Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peritoneovenous shunting for the treatment of malignant ascites has become increasingly popular. This technique can be complicated by tumor embolization, congestive heart failure, and disseminated intravascular coagulation. Arterial thromboembolism has been encountered in two patients following LeVeen shunt insertion. Recurrent bilateral femoral artery thromboemboli and a cerebrovascular accident occurred in one patient and cerebrovascular thromboembolism developed in a second patient. Major arterial embolization is potentially a serious, although infrequent, complication of peritoneovenous shunting in patients who have malignant ascites.
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PMID:Arterial thromboembolic complications of peritoneovenous shunting for malignant ascites. 620 87

Hemorrhagic infarction of the basal ganglia was observed in 2 young adult patients with acute leukemia who presented with progressive hemiparesis combined with severe mental alterations. In case 1 (AML) lethal infarction due to thrombosis of both internal cerebral veins occurred during induction therapy for relapsed leukemia; in case 2 (cALL) a devastating stroke probably due to deep cerebral venous thrombosis happened during the third remission. Neither of them had hyperleukocytosis, signs of infection, disseminated intravascular coagulation or CNS leukemia. We discuss long-term glucocorticoid therapy (case 1) and combined prophylactic CNS treatment (case 2) as possible risk factors for cerebrovascular thrombosis in acute leukemia.
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PMID:Hemorrhagic infarction of the basal ganglia. An unusual complication of acute leukemia. 664 5

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

The data on one of sepsis variations, bacterial or endotoxin shock (BS) are presented. BS is caused by gram-negative flora among which the first place belongs to E. coli, but may also be caused by gram-positive bacteria. BS is characterized by an acute onset with chills, hyperthermia, leukocytosis and early development of circulatory collapse which may cause early death of the patient. The direct of mediated effect of endotoxin on the vascular wall causing paralytic distention of the microcirculatory bed with deposition of the blood in it is recognized in the pathogenesis of BS. Subsequently, under conditions of hypoxia and acidosis disorders of hemocoagulation develop in the form of disseminated intravascular coagulation which may result in cortical necrosis of the kidneys, necrosis and apoplexy of the adrenals, hypophysis, acute ulcers in the gastrointestinal tract, necroses and hemorrhages in some other organs.
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PMID:[Bacterial (endotoxic) shock]. 699 29

Patients with classical heat stroke are different in many ways from those with exertional injury; contrasts included difference in demographic factors, prior general health, in-hospital complications and laboratory abnormalities (lactate, liver enzymes, pH, electrolytes). Severe hyperkalemia, acute renal failure, rhabdomyolysis and disseminated intravascular coagulation often dominate the course of patients with exertional heat stroke but are uncommon in those with classical heat stroke (Table 4). While lactic acidosis is the rule in exertional injury, it is somewhat unusual in patients with classical heat stroke and when above 3 mmoles/L predicts a poor outcome or death. In spite of the advanced age and multiple medical problems of the patients with classical heat stroke, careful attention to early and aggressive cooling and scrutiny for potential complications can result in salvage of most patients.
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PMID:Epidemic classical heat stroke: clinical characteristics and course of 28 patients. 707

A patient with moderately severe heat stroke was studied with particular attention to changes in haemostasis. Activation of fibrinolysis, a probable failure of hepatic synthesis of coagulation factors and severe thrombocytopenia were observed, but there was no definite evidence for disseminated intravascular coagulation (DIC). It is suggested, however, that in heat stroke of greater severity the more extensive tissue breakdown may lead to DIC. If DIC is superimposed on the above changes in haemostasis it is likely to be both sudden and overwhelming.
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PMID:Haemostasis in heat stroke. 712 69

Sixty-five patients with a bleeding disorder and coexistent neurologic abnormalities were examined over a 4-year period to determine: (1) the CNS pathology due to disseminated intravascular coagulation (DIC); (2) the clinical setting in which CNS dysfunction due to DIC occurs; and (3) the neurologic complications of DIC as opposed to those patients dying with concurrent DIC. Criteria for inclusion in the study were the combination of: (1) a neurologic disorder in a patient with clinical evidence of a bleeding disorder; and (2) evidence of DIC by laboratory criteria or the detection of fibrin thrombi in multiple organs at postmortem. Twenty-four of 65 patients met these diagnostic criteria, including 14 men and 10 women, aged 24 to 84 years. Autopsies were obtained in 17 patients. These patients were divided into two groups Group I consisted of 10 patients with evidence of cerebral bleeding or infarction at the onset of DIC. Group II consisted of 14 patients who met the diagnostic criteria for DIC but did not demonstrate postmortem evidence of hemorrhage or infarction in the brain. Patients with malignancy who present with findings suggestive of a large-vessel stroke are likely to have DIC and nonbacterial thrombotic endocarditis. The most common neurologic complications of DIC are large vessel occlusion, obtundation and coma, subarachnoid hemorrhage, and multiple cortical and brainstem hemorrhages and infarction.
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PMID:Neurologic complications of disseminated intravascular coagulation. 720 75

Ten cases of death due to heat stroke are described. They were all young men who collapsed during running exercise or route march and died in hospital later. Post-mortem examination was carried out in all cases. Death was due to disseminated intravascular coagulation with widespread microthrombus formation and coagulative necrosis involving many organs. Meteorological studies showed that at the time of the collapse the environmental temperature was higher than average although it may have been in the morning or evening.
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PMID:Acute heat stroke deaths. 722 95

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
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PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67

Heat stroke in distance runners is increasing in frequency. A case is reported of a 41-year-old man who collapsed during a 10-km "fun run" held when the temperature was 31.6 degrees C and the humidity 80%. Acute renal failure (serum creatinine level 1530 mumol/l [17.3 mg/dl]), rhabdomyolysis, disseminated intravascular coagulation and hepatic damage complicated the clinical picture. Repeated peritoneal dialysis and one cycle of hemodialysis because of a very high serum level of uric acid (1.23 mmol/l [20.7 mg/dl]) were required. Although the illness was prolonged, recovery was almost complete, and 4 months after the man's collapse the serum creatinine level had fallen to 133 mumol/l (1.5 mg/dl).
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PMID:Exertional heat stroke: the runner's nemesis. 738 6


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