Gene/Protein Disease Symptom Drug Enzyme Compound
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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 intricacies of the pathophysiology of eclampsia are still unknown. The major symptoms of our 37 year old para 3 are convulsions, hypertension, complete anuria and gastro-intestinal haemmorhage as a result of disseminated ;ntra-vascular coagulation (D.I.C.). The interdisciplinary therapeutic measures are discussed, in the course which special attention is given to the favourable influence of dopamine on renal failure and the complicating gastro intestinal haemmorhage.
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PMID:[Intensive care medicine in severe eclampsia (author's transl)]. 31 2

The risk of adverse reactions to 3,4-methylenedioxymethamphetamine (MDMA), more commonly known as "ecstasy", is now widely known in both the USA and UK, but the patterns of illness remain varied. We report our experience during 1990 and 1991. There has been a recent increase in cases of severe toxicity following recreational misuse of small amounts of MDMA. Among 7 fatalities, the pattern of toxicity included fulminant hyperthermia, convulsions, disseminated intravascular coagulation, rhabdomyolysis, and acute renal failure. Until now, there have been few reports of this type of toxicity from MDMA, which may be related both to the potential of the drug to alter thermoregulation and to the circumstances of misuse. In addition, we have monitored 7 cases of hepatotoxicity and suspect that the frequency of this complication is increasing; a history of MDMA misuse should be sought in young people presenting with unexplained jaundice or hepatomegaly. We also describe 5 subjects involved in road traffic accidents in whom MDMA was identified. Misuse of MDMA can have severe acute toxic effects; few data are available concerning long-term morbidity, and this deserves close monitoring in future.
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PMID:Toxicity and deaths from 3,4-methylenedioxymethamphetamine ("ecstasy") 135 18

Recent progress in elucidating the complex and heterogeneous interactions between malignancy and coagulation or fibrinolysis reactions in humans has clarified the pathogenesis of disseminated intravascular coagulation that occurs with malignancy and has revealed evidence for two distinct pathways of growth regulation based on production by tumor cells of initiators of thrombin formation versus plasminogen activators. We have proposed a preliminary classification of tumors (see Table 2) based on these interactions. Type I tumors are those in which the tumor cells are associated with an intact coagulation pathway that leads to thrombin formation at the tumor periphery but in which the tumor cells lack u-PA. Examples of tumors in this category include SCCL, malignant melanoma, and renal cell carcinoma. Type II tumors are those in which the tumor cells express u-PA but lack an associated coagulation pathway leading to thrombin formation. Examples of type II tumors include prostate cancer, colon cancer, breast cancer, and N-SCLC. Type III tumors are those that express neither of these pathways, or exhibit some other pattern of interaction. Obviously, this formulation must be regarded as hypothetical. However, this concept fits with the limited data available to date from clinical trials. More importantly, this hypothesis can be tested further by means of intervention aimed at interrupting pathways relevant to specific tumor types. Characterization of additional tumor types by the methods described should permit amplification of this classification of tumors and other patterns of interaction may be defined. Exploration of the coagulation-cancer interaction holds considerable promise for gaining new understanding of both the coagulation mechanism and tumor biology. Most intriguing is the prospect that imaginative approaches to cancer treatment may be devised that are not only relatively nontoxic and low cost, but also effective.
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PMID:Pathways of coagulation/fibrinolysis activation in malignancy. 157 11

Serial EEGs have been carried out during the acute phase of haemorrhagic shock and encephalopathy syndrome (HS&E) in 22 infants and children aged 3 months to 14 years. Most patients presented with fits and coma and all had shock with bleeding and disseminated intravascular coagulation (DIC). The initial EEG showed prolonged runs of often rhythmic discharges which fluctuated in amount and amplitude with varying distribution and morphology ("electrical storms"). Over a period of days the "electrical storms" gradually decreased leaving only low amplitude EEG activities or evolving to electrocerebral silence (7 cases). Fifteen patients died and all five children with multifocal "electrical storms" who survived showed gross neurological handicap. The rather distinctive EEG pattern is unusual in the context of an acute encephalopathy outside the neonatal period although similar "electrical storms" may be seen in a less extreme form in infants and children with other conditions associated with DIC. This EEG pattern presumably reflects changes in the cerebral microcirculation which in HS&E are usually relentlessly progressive and associated with devastating cortical damage.
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PMID:EEG features and their evolution in the acute phase of haemorrhagic shock and encephalopathy syndrome. 177 15

We observed 73 patients with the hemolytic uremic syndrome (HUS) in 9 years (1980-1988), comprising 34% of patients with acute renal failure treated over the same period. There were 53 boys and 20 girls; 59% were below the age of 2 years and 33% between 2 and 5 years. Acute, usually severe dysentery, responding poorly to various antibiotics, was the prodromal illness in 80%, whereas 12% had watery diarrhea. Most patients had severe renal involvement with anuria in 56% and oliguria in 30%. A polymorphonuclear leukocytosis was present in 85% of cases, but had no correlation with the highest levels of blood urea. Coagulation abnormalities suggesting consumption coagulopathy were found in 24 of 30 cases. The results of stool culture showed Shigella species in 7 cases and nontyphoidal Salmonella in 9. Escherichia coli were isolated in 11 cases, but were not further characterized. Renal biopsy showed total or patchy cortical necrosis in 20 of 50 cases. The patients were managed with supportive care, including transfusion of fresh blood or plasma and dialysis as required. The mortality was 60%, being chiefly related to the duration of renal failure and presence of renal cortical necrosis, whereas persistent dysentery and infections were complicating factors. The presence of convulsions and coagulation defects had no relation to the outcome. Our observations indicate that HUS in children in northern India is mostly related to dysentery, likely to be shigellosis, and is usually associated with severe renal damage and a high death rate.
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PMID:Hemolytic uremic syndrome in children in northern India. 186 81

Meningococcal sepsis with cardiovascular manifestations is one of the leading causes of pediatric intensive care admission (14.85%) in our area. We carried out a two phase study over period of 10 years from 1979 to 1988, involving a retrospective analysis of clinical and analytical manifestations in order to determine a prognostic score of the severity of meningococcal infections in our area. A total of 86 cases were studies over a two year period. After establishing the prognostic score, we applied a previously assayed therapeutic protocol, based on the number of criteria of severity, in 170 children selected as having the same criteria. The factors of seriousness considered were: Appearance of the first symptoms less than 12 h. previously, appearance of petechia less than 6 h. previously, hyperthermia, shock at admission, absence of meningitis, fulminating course of purpura and convulsions, leukopenia less than or equal to 5,000 mm3, prothrombin activity less than or equal to 45%, platelets less than or equal to 75,000 mm3, fibrinogen less than or equal to 250 mgrs% and FPD greater than 40 micrograms/ml (p less than or equal to 0.01 (CHI SQUARE]. In the first phase of study, overall mortality was associated with the presence of three criteria, and was highest when more than seven criteria were present. The results indicate that mortality from meningococcal sepsis is linked to fulminating deterioration of hemodynamics and DIC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Meningococcal sepsis in our area. Study of the disease severity factors and therapeutic management over a 10-year period]. 188 8

The infant or child who presents to the Emergency Department with bacterial meningitis may have nonspecific vague symptoms with few signs of serious illness. However, the disease is often rapidly progressive and life-threatening, and may be associated with respiratory failure, circulatory failure, increased intracranial pressure, disseminated intravascular coagulation, or convulsions, any of which may lead to a fatal outcome. It is important for the triage technician in an Emergency Department to cautiously inspect each young patient who presents with illness, carefully considering whether the presenting syndrome of symptoms and signs might be consistent with early meningitis. If the young patient is triaged in a nonemergent category, then periodic assessments of the patients waiting to be seen may ensure that, when the infant or child with an obscure presentation develops evidence suggesting this diagnosis, the triage technician will promptly notify the appropriate definitive care providers who assume responsibility for immediate definitive evaluation and stabilization. Changes in delivery of lifesaving care to the life-threatened child are being impacted by current advances in the understanding of the biochemical basis of disease at the cellular and subcellular levels. Endotoxin release into the blood causes increased production of kinins, which results in vasodilatation and increased vascular permeability. Members of the leukotriene family may also enhance vascular permeability as well as produce augmented leukocyte aggregation to vascular endothelium, vasoconstriction, and bronchoconstriction. Endotoxin activates the complement cascade and induces platelets to form reversible aggregates that may be trapped in the pulmonary microcirculation; and endotoxemia-activated platelets release serotonin, which may be associated with pulmonary hypertension. Now that we have antibiotics that are effective against organisms whose degradation produces endotoxin, there is interest in lessening the host inflammatory response to endotoxin through use of dexamethasone as an anti-inflammatory agent. Clinical trials have revealed that patients who received dexamethasone became afebrile earlier and were less likely to acquire deafness after bacterial meningitis. Because administration of antibiotics is the current specific medical therapy for this life-threatening microbial invasion, it is reasonable to continue to strive to shorten the interval between recognition of disease and specific therapy. However, new studies suggest that consequences of the complex host inflammatory response (at the cellular and subcellular level) to microbial invasion and endotoxin release from bacterial degradation are increasingly important in determining survival or severity of morbidity. Therapeutic intervention with specific antibiotics and steroid anti-inflammatory agents for modulating host responses enhances outcome.
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PMID:Emergency department stabilization of pediatric patients with bacterial meningitis. Current advances. 189 92

Malaria must be included in the differential diagnosis of all febrile patients. Malaria is classified 'complicated' or 'uncomplicated', according to clinical findings (cerebral malaria, generalized convulsions, pulmonary edema, severe anemia, hyperthermia, renal failure, haemoglobinuria, shock, spontaneous bleeding) and laboratory results (parasitemia greater than 5%, haemoglobin less than 5 g%, creatinine greater than 265 mumol/l, glucose less than 2.2 mmol/l, DIC, pH less than 7.2, bilirubin greater than 50 mumol/l). Plasmodium (P.) vivax, P. ovale and P. malariae cause uncomplicated disease as a rule, whereas P. falciparum may result in either of both. Complicated falciparum malaria is always at risk for a lethal outcome. Only microscopic evidence of malaria parasites proofs the diagnosis. The thick smear is good for screening, thin films are necessary to determine the species. Serology and cultures are not helpful in diagnosing acute malaria. Tests for drug resistance await to be applicable for emergency situations.
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PMID:[Clinical aspects and diagnosis of malaria]. 199 79

A 66-year-old male with chronic alcoholic liver injury was admitted on July 27, 1986 to our hospital with complaints of high fever, convulsion and skin erythema. He had consumed raw fish 3 days before, and had a scratch wound over the right arm and left leg because he had slipped in a small stream in the woods the day before admission. He was already in shock state with sepsis of V. vulnificus and DIC on admission. Although the treatment with ABPC, CP, CAZ, MINO for sepsis, and Heparin & Antithrombin III for DIC was immediately begun, he died only 10 hours after admission. On autopsy, the skin lesion revealed phlegmon with necrotizing angitis and the liver showed fatty changes with Mallory's body. The causative organism was detected from the blood and on autopsy from the skin wound, bile juice, liver, spleen, kidney and bone marrow, and its type was determined as a V. vulnificus serovar 4. It was suspected that the route of infection in this case was the raw fish rather than via the wound because the water in which he had been wounded was fresh water and the bacterium was not detected from the water, shells, nor moss existing there.
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PMID:[A case of fatal sepsis due to Vibrio vulnificus]. 218 37

The HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count) is a severe complication of pre-eclampsia with high risk for mother and fetus. During the last 40 months 27 parturients met the diagnostic criteria for HELLP syndrome in the University Hospital of Kiel (Tables 1-3). In 24 cases cesarean section was performed. Fetal mortality was 17.2%. In 13 women an uneventful clinical course resulted, all other patients developed complications: renal insufficiency (11 cases), disseminated intravascular coagulation (DIC) (4), intracerebral hemorrhage (1), cerebrovascular ischemia (1), eclamptic convulsions (3), reoperation due to intra- or extra-abdominal hemorrhage (4), severe blood loss ex vagina following spontaneous delivery (1), and liver rupture (1). Despite these severe complications no maternal death was observed. DIC, intrauterine death, and a rapid increase in liver enzymes are considered to be serious prognostic factors that could help to identify high-risk patients. The following recommendations for therapy of parturients suffering from HELLP syndrome are given: epidural anesthesia is not an appropriate method in HELLP syndrome because of the risk of epidural hemorrhage due to thrombopenia. At the present time general anesthesia seems to be the method of choice. Inhalation anesthetics such as halothane, enflurane, or isoflurane should probably be omitted in view of the preexisting hepatopathy. The high risk and the unpredictable postpartum course strongly indicate intensive care for parturients with HELLP syndrome. Antihypertensive, antieclamptic therapy and prophylactic measures to avoid renal insufficiency or hemorrhage (e.g. early substitution of erythrocytes, thrombocytes, and coagulation factors) deserve special attention. Co-operation between obstetrician and anesthesiologist is essential to obtain optimal therapy for these high-risk patients.
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PMID:[Anesthesia and intensive therapy of pregnant women with the HELLP syndrome]. 231 3


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