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

The local and generalized Shwartzman reactions are models of thrombohemorrhagic skin necrosis and DIC, respectively. An intravenous preparatory injection of endotoxin followed by an intradermal injection of endotoxin 24 hours later elicits a thrombohemorrhagic lesion only at the site of intradermal injection of endotoxin in the local Shwartzman reaction. Two intravenous injections of endotoxin spaced 24 hours apart induced a systemic generalized Shwartzman reaction characterized by coagulopathy, petechial hemorrhages, microthrombi, and decreased circulating platelets similar to DIC. Of particular interest is the observation that thrombohemorrhagic lesions of the Shwartzman reaction only develop at sites of intradermal injections of endotoxin. Microthrombi composed of platelets and leukocytes only adhere or accumulate in dermal vessels after an intradermal injection of endotoxin. Prior to the endotoxin injection, biopsies of skin show normal vessels without microthrombi or significant inflammation. Since endothelial cells line the small vessels in the dermis, where a Shwartzman reaction appears to be initiated, it is likely that endothelial cells are important for initiating a local Shwartzman reaction. IL-1 and TNF can substitute for the intradermal injection of endotoxin in the local Shwartzman reaction, induce endothelial cells to become thrombogenic, and can induce the expression of cell adhesion molecules on endothelial cells making endothelial cells more sticky for leukocytes. These observations suggest that endothelial cells play a central role in the local Shwartzman reaction and may be important in understanding diseases associated with thrombohemorrhagic skin necrosis.
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PMID:Shwartzman reaction. 228 21

Hematological and coagulating parameters were examined in 53 patients in an attempt to find possible evidence of disseminated intravascular coagulation after intravascular injection of 5% ethanolamine oleate to sclerose esophageal varices. FDP-E in the peripheral blood measured by latex photometric immunoassay significantly increased from 111.2 +/- 112.9 to 234.2 +/- 178.3 ng/ml and 370.4 +/- 189.5 ng/ml one hour after the first and second sessions of sclerotherapy, respectively (p less than 0.01). The other parameters showed no significant change, except on the first day after sclerotherapy. The increase of FDP-E was closely related to fibrinopeptide A (r = 0.689, p less than 0.01) and fibrinogen (r = 0.585, p less than 0.05), before the sclerotherapy. As repeated intravariceal sclerotherapy over short time intervals can lead to a deterioration of the coagulating system, especially in patients with abnormal preoperative coagulopathy, latex photometric immunoassay for FDP-E is a rapid and useful method of monitoring alterations in the coagulating system.
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PMID:Hypercoagulopathy after repeated injection of 5% ethanolamine oleate to sclerose esophageal varices. 228 69

Coagulation studies were performed in a patient who had been bitten by a snake of the species Bothrops neuwiedi. The patient presented with hemorrhagic necrosis at the envenomization site and considerable bleeding from venous puncture sites. He developed a severe defibrination syndrome with a clottable fibrinogen level of approximately 0.1 g/l. Fibrinogen was not measurable by clotting time assay. Fibrin degradation products were greatly elevated. Treatment with antivenom caused an anaphylactic reaction within ten minutes and serum sickness after three days. In vitro experiments revealed that B. neuwiedi venom directly activates Factors II and X, but does not activate Factor XIII. In vivo consumption of Factor XIII after B. neuwiedi envenomization is ascribed to the action of Factor IIa. At low venom concentrations clotting is initiated by activation of prothrombin by the venom either directly or via Factor X activation. Treatment with heparin might be beneficial in coagulopathy secondary to snake bite by reducing circulating active thrombin. The venom contains thrombin-like proteases which cause slow clotting of fibrinogen, and plasmin-like components causing further proteolysis of fibrinogen and fibrin. Antivenom has no effect on the proteolytic action of the snake venom. The in vivo effects of antivenom are presumably caused by acceleration of the elimination of venom components from the circulation. Intravenous administration of antivenom caused normalization of blood coagulation parameters within 48 h.
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PMID:Coagulopathy after snake bite by Bothrops neuwiedi: case report and results of in vitro experiments. 229 86

We have studied the activation state of the fibrinolytic system in 39 patients with systemic meningococcal disease (SMD). Patients defined as having fulminant septicemia (n = 13) with high (greater than 700 ng/L) levels of endotoxin (LPS) in plasma and severe coagulopathy, had significantly lower functional levels of plasminogen (P less than 0.05) and alpha-2-antiplasmin (P less than 0.01) and higher antigen levels of plasminogen activator inhibitor 1 (PAI-1) (P less than 0.01), and fibrin degradation products (FDP) (P less than 0.01), but not of PAI-2 (P greater than 0.1) as compared with less severely ill patients (meningitis and meningococcemia) (n = 25). A positive correlation existed between the admission (maximum) levels of LPS and PAI-1 (r = 0.86, P less than 0.0001). Decreasing admission levels of platelets were associated with increasing levels of PAI-1 (r = -0.55, P less than 0.001). After initiation of treatment with antibiotics and fresh frozen plasma, the PAI-1 levels declined rapidly. PAI-1 levels greater than 360 micrograms/L on admission predicted the development of a severe septic shock combined with renal impairment correctly in 12 of 13 patients (92%). None of 25 patients without multiple organ failure had PAI-1 levels greater than 260 micrograms/L. PAI-1 levels greater than 1850 micrograms/L were associated with 100% fatality. The results suggest that in the early phase of fulminant meningococcal septicemia an extensive plasmin generation occurs. On admission, however, high levels of PAI-1 seem to inhibit the plasmin generation, and thereby promote DIC.
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PMID:Plasminogen activator inhibitor 1 and 2, alpha-2-antiplasmin, plasminogen, and endotoxin levels in systemic meningococcal disease. 231 89

The coagulation profile of 25 patients with brain tumours was studied preoperatively, intraoperatively and postoperatively. Ten patients had abnormal coagulation status preoperatively. Surgical intervention led to either an alteration of preexisting abnormality or appearance of new coagulation abnormality. Disseminated intravascular coagulation and fibrinolysis occurred with equal frequency in patients with meningiomas and gliomas. The alterations as a result of surgery were transient and compensated rapidly.
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PMID:Haemostatic abnormalities in brain tumours. 233 75

Derangements of hemostasis and hemocoagulation in patients with malignancies are known as paraneoplastic syndrome. Their origin, however, has not been unequivocally established and explained, and data on their occurrence are controversial. Examination of 157 patients with different malignant tumor diseases yielded pathological laboratory findings in 94.2%. The most frequent finding was the state of hypercoagulation in 41.0%; hypercompensated syndrome of disseminated intravascular blood clotting (DIC) was found in 10.9%, compensated DIC syndrome in 18.0%, consumptive coagulopathy in 3.8%, and in 19.2% hypocoagulation state caused by other abnormalities. The laboratory finding was normal only in 5.8% of the patients. In the light of the high occurrence rate of hemostatic and hemocoagulation changes in malignant diseases, established by laboratory analysis, the use of anticoagulants and antiaggregation substances appears to be justified in the majority of cases, both to prevent the development of these changes which may complicate the course of the malignant condition, and in preoperative care to reduce the rate of postoperative thromboses in patients with tumors.
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PMID:[Changes in hemostasis as one of the paraneoplastic manifestations]. 237 16

Disseminated intravascular coagulation (DIC) occurred after closed Ender's pinning of a pathologic fracture of the humerus in a 58-year-old man with metastatic prostatic carcinoma. A review of the oncologic and urologic literature revealed that coagulopathy can be associated with prostatic carcinoma. This association seems not to have been previously reported in the orthopedic literature.
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PMID:Disseminated intravascular coagulation complicating Ender's nailing of a pathologic fracture in prostatic carcinoma. A case report. 239 52

Coagulopathy due to tuberculosis is rare. We believe ours is only the second reported case of cavitary tuberculosis associated with disseminated intravascular coagulation. Our review of all 13 cases to date shows that the patients are generally black, middle-aged, male, alcoholic, and febrile. The tuberculosis is generally military, and is associated with a high mortality. Eight of the patients had associated adult respiratory distress syndrome. Only one (our case) had an acute tuberculous peritonitis. In six cases the coagulopathy began after the start of therapy; steroids did not appear to affect survival. The exact pathophysiologic mechanisms involved in the development of DIC are unknown.
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PMID:Disseminated intravascular coagulation in association with cavitary tuberculosis. 240

The coagulation and fibrinolytic systems were analysed parallel to the clinical evaluation in 27 attacks of acute human pancreatitis of different severity. Consumptive coagulopathy was evident from decreased platelet counts, decreased prothrombin values and consumption of fibrinogen during the first days in severe attacks. Fibrinolysis was suggested by decreased plasminogen values and the presence of fibrinogen degradation products. All main protease inhibitors of the two systems showed protease-antiprotease complexation and lower functional than quantitative values. Functional levels of the protease inhibitors were almost zero in the peritoneal fluid in severe attacks. It is concluded that severe acute pancreatitis results in consumptive coagulopathy and fibrinolysis together with a local antiprotease deficiency. All the changes are closely correlated to the severity of the disease.
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PMID:Disseminated intravascular coagulation and antiprotease activity in acute human pancreatitis. 243 83

After an accidental or intentional ingestion of lindane, clinical manifestations of poisoning may include rapid onset of nausea and vomiting, coma, seizures, respiratory failure, and death. While rhabdomyolysis, secondary renal failure, and aplastic anemia have also been reported, coagulopathies have not been observed following poisoning with this pesticide. In this case report we describe a 43-year-old female who intentionally ingested 8 oz of a 20% lindane solution. Her serum lindane concentration reached 1.3 mcg/ml and her clinical manifestations included seizures, coma, rhabdomyolysis, secondary renal failure, and disseminated intravascular coagulation. The coagulopathy presented early in her clinical course and resolved when serum lindane levels fell. The patient died 11 days after the ingestion.
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PMID:Disseminated intravascular coagulation in a case of fatal lindane poisoning. 245 26


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