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)

Heatstroke occurs during intense physical exertion or environmental exposure to heat without exertion. The ability to eliminate heat is limited by volume depletion, cardiac and vascular insufficiency, and skin disorders or protective coverings that prevent sweating and evaporative heat loss. Also, many drugs predispose patients to heatstroke by impairing normal thermoregulatory function. Critical management strategies include (1) recognition of hyperthermia, (2) rapid cooling, and (3) supportive care and observation for heat-related complications of tissue injury (eg, hepatic failure, renal failure, disseminated intravascular coagulation).
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PMID:Heatstroke. Underlying processes and lifesaving management. 154 23

Nineteen cases (male 6, female 13) of acute obstructive suppurative cholangitis (AOSC) were divided into 2 groups and were studied, Group A; over 70 yrs old (12), Group B; under 70 yrs old (7). The most frequent etiology of AOSC was choledocholithiasis (Group A 75%, Group B 43%). Urgent biliary drainage was performed in 18 cases, and which were clinically improved. The decreasing rate of bilirubin were fair in both groups and only 2 cases in Group A were dead. Concerning with the laboratory findings on admission, Group A had a higher level of BUN than Group B, and there were no other significant differences. Complications were frequently occurred in Group A (Shock 83%, DIC 83%, Renal failure 42%). The diameter of choledochus at biliary drainage was below 9 mm in 45% of cases in Group A, which implied the rapid progression to AOSC from the onset of biliary obstruction. Early diagnosis and urgent biliary drainage were essential for the management of AOSC in the old age.
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PMID:[Clinical features of acute obstructive suppurative cholangitis (AOSC) in the old age]. 157 7

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease that occurs over wide areas of Europe and Asia. Hantaviruses are the cause of this syndrome. The hallmark of HFRS is the triad of fever, hemorrhage, and renal failure. In its severe form it is associated with significant mortality. The syndrome evolves through five phases: febrile, hypotensive, oliguric, diuretic, and convalescent. The central physiologic derangement in HFRS is vascular dysfunction, manifested by impaired vascular tone and increased vascular permeability. The systemic effects of this dysfunction account for the occurrence of hypotension and shock, while local effects are probably important in the development of renal failure. Shock in HFRS has distributive and oligemic features, while renal failure has features of acute tubular necrosis. Hemorrhage is a consequence of vascular injury and a deficit of functional platelets. Vascular and platelet dysfunction are both compounded by uremia. Disseminated intravascular coagulation contributes to hemorrhage in some patients. Although hantaviruses are infectious for endothelial cells and may cause direct injury, a large body of evidence suggests that immune mechanisms play an important role in the pathogenesis of HFRS.
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PMID:Mechanisms of disease in Hantavirus infection: pathophysiology of hemorrhagic fever with renal syndrome. 167 61

This study refers to the clinical features of 11 cases of hemorrhagic fever with renal syndrome (HFRS) which was prevalent in Nagoya City University Medical School. The clinical course was divided into two parts: the febrile stage and the polyuria stage. Symptoms such as lumbago, muscular pain, general malaise and anorexia disappeared along with a fall of fever. The incubation period of this disease was estimated to be about three weeks. Polyuria, proteinuria, gastric complication and impairment of liver function seemed to be some of clinical features of this disease. There was no HFRS patient with severe renal failure in our cases. The presence of disseminated intravascular coagulation (DIC) was confirmed in 3 of these 11 cases. Therefore, it was suggested that hemorrhagic tendency of this disease might be attributed to DIC. From our experiences, the most important factor for the treatment of the severe case was the earliest detection whether they were complicated by DIC or not. If they were suspected of DIC, it could be necessary to start treatment for DIC as soon as possible. Prophylactic measures for HFRS in our animal facility could contribute to the prevention of this disease.
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PMID:Clinical studies on hemorrhagic fever with renal syndrome found in Nagoya City University Medical School. 168 5

A 44-year-old woman with a history of systemic lupus erythematosus on no steroid or immunosuppressive medication presented in septic shock complicated by renal failure and disseminated intravascular coagulation. The patient was treated with antibiotics. Liver-spleen scintigraphy with Tc-99m albumin colloid initially failed to reveal tracer accumulation in the spleen. Follow-up study after one year revealed normal tracer uptake in the spleen. The transient blockade of reticuloendothelial system by immune complexes is the most likely mechanism. Other possible mechanisms include disturbed vascular supply due to thrombosis secondary to the disseminated intravascular coagulation or vasculitis.
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PMID:Reversible functional asplenia in systemic lupus erythematosus. 174 31

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

We have compared the effects of ancrod and recombinant tissue plasminogen activator (rtPA) on nephrotoxic nephritis induced in pre-immunized rabbits by the administration of nephrotoxic globulin (NTG; sheep anti-rabbit glomerular basement membrane). We used three different doses of NTG: in each experiment three groups of six rabbits were preimmunized with normal sheep globulin and given NTG: group A received no further treatment; group B received rtPA, 2 mg/kg 12 hourly; group C received ancrod 2 U/kg 12 hourly. Animals were bled daily for estimation of plasma fibrinogen and serum creatinine, then killed on day 5 and kidneys removed for histology. 1 ml/kg of NTG caused massive glomerular necrosis, all three groups having severe renal failure. With 0.5 ml/kg of NTG, ancrod and rtPA both effectively prevented fibrin deposition in Bowman's space, but all animals had severe proliferative glomerulonephritis and marked renal failure. With 0.25 ml/kg of NTG, control animals developed severe proliferative nephritis and advanced renal failure, ancrod provided almost complete protection, and the rtPA group had renal injury and functional impairment intermediate between the other two groups. We conclude that renal failure in severe nephrotoxic nephritis is fibrin-independent, but in less fulminant nephritis renal function can be protected by defibrination with ancrod. rtPA is capable of reducing glomerular fibrin accumulation as effectively as ancrod, but provides inferior protection of renal function.
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PMID:Effects of ancrod and rtPA on fibrin accumulation, glomerular inflammation and renal function in nephrotoxic nephritis. 176 13

At the Kiel University Department of Gynaecology, 21 patients between the 21th and 39th week of gestation were treated in 1987 and 1988 following diagnosis of HELLP syndrome. At the time of diagnosis all patients presented an advanced gestosis/eclampsia. 9 patients developed the classical signs and symptoms, while hospitalised. The typical signs of gestosis, hypertension, proteinurea, oedema and hypoproteinaemia preceded the changes in laboratory values caused by the HELLP syndrome. Upper abdominal pain and increase in transaminase values occurred on the average 3.4 or 2.7 days prior to the decrease of, thrombocyte count. In 19 of the 21 cases, pregnancy was terminated by caesarean section. Severe peripartal complications occurred in 7 cases e.g. foetal death in utero (n = 3), eclampsia (n = 5), renal failure (n = 2), cerebral oedema (n = 1), intracerebral haemorrhage (n = 1), disseminated intravascular coagulation (n = 1), abdominal wall haematoma (n = 1). 6 of these patients were admitted after complications had occurred prior to admittance. All 18 infants born alive survived the neonatal period. The average birth weight was 1,571 g. 11 infants were discharged clinically normal. The remaining infants included 5 cases pointing to retinopathy and 3 cases of cerebral palsy. One infant developed post-haemorrhagic hydrocephalus.
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PMID:[Development of symptoms and perinatal complications in HELLP syndrome]. 177 22

A 54-year-old man received insertion of an acupuncture needle into the region extending from the posterior neck to the back on two occasions for the treatment of shoulder stiffness. Two weeks after the second acupuncture, he developed fever, dysarthria and mictionary disturbance, finally reaching the condition of tetraplegia. He was immediately admitted to an emergency room in our hospital, and was diagnosed as sepsis with DIC, ARDS, heart failure, renal failure, liver failure, and myelitis. After one month, he recovered with transverse myelopathy as a residual deficit. Neurological findings showed transverse myelopathy below the level of Th2 at that time. Cervical CT revealed an irregular low density at the periphery of the cervical vertebra from the C2 to C4 level. Cervical MRI revealed an irregular swelling of his spinal cord from the C2 to C7 level. We explained the mechanism of transverse myelopathy in this case as follows. After the acupuncture, he suffered a focal infection of the region of needle insertion, and then the infection expanded to the cervical vertebra, thus causing osteomyelitis, sepsis, and finally cervical myelitis. Direct injury of the spinal cord and nerve roots as a complication of acupuncture was previously reported, but indirect injury of the spinal cord due to myelitis had not been reported except our present case. Careful attentions should be paid to the complications of acupuncture.
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PMID:[A case of transverse myelopathy caused by acupuncture]. 178 54

A case of severe neonatal sepsis due to intrauterine infection with Capnocytophaga ochracea, complicated by hypotension, renal failure and disseminated intravascular coagulation, is reported. The role of Capnocytophaga as an organism of increasing importance in intrauterine and peripartum infections is discussed.
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PMID:Severe intrauterine infection due to Capnocytophaga ochracea. 179 20


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