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

Significantly increased concentrations of soluble fibrinogen/fibrin complexes were found in plasma samples from ten normal pregnant women when compared with ten non-pregnant age-matched controls. In ten women with pre-eclampsia mean soluble complex concentration was more than three times that in the age, parity, and gestation matched pregnant controls. Soluble fibrinogen/fibrin complexes are also found in the plasma of patients in various hypercoagulable and thrombotic states, including disseminated intravascular coagulation. These findings provide additional evidence that pre-eclampsia is associated with disseminated intravascular coagulation.
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PMID:Soluble fibrinogen/fibrin complexes in pre-eclampsia. 5 80

The technique of plasma fibrinogen chromatography was used to study sequential changes in coagulant and fibrinolytic activity in six patients with severe pre-eclampsia. Plasma soluble fibrinogen-fibrin complex and plasma fibrinogen-fibrin degradation product levels were measured as indices of coagulant and fibrinolytic activity respectively. Clinical deterioration antenatally was accompanied by increasing coagulant and decreasing fibrinolytic activity, while a more stable clinical picture was associated with steady coagulant and increasing fibrinolytic activity. Following delivery, a surge in fibrinolytic activity accompanied or preceded clinical recovery. The pattern of increased coagulant and diminished fibrinolytic activity would seem to favour the development of disseminated intravascular coagulation in these patients and it is possible that the balance between coagulant and fibrinolytic activity may influence the clinical course and outcome of the pregnancy.
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PMID:Sequential studies in pre-eclampsia using plasma fibrinogen chromatography. 58 2

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

Pre-eclampsia complicated by deep jaundice occurred in a previously healthy primigravida. The main aetiological factor was disseminated intravascular coagulation; this caused both haemolysis and liver cell necrosis. Liver biopsy showed fibrin thrombi in the capillaries with microhaemorrhages and loss of periportal liver cells. The jaundice was attributed to both haemolytic and hepatocellular processes. Organs other than the liver were relatively unaffected.
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PMID:Pre-eclampsia presenting with deep jaundice. 84 70

In this study of 136 women with pre-eclampsia, eclampsia, placenta previa, or abruptio placentae, 21 mothers were noted to have thrombocytopenia. Seventeen of the 21 were in the pre-eclampsia group. Of the 21 thrombocytopenic mothers, nine were associated with thrombocytopenia in the children, seven children had normal platelet counts, and five had no counts performed. Eight of the nine thrombocytopenic neonates were associated with pre-eclampsia in the mother, and five of these were not believed to have disseminated intravascular coagulation as the etiology of the platelet defect. The results suggest that thrombocytopenia is common in high-risk pregnancies in both the mother and the baby. However, the etiology of the platelet defect cannot be easily explained on the basis of a hypercoagulable state.
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PMID:The association of maternal and neonatal thrombocytopenia in high-risk pregnancies. 87 Nov 38

Our experience with consumptive coagulopathy associated with preeclampsia at North Carolina Baptist Hospital is presented. All cases of recognized consumptive coagulopathy on the obstetric service from 1969 to 1975 are reviewed and the associated obstetric entities given. Two cases of consumptive coagulopathy complicating severe preeclampsia are presented. Consumptive coagulopathy occurred in 9.1% of eclamptic patients and in 2.6% of severe preeclamptic patients. No previous incidence figures were found in the literature.
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PMID:Consumptive coagulopathy in severe preeclampsia. 94 Jun 47

The coagulation and fibrinolytic systems play a key role in maintaining the integrity and patency of the vascular compartment. Pregnancy induces extensive physiological changes in these systems, thus creating an enhanced capacity to produce fibrin and a diminished ability to remove it. Fibrin deposition localized to the uteroplacental circulation is a feature of normal pregnancy. In women with fatal eclampsia, disseminated intravascular coagulation with fibrin deposition in the renal glomeruli is well documented. The condition of preeclampsia is not well defined. Nonetheless, evidence of intravascular coagulation, as shown by elevated levels of fibrin degradation products and reduced platelet counts, has been found in many women with preeclampsia. Serial studies showed that thrombin generation, as indicated by the ratio of factor VIII-related antigen to factor VIII coagulant activity, is considerably in excess of that which occurs in normal pregnancy, and its appearance coincides with the development of the clinical features of preeclampsia. Heparin therapy has bot been proven of value in established preeclampsia, but this fact does not disprove that role that intravascular coagulation may play in the pathogenesis of the disease. A controlled trial ina high-risk group of low-dose he;arin and an antiplatelet agent from the 16th to the 18th weeks of pregnancy onwards is required to elucidate the role of intravascular coagulation in preeclapmsia and its effect on the fetus.
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PMID:The role of coagulation and fibrinolysis in preeclampsia. 100 56

A prospective study of cord blood for coagulability, evidence for disseminated intravascular coagulation (DIC), and hematocrit was done in 106 infants who were offspring of mothers with high-risk pregnancies (pre-eclampsia, diabets mellitus, third-trimester bleeders, severe erythroblastosis fetalis, maternal hypertension, fetal distress, and spontaneous premature labor). Significant changes of hypercoagulability (low AT-III and abnormal TEG) were seen in the third-trimester bleeder and premature labor groups which also had the highest incidence of IRDS and necrotizing. Infants undergoing "stress" (pre-eclampsia, fetal distress) had elevated levels of factors V and VIII but were not hypercoagulable or AT-III deficient. Except for mild thrombocytopenia, infants of the diabetic mothers, a group with increased thrombotic complications, did not show any cord blood abnormalities. Offspring of third-trimester bleeders were anemic. The EBF infants were also anemic, severely hypercoagulable, and showed coagulation changes compatible with severe liver disease and/or DIC. Mild changes compatible with intravascular coagulation were seen in six infants and were not related to the the development of IRDS.
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PMID:Cord blood coagulation studies in infants of high-risk pregnant women. 111 15

A prospective evaluation of the haemostatic mechanism was undertaken in 15 normal primigravidas and in 12 primigravidas with mild to moderately severe pre-eclampsia in order to further examine the possibility that disseminated intravascular coagulation may occur in this clinical syndrome. The only coagulation abnormality demonstrated was a prolongation of bleeding time. The data do not support the suggestion that significant disseminated intravascular coagulation is associated with pre-eclampsia. The addition of the heparinoid drug sodium pentosan polysulphate to the therapeutic regimen resulted in a significant fall in platelet factor 3 availability and in decreased aggregation against ADP but conferred no objective clinical improvement. We conclude that the drug has no place in the management of established pre-eclampsia.
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PMID:Pregnancy, pre-eclampsia and disseminated intravascular coagulation. 115 76

In view of the association between pre-eclampsia and disseminated intravascular coagulation, three patients presenting with severe pre-eclampsia before the 28th week of pregnancy were treated with heparin. In all three patients, there was deterioration of hypertension and proteinuria that necessitated the withdrawal of treatment after five to six days. During treatment, serum and urinary fibrinolytic degradation products (FDPs) continued to rise or remained unaltered, plasminogen levels showed a steady fall, and the platelet count remained at a reduced level. These data suggest that heparin was an ineffective form of treatment and did not prevent the intravascular fibrin deposition associated with severe pre-eclampsia.
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PMID:Failure of heparin therapy to affect the clinical course of severe pre-eclampsia. 118 91


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