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

Disseminated intravascular coagulation accompanied 18% of cases of acute renal failure during puerperal disorders. We studied in particular 31 cases of disseminated intravascular coagulation with renal failure due to obstetric disorders : 12 post-abortion infections, 3 retentions of a dead foetus, 5 infections, 6 cases of toxemia, 2 retroplacental hemorrhages, two hemorrhages during the third stage, one uremohemolytic syndrome. For diagnosis one relies on the clinical data (bleeding, purpura, shock, hemolysis, visceral involvement) and laboratory data, (coagulation should be supervised throughout the course). The renal lesions are either cortical necrosis, or interstitial nephritis. The analogies with experimental phenomena suggest a human equivalent of the Schwartzmann-Sanarelli syndrome.
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PMID:[Acute renal failure and consumption coagulopathy in the puerperium]. 21 7

Evaluations of 650 patients with acute lymphoblastic leukemias (A.L.L.) and of 596 patients with acute granulocytic leukemias (A.G.L.) ara analyzed. The patients were treated in the department of Professeur Jean Bernard at Saint-Louis Hospital between 1964 and 1976. In A.L.L., prognosis is influenced primarely by age, being worse in infants less than 1 year old and in adults: it is also influenced by the blastic load and by other parameters such as cytology and immunological markers which could not be studied in all patients. The correlation between high blastic load and the T lymphoblasts variety is noteworthy. Random studies are still necessary to find out the best drug combinations and the optimal duration of treatment, but the necessity for meningeal prophylaxis, reinduction treatments and of L-A sparaginase consolidation is no longer discussed. Prognostic stratification is useful for therapeutical evaluation and should load to therapeutical modulation. In acute granulocytic leukemias, age is also a significant parameter and remission rate is lower for patients over 50 years of age. Cytology and cytochemistry allow to recognize acute promyelocytic leukemias and acute monoblastic leukemias which bear specific initial risks (D.I.C. for A.P.L., renal failure for acute monoblastic leukemia) but which are highly sensitive to Daunorubicin and Rubidazone respectively. In A.M.L. remission duration is not influenced by age and seems to be improved by intermittent treatment. The role of immunotherapy is still under study.
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PMID:[Treatment of acute leukemia]. 27 98

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

Three cases of postpartum hemolytic uremic syndrome (HUS) are presented. Symptoms of acute renal failure, hypertension and microangiopathic hemolytic anemia with thrombocytopenia occurred 10, 17 and 24 days after delivery. Despite early heparin therapy in all cases, one patient went into terminal renal failure needing chronic hemodialysis, with persistent hypertension which became uncontrollable requiring bilateral nephrectomy 6 months later. The second patient had diuresis one month after starting hemodialysis, but 3 months later developed malignant hypertension. Slight improvement in renal function with persistent hypertension occurred after hemodialysis for 20 months. The third patient showed complete clinical recovery after 2 months. Pathological examination of renal tissue showed the typical lesions of thrombotic microangiopathy (TMA). However, striking differences were observed in the lesion seen in early and late specimens. Early lesions could be differenciated from infancy TMA because the medium-dize arteries were more severely involved. Late lesions were variable, ranging from minor changes in glomeruli and blood vessels, via ischemic and sclerotic lesions in glomeruli with arteriolosclerosis, to the vascular and glomerular lesions seen in malignant nephrosclerosis. There was a good correlation between the renal pathology and the clinical outcome of the patients. HUS with renal TMA as a cuase of postpartum renal failure has been reported in 49 patients with a fatal outcome in 61%. The pathogenesis of the syndrome probably involves a primary endothelial damage. This causes local renal intravascular coagulation in the presence of the usual postpartum hypercoagulable state. This is shown by the presence of fibrin-fibrinogen in glomeruli and vessels, increased plasma fibrin degradation products, thrombocytopenia and lowered levels of coagulation factors. There is little hematological or pathological evidence fo disseminated intravascular coagulation or an immune-complex disease. Hypocomplementemia seen frequently is probably due to local C3 activation via the alternative pathway.
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PMID:Postpartum hemolytic uremic syndrome: a study of three cases with a review of the literature. 38 9

Recent studies in experimental crescentic glomerulonephritis, using the technique of glomerular culture, have shown that the macrophage is a major cell type present within the glomeruli and developing crescents. It has been suggested that their accumulation is a consequence of glomerular fibrin deposition. The effect of defibrination with ancrod on the cellular events occurring in experimental crescentic glomerulonephritis in the rabbit was therefore assessed in this disease using the techniques of culture of isolated glomeruli, electronmicroscopy or renal tissue, and light microscopy. Defibrinated animals developed only minimal renal impairment, virtually no fibrin deposition in Bowman's Space and only a mild degree of crescent formation, in contrast to the severe renal failure, fibrin deposition and crescent formation that occurred in the untreated animals. The culture of isolated glomeruli and electronmicroscopy of intact renal tissue demonstrated large numbers of macrophages within and emerging from glomeruli of both defibrinated and untreated animals. However, only in untreated animals were macrophages seen to migrate into Bowman's Space, phagocytose fibrin, transform into epithelioid cells and accumulate to form crescents. These studies suggest that fibrin deposition in Bowman's Space is the major stimulus to the macrophage migration from capillary loops and accumulation in Bowman's Space. However, fibrin deposition does not appear to be the stimulus to macrophage accumulation within capillary loops as this event was not affected by defibrination.
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PMID:The effect of defibrination on macrophage participation in rabbit nephrotoxic nephritis: studies using glomerular culture and electronmicroscopy. 48 57

Disseminated intravascular coagulation is here reported as a complication of status epilepticus. Other features of this case were rhabdomyolysis, hyperthermia, myoglobinuria and renal failure.
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PMID:Disseminated intravascular coagulation in status epilepticus. 57 96

Defibrination with ancrod in nephrotoxic nephritis in rabbits. In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous phase, after extensive glomerular fibrin deposition had occurred and crescents and renal failure were developing. When further glomerular fibrin deposition was prevented by defibrination, deposited fibrin was rapidly removed, indicating that glomerular fibrin-clearing mechanisms are retained in crescentic nephritis. Defibrination had no effect on the extent of glomerular C3 deposition or on the amount of proteinuria.
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PMID:Defibrination with ancrod in nephrotoxic nephritis in rabbits. 79 57

A 14-year-old patient with heat stroke, disseminated intravascular coagulation, central nervous system dysfunction, and renal failure was treated, in addition to conventional therapy, with heparin sodium for seven days. Despite very poor prognostic signs on addmission, the patient survived the acute episode and ultimately progressed to a complete recovery.
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PMID:Disseminated intravascular coagulation in heat stroke. Response to heparin therapy. 80 83

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

The clinical and laboratory findings in four cases of acute renal failure following the onset of influenza A viral infection (Port Chalmers/1/73) are presented. Although the pathophysiologic mechanisms affecting the kidney in these cases varied, the ensuing renal failure in each patient was severe. Findings suggestive of acute myoglobinuria developed in one patient, and disseminated intravascular coagulation (DIC) occurred in another. The role of viruses in the pathogenesis of renal disease is reviewed. Despite inconclusive evidence that the influenza virus can cause human renal disease, the secondary pathways that can be triggered by viral infections may be even more significant in producing various degrees of renal dysfunction. The occurrence of renal failure during an episode of influenza represents a serious complication which may influence significantly the morbidity and mortality of patients with this viral infection.
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PMID:Influenza A viral infection associated with acute renal failure. 98 71


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