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

Seven children (aged 8--17 years) presented with a high fever, headache, confusion, conjunctival hyperaemia, a scarlatiniform rash, subcutaneous oedema, vomiting, watery diarrhoea, oliguria, and a propensity to acute renal failure, hepatic abnormalities, disseminated intravascular coagulation, and severe prolonged shock. One patient died, one had gangrene of the toes, and all have had fine desquamation of affected skin and peeling of palms and soles during convalescence. Five patients were studied prospectively. Staphylococcus aureus related to phage-group I was isolated from mucosal (nasopharyngeal, vaginal, tracheal), or sequestered (empyema, abscess) sites, but not from blood. This organism produces an exotoxin which causes a positive Nikolsky sign in the newborn mouse and which is biochemically, pathologically, and immunologically distinct from phage-group-II stapphylococcal exfoliatin.
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PMID:Toxic-shock syndrome associated with phage-group-I Staphylococci. 8 81

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

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

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

A male patient was admitted to hospital 12 h after self-poisoning with mercuric chloride. He suffered multiple complications including acute renal failure, ulcerative colitis, anaemia, disseminated intravascular coagulation, chronic sepsis and severe weight loss. Initially he responded well to resuscitative measures and intensive supportive therapy, which included ventilation of the lungs, haemodialysis, dimercaprol, antibiotics, parenteral feeding and gastrointestinal surgery. Unfortunately the sepsis was never satisfactorily eradicated despite satisfactory serum concentrations of the appropriate antibiotics. On day 43 after poisoning he had a grand mal fit; after this there were focal neurological signs and on lumbar puncture he was found to have a raised protein concentration and raised pressure in his cerebrospinal fluid. The condition of the patient rapidly deteriorated and on day 47 he died. Post-mortem examination revealed a large cerebellar abscess. The literature on mercury poisoning is reviewed.
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PMID:A case of poisoning with mercuric chloride. 49 32

In a study of 1729 consecutive autopsies, the histopathologic diagnosis of disseminated intravascular coagulation (DIC) confirmed by the presence of microthrombi in more than two organs was made in 51 cases. Among them, 38 cases (74.5%) were clinically not suspected of having DIC. Microthrombi were most frequent in the kidneys, followed by the lungs, spleen, adrenals, heart, brain, and liver, in descending order of frequency. Furthermore, a wide variety of visceral lesions was another important histologic feature of DIC. Kidney lesions assumed a position of prime importance, and special attention was given to the high frequency of acute renal failure due to so-called acute tubular necrosis and bilateral renal cortical necrosis. Infections, often associated with shock, and malignancies were the most common underlying causes of DIC. DIC is a frequent, often fatal pathophysiologic condition complicating many disorders. The true incidence of DIC at autopsy may be higher. It should be noted that demonstration of microthrombi and visceral alterations related to intravascular clotting is important for the evaluation of cases suspected of having DIC.
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PMID:Disseminated intravascular coagulation in autopsy cases. Its incidence and clinicopathologic significance. 53 Aug 89

The course of 76 consecutive patients with acute renal failure and severe intra-abdominal infection was reviewed to identify the microorganisms responsible, the factor precipitating reoperation, and prognostic indicators. Peritonitis occurred in 75 patients, 48 of whom had abscesses. Twenty-four patients (32%) survived. Anaerobes and fungi were commonly grown from blood. Gram-negative aerobic blood isolates were associated with the highest mortality. Leukocytosis, physical findings, and fever were factors that prompted reexploration whereas diagnostic procedures played an ancillary role. The finding of specifically correctable conditions at reoperation improved survival (P less than .05). Myocardial infarction and disseminated intravascular coagulation affected survival unfavorably whereas hyperalimentation had a favorable influence (P less than .05). Aggressive medical, nutritional, and surgical management results in improved survival rates in these patients.
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PMID:Intra-abdominal infection and acute renal failure. 63 17

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

Decreased platelet count and platelet adhesiveness as well as increased values of the protamine sulfate test were found in 26 patients with septic abortion (9 of them anuric). Serum fibrinogen-fibrin related antigen (FR-antigen) values, detected in 13 patients (7 of them anuric) were greatly increased although euglobulin lysis time was rather prolonged (more than 400 min). Less increased FR-antigen values were noted in 15 cirrhotic patients with enhanced fibrinolytic activity in the circulating blood (euglobulin lysis time less than 120 min). These findings suggest that an important increase of FR-antigen in serum is likely to indicate a local fibrinolytic response to an initial coagulation event. Since platelet count and adhesiveness as well as FR-antigen and protamine sulfate test were similarly changed in patients with septic abortion who developed acute renal failure and in those who did not, it seems that the above mentioned parameters are not predictive for the evolution of thrombotic deposits and for possible renal complications following an episode of disseminated intravascular coagulation.
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PMID:Serum fibrinogen-fibrin related antigen and protamine sulfate test in patients with septic abortion and acute renal failure. 94 95

A patient was transfused with a unit of red blood cells that had been frozen accidentally prior to transfusion. Although he had received approximately 60 gm of free hemoglobin intravenously, the patient's only clinical reaction was massive hemoglobinuria. The benign clinical response, in the presence of massive hemoglobinuria, is attributed to the absence of immunologic imcompatibility and, thus, failure to activate vasoactive mediators and disseminated intravascular coagulation. The case illustrates revised concepts of the pathophysiology of acute renal failure associated with hemolytic blood transfusion reactions.
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PMID:Benign hemoglobinuria following transfusion of accidentally frozen blood. 94 95


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