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

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

Two patients in a family of exertion-induced heat stroke were reported. Case 1: A 23-year-old male, paternal cousin of case 2, was admitted to our hospital because of loss of consciousness during running under a burning sun. On physical and neurological examinations, he was deeply comatose with high fever, tachycardia, and increased deep tendon reflexes. Laboratory findings disclosed rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, liver injury, and brain edema. He recovered after intensive cooling, some antibiotics, glycerol and sodium dantrolene administration. Case 2: A 19-year-old male experienced loss of consciousness and high fever during playing soccer at 15 years of age, and was admitted to a hospital. On admission, he had high fever of 38.7 degrees C, and increased serum CK level. He recovered two weeks after admission. He was readmitted to our hospital to evaluate the predisposition for malignant hyperthermia. His physical and neurological examinations showed no abnormalities. Routine laboratory findings were within normal limits. Muscle biopsy findings of cases 1 and 2 were mildly increased number of fibers with centrally placed nuclei. Caffeine test on skinned muscle fibers from the biopsies showed normal response in both type 1 and 2 fibers. The present patients were diagnosed as having exertion-induced heat stroke, but with no increased muscle fiber sensitivity to caffeine, suggesting that the pathomechanism differs from that of malignant hyperthermia induced by malfunction of sarcoplasmic reticulum.
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PMID:[Two familial cases with exertion-induced heat stroke--relationship to malignant hyperthermia]. 139 27

The analysis of 88 lethal outcomes of hemorrhagic fever with renal syndrome (HERS) showed the occurrence of adenohypophyseal hemorrhage and necrotic foci in 75.5% of cases as well as combined involvement of adenohypophysis and adrenals in 18.4%. Pathogenetically, adenohypophyseal affection is related to anatomical-physiological features of the vessels, microcirculatory disorders, acute venous congestion. Contributing factors may be acute DIC syndrome, relapsing and prolonged collapses, hyperhydration leading to brain edema and hemostasis. Uncontrollable vomiting recorded in all the deceased patients seemed to promote destruction of adenohypophysis. Clinically, this gross pathomorphology ++ was equivalent to severe form of the disease--hypopituitary coma. Proper prophylaxis of the above complications is one of the conditions entailing reduction of mortality in HFRS.
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PMID:[Analysis of fatal outcome in hemorrhagic fever with renal syndrome]. 198 56

A 20 year old woman with a severe head injury and rapidly increasing brain edema died 46 hours after the accident. There was clinical evidence of protracted shock and disseminated intravascular coagulation. The autopsy revealed a macro-embolization of brain tissue of the lungs with many central and intermediate lung artery branches occluded by cerebral tissue. Preconditions of the brain tissue embolism were a severe fracture of the skull including a traumatic rupture of the right sigmoid sinus, together with a local brain laceration and an extremely elevated intracranial pressure. Fibrin precipitations were prominent at the surfaces of the brain tissue emboli as well as in peripheral blood vessels of the lung; in the systemic circulation, intravascular coagulation was much less pronounced.
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PMID:[Massive pulmonary brain tissue embolism]. 224 9

Two patients who had cerebral aspergillosis with massive intracerebral hemorrhage were presented. Case I was a 59-year-old woman who had slight mental retardation. There was swelling in the left forehead, from which mucosal cysts of frontal sinus had been removed 2 years before her admission. She had a diagnosis of subdural abscess and radical operation was performed. Aspergillus was found in the abscess histologically. Three months after the operation, CT scan revealed multiple abscess in bilateral frontal lobe. When she lost consciousness suddenly 4 months after the operation, CT scan showed a huge intracerebral hematoma. Case 2 was a 16-year-old girl who suffered from immunological dysfunction caused by more than 6 months antibiotics-steroid treatment for pneumonitis. She lost her consciousness after complaints of severe headache. CT scan showed a heterogeneous high density area with severe brain edema in the left temporal lobe. The removal of hematoma was performed immediately. The level of her consciousness improved, but she died of the complication of DIC and renal failure 14 days after the hemorrhage. Autopsy revealed a number of aspergillomas in lungs, kidneys, gastrointestinal tract, liver and pancreas. Marked necrosis and a number of aspergillus hyphae which invaded and penetrated the wall of cerebral vessels were found in the brain tissue. It was presumed that such a huge intracerebral hematoma was caused by direct invasion and penetration into the brain of aspergillus from the blood vessels. The diagnosis of cerebral aspergillosis is made mainly by the pathological examination of the tissue obtained at surgery or autopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of cerebral aspergillosis with intracerebral hemorrhage]. 322 71

Poisoning occurred in 32 mink fed diets containing meat from cows which had been fed a polychlorinated biphenyl (PCB), Aroclor 1254. No live kits were produced and all adult mink died during a 105 day period of feeding a ration containing 3.57 ppm of PCB. At a level of 0.64 ppm of PCB in ration one of 12 mink produced three kits, all of which died during the first day after birth. Clinical signs were limited to weight loss and passage of black tarry feces. The gross lesions seen were yellowish discoloration of the liver and hemorrhage into the abdominal cavity or gastrointestinal tract. Microscopic lesions were nephrosis, fatty de-generation and necrosis of the liver, brain edema, disseminated intravascular coagulation, and fibrosis of coronary arteries. It is concluded that mink are highly sensitive to small quantities of PCB fed for an extended period of time.
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PMID:Dietary effects of polychlorinated biphenyls on mink. 427 Aug 10

A small outbreak of louse-borne relapsing fever in Khartoum (May-June 1974) provided material for a clinico-pathological study. The history of the disease in the Sudan is reviewed and the clinical and laboratory findings in 32 patients are presented. Fever, headache, jaundice, epistaxis and hepatosplenomegaly were the commonest clinical findings; thrombocytopenia was detected in 93% of cases. Although elevated levels of fibrin degradation products were found in most patients, disseminated intravascular coagulation could not be diagnosed. Hepatocellular derangement was found in 68% of cases, while 78% had high blood urea. In five autopsied bodies there was bronchopneumonia, interstitial edema with focal myocardial fibrosis, hepatic necrosis, splenic infarcts, increase in size and cellularity of the glomeruli and brain edema and congestion. Intracranial haemorrhage was found in three of the autopsied cases.
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PMID:Louse-borne relapsing fever in the Sudan. A historical review and a clinico-pathological study. 742

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.
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PMID:[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)]. 742 60

CT/MRI findings, laboratory examinations and prognoses of 42 patients with acute encephalopathy (AE) (Japan Coma Scale > or = 200) were reported. 1. Findings on CT/MRI were divided into the following 7 categories: Group 1 (normal), Group 2 (CT/MRI looked normal in acute phase, but brain atrophy developed and progressed slowly by weeks or months), Group 3 (CT/MRI looked normal within a few days after the onset of AE, but cortical laminar necrosis developed at 4-5 days after the onset), Group 4 (marked brain edema developed within 2 days after the onset of AE), Group 5 (AE with symmetric thalamic lesions), Group 6 (symmetric pallidum, lesions on MRI which appeared after brain edema disappeared), and Group 7 (the brain shrinked during acute phase, which normalized on the follow up CT/MRI). 2. Serum AST elevated in approximately 50% of the patients with AE. Sixty percent of them exhibited DIC, whose prognoses were poor. Cerebrospinal fluids (CSF) neopterin (NP) and/or interleukin (IL)-6 were elevated in all the 8 patients examined. In the two cases whose serum NP and IL-6 were measured at the same time, their values in the CSF were higher than those in the serum in one case, and almost the same in the other. In a patient with a condition mimicking hemorrhagic shock and encephalopathy, serum IL-6 concentration was very high (94,000 pg/ml). 3. Mild hypothermia (around 34 degrees C) combined with methylprednisolone pulse therapy was excellently effective on AE. A 6-year-old boy exhibited tonsillar herniation at admission recovered well to be able to run. 4. Differentiation between Reye syndrome and HSE, and the pathogenesis of AE were also discussed.
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PMID:[Infection-related acute encephalopathy: CT scan/MRI finding, laboratory examination and prognosis]. 1072 91

The case of a healthy 31-year-old woman in the 40th week of second pregnancy is presented. During preparation for an emergency caesarean section, she developed an amniotic fluid embolism (AFE) with unusual and unique features. The acute onset of disease with cardiorespiratory failure with hypotension, tachycardia, cyanosis, respiratory disturbances and loss of consciousness, suggested at first a pulmonary thromboembolism, but the appearance of convulsions led to the diagnosis of AFE. The patient died after 5 days due to an untreatable brain edema. At autopsy, AFE with the usually associated disseminated intravascular coagulation was found in the lungs, brain, left adrenal gland, kidneys, liver and heart. Eosinophilic inflammatory infiltrates were found in the lungs, hepatic portal fields and especially in the heart, suggesting a specific hypersensitivity reaction to fetal antigens. Moreover, intravascular accumulation of macrophages in the lungs also favored a non-specific immune reaction to amniotic fluid constituents.
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PMID:Amniotic fluid embolism with involvement of the brain, lungs, adrenal glands, and heart. 1273 31


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