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

Treatment of severe acute respiratory failure with extracorporeal gas exchange necessitating near complete systemic anticoagulation requires a delicate balance to be maintained between disseminated intravascular coagulation and hemorrhagic complications. The present study describes our first experience using a heparin coated extracorporeal artificial lung and circuitry during clinical extracorporeal CO2 removal. In spite of a partial thromboplastin time and activated clotting time within or close to the normal range, neither laboratory evidence for disseminated intravascular coagulation induced by the extracorporeal circuit nor thrombi in the pulmonary vasculature were found. Scanning electron microscopy of the heparin coated hollow fiber gas exchanger demonstrated only minor deposits on the surface. Use of a heparin coated artificial lung may enhance the margin of safety of extracorporeal gas exchange and ultimately broaden its indications.
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PMID:Extracorporeal CO2-removal with a heparin coated artificial lung. 322 Oct 12

Eleven of 43 nonimmune patients with falciparum malaria had one or several organ complications: cerebral malaria, acute respiratory failure, acute renal failure, secondary infection, autoimmune haemolysis, spontaneous spleen rupture, and acute pancreatitis. Parasitaemia was 0.1 to 60%. Initial antiparasitic therapy with quinine given parenterally resulted in rapid regression of parasitaemia. An additional schizonticide agent was given depending on parasitic resistance. Supportive therapy comprised intensive-care monitoring including fluid and electrolyte balance and, if necessary, early haemodialysis and (or) endotracheal intubation with PEEP breathing. In one patient with excessive parasitaemia exchange transfusion was performed. Heparin was given only in proven disseminated intravascular coagulation, corticosteroids only in persistent autoimmune haemolysis. All patients survived without suffering permanent defects. Retrospective analysis shows that, apart from rapid specific therapy, supportive treatment of the individual organ complications determines course and prognosis of complicated falciparum malaria.
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PMID:[Complicated malaria tropica: specific and supportive therapy in the imported diseases]. 351 46

Although, miliary tuberculosis is an unusual cause of severe acute respiratory failure, we describe nine patients with miliary tuberculosis who developed adult respiratory distress syndrome. This complication occurred in seven patients despite treatment with antituberculous drugs. In two patients who developed the syndrome, miliary tuberculosis was diagnosed only at postmortem. The presence of pulmonary hypertension in all cases and disseminated intravascular coagulation in seven cases suggests a possible pathophysiologic relationship with severe pulmonary vascular damage. The high mortality rate (88.8%) was associated with nonpulmonary organ system failure. Miliary tuberculosis should be considered in patients with adult respiratory distress syndrome of unknown etiology, and simple diagnostic procedures such as sputum, bronchial brushing, and gastric examination should be followed by invasive diagnostic procedures to confirm this etiology. Since untreated miliary tuberculosis is usually fatal, early recognition of this disease is of great importance, and specific therapy may play a lifesaving role.
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PMID:Miliary tuberculosis and adult respiratory distress syndrome. 358 48

Eight cases of pulmonary involvement were observed in 17 severe cases of ictero-haemorrhagic leptospirosis. Haemoptysis (7 cases) occurred on the 4th day of the infectious syndrome and was associated with other haemorrhagic manifestations in 4 cases. Cough, pain and polypnoea were not constant. Chest X-ray showed diffuse, non-specific changes, such as nodular opacities or infiltrates. Septicaemia was confirmed in all cases with acute renal failure in 7 cases and meningitis in 6 cases. Severe thrombocytopenia was demonstrated in 2 cases. Six patients recovered quickly with regression of the lung changes within 12 days. Two patients died, one of a fulminant haemoptysis related to a disseminated intravascular coagulation syndrome, and the other of acute respiratory failure. All cases were confirmed serologically. Although lung changes in leptospirosis are usually benign and mild, haemoptysis and polypnoea with diffuse radiological changes are poor prognostic factors. The pathological changes were similar to those of haemorrhagic alveolitis. These changes may be either due to the liberation of toxins or to an immunological phenomenon.
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PMID:[Pulmonary manifestations in severe ictero-hemorrhagic leptospirosis]. 363 26

The model of chest trauma accompanied by acute respiratory failure was studied on 78 guinea-pigs. Histological and electron microscopic methods have revealed a typical pattern of shock lung: combination of diffuse bilateral microfocal distelectases and microcirculation disturbances, i.e. pulmonary venular spasm accompanied by sludge, disseminated intravascular coagulation, focal hemorrhages and interstitial edema. In 5 out of 13 cases 72 hours later hyaline membranes were observed as conglomerations of eosinophilic masses of plate form, distinct from intraalveolar edema. At the ultrastructural level hyaline membranes could be identified as stripes of granular or fibrillar accumulations containing cellular organella debris, ajacent to alveolar walls.
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PMID:[Mechanism and time periods of the development of hyaline membranes in acute respiratory failure of traumatic origin]. 385 83

From the analysis of 182 consecutive surgical patients who underwent hepatectomy and/or were associated with liver cirrhosis during 1963-1982, acute respiratory failure was proved to be so much often in those patients. The case rate of this complication tends to increase according to resected size of liver tissue and severity of liver cirrhosis. Those cases showed clinical signs of pulmonary interstitial edema and were often associated with coagulopathy and endotoxemia. In order to clarify the pathophysiological mechanism of the acute respiratory failure based on liver dysfunction, a canine experimental model in which blood inflow into the liver was completely blocked was newly devised, and respiratory state in this model was analysed. The following results were obtained. The increase of EVLW (extravascular lung water) measured by modified double indicator dilution method was linear to the increase of PWP (pulmonary wedge pressure) in both liver failure group and control group. But the coefficient of the regression line was three times larger in the former group than in the latter. It suggests that permeability of pulmonary capillary was highly increased in liver failure group. All dogs with liver failure showed typical symptomes of lung edema at maximal PWP. Disseminated intravascular coagulation, consumption of neutrophils, decrease of CH50 and serum opsonin were thought to be mediators of the increase of lung vascular permeability. Steroid and PGI2 blocked the increase of the lung vascular permeability completely but not the increase of lung vascular resistance in this experimental model.
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PMID:[Acute respiratory failure based on liver dysfunction in canine liver ischemia model]. 407 3

Plasma fibronectin (FNp) concentrations were measured in 63 patients with acute respiratory failure and 28 patients with circulatory failure, using Laurell's electroimmunoassay method. Measurements were made in the acute phase and repeated in the course of the disease. The mean FNp concentration in 20 controls was 262 +/- 59 mg/l. FNp values were normal in the acute phase of chronic obstructive pulmonary disease and in cardiogenic pulmonary oedema. In contrast, they were significantly decreased in adult respiratory distress syndrome and in acute pneumonia, as well as in acute circulatory failure, notably from septic shock. FNp values were also considerably reduced in patients with severe disseminated intravascular coagulation syndrome. Clinical improvement was accompanied by a return to normal of FNp concentrations. The mortality rate was greater in patients with low FNp values than in those with normal values.
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PMID:[Acute respiratory and circulatory failure. Prognostic value of plasma fibronectin levels]. 622 Mar 70

A 49-year-old previously healthy man fell gravely ill after repeatedly eating the mushroom Paxillus involutus. Haemolysis and circulatory shock caused acute renal failure, acute respiratory failure and disseminated intravascular coagulation. The patient died three-and-a-half days after the mushroom meal in protracted shock. In addition to the signs of haemolysis, post-mortem examination revealed signs of intravascular coagulopathy in lungs, kidneys, adrenals, myocardium, liver and spleen. There were also extensive fat emboli to both lungs. An IgG antibody against paxillus involutus extract was demonstrated in the patient's serum. The immunological reaction pattern suggests primarily the formation of an immune complex, which secondarily attaches itself to the erythrocyte surface and causes intravascular haemolysis by activation of the complement chain. In the first instance the diagnosis is made from anamnestic data. In addition to adequate treatment of circulatory shock, immediate plasma separation could provide a chance of effective treatment.
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PMID:[Fatal immunohaemolytic anaemia after eating the mushroom Paxillus involutus (author's transl)]. 710 97

Acute respiratory failure is a common complication in patients with disseminated intravascular coagulation associated with sepsis. To elucidate the role of coagulation abnormalities in acute lung injury in sepsis, we investigated the effect of anticoagulants on the pulmonary vascular injury in rat induced by lipopolysaccharide (LPS). When administered intravenously, LPS (5 mg/kg body weight) significantly increased the accumulation of 111indium-labeled neutrophils in lung 30 min after administration. Subsequently, the pulmonary vascular permeability and the serum level of fibrin and fibrinogen degradation products (E) [FDP (E)] increased and remained elevated for several hours. Neither heparin alone, heparin plus antithrombin III, or dansyl-Glu-Gly-Arg-chloromethyl ketone-treated factor Xa, a selective inhibitor of thrombin generation, prevented LPS-induced vascular injury 6 hours after LPS administration, whereas these substances significantly inhibited the increase in serum FDP (E) at that time. LPS-induced pulmonary vascular injury was significantly attenuated in rats with methotrexate-induced leukocytopenia or treated with ONO-5046, a potent granulocyte elastase inhibitor, although ONO-5046 did not inhibit the LPS-induced increase in serum FDP (E). Thus, activated leukocytes play a more important role than coagulation abnormalities in the pathogenesis of LPS-induced pulmonary vascular injury in an experimental rat model of endotoxemia.
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PMID:Endotoxin-induced pulmonary vascular injury is mainly mediated by activated neutrophils in rats. 748 29

A few hours after a 15 km march a 19-year-old man developed a fever of 40 degrees C, accompanied by hemoptysis, tarry stools and pain in the thigh. On physical examination there was tenderness and swelling over the shoulders, upper arms and thighs as well as petechiae, bruises, hepatomegaly, pain on percussion over the kidney region and signs of hypovolaemia. There was leukocytosis (18,800/microliters) and increased creatinase activity (3900 U/l, rising to 66,300 U/l after 24 h). The platelet count fell from 147,000 to 11,000/microliters, the fibrinogen level to 0.25 milligrams. On the second day serum creatinine was 4.1 mg/dl, urine volume 50 ml/24 h, urinary myoglobin concentration 120,000 micrograms/l. The Quick value dropped to under 3%, while liver enzymes and bilirubin concentration rose. The rhabdomyolysis caused acute respiratory failure, despite symptomatic treatment of the acute renal failure and consumption coagulopathy, but after 8 weeks of intensive treatment the patient was discharged without symptoms. No cause other than the preceding physical exertion was found for the rhabdomyolysis. Muscle biopsy revealed unspecific changes 4 1/2 months after discharge.
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PMID:[Complications of an idiopathic rhabdomyolysis (Meyer-Betz syndrome) after physical exertion]. 786 81


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