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

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

Perfusion is more critical than oxygen in the maintenance of cell viability. A high hematocrit or high fibrinogen level increases blood viscosity and predisposes to disseminated intravascular coagulation. It is recommended that a hematocrit of about 30 be maintained in periods of circulatory stress such as shock or extracorporeal circulation.
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PMID:Importance of capillary perfusion. 49 56

Disseminated intravascular coagulation was induced in dogs by infusion of tissue thrombokinase. Its course was followed by coagulation tests, determination of the rate of microthrombosis, and measurement of organ functions and oxygen consumption. The therapeutic result of streptokinase administration at an early stage of pathological changes is demonstrated by improvement of the disturbed organ functions and oxygen supply as well as by the decrease in plasma-haemoglobin level. When streptokinase was administered at an advanced stage of organ damages, they remained irreversible, although repatency of the microvasculature had been reached.
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PMID:[Experimental therapy of disseminated intravascular coagulation by streptokinase administration]. 51

Combined injuries occur in a great number. More than half of the deaths in accidents are caused by combined injuries. In more than 70 per cent of these, brain injury is the decisive lethal factor. Shock, respiratory disturbances, signs of fat embolism, coagulation disturbances have to be assessed first. The primary shock therapy begins with the filling up of the volume by colloid solutions. If internal bleedings are the cause of the shock, they must be treated first. Respiratory insufficiencies are mainly due to thorax injuries. Although systematic treatment cannot remove the fact of a fat embolism, it can keep its pathophysiological consequences within certain limits. Among the coagulation disturbances, special attention should be paid to the consumption coagulopathy. As regards the brain, attention should be paid to the increase in intracranial pressure as well as to increase in body temperature, decrease in oxygen saturation, and the like, the combination of which often has a deleterious effect. In the timing, the shock therapy is followed by an orientating examination (including state of consciousness, possible internal haemorrhages, bone fractures, etc.), provisional immobilisation, pain relieving and, when required, sedation. Intracranial complications must be looked for in all their phases. Osteosynthesis is not carried out as part of the primary treatment but usually only one week later. Open brain injuries have no priority but intracranial haematomas have an absolute priority. Surgical treatment of liquor fistulas should only be carried out in the acute phase when extensive impression fractures are present at the same time.
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PMID:[Timing in the treatment of multiple injuries]. 55 Jun 45

The exposure of rats to 100% oxygen at 1 atmosphere leads to a prolongation of prothrombin times and activated partial thromboplastin times. This development is associated with a consumption of factor XII, VIII, and VII activities and with the appearance of fibrin monomers and fibrinogen degradation products. Lead acetate enhances all oxygen-induced changes of the coagulation systems drastically. The O2 survival time of chicks which are naturally deficient in factor XII is greatly increased over that of rats and is not affected by lead acetate. Oxygen survival times of rats suffering from chronic respiratory disease (CRD) are also significantly increased when compared with normal rats. It appears that consumptive coagulopathy and disseminated intravascular coagulation are early events in oxygen exposure, and that their development is accelerated by lead ions.
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PMID:Oxygen-induced consumptive coagulopathy and its enhancement by lead acetate. 57 13

The role of disseminated intravascular coagulation (DIC) in the pathogenesis of adult respiratory distress syndrome (ARDS) was studied in the experimental animals. ARDS was simulated in dogs by the administration of various doses of Escherichia coli endotoxin (Difco). The alveolar surface activity in the group which received lethal dose of endotoxin (3 mg/kg) exhibited no significant alterations with mild pulmonary insufficiency and little pathologic change five hours after the induction of shock. On the other hand, a significant decrease in alveolar surface activity was found to develop in the group which received sublethal dose of endotoxin (1 mg/kg) accompanying enlarged alveolar-arterial oxygen tension differences (A-aDO2) and elevated pulmonary vascular resistance after 24 hours. These changes occurred concomitantly with pathologic findings of DIC, interstitial edema and atelectasis. The disturbance in ventilatory function observed in prolonged shock appeared to be related to the impairment of pulmonary microcirculation caused by DIC and subsequent hypoxia of lung tissue which led to a loss of alveolar surfactant.
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PMID:Disseminated intravascular coagulation in the pathogenesis of adult respiratory distress syndrome: 2. Experimental study. 60 93

Two cases of infants with shock are presented. Cardiac output was determined in both with dilution dye using an auricular oxymeter, with three determinations: at 0, 30 and 60 minutes while receiving intranvenous fluids. At the same time, blood gases and blood lactatewere determined. The first case showed hypodynamic shock secondary to hypovolemia due to severe dehydration, associated to low central venous pressure, low arterial tension, increased peripheral resistance and increased arteriovenous difference of oxygen. The second case was a newborn with sepsis and disseminated intravascular coagulation with hyperdynamic shock with very high cardiac output, low peripheral resistance and low arteriovenous difference of oxygen. Both cases had an initial increase of lactate and a mild decrease at the end of the period of clinical observation.
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PMID:[Hemodynamometabolic changes in shock in infants. Report of 2 cases]. 62 52

Male rats of 260 g were exposed to hyperbaric conditions of oxygen with different partial pressures and the changes of the haemostasis were studied. In 100% oxygen at 2 ATA, the animals died within 48 h. In 100% oxygen at 1 ATA, death occurred only after 3 d; however, in 24-48 h there developed disseminated intravascular coagulation (DIC). At the same time uncompensated acidosis of 7.34 +/- 0.02 was measured. Perivascular bleeding could be histologically demonstrated in different organs. The mixture of 60% oxygen and 40% nitrogen caused only a minimal DIC while a mixture of 40% oxygen and 60% nitrogen caused no changes in the haemostasis. Volunteer young males exposed to the mixture of 60% oxygen and 40% nitrogen, developed the beginning symptoms of DIC, which made it necessary to stop the experiments.
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PMID:Disseminated intravascular coagulation developed in hyperbaric oxygen. 65 96

Shock continues to be associated with a high mortality rate primarily because of delays in diagnosis and therapy. To diagnose shock early, and thereby increase the chances of reversal before there is extensive deterioration of vital organs, one should look for any decrease in pulse pressure, urine output, urine sodium concentration, alertness or any increase in urine osmolarity, tachypnea or tachycardia. Systolic hypotension, oliguria, metabolic acidosis and a cold clammy skin are late signs of shock. The pathophysiology of early hypovolemic shock includes hyperventilation, vasoconstriction, cardiac stimulation, fluid shifts into the vascular system and platelet aggregation. Late shock is characterized by lysosomal breakdown, subsequent release of kinins (especially bradykinin), impaired cell metabolism and organ function, fluid shifts out of the vascular system because of capillary endothelial damage and intravascular coagulation. The primary cause of shock should not be neglected in favor of treating signs, symptoms, and laboratory data. The resuscitation from the shock process itself involves correction of pathophysiologic changes, based on objective trends and responses rather than isolated measurements. A suggested outline of therapies in order of their use includes: 1) correction of the primary problem; 2) ventilation and oxygen; 3) fluid-loading: 4) inotropic agents; 5) correction of acid-based and electrolyte abnormalities; 6) steroids ("physiologic" or "pharmacologic" doses); 7) vasopressors (especially in elderly, severely hypotensive patients); 8) vasodilators (if excess vasoconstriction); 9) diuretics (if oliguric in spite of the above), and 10) heparin (if DIC). The most common errors are 1) late diagnosis; 2) inadequate control of the primary problems; 3) inadequate fluid loading; 4) delayed ventilator assistance, and 5) excessive reliance on and use if vasopressors and diuretics.
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PMID:Shock in the emergency department. 79 60

Consumptive coagulopathy and disseminated intravascular coagulation can be observed in rats exposed to 4 ata of oxygen. These events clearly precede the death of the animal and appear to be initiated by an activation of coagulation factor XII (Hageman). The onset and the extent of consumptive coagulapathy are greatly enhanced by a single and low intravenous dose of lead acetate. Mechanisms of activation of the intrinsic coagulation system and its role in oxygen toxicity are being discussed.
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PMID:Consumptive coagulopathy as biochemical mechanism in oxygen toxicity and its enhancement by lead(II) ions. 91 46


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