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

Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12 h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.
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PMID:Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response. 169 May 34

A 70-year-old previously healthy woman was admitted with a 1-day history of malaise, sore throat, nausea, vomiting, rigors, and confusion. She was found to be in septic shock with purpura fulminans and disseminated intravascular coagulation. She died within 36 hours of admission. Blood cultures grew Neisseria meningitidis group Y. Necropsy revealed evidence of shock and bilateral adrenal hemorrhage.
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PMID:Purpura fulminans and adrenal hemorrhage due to group Y meningococcemia in an elderly woman. 190 68

The syndrome of haemolysis, elevated liver enzymes and low platelets (HELLP Syndrome) is a consequence of severe preeclampsia/eclampsia. The clinical course is characterized by an unusual presentation with abdominal pain, and manifestations of inadequate haemostasis and excessive bleeding are common. Maternal and perinatal morbidity and mortality are high. We report our experience with 33 patients over a five-year period. The mean gestational age (GA) of the pregnancies was 34 +/- 2.8 wk including 11 patients who delivered 12 neonates of less than 34 wk GA. The most common presenting complaints were right upper quadrant or epigastric pain in 25 patients (76%) and nausea or vomiting in 14 patients (42%). Diagnosis was missed or delayed in 12 patients (36%). Thirty-one patients (94%) were delivered by Caesarean section and a deteriorating maternal condition was the most common indication for operative delivery. Twenty-three patients received general anaesthesia, eight received epidural anaesthesia and there were no complications related to the anaesthetic. There was clinical evidence of abnormal haemostasis: seven patients had excessive blood loss at Caesarean section, two had postpartum haemorrhage, three developed DIC and four developed wound haematoma. The average decrease in haemoglobin concentration was 32 g.L-1 and twelve patients (36%) received blood transfusions. There was one stillbirth. There were no neonatal deaths but morbidity was prominent and related primarily to prematurity. Delayed or missed diagnosis is common in HELLP syndrome and a premature delivery by Caesarean section is usual.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Obstetrical anaesthesia for patients with the syndrome of haemolysis, elevated liver enzymes and low platelets. 173 44

A 20-year-old female presented with sudden onset of abdominal pain, diarrhoea and vomiting progressing to fever, tachycardia and mild hypotension. Within 12 hours, a petechial rash appeared on the face and abdomen, spreading to the extremities. Laboratory findings confirmed the diagnosis of acute meningococcaemia. Clinical features of endotoxic shock, vasculitis and skin necrosis rapidly ensued. Aggressive treatment to control the septicaemia, disseminated intravascular coagulation and unstable cardiovascular state ultimately proved successful. Approximately 6 weeks later, amputation of some of the digits and extensive skin grafting were carried out in the Regional Burns Unit. However, serious psychological side effects gradually began to appear which required urgent psychiatric intervention. For an active young woman the challenge of coping with such a severe illness and coming to terms with the disability and disfigurement resulting from it was almost overwhelming. It was, perhaps, particularly hard because of the threat posed to her ambition to complete her nursing education and become a nurse. Little was found in the nursing literature on acute meningococcaemia. But this illness provides considerable challenges not only to those who suffer from it, but also to those who nurse them. A final brief review of published literature on acute meningococcaemia and the clinical manifestations and outcome of it is provided for those who wish to know more about it.
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PMID:Acute meningococcaemia: a case study. 232 67

A previously healthy 35-year-old woman was seen at 37 weeks' gestation with a 10-day history of fever, vomiting, diarrhea and malaise. Serum laboratory findings included elevation of serum bilirubin and AST, prolongation of serum prothrombin time and a positive monospot. A tentative diagnosis of acute fatty liver of pregnancy was made, and a healthy male infant was delivered by emergency cesarean section because of fetal distress. Over the subsequent 3 days, acute progressive oliguric renal failure, disseminated intravascular coagulation, hypoglycemia requiring intravenous dextrose infusion and pancreatitis developed; her mental status progressed to stage III encephalopathy. Quantitative computed tomography estimated the liver volume to be 770 cm3. The decision to proceed with orthotopic liver transplantation was made on the basis of progressive clinical deterioration despite aggressive support and because of her small liver size. After transplant, the patient's multisystem failure rapidly reversed. Histopathological examination of the native liver demonstrated predominantly zone 3 microvesicular steatosis with characteristic ultrastructural changes consistent with acute fatty liver of pregnancy. Southern blot analysis for Epstein-Barr virus DNA was negative. We conclude that orthotopic liver transplantation should be considered for the small group of patients with fulminant hepatic failure associated with acute fatty liver of pregnancy who manifest signs of irreversible liver failure despite delivery of the fetus and aggresive supportive care.
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PMID:Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation. 240 63

Clinical symptoms and laboratory measures of renal and liver function, coagulation, and inflammatory parameters were prospectively studied in 74 hospitalized patients (14-74 years of age) with serologic evidence of nephropathia epidemica. The most common clinical findings were acute onset of symptoms, fever (greater than or equal to 38 degrees C), thirst, headache, nausea, back pain, vomiting, myalgia, and abdominal pain. Twenty-seven patients (37%) had hemorrhagic manifestations, i.e., epistaxis, melena, hematemesis, petechial bleeding, macroscopic hematuria, or metrorrhagia. Disseminated intravascular coagulation developed in four patients. Fifty-one percent had thrombocytopenia. Proteinuria was recorded for all patients, while hematuria and glucosuria were noted for 85% and 58%, respectively. Serum creatinine levels were elevated in 71 (96%) of the patients. Levels of C-reactive protein or erythrocyte sedimentation rates were elevated in all cases, usually to levels found in serious bacterial diseases. Sixty-six (89%) of the patients were followed for up to 7 months, at which time all had recovered clinically. No patient died or required dialysis. We conclude that nephropathia epidemica in Sweden has a clinical picture similar to that of hemorrhagic fevers in other parts of the world, but with a milder course and a better prognosis.
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PMID:Clinical characteristics of nephropathia epidemica in Sweden: prospective study of 74 cases. 257 3

Three cases of chronic subdural hematoma (CSH) following advanced cancer are reported. Case 1. A 54-year-old male patient was referred to our clinic in a semicomatose state. Bilateral CSH was evacuated through a pair of burr holes, and consciousness was recovered. However, subependymal hemorrhage occurred at the third ventricle 6 days after the operation. Hematological examination revealed thrombocytopenia. He died 12 days after operation because of hemorrhage in the lung. Postmortem examination disclosed metastatic adenocarcinoma of unknown origin to the dura mater, lymph nodes, lung and bone marrow. Case 2. A 50-year-old male patient who was diagnosed as having gastric cancer was referred to our clinic in a state of deep coma. CT scan revealed CSH and putaminal hemorrhage at the left side. Hematological examination revealed disseminated intravascular coagulation (DIC). After the subdural hematoma was evacuated, the putaminal hematoma enlarged and hemorrhagic infarction at the left temporo-occipital lobes occurred. He died 2 days after operation. Autopsy was not carried out, but histological examination revealed poorly differentiated malignant cells in the outer membrane of the subdural hematoma. Case 3. A 53-year-old female patient who had a history of gastric cancer operated on 4 years ago was admitted to our clinic complaining of headache and vomiting. CT scan revealed bilateral subdural hematoma. Following a pair of burr-holes and irrigation of the hematoma, hemorrhage recurred alternatively at the left side on the 6th and at the right side on the 27th day after the operation. Hematological examination revealed DIC, and bone marrow puncture disclosed metastasis of the adenocarcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic subdural hematoma following advanced cancer: report of three cases]. 258 17

Endotoxins (lipopolysaccharides, LPS) are potent bacterial poisons always present within the intestines in considerable amounts. Several pathophysiological conditions such as hypovolaemia, hypoxia, intestinal ischaemia, burns and radiation lead to a breakdown in the barrier and depending upon the extent of the injury, endotoxins enter the systemic circulation in increasing amounts. Antibiotics do not inactivate the endotoxins which continue to exert their toxic effects leading to nausea, vomiting, diarrhoea, fever, disseminated intravascular coagulation, vascular collapse and organ failure. When nonabsorbable antibiotics are given prior to the insult, systemic endotoxaemia is prevented. Immunotherapy, using anti-lipopolysaccharide IgG, inactivates plasma endotoxins, destroys gram-negative bacteria and opsonises them and may become a major form of therapy. An outline of endotoxin and anti-lipopolysaccharide and its importance to the anaesthetist and intensive care specialist is presented.
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PMID:Endotoxins and anti-endotoxins (their relevance to the anaesthetist and the intensive care specialist). 265 93

A full-term male neonate, weighing 2540 g at birth, was admitted to hospital on day 2 because of vomiting and severe dehydration. Duodeno-duodenostomy was performed on day 5 for congenital duodenal atresia. The child was well postoperatively until day 9, when he developed fever. Intermittent fever continued despite treatment with several antibiotics. He became seriously ill on day 15 and developed disseminated intravascular coagulation. Treatment with antifungal drugs (amphotericin B and 5-flucytosine) was effective for systemic candidiasis, but candida endophthalmitis developed. There was a persistent vitreous lesion in the left eye, which after cessation of therapy has been improving gradually. Systemic candidiasis and candida endophthalmitis should be considered in neonates who develop signs of sepsis postoperatively.
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PMID:Systemic candidiasis with DIC and candida endophthalmitis in a postoperative neonate. 269 30

To further define the clinical, pathologic, and biochemical features of hemorrhagic shock and encephalopathy syndrome, we studied 25 affected children (aged 3 months to 14 years) admitted to a single center between 1982 and 1985. A prodromal illness comprising vomiting, diarrhea, listlessness, and fever was present in 84% of the cases. Acute onset of shock, convulsions and coma, bleeding (or laboratory evidence of disseminated intravascular coagulation), elevated plasma activity of hepatic enzymes, acidosis, and impaired renal function was present in every case. Twenty patients died, and all the survivors are neurologically damaged. At postmortem examination, intravascular microthrombi coexisting with hemorrhages and petechiae were found in most organs. Centrilobular liver necrosis and cerebral edema were prominent features. No microbiologic cause for the disorder was identified, but decreased plasma levels of the protease inhibitors alpha 1-antitrypsin and alpha 2-macroglobulin, together with increased levels of circulating proteolytic enzymes, were frequently present. An overrepresentation of the uncommon variant phenotypes of alpha 1-antitrypsin was found in first-degree relatives of affected patients (four had the MZ phenotype, and one each the MS or MC phenotype, of 19 relatives studied). Abnormal accumulation of alpha 1-antitrypsin was detected immunohistochemically in the livers of six of the patients. Defective protease inhibitor production or release may be involved in the pathogenesis of the disorder.
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PMID:Hemorrhagic shock and encephalopathy: clinical, pathologic, and biochemical features. 276 14


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