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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 intricacies of the pathophysiology of eclampsia are still unknown. The major symptoms of our 37 year old para 3 are convulsions, hypertension, complete anuria and gastro-intestinal haemmorhage as a result of disseminated ;ntra-vascular coagulation (D.I.C.). The interdisciplinary therapeutic measures are discussed, in the course which special attention is given to the favourable influence of dopamine on renal failure and the complicating gastro intestinal haemmorhage.
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PMID:[Intensive care medicine in severe eclampsia (author's transl)]. 31 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

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

The DIC syndrome is the most common cause of an abnormal hemorrhage tendency during pregnancy and the puerperium and reflects systemic activation of the coagulation cascade by circulating thromboplastic material, with secondary activation of the fibrinolytic system. Its presence in a pregnant patient almost invariably is evidence of an underlying obstetric disorder such as abruptio placentae, eclampsia, retention of a dead fetus, amniotic fluid embolism, placental retention or bacterial sepsis. Diagnosis of the DIC syndrome rests on the demonstration of reduced levels of fibrinogen and platelets, prolongation of the thrombin, prothrombin and partial thromboplastin times, and the presence of fibrin/fibrinogen degradation products (FDP) in the serum. Therapy consists of prompt removal of the source of procoagulant material, replacement of depleted clotting factors and, in some cases, anti-coagulation with heparin.
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PMID:Disseminated intravascular coagulation in pregnancy. 91 82

Three hundred sixty-five cases of eclampsia, including 49 women who died, were analyzed in order to determine factors which led to death. The age of the patient was clearly the most important factor. Older women tended to have coexisting renal and vascular disease and also manifested more hematologic abnormalities, in particular, disseminated intravascular coagulation. Other important factors leading to death were twin pregnancies, delay in hospitalization, failure to terminate the pregnancy, and the physician's unawareness of the severity of the mother's disease. The mortality after cesarean section was the same as in women delivered vaginally.
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PMID:Factors that influence maternal mortality in eclampsia. 100 51

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

Alternations in the coagulation mechanism were looked for in a population of eclamptic women, most of when were young, nulliparous, and without evidence of chronic vascular disease, and all of whom survived. Thrombocytopenia was identified in 29% of these women. A prolonged plasma thrombin time was demonstrated in 51% yet elevated fibrinogen-fibrin degradation products in serum were uncommon, as was fibrin monomer in plasma. Overt microangiopathic hemolysis was rare. It is concluded that disseminated intravascular coagulation, when it does occur in eclampsia, is the consequence of the disease rather than the cause. Moreover, endothelial damage, rather contents, probably initiates the thrombocytopenia and other coagulation changes.
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PMID:Does coagulation have a causative role in eclampsia? 100 57

A case of acute renal failure associated with disseminated intravascular coagulation occurring immediately post partum is reported. The aetiological role of the associated eclampsia together with evidence for a hypersensitivity reaction to ampicillin is discussed.
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PMID:Postpartum renal failure associated with eclampsia and penicillin hypersensitivity. 119 92

The maternal coagulation mechanism has been investigated in an effort to identify its role, if any, in the pathogenesis of eclampsia. Thrombocytopenia was identified in 28 of 95 cases (29 per cent), a prolonged thrombin time in 19 of 38 (50 per cent), abnormally elevated serum fibrinogen-fibrin degradation products in two of 65 (3 per cent), and circulating fibrin monomer in one out of 20 (5 per cent). Overt hemolysis was rare (2 per cent). Thus the pattern as well as the degree of change in the maternal coagulation mechanism differed remarkably from that typical of severe abruptio placentae and of prolonged retention of a dead fetus, the classic obstetric models of fast and slow disseminated intravascular coagulation. It is concluded that the coagulation changes when present in eclampsia are effect rather than cause. Moreover, the changes may evolve primarily from platelet adherence at sites of vascular endothelial damage as the consequence of segmental vasospasm and vasodilatation rather than be triggered by the escape of thromboplastin from the placenta into the maternal circulation.
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PMID:Coagulation changes in eclampsia: their frequency and pathogenesis. 125 45

Current concepts of the etiology, pathophysiology, clinical and laboratory diagnosis, and management of fulminant and low-grade DIC have been presented. Considerable attention has been devoted to interrelationships within the hemostasis system. Only by clearly understanding these pathophysiologic interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and will remain so until more is published about specific therapeutic modalities and survival patterns. Also, therapy must be highly individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis, and hemodynamic and other clinical parameters. Many syndromes that are organ-specific share common pathophysiology with DIC but are typically identified as an independent disease entity, such as hemolytic uremic syndrome, adult shock-lung syndrome, eclampsia, and many other isolated "organ-specific" disorders.
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PMID:Disseminated intravascular coagulation. 145 11


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