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)

We present a case of a 11/2-year-old boy with toxic enteritis, consecutive consumption coagulopathy, and sever brain damage. During the acute phase we found high activity of the BB isoenzyme of creatine kinase in cerebrospinal fluid, but not in the serum. Isoenzyme MM could also be found in the spinal fluid (37.9% of the total activity). We conclude that analysis for creatine kinase isoenzymes in spinal fluid is of clinical importance.
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PMID:Creatine kinase isoenzymes in cerebrospinal fluid in a case of brain damage. 94 52

Venom from newborn Bothrops asper snakes has higher lethal, hemorrhagic, edema-forming, proteolytic and defibrinating activities than venom from adult B. asper specimens. Electrophoretic analysis confirmed the variation between these venoms. Intramuscular injection of 100 micrograms of venom from newborn specimens in mice induced defibrination, together with moderate increments of serum levels of lactate dehydrogenase, creatine kinase, hemoglobin and total proteins. A conspicuous hemorrhage developed in injected muscle rapidly after envenomation, probably due to a drastic alteration in capillaries and larger blood vessels. Other histological alterations included moderate myonecrosis, lung collapse and prominent renal damage, characterized by tubular necrosis and hyalinization. Polyvalent antivenom effectively neutralized lethal, hemorrhagic and indirect hemolytic activities of newborn B. asper venom, although requiring higher antivenom doses than neutralization of venom from adult B. asper.
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PMID:Pathological and biochemical changes induced in mice after intramuscular injection of venom from newborn specimens of the snake Bothrops asper (Terciopelo). 144 Jun 47

Because an increasing number of patients were arriving at our emergency room with cocaine intoxication and rhabdomyolysis, we reviewed our experience with such patients. We identified 39 patients seen at our institution over an eight-year period with acute rhabdomyolysis after cocaine use. The patients' mean creatine kinase level was 12,187 U per liter (range, 1756 to 85,000). Thirteen of the 39 patients (33 percent) had acute renal failure; 6 of them died. In comparison to the patients with normal renal function, those with renal failure were more often admitted with profound hypotension (46 vs. 4 percent; P less than 0.001), hyperpyrexia (69 vs. 15 percent; P less than 0.001), and markedly elevated serum creatine kinase levels (mean, 28,084 vs. 7931 U per liter; P less than 0.01). Disseminated intravascular coagulation developed in seven patients with renal failure. All six deaths were in this group. Severe hepatic dysfunction was found in 11 patients with renal failure. We conclude that cocaine intoxication can cause acute rhabdomyolysis with acute renal failure, severe liver dysfunction, and disseminated intravascular coagulation and that the mortality rate among patients with this syndrome is high.
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PMID:Acute rhabdomyolysis associated with cocaine intoxication. 341 85

A rare isozyme of serum creatine kinase (CK) migrating cathodic to CK-MM on electrophoresis was found in a 30-year-old male with stomach cancer complicated by disseminated intravascular coagulation leading to massive upper gastrointestinal bleeding and marked anemia. Serum CK activity rose to a maximum of 374 U/l without detectable CK-MB isoenzyme. The patient was also characterized by a marked increase in serum lactate dehydrogenase (all isozymes elevated) and by preferential leakage of mitochondrial aspartate aminotransferase and glutamate dehydrogenase, indicating the presence of extensive tissue damage involving mitochondria. Skeletal muscle mitochondria were considered the most likely source of the additional CK isozyme.
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PMID:Cathodic isozyme of serum creatine kinase in a case of stomach cancer complicated by disseminated intravascular coagulation. 744 49

Acute exertional rhabdomyolysis is caused by a skeletal muscle injury that results in the release of myoglobin and other cellular contents into the circulatory system. Recent reports suggest that acute exertional rhabdomyolysis is more common and more serious than previously realized. Mild to moderate acute exertional rhabdomyolysis can result in hyperkalemia, hypernatremia, lactic acidosis and hyperphosphatemia. Disseminated intravascular coagulation, renal failure and compartmental syndrome may also occur. The physician should maintain a high index of suspicion for acute exertional rhabdomyolysis in patients who present with symptoms of an overexertion injury, most commonly pain and swelling in the affected muscles. Special attention should be given to evaluating the history for occupational, recreational, environmental and medical risk factors for rhabdomyolysis. Screening may be performed with a simple urine dipstick test; if the urine is orthotoluidine-positive, the diagnosis should be confirmed with measurement of the serum creatine kinase level. Early intervention with aggressive hydration and close monitoring for metabolic, renal or hematologic complications may prevent serious injury or death.
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PMID:Acute exertional rhabdomyolysis. 762 24

In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin < 5 g/dl (0/12), < 8 g/dl (2/12); serum creatinine > 265 mumol/l (3/12); blood glucose < 2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH < 7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia > 5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia < 30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12), < 125 mmol/l (2/12); rhabdomyolysis with creatine kinase > 1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intensive care aspects in severe tropical malaria: clinical aspects, therapy and prognostic factors]. 777 Jul 59

Although rare, exertional collapse and sudden death are the most serious potential complications of sickle cell trait. Studies suggest that this condition may occur in susceptible persons when poor physical conditioning, dehydration, heat stress or hypoxic states precipitate sickling of the abnormal erythrocytes. Sickling leads to endothelial damage, which can cause vasoconstriction, disseminated intravascular coagulation and local tissue damage. Cardiac effects include acute ischemia and arrhythmias. Muscle damage results in acute compartment syndromes and release of myoglobin into the circulation. Acute renal failure is possible. Diagnosis is based on a high index of suspicion, and characteristic presentation and laboratory findings, including myoglobinuria, hyperkalemia, hypocalcemia, hyperphosphatemia and elevated creatine kinase levels. The differential diagnosis includes pulmonary embolism, acute cardiac events, anaphylaxis and heat stroke. Management is based on stabilization, rehydration, and the treatment and prevention of complications.
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PMID:Exertional collapse and sudden death associated with sickle cell trait. 904 99

We report a rare case of spontaneously developing generalised gas gangrene with massive rhabdomyolysis after a cholecystectomy and drainage of a hepatic abscess. On preoperative physical examination the patient appeared severely ill and was icteric and oliguric. Laboratory evaluation showed signs of systemic inflammation, elevated lactate levels, evidence of disseminated intravascular coagulation (DIC), and increased levels of serum creatine kinase (CK) activity. Abdominal ultrasound and endoscopic retrograde cholangiography showed a gallbladder perforation and a hepatic abscess. Cholecystectomy and drainage of the abscess was performed immediately and without technical problems. After postoperative admission to the intensive care unit, the patient showed evidence of generalised myonecrosis with subcutaneous gas formation and acute renal failure. Initially, there were few other signs of systemic toxicity; the patient was not hypotensive and the pulmonary gas exchange was normal. Within hours diffuse swelling of his right leg developed with cutaneous gangrene and a compartment syndrome. After fasciectomy and extensive surgical debridement, uncontrollable bleeding due to DIC developed from the fasciectomy site, which finally required exarticulation of the leg at the hip joint. At this point, multiple organ failure including severe adult respiratory distress syndrome was present. Two days after cholecystectomy, the patient died from hypoxic cardiocirculatory failure. Clostridium perfringens was repeatedly isolated from the wounds. Besides gas gangrene, the differential diagnosis of such infections includes localised clostridial cellulitis, nonclostridial anaerobic cellulitis caused by mixed aerobes and anaerobes, and type I or type II necrotising fasciitis. Patients with systemic necrotising infections should be treated with broad-spectrum antimicrobial regimens (penicillin G, 3rd generation cephalosporins, clindamycin, and aminoglycosides). An otherwise unexplained elevation of serum CK activity in the presence of acute cholecystitis may suggest haematologic spread of an aggressive myolytic agent and the beginning of myonecrosis. This should prompt immediate surgical exploration after establishing broad-spectrum antibiotic coverage. The role of hyperbaric oxygen treatment in this situation remains to be established. If hyperbaric oxygen is to be employed, it should neither delay surgical exploration nor jeopardize the patient with the hazards of an interhospital transport.
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PMID:[Generalized gas gangrene infection with rhabdomyloysis following cholecystectomy]. 916 65

Five of fourteen patients with multiple system atrophy (MSA) experienced a total of eight episodes of malignant syndrome, three episodes in 1, two episodes in 1 patient, and a single episode in each of the other patients. Four patients had extrapyramidal symptoms and required antiparkinson therapy, including dopaminergic agonists. Five episodes occurred in the summer season. Two were caused by decreased or irregular doses of antiparkinson drugs, one by administration of an antidepressant drug, three by complications, and two by elevation of body temperature of environmental origin. A patient without parkinsonism became febrile after administration of droxidopa, which may be a central pyrogenic substance that acts via the noradrenergic system. Administration of dopaminergic drugs and dantrolene sodium was followed by recovery in four episodes in three patients. One patient manifested dysautonomia after recovery from the malignant syndrome. Another patient with high serum creatine kinase levels and myoglobinuria developed renal failure requiring hemodialysis. Another patient died of DIC. Besides withdrawal of dopaminergic agents, which alter monoaminergic neuron activity, stress to the body and heating by a variety of factors tend to trigger the malignant syndrome in MSA.
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PMID:[Malignant syndrome in multiple system atrophy]. 919 91

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


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