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

In addition to the typical manifestations of thrombotic-thrombocytopenic purpura like thrombocytopenia, haemolysis, fever, coma and renal failure, signs of a beginning DIC could be seen in a patient after abdominal surgery. Haemostatic, cardiovascular and respiratory data are presented. Pulmonary angiography by using a Swan-Ganz-catheter revealed multiple filling defects reversible with therapy. Treatment with fresh whole blood aggravated thrombocytopenia. Daily infusions of fresh frozen plasma combined with heparinisation and antithrombin III because of DIC, induced haematologic remission. Renal failure and cerebral symptoms could not be influenced. Diagnosis, monitoring and therapy are discussed.
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PMID:[Partial remission of fulminant thrombotic-thrombopenic purpura (Moschcowitz syndrome) by infusion of fresh plasma]. 375 26

Following the administration of fluphenthixol (a depot phenothiazine) for a psychotic illness, a 44-year-old woman developed weakness, rhabdomyolysis and renal failure, together with hyperthermia (42 degrees C) and signs of both autonomic and central nervous system dysfunction. She died following massive intestinal haemorrhage, intra-abdominal sepsis and probable disseminated intravascular coagulation. A diagnosis of neuroleptic malignant syndrome had been made, but treatment with dantrolene sodium was probably instituted too late to prevent the progress of the complications she had developed. This syndrome, which follows the use of phenothiazines or butyrophenones, is rare, potentially fatal and probably underdiagnosed. It has been likened to malignant hyperthermia, but a review of the literature points to many differences. Both dantrolene sodium and dopaminergic drugs (bromocriptine, amantidine and L-dopa) have been shown to be efficacious and their continued use, despite a failure in this case, is advocated until more is known about this syndrome.
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PMID:The neuroleptic malignant syndrome. Case report with a review of the literature. 382 73

Acute leukemias with high white blood count have a poor immediate prognosis and the treatment must be started within the first hours following diagnosis. It is necessary to prevent and to treat the severe metabolic disorders observed during induction treatment of acute lymphoblastic leukemia with WBC greater than or equal to 100,000/mm3. We analysed all the metabolic disorders in a retrospective study of 45 patients in order to determine their adequate prevention and treatment. Prevention of hyperuricemia and of secondary renal failure is now possible with urate oxidase, allowing an aggressive and rapid induction. Hyperkalemia can be prevented by urinary alkalinization and hyperphosphoremia with hypocalcemia by high dose intravenous calcium therapy. Renal failure is often transitory and functional. Disseminated intravascular coagulation is treated by heparin and platelets infusion and severe hyperglycemia requires insulin therapy.
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PMID:[Acute hyperleukocytic lymphoblastic leukemia (greater than or equal to 100,000 leukocytes/mm3). Metabolic changes during induction treatment. Study, prevention and treatment]. 385 53

In spite of all the scientific and technical advances in recent years, shock that is not rapidly correctable with fluid can have a morbidity rate exceeding 80%. Consequently awareness of such precipitating factors as sepsis and early diagnosis and treatment are essential. Treatment should be rapid and should follow a previously outlined protocol. Such protocols should include correction of the precipitating problem and aggressive resuscitation to assure adequate ventilation and oxygenation of the blood and optimal oxygen delivery to the tissues. Fluid and blood should be given as needed until filling pressures begin to rise rapidly with further fluid infusion. With hemorrhagic shock in previously healthy individuals, a hemoglobin level of 10.0 g/dL is usually adequate. In older, septic, or cardiogenic shock patients, a hemoglobin level of 12.5 to 14.0 may be preferable. If an optimal preload does not increase cardiac output to normal or higher levels, inotropic agents should be used. If shock still persists, one must be sure that the arterial pH is not excessively high or low. Glucocorticoids may then be given in low dose (200 mg hydrocortisone) in case some degree of adrenal insufficiency is present. They can also be given in high doses (equivalent to 150 mg/kg hydrocortisone) early in septic shock primarily to prevent excess complement activation and to preserve membrane integrity. Vasopressors may occasionally be required if there is excessive vasodilation, especially if there is persistent hypotension in the presence of high-grade coronary or cerebral artery stenosis. Vasodilators may be used to try to correct myocardial ischemia (nitroglycerin), excessive preload (nitroglycerin), or excessive afterload (nitroprusside or hydralazine). Combinations of vasodilators and inotropic agents may be required in some patients with high systemic vascular resistance and persistently low cardiac outputs. Mechanical assist with IABP can be of great value in persistent cardiogenic shock. Diuretics may occasionally help prevent renal failure in patients who are persistently oliguric after blood flow and pressure are restored. Heparin is occasionally of value if DIC develops with no concomitant fibrinolysis. Antibiotics are important in septic shock and may also be important if persistent shock has reduced gastrointestinal mucosal integrity so that bacteria and bacterial products can enter the portal system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Science and shock: a clinical perspective. 389 56

Because of the importance of the renin-angiotensin system in renal homeostatic mechanisms, the effect of angiotensin administration upon disseminated intravascular coagulation has been studied in rabbits. An infusion of angiotensin II (0.1 mug/kg/min for 2 hours) produced neither histologic abnormalities in the kidneys nor an elevation of creatinine. After an infusion of thrombin (2.0 units/kg/min for 2 hours) only 3 of 10 rabbits, when sacrified 24 hours later, showed histologic lesions comprised of occasional fibrin thrombi and foci of tubular necrosis. Creatinine levels did not rise. In contrast, the combination of angiotensin and thrombin resulted in renal lesions in 12 of 14 animals. Four had frank cortical necrosis, while combinations of tubular necrosis, glomerular thrombosis and segmental glomerular infarction occurred in the others, together with elevated creatinine levels. Blockade of alpha-adrenoreceptors with phenoxybenzamine in 12 animals did not prevent either these histologic changes or creatinine elevation, showing that the effect of angiotensin was independent of alpha-adrenoreceptor stimulation. The synergistic interaction between angiotensin and disseminated intravascular coagulation was not explained by differences in the consumption of plasma fibrinogen but apparently was due to localization of fibrin thrombi within glomerular capillaries by the vasomotor actions of angiotensin, as has previously been shown to occur with alpha-adrenoreceptor simulation. Such a mechanism might contribute to renal glomerular deposition of fibrin in acute ischemic renal failure.
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PMID:Interaction of angiotensin with disseminated intravascular coagulation: a possible mechanism in the genesis of acute renal failure. 435 49

Eight patients with E. coli septicaemia had oliguric renal failure which was associated with haematological evidence of intravascular coagulation. Five of these patients also had the characteristic blood picture of microangiopathic haemolytic anaemia. In an attempt to prevent further deposition of fibrin, intravenous heparin was administered to six patients, three of whom recovered fully and three died. The diagnosis of intravascular coagulation was subsequently confirmed by histological examination of necropsy material and it is suggested that some of the complications of E. coli septicaemia may be attributable to disseminated intravascular coagulation.
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PMID:Intravascular coagulation and E. coli septicaemia. 457 93

If there are adverse reactions following blood transfusion accurate intervention is necessary. Symptomatical therapy has to start independent from the origin of transfusion reaction. Specific therapy should base on laboratory results. Symptoms, their frequency and severity, are described and therapeutic strategy is outlined. Severe transfusion reaction leading to shock, disseminated intravascular coagulation and renal failure needs intensive care.
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PMID:[Therapy of adverse transfusion reactions]. 610 31

Patients with severe viral infections such as Lassa or Ebola may be denied adequate laboratory investigations because of justifiable fears among laboratory staff. This study in monkeys was designed to provide comprehensive haematological and biochemical monitoring in a contained environment during all stages of Ebola infection. Marked neutrophilia, depletion of lymphocytes, and early failure of platelet aggregation preceded a consumption coagulopathy with a microangiopathic haemolytic anaemia, thrombocytopenia, and failure of prostacyclin production by vascular endothelium. Liver dysfunction was moderate but in conjunction with the dehydration and hypoalbuminaemia could be expected to precipitate renal failure and shock. It seems reasonable to anticipate successful patient support with a patient management isolator and treatment with platelet transfusions, fresh frozen plasma, and possibly prostacyclin when haemostasis is defective during this otherwise self-limiting illness.
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PMID:Haematological and biochemical monitoring of Ebola infection in rhesus monkeys: implications for patient management. 613 2

To investigate the nature and role of coagulation and complement alterations in the pathogenesis of Korean hemorrhagic fever (KHF), the profiles from the early stages in 27 male patients were serially evaluated. Evidence of disseminated intravascular coagulation (DIC) was observed in 14 of the 27 patients (51.8%) sometime during the course of the disease. The earlier the coagulation tests were performed, the more frequently the evidence of DIC was found. The mean serum C3 concentration was significantly decreased during the early stages, while serum C4 concentrations revealed no significant variation. A significant decrease of the serum C3 concentration, however, was found only in the group with DIC. Korean hemorrhagic fever (KHF) is an acute, systemic disease characterized by fever, hemorrhagic manifestations, and renal failure. This disease has been known to occur from the Pacific Ocean to the Baltic Sea under various synonyms and toponyms including epidemic hemorrhagic fever, hemorrhagic nephrosonephritis and hemorrhagic fever with renal syndrome. Recent investigations demonstrated the identity of these conditions described from Korea, the Soviet Union, Japan, and China. Nephropathia epidemica of Scandinavia was also revealed to have a close serological relation to this disease, but with antigenic differences. The etiologic agent was identified in 1978 by Lee et al., who isolated a viral antigen from a field mouse, Apodemus agrarius coreae, which is the natural reservoir of this disease in Korea. The KHF or Hantaan virus has been propagated in cell cultures and observed electronmicroscopically. In thin sections, the virus was detected within the cytoplasmic granular matrices (viroplasms) of the infected cells. Virus particles were spherical and had an extremely electron-dense core. Negative-contrast staining showed that the virus had an icosahedral structure and annular surface capsomeres. The morphology and morphogenesis of the virus were similar to those of the orbiviruses. The characteristic pathologic findings observed in fatal cases of KHF are congestion and hemorrhage of the renal medulla, hemorrhage in the right atrial wall of the heart, and hemorrhage and necrosis in the anterior lobe of the pituitary gland. The microscopic characteristics of these lesions consist of hemorrhage, coagulation necrosis, and mononuclear cell infiltration. The clinical course of typical KHF may be divided into five phases, each designated for a characteristic physiologic aberration; febrile, hypotensive, oliguric, diuretic, and convalescent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Disseminated intravascular coagulation in Korean hemorrhagic fever. 614 86

Acute necrotizing pancreatitis developed in 5 of 405 patients who underwent renal transplantation. All five patients were taking immunosuppressive medication (azathioprine and steroids). Three patients also received rabbit antithymus serum. Alcohol ingestion or cholelithiasis did not play any causative role in the pancreatitis, which began between 7 days and 13 months after renal transplantation. The delay from the time of admission for pancreatitis to surgical exploration was a mean of 17 days. Operative findings included pancreatic necrosis, hemorrhage and abscess formation. All five patients died of the complications of necrotizing pancreatitis--persistent sepsis, respiratory and renal failure, upper gastrointestinal bleeding and disseminated intravascular coagulation. This review demonstrates that prolonged conservative therapy in renal transplant patients with necrotizing pancreatitis is associated with high mortality. The authors believe that earlier surgical intervention will lead to increased survival.
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PMID:Necrotizing pancreatitis in renal transplant patients. 618 Aug 18


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