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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 coagulation system was studied in twenty-seven patients undergoing second-trimester abortion induced by intra-amniotic prostaglandin (P.G.) E2 alone and in combination with a hypertonic solution of urea or glucose. Changes consistent with intravascular coagulation, namely a rise in fibrin degradation products and a fall in plasma-fibrinogen and platelet-count, were observed in those patients treated using P.G.E2 with hypertonic urea. Similar but less pronounced changes were found in the group treated using P.G.E2 with hypertonic glucose. In patients treated with P.G.E2 alone no changes suggestive of intravascular coagulation were detected. One patient treated using P.G.E2 with hypertonic urea who did not abort for 26 hours demonstrated changes indicative of a pronounced degree of disseminated intravascular coagulation. These findings show that when abortion is induced using P.G.E2 and a hypertonic solution, particularly hypertonic urea, disseminated intravascular coagulation can occur as a result of a hypertonic agent being used.
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PMID:Coagulation changes during second-trimester abortion induced by intra-amniotic prostaglandin E2 and hypertonic solutions. 5 53

Studies of coagulation were performed prospectively in 41 patients with mild to moderately severe acute pancreatitis. Six patients (15%) presented with coagulation data suggestive of defibrination; two of them had clinical signs of bleeding. No other cause than pancreatitis was found in these 6 patients to account for coagulation abnormalities. Comparing the patients who presented defibrination to those who did not, no difference was observed in clinical course and admission values of serum amylase, fibrinogen, urea, calcium, glucose, transaminase levels, white blood cell count and arterial partial pressure of oxygen. Platelets counts and serum creatinine levels were respectively lower and higher in the first group of patients.
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PMID:[Defibrination syndrome during acute pancreatitis: 6 cases. Prospective studies of coagulation in 41 patients (author's transl)]. 46 Nov 54

137 patients (92 men and 45 women) with an average age of 58 years (range: 19 to 90 years) were hospitalised between January 1970 and June 1977 for acute aortic dissection. In 107 patients (and in 91 cases during the first 24 hours of hospitalisation) aortography was performed. This examination was found to be greatly reliable when its findings were compared with those at surgical exploration. In the absence of surgical treatment, 69 patients died and 5 survived. Amongst the patients undergoing surgery, 37 died and 27 survived. With the exception of type III dissections, survival appeared to be markedly increased by surgical treatment. Preoperative factors indicative of a poor prognosis included a neurological deficit of central origin, oligoanuria, raised blood urea, disseminated intravascular coagulation and dissection of the superior mesenteric artery or the coeliac trunk.
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PMID:[Acute aortic dissection. Prognostic factors, therapeutic indications. 137 cases (author's transl)]. 49 51

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

Under the proper experimental conditions, disseminated intravascular coagulation,"an intermediary mechanism of disease," results in the classic endotoxin-induced generalized Shwartzman reaction. Other substances, such as liquoid, a highly negatively charged anticoagulant, trigger a generalized Shwartzman reaction-like phenomenon in rabbits. We studied the effects of a single high intravenous dose of liquoid (12.5 mg.) upon the rat's coagulation and complement systems and their correlation with the kidney morphology by light, fluorescence, and electron microscopy. Thrombin time was prolonged; fibrinogen, plasminogen, and factors VIII and XII concentrations were markedly decreased, whereas fibrin degradation products were increased in the experimental animals when compared with the saline-injected controls (p greater than 0.001). Total hemolytic complement, hemolytic activity of terminal components (C3 to C9), and C3 protein concentration were significantly reduced (p greater than 0.001). The liquoid-injected rats developed cortical necrosis and manifested oliguria and anuria, with elevated blood urea nitrogen levels, when survival was longer than 3 hours. Histologically, thrombi of fibrin-like material filled the glomerular capillaries. Deposits of fibrin, and also of immunoglobulin G and C3, were readily identifiable by specific immunofluorescence, Linear or granular fluorescent deposits (or both) along the glomerular basement membranes and in the mesangium were observed. Electron microscopy demonstrated necrosis of glomeruli and abundant thrombi of fluffy, compact granular, or fibrillar electron-dense material. No typical fibrin periodicity was detected. These experiments support the concept of activation of the coagulation and the complement systems. We postulate that liquoid produced not only a consumptive coagulopathy in the rat but also a direct or perhaps anindirect activation of complement. Whether this latter has occurred through the classic or an alternate pathway remains to be elucidated.
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PMID:Disseminated intravascular coagulation induced by liquoid in the rat. I. Correlation of hematologic and complement abnormalities with renal lesions studied by light, fluorescence, and electron microscopy. 112 10

The protective effects of anticoagulants in nephrotoxic nephritis in rabbits have been studied, using various doses of heparin and defibrination with ancrod. Massive doses of heparin (2000 units/kg/day) were required before significant reduction in glomerular fibrin deposition, extracepillary cell proliferation and urea retention occurred. Doses of 300 and 1000 units/kg/day were insufficient to modify fibrin deposition and cell proliferation. Defibrination with ancrod provided protection, judged by histological and functional criteria, comparable to 2000 units of heparin/kg/day; but fibrin could still be demonstrated in the glomeruli of animals treated with 2000 units of heparin/kg/day, contrasting with the virtual absence of fibrin in animals given ancrod.
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PMID:A quantitative evaluation of anticoagulants in experimental nephrotoxic nephritis. 121 1

Quantitative studies of the effects of defibrination (with ancrod) have been undertaken in two forms of allergic glomerular damage, nephrotoxic serum nephritis and acute serum sickness in rabbits. No differences in intrarenal fixation of nephrotoxic antibody, complement activation or host antibody response were detected between defibrinated and untreated rabbits with nephrotoxic serum nephritis. Defibrination prevented intraglomerular fibrin deposition in this disease; but some glomerular damage as shown by a rise in blood urea and endothelial proliferation still occurred in defibrinated animals. No differences in immune elimination of BSA, circulating immune complex formation or intrarenal localization of immune complexes were noted in defibrinated animals with acute serum sickness. No intraglomerular fibrin deposition was detected in treated or untreated animals in this disease model. It is concluded that the protective effects of ancrod are directly related to defibrination, and not to any other modification of allergic events.
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PMID:The effects of defibrination with ancrod in experimental allergic glomerular injury. 121 11

We observed 73 patients with the hemolytic uremic syndrome (HUS) in 9 years (1980-1988), comprising 34% of patients with acute renal failure treated over the same period. There were 53 boys and 20 girls; 59% were below the age of 2 years and 33% between 2 and 5 years. Acute, usually severe dysentery, responding poorly to various antibiotics, was the prodromal illness in 80%, whereas 12% had watery diarrhea. Most patients had severe renal involvement with anuria in 56% and oliguria in 30%. A polymorphonuclear leukocytosis was present in 85% of cases, but had no correlation with the highest levels of blood urea. Coagulation abnormalities suggesting consumption coagulopathy were found in 24 of 30 cases. The results of stool culture showed Shigella species in 7 cases and nontyphoidal Salmonella in 9. Escherichia coli were isolated in 11 cases, but were not further characterized. Renal biopsy showed total or patchy cortical necrosis in 20 of 50 cases. The patients were managed with supportive care, including transfusion of fresh blood or plasma and dialysis as required. The mortality was 60%, being chiefly related to the duration of renal failure and presence of renal cortical necrosis, whereas persistent dysentery and infections were complicating factors. The presence of convulsions and coagulation defects had no relation to the outcome. Our observations indicate that HUS in children in northern India is mostly related to dysentery, likely to be shigellosis, and is usually associated with severe renal damage and a high death rate.
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PMID:Hemolytic uremic syndrome in children in northern India. 186 81

A 39-month clinical study of leptospirosis was undertaken at the Queen Elizabeth Hospital, Barbados. Eighty-eight patients had a confirmed diagnosis of the disease during the period. The major serogroups identified were autumnalis (including a new serovar bim), icterohaemorrhagiae, ballum and canicola. The majority of patients presented with jaundice (95%,) anorexia and headaches (85%), fever (76%) and conjunctival suffusion (54%). While abnormal creatinine levels were seen in 49% of patients on admission, only 16% were judged to have had renal failure. The urine to plasma urea ratio showed high sensitivity and specificity in the diagnosis of pre-renal azotemia. Cardiac arrhythmias and myocarditis occurred in 18% of patients and pericarditis in 6%. An elevated serum amylase was found in 65% of cases. The bilirubin level took 5.5 weeks to return to normal. Thrombocytopenia was shown not to be due to a disseminated intravascular coagulation, and a randomised trial of high dose penicillin did not reveal any benefit to jaundiced patients. The overall mortality during the study was 5.7%.
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PMID:Leptospirosis in Barbados. A clinical study. 233 95

The clinical and laboratory characteristics of a severe form of hemorrhagic fever with renal syndrome (HFRS) in Greece are presented. Twenty-seven patients with serologically confirmed HFRS were studied; 10 required renal dialysis, six had hemorrhagic manifestations, and four died. In patients with hemorrhagic manifestations, the platelet counts were generally less than 100,000 cells/microL. In three patients findings were compatible with disseminated intravascular coagulation. Laboratory investigation showed a consistent rise in levels of serum urea nitrogen and creatinine beginning on the fifth or sixth day of illness and reaching a maximum level between the ninth and 12th days of illness. The disease in Greece more closely resembles the Asian form of HFRS (Korean hemorrhagic fever) than the Scandinavian form of the disease (nephropathia epidemica) because of the high mortality rate, the occurrence of hemorrhagic manifestations, and the severity of the clinical disease.
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PMID:Hemorrhagic fever with renal syndrome in Greece: clinical and laboratory characteristics. 256 79


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