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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 most frequent obstetrical cause of coagulation disorders as disseminated intravascular coagulation is placental abruption, which can be found in women without any apparent clinical disturbances or in the state of established preeclampsia. Hypertension occurs in 5-8% of all pregnancies and may be complicated by preeclampsia. Preeclampsia is a complex clinical syndrome with insufficiently clear pathophysiology based on the damage of the vascular endothelium. As a result of this, generalized endothelial disruption in preeclampsia, a multiorgan dysfunction, can develop, most frequently reflected in the clinical presentation with haematological and renal disturbances and with a disordered function of the liver and central nervous system. We are presenting a case of a gravid woman with poorly regulated hypertension that resulted from development of preeclampsia, later complicated by placental abruption and disseminated intravascular coagulation (DIC) with multi-organ dysfunction. The importance of rapid recognition of coagulation disorder and the attempt at surgical treatment aiming at removal of the triggering mechanisms of DIC was shown, suggesting all the symptomatic therapeutic measures would be ineffective. Although our patient was surgically treated in the phase of generalised disorder characterised by development of coma, acute respiratory distress syndrome and renal insufficiency when mortality was 70%, the recovery of functions of all involved organs was achieved, except for the renal function that required chronic haemodialysis treatment.
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PMID:[Multiorgan dysfunction in a gravid woman with placental abruption and disseminated intravascular coagulation]. 1792 41

We describe a 26-year-old female patient, who had attempted suicide with Endosulfan, and who presented to the Emergency Department with status epilepticus. She subsequently developed hypotension refractory to inotropes, intravascular hemolysis, disseminated intravascular coagulation (DIC), metabolic acidosis and, finally, cardiac arrest and death. Endosulfan is a chlorinated insecticide that causes central nervous system hyperstimulation. It is absorbed from the gastrointestinal tract, skin, and respiratory tract, and leads to nausea, vomiting, paraesthesia, giddiness, convulsion, coma, respiratory failure, and congestive cardiac failure. Hepatic, renal and myocardial toxicity, agranulocytosis, aplastic anemia, cerebral edema, DIC, thrombocytopenia, and skin reaction also have been reported. Management includes decontamination of skin and gastrointestinal tract, supportive care including treatment of status epilepticus, dysrhythmias, and mechanical ventilation. Mortality and morbidity rates are very high and there is no specific antidote. Atropine and catecholamines should be avoided.
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PMID:Endosulfan poisoning with intravascular hemolysis. 1797 61

Malaria remains a highly prevalent disease in more than 90 countries and accounts for at least 1 million deaths every year. Plasmodium falciparum infection is often associated with a procoagulant tonus characterized by thrombocytopenia and activation of the coagulation cascade and fibrinolytic system; however, bleeding and hemorrhage are uncommon events, suggesting that a compensated state of blood coagulation activation occurs in malaria. This article (i) reviews the literature related to blood coagulation and malaria in a historic perspective, (ii) describes basic mechanisms of coagulation, anticoagulation, and fibrinolysis, (iii) explains the laboratory changes in acute and compensated disseminated intravascular coagulation (DIC), (iv) discusses the implications of tissue factor (TF) expression in the endothelium of P. falciparum infected patients, and (v) emphasizes the procoagulant role of parasitized red blood cells (RBCs) and activated platelets in the pathogenesis of malaria. This article also presents the Tissue Factor Model (TFM) for malaria pathogenesis, which places TF as the interface between sequestration, endothelial cell (EC) activation, blood coagulation disorder, and inflammation often associated with the disease. The relevance of the coagulation-inflammation cycle for the multiorgan dysfunction and coma is discussed in the context of malaria pathogenesis.
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PMID:Blood coagulation, inflammation, and malaria. 1826 2

Coagulation disorders are a well known complication in patients with head injuries. A prospective study was undertaken to determine the incidence and prognostic value of haemostatic abnormalities in this group of patients. Clotting mechanisms in 105 patients with an isolated head injury were evaluated using platelet count (PC), prothrombin time (PT), activated partial thromboplastin time (APPT), thrombin clotting time (TCT), plasma fibrinogen concentration (Fib), level of fibrin-fibrinogen degradation products (FDP) and increased consumptive coagulopathy grade (ICCG) in the first 24 h after injury. The clinical severity of the head injuries was represented by the post-resuscitation Glasgow coma score (GCS) divided into four coma groups (CG). Test results were compared between two outcome groups of patients: discharged and dead. The incidence of disseminated intravascular coagulation (DIC) by laboratory criteria in the two groups was 12% and 38%, respectively. The differences between mean values of the discharged and dead patients for GCS, APTT, FDP and ICCG were statistically significant (P < 0.001). There was a very strong correlation between the GCS and values of the FDP, APTT, TCT and ICCG (P < 0.01). Stepwise logistic regression analysis demonstrated that GCS, FDP level, and ICCG predicted outcome in 84% of cases. Other tests did not provide additional predictive value. We conclude that evaluation of coagulation and fibrinolysis in patients with head injuries is not only important in identifying the occurrence of coagulopathy, but also useful in predicting head injury outcome.
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PMID:Role of coagulopathy in patients with head trauma. 1863 59

Influenza-associated encephalopathy (IAE) usually occurs in children aged <5 years. Adult cases of IAE are very rare and, thus far, no definite adult autopsy case has been reported. Here, we present the first definite adult autopsy case of IAE. A 76-year-old man presented with sudden coma a day after the onset of fever caused by infection with influenza type A virus. Soon after admission, his condition was complicated by DIC, shock, and multiple organ failure, and he was diagnosed with IAE. Oseltamivir administration and steroid pulse therapy were performed but these proved to be ineffective. The patient died about 24 hours after the onset of encephalopathy. The autopsy revealed massive brain edema and diffuse increase of amoeboid glias without inflammatory cell infiltration. Influenza type A/Hong Kong virus (H3) was isolated from his lungs. Serum IL-6 level was extremely high (35,800 pg/ml; normal, 0.221-4.62 pg/ml). The clinical course, and the laboratory and pathological findings of this adult case resembled those of a typical childhood-onset IAE, suggesting the same pathogenesis. During the influenza season, IAE should be taken into account for differential diagnosis in adult patients with altered mental status and fever.
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PMID:[Elderly autopsy case of influenza-associated encephalopathy]. 1908 26

HELLP (haemolysis, elevated liver enzymes, and low platelet count) syndrome can result in a fatal intracranial haemorrhage during the perinatal period. We report treatment of a 32-year-old primigravida who fell into a deep coma during labour with fetal distress, complicated by a spontaneous acute subdural haematoma and intracerebral haemorrhage. Simultaneous emergency operations, evacuation of the acute subdural haematoma and a caesarean section, were performed, during which a diagnosis of HELLP syndrome with disseminated intravascular coagulation was made. Both mother and infant recovered, though hemiparesis persisted in the mother. Patients with HELLP syndrome should be managed as high-risk, which requires an excellent working relationship of the physicians involved. Prompt recognition of intracranial haemorrhagic complications and neurosurgical intervention are particularly important.
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PMID:Spontaneous acute subdural haematoma and intracerebral haemorrhage in patient with HELLP syndrome: case report. 1939 Jul 78

Here in we report the case of a patient who displayed a classic heat stroke with multiple organ dysfunction and hypercoagulable state resistant to conventional whole body cooling and antipyretic therapy, and necessitating the use of hyperbaric oxygen therapy (HBOT) to rescue him from death. A 49-year-old male laborer, suffering from heat stroke syndromes (e.g., hyperpyrexia, seizure and coma, and hypotension), was admitted to an emergency unit of a medical center hospital. The patient displayed multiple organ dysfunction with rhabdomyolysis, hepatic, renal, respiratory, and cerebral dysfunction, and disseminated intravascular coagulation (DIC). Both hyperpyrexia and multiple organ dysfunction were resistant to conventional treatment measures. HBOT was adopted to rescue the patient from heat stroke-induced death. Before HBOT, analyses of serum revealed hypercoagulable state or DIC as well as signs of rhabdomyolysis, and renal and hepatic failure. In addition, pulmonary edema, coma, hypotension, and hyperpyrexia occurred. HBOT was used successfully to combat these syndromes and to rescue the patient from heat stroke death. This case suggests that HBOT is useful for treatment of heat stroke with multiple organ dysfunction.
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PMID:A hyperbaric oxygen therapy approach to heat stroke with multiple organ dysfunction. 1977 3

Amanita phalloides is responsible for the majority of the fatalities caused by mushroom poisoning. It causes damage in liver, kidneys and rarely pancreas, causing encephalopathic coma, disseminated intravascular coagulation, hemorrhage and hypovolemic shock. However, its effect on cardiac functions has not been established yet. In this case report, we aimed to present a female patient poisoned by A. phalloides mushroom complicated with multi-organ failure and cardiogenic shock due to advanced left ventricular systolic dysfunction. This case report was the first to show a successful treatment of cardiogenic shock due to mushroom poisoning with intra-aortic balloon counterpulsation, whereas she did not respond to other therapies.
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PMID:A case report of an unusual complication of Amanita phalloides poisoning: Development of cardiogenic shock and its successful treatment with intra-aortic balloon counterpulsation. 1985 78

A 41-year-old male, with no previous medical history, was admitted to our intensive care unit with severe isolated neurotrauma and a Glasgow Coma Scale of E1-M1-V1, mid-dilated unreactive pupils and severe abnormalities on the brain CT-scan. A severe syndrome of disseminated intravascular coagulation (DIC) and non-oliguric renal insufficiency developed. Following clinical and neurophysiological examination the patient was declared brain-dead, and the family gave permission for organ donation. The left kidney was transplanted and functioned well immediately. However, in view of the DIC and renal function disorders the right kidney was not considered usable for transplantation elsewhere. Pathological examination revealed many fibrin thrombi in the glomerular capillaries and acute tubular necrosis. This case supports the view that thrombotic microangiopathy in kidneys of patients with DIS, even with renal function impairment, is not an a priori reason for excluding donation.
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PMID:[Kidney donor with severe disseminated intravascular coagulation: transplantation however successful]. 1985 87

Acute renal failure, disseminated intravascular coagulation (DIC), acute respiratory distress syndrome (ARDS), hypoglycemia, coma, or epileptic seizures are manifestations of severe Plasmodium falciparum malaria. On the other hand, Plasmodium vivax malaria seldom results in pulmonary damage, and pulmonary complications are exceedingly rare. We report the case of a 42-year-old male living in a malaria-endemic area who presented with ARDS and was diagnosed as having Plasmodium vivax malaria. A diagnosis of Plasmodium vivax malaria was established by a positive Plasmodium LDH immunochromatographic assay while a negative PfHRP2 based assay ruled out P. falciparum malaria. After specific anti-plasmodial therapy and intensive supportive care, the patient recovered and was discharged from hospital. The use of NIPPV in vivax-malaria related ARDS was associated with a good outcome.
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PMID:Plasmodium vivax malaria: an unusual presentation. 1988 Nov 94


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