infections (23 cases) or various stresses: acute hemolysis, shock, severe hepatic failure, intoxications, acidosis, heat-stroke... Consumption coagulopathy is intricated with the general stress which induces it, and with the visceral lesions induced by the stress and which can be aggravated by the consumption coagulopathy. The state of shock is observed in 76% of the cases, the haemorrhagic syndrome in 73%. Acute hemolysis and the clinical signs evocative of disseminated intravascular coagulation (cutaneous signs) are more rare. Following the initial manifestations, visceral complications may develop: renal, hepatic, respiratory, neurological, digestive. The evolution of the biology must be carefully studied. The diagnosis is made on both clinical and biological data. Etiological and pathophysiological treatment should be carried out. In our series, controlled and adapted heparin therapy was given systematically.
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PMID:[Acute consumption coagulopathies. 120 cases]. 99 6

In accordance with the clinical and coagulographic data on 172 patients with ischemic brain stroke (IBS), the authors developed a method of the use of some medicamentous agents (heparin, platelet inhibitors, fresh-frozen blood plasma, plasminogen activators, proteolytic enzymes), adapted to concrete characteristics of the coagulation status at different stages of brain infarction formation and permitting the rate of lethal outcomes to be reduced. In disseminated intravascular coagulation seen in patients with the gravest patterns of IBS, heparin may be indicated.
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PMID:[Revising the principles and improving the methods of differential therapy of ischemic stroke]. 131 50

Two patients in a family of exertion-induced heat stroke were reported. Case 1: A 23-year-old male, paternal cousin of case 2, was admitted to our hospital because of loss of consciousness during running under a burning sun. On physical and neurological examinations, he was deeply comatose with high fever, tachycardia, and increased deep tendon reflexes. Laboratory findings disclosed rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, liver injury, and brain edema. He recovered after intensive cooling, some antibiotics, glycerol and sodium dantrolene administration. Case 2: A 19-year-old male experienced loss of consciousness and high fever during playing soccer at 15 years of age, and was admitted to a hospital. On admission, he had high fever of 38.7 degrees C, and increased serum CK level. He recovered two weeks after admission. He was readmitted to our hospital to evaluate the predisposition for malignant hyperthermia. His physical and neurological examinations showed no abnormalities. Routine laboratory findings were within normal limits. Muscle biopsy findings of cases 1 and 2 were mildly increased number of fibers with centrally placed nuclei. Caffeine test on skinned muscle fibers from the biopsies showed normal response in both type 1 and 2 fibers. The present patients were diagnosed as having exertion-induced heat stroke, but with no increased muscle fiber sensitivity to caffeine, suggesting that the pathomechanism differs from that of malignant hyperthermia induced by malfunction of sarcoplasmic reticulum.
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PMID:[Two familial cases with exertion-induced heat stroke--relationship to malignant hyperthermia]. 139 27

Disseminated intravascular coagulation (DIC) may cause multiple organ failure. Although DIC may cause capillary occlusion in any and all organs, the lungs, liver, kidneys, gut, heart and brain are particularly affected. Focal brain necrosis can also be caused by DIC. Fibrinolytic therapy will often restore significant blood flow to the capillaries of the lungs. This results in significant increase in lung function because the lung is more resistant to actual necrosis and will resume function once circulation is restored. Administration of fibrinolytic therapy will also prevent liver and kidney failure if started within four hours after trauma. This therapy, when given in low doses intravenously over a twenty-four hour period, has little effect on the coagulation mechanism, and abnormal bleeding, therefore, has not been a concern. It is speculated that if plasminogen activators are effective and safe for treating the intravascular clots of DIC, then perhaps they would be effective in treating other types of intravascular coagulation in the brain, such as various types and degrees of stroke.
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PMID:Organ damage in shock, disseminated intravascular coagulation, and stroke. 147 53


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