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

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

Endotoxins of gram-negative bacteria and of intestinal origin, insufficiently cleared by the hepatic reticulo-endothelial system are of an increasing interest within the pathogenesis of liver diseases. With purpose to obtain data concerning incidence and course of endotoxaemia in patients with liver cirrhosis an unselected group of these patients, sequentially admitted, was investigated by means of the Limulus-gelation test, regarded as most sensitive to endotoxins. At the admittance, 65% of the patients had endotoxaemia, further 14% developed endotoxaemia later. In total 79% of the patients investigated had endotoxaemia.---Bleeding from oesophageal varices was associated with endotoxaemia in 78%, functional renal impairment in 75%, consumption coagulopathy in 81%, encephalopathy in 77% and a pyrogen reaction in 82% of the patients. Regarding the Limulus assay, the dilution technique was more sensitive in detection of free endotoxaemia as opposed to the chloroform extract. It is concluded from the results that endotoxaemia in patients with liver cirrhosis is frequent and has to be viewed as relevant within the pathogeneses of chronic liver diseases.
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PMID:[Endotoxinemia in liver cirrhosis]. 96 Sep 7

A 39 year old woman presented with a short history of bloody diarrhoea. She subsequently developed microangiopathic haemolysis, platelet consumption, and renal impairment. Initial investigations suggested underlying Crohn's disease of the terminal ileum complicated by sepsis and disseminated intravascular coagulation. However, after resection of a perforated caecum and terminal ileum, the diagnosis of thrombotic thrombocytopenic purpura was made. There was weak serological evidence of yersinia infection, this may have caused the early localisation of the lesions to the terminal ileum. This is believed to be the first report of thrombotic thrombocytopenic purpura affecting the small bowel alone at presentation.
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PMID:Thrombotic thrombocytopenic purpura mimicking acute small bowel Crohn's disease. 162 73

Acute infections with group A beta-hemolytic streptococcus normally take a favourable course under therapy with penicillin. Only in a few cases has a completely different manifestation been described with multisystem failure similar to toxic shock syndrome induced by Staphylococcus aureus. We report on 4 patients (1990/91) who showed this manifestation in spite of immediate antibiotic therapy. In 3 patients the suspected portal of entry was the skin, in 1 patient it was unknown. Group A streptococci were grown from blood cultures from all 4 patients. Without an underlying immune deficiency all 4 patients (age 22, 24, 38 and 51) went into septic shock with high fever, hepatic and renal impairment, diarrhea, DIC and cerebral confusion. 2 patients died within a few days after developing acute respiratory distress syndrome and cerebral edema. All strains isolated from the patients were penicillin-sensitive, group A streptococci. 3 of them were M-type 1, which are known to be more invasive. The bacteremia by itself is not sufficient to explain all complications and the high mortality rate. It is probable that streptococcal toxins, such as pyrogenic exotoxin A, streptolysin O, or a new unknown one, play a decisive role.
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PMID:[Toxic shock syndrome in infection due to Streptococcus pyogenes]. 173 21

This is a very rare case report of Goodpasture's syndrome with IgA antibasement membrane antibody. A 43-year old male was admitted because of severe dyspnea with slight hemoptysis. Chest X-ray demonstrated extensive bilateral infiltrates with air bronchogram, predominantly in the right lung. Laboratory data on admission showed severe anemia and moderate renal impairment. The pulmonary infiltrates resolved spontaneously within 10 days. Goodpasture's syndrome or collagen vascular disease was suspected and he underwent a percutaneous renal and transbronchial lung biopsy. The renal biopsy showed crescent formation affecting 70-80% of glomeruli. Linear IgA deposits, but not IgG, were demonstrated along the glomerular basement membrane by the direct immunofluorescence procedure. The lung biopsy contained many hemosiderin-laden macrophages in the lumen of the alveoli and showed mild thickening of alveolar walls. However, linear immunoglobulin deposits on the alveolar capillary basement membrane were not demonstrated by direct immunofluorescence. The diagnosis of Goodpasture's syndrome with IgA antibasement membrane antibody was made. His serum was negative for antibasement antibody by indirect immunofluorescence. He was treated with prednisone, 30 mg daily. His pulmonary symptoms and anemia improved markedly, but his renal function did not change. Thirteen months after his first admission, he suffered from severe bacterial pneumonia, which was complicated by disseminated intravascular coagulation. He died of respiratory failure. Autopsy was rejected.
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PMID:[A case of Goodpasture's syndrome with IgA antibasement membrane antibody]. 221 6

We have studied the activation state of the fibrinolytic system in 39 patients with systemic meningococcal disease (SMD). Patients defined as having fulminant septicemia (n = 13) with high (greater than 700 ng/L) levels of endotoxin (LPS) in plasma and severe coagulopathy, had significantly lower functional levels of plasminogen (P less than 0.05) and alpha-2-antiplasmin (P less than 0.01) and higher antigen levels of plasminogen activator inhibitor 1 (PAI-1) (P less than 0.01), and fibrin degradation products (FDP) (P less than 0.01), but not of PAI-2 (P greater than 0.1) as compared with less severely ill patients (meningitis and meningococcemia) (n = 25). A positive correlation existed between the admission (maximum) levels of LPS and PAI-1 (r = 0.86, P less than 0.0001). Decreasing admission levels of platelets were associated with increasing levels of PAI-1 (r = -0.55, P less than 0.001). After initiation of treatment with antibiotics and fresh frozen plasma, the PAI-1 levels declined rapidly. PAI-1 levels greater than 360 micrograms/L on admission predicted the development of a severe septic shock combined with renal impairment correctly in 12 of 13 patients (92%). None of 25 patients without multiple organ failure had PAI-1 levels greater than 260 micrograms/L. PAI-1 levels greater than 1850 micrograms/L were associated with 100% fatality. The results suggest that in the early phase of fulminant meningococcal septicemia an extensive plasmin generation occurs. On admission, however, high levels of PAI-1 seem to inhibit the plasmin generation, and thereby promote DIC.
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PMID:Plasminogen activator inhibitor 1 and 2, alpha-2-antiplasmin, plasminogen, and endotoxin levels in systemic meningococcal disease. 231 89

Acute renal failure (ARF) is regarded as relatively uncommon in preeclampsia-eclampsia (PE-E) and, in any event, of moderate degree or reversible. Cortical necrosis is reported as rare, even in fatal cases. Little light has as yet been shed on the mechanisms responsible for ARF in PE-E. This paper describes 17 cases observed over the last 15 years, in which cortical necrosis (3 histological and 2 clinical diagnoses) was relatively frequent (29.4%). The severity of renal impairment did not appear to be related to chronological age, parity, period of pregnancy in which PE-E commenced and its duration prior to delivery, presence of frank eclamptic crises or the concomitance of earlier vascular or renal disease (p greater than 0.05). The superimposition of abruptio placentae (AP) was the only clinical factor significantly correlated with cortical necrosis (p greater than 0.05). The association PE-E + AP seems to be a particularly unfavorable prognostic sign for the kidney owing to the contribution of additional damage mechanisms (vasospasm, disseminated intravascular coagulation, hemorrhagic shock) furnished by AP, while PE-E itself prepares the ground for AP. The fact that PE-E is difficult to diagnose when AP is the onset symptom may be responsible for the underestimation of its contribution towards the induction of severe renal damage.
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PMID:Acute renal failure in preeclampsia-eclampsia. 342 11

We report a fatal case of heatstroke in an obese boy who developed multi-organ failure. Six other cases of exertional heatstroke admitted to our hospital over the last 5 years were also reviewed. All of them showed some degree of renal impairment. The causes of renal failure are multifactorial, with rhabdomyolysis being the major mechanism. All cases except one responded to alkaline diuresis without the need for dialysis. Continuous venovenous hemofiltration appeared to be a good alternative in hemodynamically unstable patients. Renal function recovered completely after varying intervals in all surviving cases. Interestingly, rhabdomyolysis in our heatstroke patients was usually associated with hypokalemia or normokalemia instead of hyperkalemia. Mortality in our series was largely related to the long duration of hyperthermia and coma, the severity of disseminated intravascular coagulation, and the presence of cardiogenic shock and severe acidosis.
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PMID:Renal failure and heatstroke. 764 68

Hemorrhagic shock and encephalopathy syndrome (HSES) is a sudden-onset symptom complex occurring in previously healthy infants and children. It was first described in 1983 in the United Kingdom in 10 infants. Subsequently, > 140 cases have been reported worldwide, although no cases have been previously reported in the forensic literature. Typically the child presents with fever, shock, encephalopathy with coma and seizures, evidence of hemorrhage, and diarrhea. Laboratory investigation reveals falling hemoglobin and platelet counts, renal impairment, evidence of disseminated intravascular coagulation, metabolic acidosis, and raised serum transaminases. Microbiological cultures are uniformly negative. The condition has a high mortality and morbidity. The etiology is unknown and may be multifactorial. However, hyperpyrexia appears to play a central role in pathogenesis. The diagnosis of HSES in the deceased child is one of exclusion and requires a careful antemortem history as well as a thorough autopsy with toxicological and microbiological investigations. A case of HSES is reported and the literature reviewed.
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PMID:Hemorrhagic shock and encephalopathy syndrome. An unusual cause of sudden death in children. 909 7

The spectrum of clinical severity for scrub typhus ranges from inapparent, mild, to severe or fatal. The pathologic changes are focal or disseminated multiorgan vasculitis of the small blood vessels, a fact that helps explain the great diversity of clinical manifestations that can be encountered. We reported a case of scrub typhus with unusual and serious multiorgan involvement, including tubulointerstitial nephritis (TIN) with acute renal failure (ARF), interstitial pneumonitis with adult respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), liver function impairment, upper gastrointestinal bleeding, prolonged hyperamylasaemia and hyperlipasaemia. Chloramphenicol administration rapidly altered the clinical course, but with sequelae of renal impairment and prolonged hyperamylasaemia and hyperlipasaemia for 10 months.
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PMID:Scrub typhus associated with multiorgan failure: a case report. 957 50


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