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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 pathophysiologic mechanism of fat embolism syndrome (FES) has been thought to depend on mechanical blockage of capillaries by fat emboli or on the toxic effect of free fatty acids on the capillary endothelium. Aggregation of platelets, microembolism, disseminated intravascular coagulation, and vasoactive amines are considered to be involved. The question of why some patients develop fat embolism while other patients with similar injuries do not remains to be solved. Blood tests in ten patients who developed FES and their reaction to stress were compared to the same tests in ten patients with similar injuries without FES at least 1 year after trauma. The following were measured: blood Hb, leucocytes, platelets, protein and lipid electrophoresis, ACTH, cortisol, TSH, GH, insulin, glucose, NEFA, certain coagulation and fibrinolytic studies, alpha 1 antitrypsin, and antithrombin III. The platelet values, especially after stress, and P + P values were higher in the FES-patients. The alpha-beta lipoprotein ratio was lower and the blood glucose values were higher in half of those FES-patients in whom a diabetic heredity was discovered. The U-catecholamines were also somewhat higher in the FES-patients. Disturbances of the lipid and carbohydrate metabolism as well as a high platelet count and high P + P values may predispose to thrombosis and DIC. More numerous petechiae in Rumpel-Leede's stasis test in fat embolism patients suggest increased capillary fragility. Low growth hormone values in FES-patients and a different cortisol reaction to stress compared to control patients suggests a disturbed neurohumoral regulation in FES.
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PMID:Stress hormones, lipids, and factors of hemostasis in trauma patients with and without fat embolism syndrome: a comparative study at least one year after severe trauma. 735 96

Disseminated intravascular coagulation is a very rare complication of diabetic ketoacidosis. Central nervous system palsy but not peripheral neuropathy has been reported in these patients. On the other hand, signs of peripheral neuropathy may also be present at the onset of diabetes, but they are usually reversible within a few days after correction of the metabolic derangement. We describe an unusual case of mononeuritis multiplex syndrome still present after 2 months of follow-up in a child with diabetic ketoacidosis complicated by disseminated intravascular coagulation at the onset of insulin-dependent diabetes. These neurological impairments may be consistent with functional neural lesions due to vasa nervorum thrombosis and prolonged ischaemia.
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PMID:Disseminated intravascular coagulation and severe peripheral neuropathy complicating ketoacidosis in a newly diagnosed diabetic child. 782 59

1. Injection of lipopolysaccharides (LPS) or endotoxin into mice and rats induces a prolonged increase in serotonin (5-hydroxytryptamine: 5HT), predominantly in the liver. 2. The 5HT increase reflects the accumulation of platelets in the sinusoidal and perisinusoidal Disse spaces (spaces between endothelial cells and hepatocytes) in the liver. 3. Most of the platelets which accumulated in these spaces still retained their intact structure and a large amount of 5HT. 4. Interleukin-1 and/or tumor necrosis factor also induce the platelet response. 5. Kupffer's cells play a key role in this platelet response. 6. Anti-platelet drugs currently used, except for anti-inflammatory steroids, were ineffective in preventing the platelet response. 7. This platelet response is different from the well known platelet aggregation. 8. The possible involvement of this platelet response in insulin-independent hypoglycaemia, disseminated intravascular coagulation, septic shock, hepatitis, Shwartzman type reactions or self-defense mechanisms is discussed.
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PMID:Active translocation of platelets into sinusoidal and Disse spaces in the liver in response to lipopolysaccharides, interleukin-1 and tumor necrosis factor. 827 Jan 61

Various hemostatic abnormalities have been reported and excess activation of coagulation factors, such as prothrombin, factor VII, factor IX, and factor XI, have been detected in thrombotic diseases states by various assay systems. We recently developed the enzyme-linked differential immunoassay for activated factor XI-alpha 1 antitrypsin complex (FXIa-alpha 1 AT) and applied it with other assays for activated factors such as thrombin-antithrombin III complex (TAT) to detect the hypercoagulable state in clinical samples. In patients with DIC, the FXIa-alpha 1 AT level in plasma increased before onset of DIC. In patients with non-insulin-dependent diabetes mellitus, FXIa-alpha 1AT and TAT levels were increased in the patient plasma. FXIa-alpha 1AT was related to the severity of urinary albumin excretion, whereas TAT was not. Plasma FXIa-alpha 1AT levels were significantly increased in patients with angiographically proven coronary artery disease, and showed a positive correlation with TAT, fibrinogen, and Lp(a). Evaluation of activated coagulation factor provides useful information on the diagnosis of thrombotic disease.
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PMID:[Activated coagulation factors in various thrombotic diseases]. 856 28

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91

A 61-year-old man with a history of hypertension and diabetes mellitus had a tooth extracted. Nine days later, he was admitted to the hospital with complaints of high fever, dyspnea, and anterior chest pain. Physical examination revealed a drowsy man with a fever of 38.2 degrees C, blood pressure of 66/44 mmHg, and marked redness and swelling from the neck to anterior part of the chest. Laboratory examination indicated severe infection and multiple organ failure, consisting of cardiac, respiratory, renal, and hepatic failure, with disseminated intravascular coagulation. Chest X-ray and CT-scan films showed abscesses extending from the neck to the mediastinum, and bilateral pleural effusion. Immediately, he was treated with catecholamines, furosemide, mechanical ventilation with a high concentration of oxygen, continuous drainage, repeated skin incisions, and broad-spectrum antibiotics. In addition, steroid pulse therapy was administered for persistent respiratory failure. On the 28th hospital day, a fistula developed between the trachea and the mediastinum, and an intratracheal tube had to be inserted through the fistula. On the 212 th hospital day, after intravenous hyperalimentation, continuous intravenous insulin infusion, and administration of broad-spectrum antibiotics, catecholamines, and furosemide, the patient was weaned from mechanical ventilation. A restrictive ventilatory defect due to ankylosis and atrophy of underused muscles was noted after weaning, but the PaO2 was high with a low dose of oxygen (1 to 2 l/min), and 21 months later, the blood gases were normal while the patient was breathing room air. As of January, 1996, he was undergoing rehabilitation to promote his recovery from ankylosis, muscle atrophy, and speech dysfunction.
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PMID:[Recovery from descending necrotizing mediastinitis and multiple organic failure after seven months of mechanical ventilation]. 893 49

Autologous islet transplantation after pancreatectomy has been used in the surgical management of patients with intractable pain secondary to chronic pancreatitis. Total or near total pancreatectomy invariably leads to exogenous insulin dependence in these patients unless they undergo islet transplantation. Transplantation of autologous islet cells harvested from the patient's pancreas into the liver through portal vein infusion has led to long-term euglycemia in 30% to 50% of patients. We report the development of disseminated intravascular coagulation and fatal hemorrhagic shock in a 36-year-old woman after total pancreatectomy and autologous islet transplantation through retrograde infusion into the splenic vein. We report the clinical and pathological findings and discuss the possible pathophysiological mechanisms involved in the development of disseminated intravascular coagulation after this procedure.
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PMID:Fatal disseminated intravascular coagulation after autologous islet transplantation. 938 36

Pyogenic osteomyelitis is often accompanied by diabetes, but the disease in the clavicula has rarely been reported. We describe an unusual case of a 53-year-old man with poorly controlled non-insulin-dependent diabetes mellitus who presented with pyogenic clavicular osteomyelitis and developed DIC and acute renal failure. A 67Ga scintigram revealed an abnormal accumulation of the isotope in the right clavicula, where magnetic resonance imaging (MRI) showed inflammatory changes. This suggests that a 67Ga scintigram and MRI are of clinical value for the early diagnosis of the disease. Antibiotic chemotherapy with gamma-globulin and gebexate mesilate, and hemodialysis almost cured his serious condition.
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PMID:Pyogenic clavicular osteomyelitis associated with disseminated intravascular coagulation and acute renal failure in a patient with non-insulin-dependent diabetes mellitus. 939 43

A 66-year-old woman with a 7-year history of Parkinsons' disease was admitted to our hospital because of a high fever and disturbance of consciousness. She had been treated with levodopa/benserazide hydrochloride and trihexyphenidyl hydrochloride until admission. On admission, the patient was comatose, her temperature was 40.5 degrees C, her blood pressure was 54/-mmHg, and her pulse rate was 130 beats/min. Laboratory tests showed leukocytosis, a high level of creatine kinase in serum and evidence of hyperosmolar non-ketotic diabetic coma (blood glucose, 1,080 mg/dl) and of disseminated intravascular coagulation (DIC). A continuous insulin infusion, antibiotics, nafamostat mesilate, and urinastatin were given, after which the DIC, hyperglycemia, and the level of consciousness were improved. However, levels of creatine kinase, myoglobin, transaminase, and amylase in serum continued to increase, and multiple organ failure was suspected. Furthermore, she became less responsive, diaphoretic, and tremulous; fever and mild rigidity developed. The peak creatine kinase and myoglobin were 11,095 U/l and 12,520 ng/ml, respectively. A diagnosis of malignant syndrome was made, and treatment with levodopa/carbidopa and dantrolene was begun. Within several days, the clinical and laboratory findings improved. We report here a rare case of malignant syndrome associated with DIC followed by diabetic coma in an elderly patient with Parkinsons' disease during L-dopa therapy. Timely diagnosis and treatment of malignant syndrome are important in the management of elderly patients with Parkinsons' disease, because DIC and multiple organ failure may occur in the early stages of malignant syndrome.
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PMID:[Malignant syndrome associated with disseminated intravascular coagulation and a high level of amylase in serum, followed by diabetic coma in an elderly patient with Parkinson's disease during L-dopa therapy]. 958 93

Haemorrhagic shock and encephalopathy syndrome (HSES) is a devastating disorder affecting infants. So far no cases have been reported in Switzerland. It is characterised by the abrupt onset of hyperpyrexia, shock, encephalopathy, diarrhoea, disseminated intravascular coagulation (DIC) and renal and hepatic failure in previously healthy infants. Severe hypoglycaemia has been repeatedly reported in association with HSES. However, the pathophysiology of the hypoglycaemia is not clear. We report on two infants (2 and 7 months old) with typical HSES, both of whom were presented with nonketotic hypoglycaemia. In the first case, plasma insulin was 23 pmol/l at the time of hypoglycaemia (0.1 mmol/l). In the second case, increased values for interleukin-6 (IL-6) (319 pg/ml) and IL-8 (1382 pg/ml) were found 24 hours after admission, whereas IL-1 and tumour necrosis factor-alpha (TNF-alpha) were not measurable. Alpha-1-antitrypsin was decreased (0.6 g/l). In hyperpyrexic, unconscious and shocked infants, HSES should be considered and hypoglycaemia should be specifically looked for. Hypoglycaemia is not caused by hyperinsulinism but may be secondary to the release of cytokines.
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PMID:Haemorrhagic shock and encephalopathy syndrome: report of two cases with special reference to hypoglycaemia. 1070 Dec 32


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