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

We have reported a case of neuroleptic malignant syndrome (NMS) in a patient with historical and clinical features suggestive of heat stroke or sepsis and adult respiratory distress syndrome (ARDS). ARDS and disseminated intravascular coagulation may be important, atypical signs encountered early in NMS and complicating its recognition.
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PMID:Neuroleptic malignant syndrome presenting as adult respiratory distress syndrome and disseminated intravascular coagulation. 335 84

Two cases of complete sagittal sinus occlusion with multiple brain hemorrhages, elevated intracranial pressure, and disseminated intravascular coagulation are described. These patients were successfully managed using pentobarbital-induced coma to ameliorate intracranial pressure elevation. This therapy was combined with monitoring of intracranial pressure and intermittent drainage of cerebrospinal fluid to further control intracranial pressure elevations. Thrombus and coagulopathy resolved with pentobarbital alone in one patient and after pentobarbital plus heparin therapy in the second patient. It is suggested that cases of severe distal sagittal sinus thrombosis with brain hemorrhage and intracranial hypertension may benefit from combined pentobarbital coma and intraventricular drainage. This allows for stabilization of bleeding tendencies before instituting heparin therapy when necessary. Management of sagittal sinus thrombosis with barbiturates or ventricular drainage is best performed in an intensive care unit environment with continuous monitoring of intracranial pressure and substantial electrophysiologic and neuroradiologic support.
Stroke 1988 Jul
PMID:Treatment of sagittal sinus thrombosis associated with cerebral hemorrhage and intracranial hypertension. 338 62

A multiinstitutional review of 10 pregnancies complicated by septic shock was undertaken to identify the clinical characteristics and hemodynamic alterations associated with this condition. Prolonged rupture of membranes with the subsequent development of chorioamnionitis or postpartum endometritis were risk factors that commonly preceded the diagnosis of septic shock. The majority of septic shock cases occurred during the puerperium. There were two maternal deaths in this selected series. Associated complications included pulmonary edema, adult respiratory distress syndrome, disseminated intravascular coagulation, pulmonary emboli, and cardiac arrest. The primary hemodynamic derangements were reduced systemic vascular resistance with depressed myocardial function. The mean initial systemic vascular resistance index in eight surviving women was 885 +/- 253 dyne.sec/cm5.m2. Despite an overall presenting cardiac index of 4.20 +/- 2.01 L/min/m2, five patients (50%) had evidence of myocardial depression based on analysis of their left ventricular function curves. Mean arterial pressure, systemic vascular resistance, and left ventricular stroke work index all showed significant improvement after therapy. A hemodynamic algorithm based on volume therapy, inotropic agents, and peripheral vasoconstrictors is offered. This therapeutic approach is designed to optimize cardiac performance and maintenance of organ perfusion in the critically ill patient with septic hypotension during pregnancy.
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PMID:Septic shock during pregnancy. 340 99

Coagulation parameters were initially monitored in 8 patients receiving whole body hyperthermia (WBH). Patients were heated by the warm water blanket technique to 41.8 degrees C (Tmax), maintained at this temperature for 2 hours, then allowed to cool. A fall in platelets was apparent by the time Tmax was achieved and continued during the 18 hours after WBH. Levels of beta-thromboglobulin (BTG) and platelet factor 4 rose by 56% and 191% by the end of treatment but returned to baseline 18 hours later. Fibrinogen, plasminogen and alpha 2-antiplasmin levels declined and FDP and fibrinopeptide A (FPA) levels increased during WBH. Factor XII and Factor VIII:C fell moderately during WBH while Factors VIII R:Ag, VIII:RC and V did not change or showed a late rise. Factor VII levels fell in 7 of 8 patients, reaching levels of 30% of normal in four. To better define the sequence of these coagulations perturbations, earlier and more frequent timepoints were studied in an additional 3 patients. This revealed that decreases in fibrinogen and plasminogen and increases in FPA and BTG occur very early (by the time the patient reaches 39 degrees C). On the other hand, a decrease in Factor VII activity was not apparent until patients had reached Tmax. WBH is therefore associated with a consumption coagulopathy. Possible mechanisms are discussed and extrapolations to the situation seen in heat stroke are suggested.
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PMID:Activation of coagulation during therapeutic whole body hyperthermia. 373 68

Progressively increasing heat stress ultimately results in heat stroke, a medical emergency leading to death if not treated properly. Initially in heat stress, enormous increases in blood flow and volume in skin (and muscle if exercising) are achieved by the diversion of blood away from the splanchnic bed, kidneys, and probably fat and muscle, and in some species such as man, there is also an increase in cardiac output. The onset of heat stroke is thought to involve a decrease in central venous pressure, which is defended by constriction in both arterioles and veins of the skin via low-pressure baroreceptors in the cardiopulmonary region. Body heat loss is thereby reduced and the consequent rise in body temperature causes death due to thermally evoked critical changes in central nervous system activity and/or fatal embolization following disseminated intravascular coagulation and erythrocyte sphering. Evidence is presented, which supports the proposal that cardiac filling pressure is the limiting factor in adjusting to heat stress.
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PMID:A case supporting the proposal that cardiac filling pressure is the limiting factor in adjusting to heat stress. 375 Nov 32

Fifty two consecutive patients with heat stroke were examined for evidence of adult respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC). Twelve patients were found to have ARDS (incidence of 23 percent) of whom nine (75 percent) died. All of these 12 patients had DIC as compared to only one among the 40 patients without ARDS. Review of the evidence in literature linking ARDS and DIC and our own observations in this study lead to the conclusion that the coagulopathy may be an essential mediator of lung damage in heat stroke and is a reliable marker of its occurrence. This suggests the possibility that screening of heat stroke victims for DIC may identify patients at increased risk of developing overt ARDS and allow early institution of measures which may possibly improve survival.
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PMID:Adult respiratory distress syndrome and disseminated intravascular coagulation complicating heat stroke. 375 68

21 patients (aged 28-81 years) with recent subarachnoid hemorrhage (10 saccular aneurysms, 3 arteriovenous angiomas, 8 normal angiograms) were continuously infused with tranexamic acid at a dosage of 5 g daily for up to 14 days. Therapy was surveyed by daily measurement of the available plasminogen activity (aPl) with the chromogenic substrate S-2251 and by a modified bioassay, whereby the concentration of tranexamic acid was determined thrombelastographically and expressed as antifibrinolytic equivalent. In addition, a battery of blood coagulation tests was performed daily. 5 patients died, 1 after postoperative stroke, 3 as a result of general complications during intensive care treatment, but only 1 due to rebleeding. 4 patients were successfully operated during the first week, 1 patient after 2 weeks. aPl fell from 99.2% (SEM 3.0%, n = 21) before treatment to 72.9% (SEM 3.5%, n = 21) after 24 h and to the therapeutic level between 50 and 60% from day 2 on. The mean steady state of the antifibrinolytic equivalent corresponded to about 150 micrograms/ml of tranexamic acid during infusion. Intra- and interindividual changes were relatively small for aPl, when compared with the antifibrinolytic equivalent measured by the bioassay. In 2 elderly patients tranexamic acid infusion had to be terminated because of clinical and laboratory signs of disseminated intravascular coagulation, whereby aPl fell below the therapeutic range, elucidating that this method is a sensitive indicator for a hypercoagulable state and useful for the surveillance of therapy with antifibrinoltic agents.
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PMID:Monitoring of antifibrinolytic treatment in subarachnoid hemorrhage. 399 57

Plasma fibronectin concentrations were significantly (P less than 0.001) below the reference range in dogs with disseminated intravascular coagulation (DIC) secondary to nonlymphomatous neoplasia, acute necrotizing pancreatitis, sepsis, chronic active hepatitis, and heat stroke. There was no statistical evidence of a group effect. Decrease in fibronectin concentration was associated with severe DIC, although no attempt was made to correlate fibronectin concentration with prognosis. These findings parallel those reported for severely ill human beings with diseases associated with DIC. They exemplify the potential of spontaneous diseases in animals as models for the study of human disease.
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PMID:Plasma fibronectin concentrations in dogs with disseminated intravascular coagulation. 400 93

Blood coagulation and fibrinolysis were assessed in 55 cases of heat stroke who presented with or without bleeding tendencies during the Makkah pilgrimage of 1983. 17 patients were identified to have evidence of disseminated intravascular coagulation (DIC). Bleeders with DIC had a higher incidence of shock and a higher mortality when compared to non-bleeders. Thrombocytopenia and liver cell damage were not limited to cases with DIC. Coagulation factors and serum enzyme studies suggested non-specific tissue damage as the trigger mechanism for DIC possibly proceeding through the extrinsic system of blood clotting. We conclude that the breakdown of haemostasis in heat stroke is multifactorial: thrombocytopenia, liver cell damage and DIC.
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PMID:Blood coagulation and fibrinolysis in heat stroke. 406 8

A treatment modality of a new original design was used in 87 survivors of ischemic stroke. Apart from the standard remedies, the authors administered drugs affecting the syndrome of disseminated intravascular coagulation, such as dipyridamole, glutamic acid and phytin, with heparin and freshly frozen plasma containing antithrombin III employed in grave cases. Hemostatic parameters in the study patients were observed to normalize more rapidly compared with the control group.
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PMID:[Treatment of the syndrome of disseminated intravascular coagulation in ischemic strokes]. 615 May 90


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