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

Hypertension during pregnancy and its complications are the most important cause of maternal and foetal death and morbidity. The chronic primary hypertension can be differentiated from the dysgravidia by anamnestic, biological, clinical and technical investigations. However the diagnosis remains difficult and the renal needle biopsy can help to ascertain it. The pathogenesis of dysgravidia is still obscure: the placental ischemia leads to a slow disseminated intravascular coagulation state with renal injury, while a vascular hyperreactivity leads to an increase of the resistance, a relative hypovolemia and lowering of cardiac output. The treatment and remote prognosis of the hypertensive disease associated with the pregnancy are summarized. The antihypertensive drugs improve the maternal prognosis while jeopardize the foetal outcome.
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PMID:[Hypertension and pregnancy]. 30 56

Neonatal nonbacterial thrombotic endocarditis (NBTE), a rare disorder yet to be diagnosed antemortem, is described in two infants. The first infant was postmature and suffered from polycythemia and meconium aspiration. The meconium-stained placenta manifested evidence of ischemia and disseminated intravascular coagulation (DIC). The second patient was delivered near term by cesarean section, and hyaline membrane disease developed. The pathogenesis of NBTE may relate to perinatal hypoxia with transient tricuspid insufficiency, polycythemia, and DIC.
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PMID:Neonatal nonbacterial thrombotic endocarditis. 58 32

Presentation of a case of disseminated intravascular coagulation with micro-angiopathic hemolytic anemia, associated with a micro-carcinoma of the prostate. In the absence of other etiology it is postulated that the carcinoma was responsible for the hematological disturbance in spite of its small size andlack of either metastases or mucin secretion. The unusual discovery in this disease of bony necroses of the vertebrae, which are attributed to ischemia following micro-thromboses, is also discussed.
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PMID:[Disseminated intravascular coagulation with microangiopathic hemolytic anemia and bone necrosis associated with a prostatic microcarcinoma]. 70 6

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.
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PMID:Coagulopathy following experimental cerebral ischemia. 84 91

A patient with a relatively localized occult carcinoma of the lung and hemorrhage secondary to chronic disseminated intravascular coagulation (DIC) which continued for eight months is described. Despite continuing DIC two major operations were performed without excessive blood loss. Preoperative heparinization, in vitro clotting of the arterial graft, and temporary postoperative reversal of systemic heparin were utilized for abdominal aortic aneurysm resection. Blood product replacement therapy facilitated an emergency laparotomy. The patient was also managed successfully for several months without anticoagulant therapy. A hypothesis that vascular thrombi are not a necessary prerequisite for DIC is proposed. This hypothesis is based on the absence of thrombi or evidence of ischemia in this patient and in others and is supported by experimental observations made by other investigators.
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PMID:Case report: chronic disseminated intravascular coagulation due to occult carcinoma. 90 Jan 58

The significance and frequency of fibrin thrombi (FT), the pathological hallmark of disseminated intravascular coagulation (DIC), in ischemic intestine were analyzed in a retrospective study of the infarcted bowel of patients with occlusive mesenteric ischemia (OMI) and nonocclusive mesenteric ischemia (NOMI). Representative intestinal sections were studied from 10 patients with NOMI of the small and/or large bowel and 12 patients, with OMI of varied etiology. Three patients with inflammatory bowel disease and 1 patient with DIC and bowel necrosis were also studied. Routine hematoxylin and eosin stains for fibrin were prepared for each specimen. The number of FT was quantitated. FT were identified in each of the 10 cases of NOMI; however in only 2 were they prominent. FT were identified in 6 of the 12 cases of OMI and in 4 of these 6 they were a prominent feature. Rare FT were present in the cases of inflammatory bowel disease and did not correlate with the inflammatory process. No FT were present in the intestinal sections of the DIC case. FT are a nonspecific feature of necrosis and can be identified in both occlusive and nonocclusive ischemic bowel disease. Their presence in the intestine of NOMI therefore cannot be used to implicate DIC as the primary cause of this entity.
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PMID:Disseminated intravascular coagulation in nonocclusive mesenteric ischemia: the lack of specificity of fibrin thrombi in intestinal infarction. 99 77

A 10-year-old boy presenting with recurrent successive events of peripheral arterial occlusion in both legs, more prominent on the left side, was diagnosed as having acute promyelocytic leukemia. Histological examination of the occluding material showed that it was composed of leukemic blast cells. The boy underwent five operations. Each time the arterial flow was reestablished by removing cylindrical hollow white material obstructing the lumen. However, after the last operation, irreversible ischemia developed, necessitating an above-knee amputation. There was no evidence of disseminated intravascular coagulation. Three months later a right lumbar sympathectomy was performed for relief of causalgic-ischemic pains, with successful results. Preoperative angiography demonstrated irregular narrowing of the right iliac arteries and tibioperoneal trunk stenosis.
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PMID:Recurrent peripheral arterial occlusion by leukemic cells sedimentation in acute promyelocytic leukemia. 162 46

The purpose of this study was to determine whether normal fibrinogen contributes to the development of myocardial reperfusion injury by acting as a substrate in vivo for neutrophil adhesion. This was tested in a dog model of acute myocardial infarction that used pentobarbital anesthetized dogs subjected to 90 min regional myocardial ischemia and 5 h reperfusion. Dogs were treated with 1 unit/kg Ancrod (venom from the Malayan pit viper, Agkistrodon rhodostoma) or vehicle i.v. 60 min after left circumflex coronary artery occlusion. Therapeutic defibrination was verified in Ancrod-treated dogs by measurements of clottable fibrinogen, alpha-2 antiplasmin and plasminogen, by the activated partial thromboplastin time and by immunoelectrophoresis. Fibrinogen was depleted to below detectable limits of the assay (less than 0.05 mg/ml) after treatment with Ancrod. The defibrination effect was accomplished by the expected activation of the fibrinolytic system: alpha-2 antiplasmin was decreased by 10% and plasminogen activity was decreased by 30% with Ancrod treatment. There were no measureable differences between the two treatment groups in heart rate, mean arterial blood pressure, rate pressure product or circumflex coronary blood flow throughout the 90 min of regional ischemia or during the 5 h of reperfusion. The relative severity of ischemia between the two treatment groups was similar when assessed with radiolabeled microsphere measurement of myocardial blood flow. The accumulation of neutrophils (measured by myeloperoxidase activity) within the myocardium after reperfusion was not reduced by prior depletion of fibrinogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic defibrination with ancrod does not protect canine myocardium from reperfusion injury. 170 37

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

The origin of pre-eclampsia lies in uteroplacental ischemia due to an anomaly of the "vascular insertion" of the placenta. Although the cause of this anomaly remains unknown, it would appear to include both a genetic and an immunological origin possibly favourised by special underlying conditions and certain obstetric circumstances. Prostaglandin imbalance (in particular prostacyclins and Thromboxane A2) appears to be one of the chief factors governing these anomalies. One of the consequences of these mechanisms is the onset of hypertension but other disturbances are essential features. In particular, disseminated intravascular coagulation may occur leading to the release of numerous microthrombi which cause placental (leading to chronic fetal distress), renal, hepatic and cerebral lesions.
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PMID:[Physiopathological elements of pre-eclampsia and the role of the main complementary tests]. 176 67


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