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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 injection of a sublethal bolus of E. coli into conscious swine produces an early increase in PAP and a decrease in LAP. This hemodynamic effect may be secondary to the pulmonary venous constriction seen in other species, or may relate to demonstrated multiple pulmonary microemboli. Hypoxemia developed in only four of 17 animals although all endotoxin-treated swine showed interstitial edema and elevated wet/dry weight ratios with normal pulmonary surfactant. In addition, endotoxin-treated swine developed signs of disseminated intravascular coagulation, with renal cortical infarcts in 44%, and coronary arterial thrombi in 28% including one transmural myocardial infarction. This effect was observed in the absence of prolonged hypotension in swine and should provide a useful model for further study of the relationship of endotoxin to disseminated intravascular coagulation.
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PMID:Hemodynamic and respiratory responses of conscious swine to E. coli endotoxin. 0 64

The relationship between factor VIII (AHF) procoagulant activity and factor VIII-related antigen were examined in patients with disseminated intravascular coagulation (DIC), pulmonary embolism (PE), and coronary artery disease with or without myocardial infarction (MI). It was found that 13 of 13 patients with DIC, 17 of 17 patients with PE, and 10 of 12 patients with MI possessed a significantly elevated factor VIII-related antigen to factor VIII activity ratio (VIII-ratio). The VIII-ratio returned to normal in each of 2 patients with DIC and 1 paitent with PE after treatment with heparin, heparin and alpha-amino-caproic acid, and heparin and coumadin respectively. In contrast, the VIII-ratio was slightly elevated only in 1 of 15 patients with coronary artery insufficiency without MI. In in vitro studies, after treatment of plasma with thrombin or plasmin, factor VIII activity was lost, whereas the amount of factor VIII-related antigen remained the same or was even increased when measured by agarose quantitative immunoelectrophoresis. These observations have led us to conclude that an elevated VIII-ratio is a very sensitive indicator of intravascular coagulation.
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PMID:In vivo and in vitro effects of thrombin and plasmin on human factor VIII (AHF). 13 71

The hemodynamic response to slow and rapid defibrination was sutdied in anesthetized beagle dogs, with the following results: 1. Slow defibrination was a benign procedure that had little or no effect on the hemodynamic variables studied. 2. Rapid defibrination induced statistically significant decreases in cardiac output, stroke volume, and mean aortic arterial pressure. 3. Bradycardia, a drop in mean left v"ntricular pressure, cardiac and minute work indices, an increase in pulmonary artery pressure, and a drastic rise in pulmonary and systemic vascular resistances were also observed. Although physiologically apparent, these changes were not statistically significantly different from control levels. 4. Pulmonary capillary wedge pressure, left ventricular end-disatolic pressure, arterial pH, and blood gases were not altered by rapid defibrination. 5. In view of the similarities between the hemodynamic changes observed after rapid defibrination and acute myocardial ischemia, the role of decreasing fibrinogen concentrations and blood viscosity in aucte myocardial infarction and the sudden death syndrome is questioned.
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PMID:Hemodynamic effects of slow and rapid defibrination with defibrizyme, the thrombin-like enzyme from venom of the timber rattlesnake. 23 15

Seven elderly cases with reversible electrocardiographic changes simulating acute myocardial infarction in the absence of gross myocardial infarction on postmortem examination were observed following the blood transfusion. The underlying diseases were cancer of gastrointestinal tract or gall bladder in 4, gastric ulcer in 2, and 1 of pseudomembranous enterocolitis. The electrocardiogram revealed the abnormal Q waves with monophasic ST elevation and following coronary T inversion. These findings lasted only for 2 to 7 days and returned to the previous normal tracings. The hematocrit was elevated from 28.9 to 47.7 after the blood transfusion of 800 to 1,800 ml. The disseminated intravascular coagulation was shown in 5 cases. GOT levels were within normal ranges except 1 case. Pathological findings in cases with recent electrocardiographic changes were characterized by the mural thromboses, extending into the myocardium through the Thebesian vein. The focal small necroses of the adjacent myocardium or around the thrombosis of small vessels were also observed. In the later phase the fine interstitial fibrosis took place after the resorption of the thrombi and necrotic foci. From these clinical and pathological findings we proposed a new concept of reversible myocardial infarction induced from the hypercoagulability, disseminated intravascular coagulation, and elevated hematocrit.
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PMID:Acute reversible myocardial infarction after blood transfusion in the aged. 30 Aug 14

Affinity chromatographic studies using insolubilized fibrinogen (fibrinogen-agarose) revealed that fibrin monomer present in plasma is selectively adsorbed to fibrinogen-agarose and may be quantitatively estimated following desorption. Analysis of plasma samples from patients with myocardial infarction, cirrhosis of the liver malignant diseases and DIC confirmed the presence of considerable amounts of fibrin monomer revealing concentrations between 3 and 15 mg/100 m1 plasma as compared to normal plasma (1.96 +/- 0.37 mg/100 m1, = 27). The method is suitable for the assessment of hypercoagulable states. Standard conditions for the procedure were evaluated using 3H-labelled fibrinogen and fibrin monomer.
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PMID:Detection of thrombin-induced fibrinogen derivatives in thrombotic states. 61 80

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

Therapeutic defibrination by Arwin was induced in a group of nine patients suffering from unstable angina combined with hyperfibrinogenaemia and in a further six patients who developed hyperfibrinogenaemia accompanied by angina pectoris after thrombolytic therapy with streptokinase for recent myocardial infarction. In patients of the former group with unstable angina a mean pretreatment plasma fibrinogen concentration of 4.9 g/1 was lowered to 1.4 g/l over a period of four weeks, whilst in the latter group, the plasma fibrinogen was lowered from 5.7 g/l to 2.0 g/l over 10 days. In all cases a remarkable improvement in the severe anginal symptoms was achieved already at fibrinogen levels within the lower range of normal. This improvement outlasted the period of therapy in most patients. Two patients died following acute myocardial infarction; one of the patients with unstable angina died 15 months after Arwin therapy and the second patient discontinued therapy after one week and died three weeks later.
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PMID:[Therapeutic defibrination by arwin in unstable angina pectoris combined with hyperfibrinogenaemia (author's transl)]. 71 35

Six cases of coronary embolism and myocardial infarction associated with nonbacterial thrombotic endocarditis were seen at the Mount Sinai Hospital over a ten-year period. Every patient had an underlying malignant neoplasm. The vegetations were found on aortic, mitral, tricuspid and pulmonic valves and were located on the free or closure margins. The clinical diagnosis of this condition is difficult because of simultaneous embolization to the brain, causing widespread neurologic symptoms, but could be made by electrocardiographic and serum enzyme studies. Myocardial infarction caused the deaths of three patients. The relationship between nonbacterial thrombotic endocarditis, hypercoagulability, and disseminated intravascular coagulation is discussed.
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PMID:Coronary embolism and myocardial infarction associated with nonbacterial thrombotic endocarditis. 90 73

In patients with angina pectoris and acute myocardial infarction different signs of disseminated intravascular coagulation were found, their intensity depending on the severity of the clinical course. In myocardial infarction with a complicated course and, especially, in shock signs of disseminated intravascular microthrombus formation were revealed, its criteria including, according to the author's data, reduced platelets count, factor V activity, shortening of platelets life and period of labelled fibrinogen circulation, appearance of large quantities of the fibrin-monomer complex.
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PMID:[Disseminated intravascular coagulation in myocardial infarct]. 102 34

A case of life-threatening adverse effects following intravenous administration of a non-ionic contrast medium is reported. The patient, a 68-year-old diabetic hypertensive male with dyspnoea and cough had an abnormal chest radiograph, revealing congestive heart failure and an enlarged right hilum. Computed tomography (CT) of the chest was performed using 100 cm3 of intravenous iopamidol. Within half an hour the patient developed abdominal cramping, vomiting, and diarrhoea, followed by hypotension, tachycardia, fever to 40 degrees C, and delirium. His course was complicated by disseminated intravascular coagulation, rhabdomyolysis, renal failure, respiratory arrest, and atrial fibrillation. There was no evidence of infection, neoplastic disease, or myocardial infarction. Over the next month the patient slowly recovered. One other case report implicates a contrast agent with a similar syndrome. The features of this case fulfil the criteria for a probable adverse drug reaction of a type and severity rarely encountered.
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PMID:Case report: multisystem failure following intravenous iopamidol. 139 88


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