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

As the initial problems of trauma have been resolved, patients may survive the immediate period following critical injury only to succumb later to the effects of sepsis. We previously noted a correlation between multiple organ failure and intravascular clotting. The present study evaluated the incidence of infection complications following proven disseminated intravascular coagulation. Detailed analysis of multiple clotting factor changes following critical surgical illness (Factors I, II, V, VIII, IX, X, XI, and platelets, fibrin degradation products and plasminogen) were carried out prospectively in 48 patients. Twenty-one of the 48 were classified as having a severe degree of intravascular coagulation on the basis of hematologic evidence. Only one survived without evidence of infection; 16 showed changes consistent with a moderate degree of intravascular coagulation, and ten subsequently developed evidence of infection. Of the 11 patients with minimal evidence of intravascular coagulation, infection developed in only one.
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PMID:The relationship between sepsis and disseminated intravascular coagulation. 70 5

In 40 out of 45 children dead from sepsis in 1974--1976 the development of the syndrome of disseminated intravascular coagulation was proved on the grounds of the pathologic picture. In 27 cases histological changes were combined with characteristic clinico-laboratory manifestations of the syndrome. The latter was not found in 10 children who died of a severe local purulent process.
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PMID:[Disseminated intravascular coagulation syndrome in sepsis in infants]. 70 15

We have reviewed 53 cases of disseminated intravascular coagulation (DIC) in the newborn, including 29 cases that were confirmed at autopsy. Factors predisposing to DIC included maternal complications (60%), low Apgar scores (30%), hyaline membrane disease (62%), and sepsis (26%). Diagnostic criteria common to autopsy-proved cases included presence of fibrin degradation products, low factor V activity, a prolonged prothrombin time, and a prolonged partial thromboplastin time and/or thrombocytopenia. There appeared to be no difference in coagulation response or in mortality among patients treated with different therapeutic regimens. Survivors were older gestationally, had higher birth weights, and higher Apgar scores.
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PMID:Disseminated intravascular coagulation in the newborn. 76 May 11

Of 35 newborn infants who died from an infection 19 had postmortem evidence of massive pulmonary hemorrhage. All but 1 of the 19 had evidence of antimortem formation of intravascular fibrin clots in lung tissue. Seventeen infants had low platelet counts. Of the 11 infants in whom coagulation studies were done, 8 had evidence of disseminated intravascular coagulation (DIC) during life. Vasculitis in the lungs, associated with fibrin clots and hemorrhages, was detected in two infants. It is postulated that sepsis is an important cause of hemorrhage in the newborn, probably as a result of the development of DIC.
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PMID:Massive pulmonary hemorrhage in neonatal infection. 76 37

In childhood hyperpyrexia is the most important factor causing the irreversibility of shock. The combination of high fever and circulatory impairment is more frequent during the first years of life. This behaviour is due to the high resistance of the arterial system in infancy. Marked general vasoconstriction increases the risk of a reduction in circulation and of heat loss, and causes hypoxia and rise of fever. The further course of shock is largely determined by microcirculatory failures. Under hyperpyrexia the disturbance of homeostasis can be intensified by shivering, blocking of perspiratio sensibilis, hyperosmolarity, brain edema, and DIC. In most cases of meningococcal sepsis shock and DIC begin with vasoconstrictive centralisation of circulation. The high-output-shock is extremely rare in children with high fever. The control of all important functions of a febril child in shock is the best baseline for the treatment. It is necessary in all shock patients in hyperpyrexia to reduce the fever and to repair the peripheral circulation. The therapy consists of antipyretic drugs, physical cooling, infusions of buffer-bases, dopamine, antibiotics and so on. In DIC heparin or streptokinase are indicated. In severe circulatory impairment combined with high fever prednisone is useful, in brain edema dexamethasone. The fatality rate of our cases has been diminished by a systematic therapy of hyperpyrexia and shock from 10 to 3 percent.
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PMID:[Hyperpyrexia and shock (author's transl)]. 77 99

This chapter has provided a review of available literature regarding alterations of hemostasis associated with CPB. The primary pathology of altered hemostasis during CPB appears to be two-fold: (1) a functional platelet defect of unclear etiology, which occurs in virtually all patients, and (2) a primary hyperfibino(geno)lytic defect which occurs in the majority of patients undergoing cardiopulmonary bypass. Significant thrombocytopenia does not appear to be a consistent problem, and is probably a function of perfusion technics; this may, however, be an important source of hemorrhage in some instances. Although hyperheparinemia, heparin rebound, and protamine excess have occasionally been incriminated as sources of hemorrhage during CPB, no well documented cases appear in the literature. Likewise, although DIC gained popularity in early reports of CPB hemorrahge, it appears that this syndrome rarely, if ever, arises as a consequence of CPB alone; it can be seen, however, in CPB patients who are provided a triggerin situation for DIC, such as shock, sepsis, or hemolytic transfusion reaction. It is likely that many reported alterations of hemostasis during CPB which were concluded to represent DIC actually were due to hyperfibino(geno)lysis. The key to prevention of CPB hemorrhage rests simply in obtaining an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies in both patient and family; of equal importance is a careful history regarding antiplatelet drugs. A careful physical examination, searching for clues of a real or potential bleeding diathesis, also can often prevent catastrophic cases of CPB hemorrhage. Lastly, an adequate presurgical laboratory screen must be performed; in addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a thrombin time and standardized template bleeding time must be added. The addition of these two simple modalities will insure against significant defects in fibrinogen, the fibrinolytic system, vascular function, and platelet function. When CPB hemorrhage occurs, simple laboratory screening will usually allow for a quick hemostasis evaluation. The parameters recommended in this review will distinguish between surgical and nonsurgical bleeding and should, therefore, allow for a quick decision regarding necessity for reexploration and the adequacy of hemostasis if reexploration is needed. In addition, this screen will distinguish between difficulties with heparin, protamine, and the fibrinolytic system. The vast majority of nonsurgical hemorrhages during CPB is due to a functional platlet defect, primary hyperfibrino(geno)lysis, or a combination of these. The quick administration of platelet concentrates, while awaiting laboratory evaluation, will control or significantly blunt most instances of CPB hemorrhage. If platelets fail to control bleeding, and reasonable laboratory evidence of primary hyperfibrino(geno)lysis is present, antifibrinolytics should then be used...
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PMID:Alterations of hemostasis associated with cardiopulmonary bypass: pathophysiology, prevention, diagnosis, and management. 79 78

Diagnosis of disseminated intravascular coagulation (DIC) was made in 64 cases (16.2%) among a total of 395 autopsy cases. There were 31 men and 33 women. Their ages ranged from 31 to 91 years (mean 76.3). Underlying diseases were mainly malignancy and sepsis. Fresh cardiac lesions were found in 40 cases (62.5%). Coronary thrombosis was found in 13 cases (20.3%) and myocardial necrosis in 24 cases (37.5%), with acute myocardial infarction in 9 and focal necrosis in 15. Nonbacterial thrombotic endocarditis was found in 17 cases (26.6%), mural thrombi in 11 (17.2%), and bleeding of the heart in 11 (17.2%). Platelet count, fibrinogen and euglobulin lysis time were not correlated with myocardial necrosis nor coronary thrombosis. Increase of fibrin degradation products correlated with the presence of coronary thrombosis with or without myocardial necrosis. DIC was found with a high incidence in the aged, and many of them were complicated with fresh cardiac lesions. Development of acute myocardial infarction depends on the small thrombi in the severe stenosis of the main coronary arteries or on the multiple microthrombi in the peripheral coronary branches.
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PMID:A clinicopathological study on cardiac lesions in 64 cases of disseminated intravascular coagulation. 84 48

A case of pneumococcal sepsis with DIC is reported. The patient had hyposplenism from thorium dioxide administration 23 years previously. Evidences of consumptive coagulopathy were verified by clinical manifestations of shock, generalized petechiae, abnormal hemostatic studies, and autopsy findings. The possible pathogenetic mechanism(s) of DIC in hyposplenism and pneumococcemia are reviewed.
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PMID:Hyposplenism and disseminated intravascular coagulation (DIC) in fulminant pneumococcal sepsis. 88 88

A critically ill patient with disseminated intravascular coagulation (DIC) secondary to gram negative septicemia is reported. Low dose (5-10 mu/kg/h) heparin by intravenous infusion promptly inhibited intravascular coagulation, as reflected by laboratory studies. Fibrin monomer (FM) became undetectable, concentration of fibrin degradation products (FDP) fell, fibrinogen rose, and the activated partial thromboplastin time (PTT) shortened. Unintentional, temporary interruption of heparin resulted in transient return of abnormal laboratory values. The patient went on to make a complete recovery. Although the therapeutic contribution of heparin could not be proven in this patient, the laboratory data suggested that it was a valuable adjunct and in the dosage given unlikely to potentiate bleeding. The monitoring of heparin therapy in DIC by measurement of FDP, FM, and fibrinogen rather than clotting time is recommended.
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PMID:Case report: low-dose intravenous heparin in the treatment of disseminated intravascular coagulation. 91 96

The study included 28 infants with infectious gastroenteritis who evolved with disturbances of coagulation and in whom laboratory tests were practiced by micromethods through capillary puncture. The most frequently seen abnormality was a combination of vitamin K dependent factors deficiency with thrombocytopenia. Another observation in our study is that hypofibrinogenemia in infants with infectious gastroenteritis is not always secondary to disseminated intravascular coagulation. A decrease in fibrinogen in these cases is explained by a lack in synthesis of this factor in infants with malnutrition since out of 16 malnourished infants, 75% evolved with hypofibrinogenemia, while eutrophic infants evolved with normal fibrinogen. The disseminated intravascular coagulation syndrome was seen more frequently in patients with infectious gastroenteritis complicated with septicemia and shock, 57% of the patients did not show manifestations of bleeding nor of thrombosis which justifies in these cases a systematic investigation of the coagulation mechanism.
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PMID:[Blood coagulation disorders in infants with infectious gastroenteritis]. 91 59


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