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)

Eighteen patients whose mean age was 61 years were referred to us with acute aortic occlusion from 1977 to 1985. Ten patients had cardiac emboli (group I) and eight had aortoiliac occlusive disease (group II). Fourteen of these patients had paresis or paralysis. Diagnosis was prompt but the time lapse from onset of symptoms to revascularization averaged 18 hours (group I, 10.3 hours; group II, 26.1 hours). All 10 patients in group I had embolectomy alone; of the eight patients in group II, two had transfemoral thrombectomy and six had bypass procedures. The perioperative mortality rate was 40% in group I and 62.5% in group II. Complications developed in 12 patients (nine died); renal failure occurred in 11, compartment syndrome in nine, adult respiratory disease syndrome in three, acute myocardial infarction in three, disseminated intravascular coagulation in two, and paraplegia in one. No amputations were required in the nine survivors and limb function was restored in eight of these patients. Acute aortic occlusion sets in motion a chain of events that threatens life and limb. Prompt diagnosis and revascularization by the simplest operation are required to decrease morbidity and mortality.
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PMID:Acute aortic occlusion--a multifaceted catastrophe. 374 30

By damaging cell membrane integrity, acute rhabdomyolysis leads to electrolyte shifts according to the concentration gradients and the liberation of intracellular substances. Diagnosis is confirmed by the presence of a high serum creatinkinase activity (CK) and myoglobinuria. For clinical purposes myoglobinuria is demonstrated by a blood-positive dipstick in the absence of hematuria or hemoglobinuria. Rhabdomyolysis is usually acquired and is rarely due to hereditary enzyme defects. The authors report on 61 patients admitted in the last 15 years with rhabodomyolysis. In the past 4 1/2 years the diagnosis was suggested by CK greater than 5000U/1 in 49 patients, representing 1.6% of all admissions in the departments of medicine and surgery. Originally described in crush situations, rhabdomyolysis has been observed with increasing frequency as a consequence of muscular stress and self crush due to coma or hemi- and paraplegia during the last decades. 24% of the patients with this diagnosis had had an intoxication, and in 70% there were multiple simultaneous causes. Autoimmune diseases, infections of bacterial, viral and fungal origin, endocrinopathies, and thermic and ischemic injuries can also provoke rhabdomyolysis. As a consequence of fluid shift into the damaged muscle a compartment syndrome may lead to vascular or neural defects. In 80% of cases there is initial hypocalcemia, turning later into hypercalcemia. Other frequent electrolyte disorders accompanying rhabdomyolysis are hyperkalemia, hyperphosphatemia and a widened anion gap. 6 of 13 patients showed the typical blood changes found in patients with disseminated intravascular coagulation. Acute renal failure developed in 30 patients, 15 of whom underwent dialysis or hemofiltration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute rhabdomyolysis]. 395 76

Idiopathic purpura fulminans usually occurs in young children and is frequently preceded by a preparatory viral or bacterial infection. Following a severe streptococcal pharyngitis, an 8-year-old boy developed purpura fulminans with disseminated intravascular coagulation and severe protein S deficiency (total antigen < 0.05 u/ml). Despite generous plasma infusions, skin necrosis progressed rapidly into compartment syndrome which required fasciotomy and skin grafting and resulted in the loss of three digits of the right foot. Total protein S remained low for over a month despite plasma supplementation and complete normalization of protein C levels. A polyclonal anti-protein S IgG was demonstrated in the patient's plasma, which decreased to 25% of baseline titre after 1 month and was undetectable 6 months after purpura fulminans, when plasma protein S had returned to normal. Transient, isolated and severe deficiencies of protein S have been reported in patients with idiopathic purpura fulminans and a previous preparatory infection. Autoimmune protein S deficiency may play a key role in the aetiopathogenesis of idiopathic purpura fulminans.
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PMID:Severe autoimmune protein S deficiency in a boy with idiopathic purpura fulminans. 773 61

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

Acute infectious purpura fulminans (AIPF) is a rare syndrome of hemorrhagic infarction of the skin, extremity loss, and intravascular thrombosis. It progresses rapidly and is accompanied by disseminated intravascular coagulation and vascular collapse. The victims often succumb to the disease. Our objective was to investigate the clinical manifestations, outline the clinical course, and delineate factors related to mortality among the patients with AIPF. Patients diagnosed with AIPF over a 15-year period were reviewed retrospectively for patient history, comorbid conditions, progression of clinical course, and medical and surgical management. The vast majority of the patients were under the age of 7; however, the disease process can be seen in adults. The overall mortality rate was 43 per cent. The major predisposing factors were history of recent upper respiratory infection, recent surgery or childbirth, young age, and absence of a spleen. The most common clinical manifestations were skin discoloration, disseminated intravascular coagulation, fever, and septic shock. The most common bacteria cultures were Neisseria meningitidis, Hemophilus influenzae, and Streptococcus pneumoniae. There appears to be a higher mortality in patients who did not undergo a surgical intervention. Compartment syndrome needs to be evaluated early on in the presentation. Rapid diagnosis, intensive care unit management, and prompt surgical consultation and debridement may decrease the mortality.
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PMID:Acute infectious purpura fulminans: a 15-year retrospective review of 28 consecutive cases. 1257 89

Rhabdomyolysis is a disorder characterized by acute damage of the sarcolemma of the skeletal muscle leading to release of potentially toxic muscle cell components into the circulation, most notably creatine phosphokinase (CK) and myoglobin, and is frequently accompanied by myoglobinuria. Therefore, the term myoglobinuria is often used interchangeably with the term rhabdomyolysis. This disorder may result in potential life-threatening complications such as acute myoglobinuric renal failure, hyperkalemia and cardiac arrest, disseminated intravascular coagulation, and compartment syndrome. The condition is etiologically heterogeneous and may result from a large variety of diseases affecting muscle membranes, membrane ion channels, and muscle energy supply including acquired causes (e.g., exertion, crush injury and trauma, alcoholism, drugs, and toxins) and hereditary causes (e.g., disorders of carbohydrate metabolism, disorders of lipid metabolism, or diseases of the muscle associated with malignant hyperthermia). In many patients with idiopathic recurrent rhabdomyolysis, specific inherited metabolic defects have not been recognized up to now.
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PMID:[Rhabdomyolysis and myoglobinuria]. 1279 89

Rhabdomyolysis is a severe clinical symptom of variable etiology. Acquired factors of exogenous origin such as traumata and endogenous metabolic disturbances have to be separated from hereditary disease as causative mechanism. Most frequently, exertional stress during hyperthermia, traumatic damage or ethanol abuse are observed. Almost independent of the diverse initial events, the pathogenesis follows a common final pathway with intracellular calcium accumulation and ATP depletion. Clinical symptoms vary. Seldom, the classical triad of muscle pain, weakness, and dark urine is observed. Recurrent episodes should raise suspicion of an inherited disorder. Severe complications are hypovolemia, electrolyte disorders with hyperkalemia and hypocalcemia resulting in life threatening arrhythmias, a compartment syndrome, disseminated intravascular coagulation and acute renal failure, which is frequently oligo-anuric. In combination with often severe underlying disease, renal failure causes death in 1/5 of the patients. The diagnosis is made with the determination of serum creatine kinase and the myoglobin levels in plasma and urine. Therapeutic options are to correct the hypovolemia with sufficient fluid supply, the prevention of oliguria using loop diuretics, alkalinization of the urine, normalization of serum electrolytes with reduction of hyperkaemia, and decompression of compartment syndromes. An underlying disease should be evaluated to initiate specific therapeutical and preventative steps. Avoiding pre-disposing factors by identifying the mechanisms of disease will reduce the occurrence of rhabdomyolysis with its still high mortality.
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PMID:[Rhabdomyolysis]. 1295 32

Rhabdomyolysis is defined as a syndrome resulting from skeletal muscle injury with release of muscle cell contents into the plasma. One of the main causes of rhabdomyolysis is eccentric exercise against high resistance. There are mechanical as well as metabolic causes in exercise induced rhabdomyolysis. The mechanical aspect includes high physical tension on the muscle fiber and the metabolic causes include lack of available ATP and disturbance in intracellular electrolyte balance, especially calcium. The clinical picture of rhabdomyolysis may include muscle soreness, reduction of the range of motion, decreased muscle strength, black urine and, in severe cases, acute renal failure. Laboratory results may include delayed high levels of muscle enzymes in the plasma, myoglobinemia and myoglobinuria, disturbance in blood electrolyte balance, and in severe cases, disturbance in coagulatory function and DIC. Compartment syndrome may also be part of severe rhabdomyolyis. The main treatment for rhabdomyolysis is fluids administration and maintaining urination, in order to preserve renal function. In severe compartment syndrome fasciotomy may be necessary. There is a wide variability in the severity of rhabdomyolysis. This variability is not completely understood but may be related to the level of physical fitness, morphometrical characteristics and gender. In order to prevent exercise induced rhabdomyolysis, a gradual training program should be maintained providing enough recovery time, preserving fluid balance, and avoiding extreme eccentric exercise and exercise in high heat load.
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PMID:[Exercise induced rhabdomyolysis--characteristics, mechanisms and treatment]. 1571 20

A four-month-old infant was hospitalized because of RSV bronchiolitis. Two days after presentation he developed rhabdomyolysis, most probably as a result of multiple factors (hyperthermia, hypovolemia/dehydration, hypernatremia, metabolic acidosis), followed by severe complications including acute renal failure, hepatic dysfunction and disseminated intravascular coagulation. Under sufficient fluid supply he recovered completely. In rhabdomyolysis clinical symptoms vary. Seldom, the classical trial of muscle pain, weakness, and dark urine is observed. Severe complications are hypovolemia, electrolyte disorders, a compartment syndrome, disseminated intravascular coagulation and acute renal failure, which causes death in 20% of the patients, although non-traumatic causes seem to have better outcome. The mainly therapeutic option is to correct the hypovolemia with sufficient fluid supply.
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PMID:[More than muscle stiffness]. 1660 71

Purpura fulminans is a syndrome characterized by hemorrhagic infarction of the skin and underlying soft tissue as a result of disseminated intravascular coagulation and intravascular thrombosis. In this study, the authors report their experience with surgical intervention for acute infectious purpura fulminans (AIPF). A retrospective chart review was performed including all patients diagnosed with AIPF from January 1, 2006, to December 31, 2008, and treated at an academic medical center. Primary endpoints of interest were overall survival rate and the need for and level of eventual amputation. Improvement in limb perfusion was included as a secondary endpoint. Nine patients were diagnosed with AIPF at the authors' institution during a 3-year period, and seven of these diagnoses were made within 12 months. Overall mortality was 44% (5/9). Amputation was required in 80% of survivors (4/5). All patients explored within 24 hours of diagnosis had evidence for compartment syndrome with visible bulging muscle on fascial release. AIPF is a devastating disease with significant mortality and morbidity primarily related to the loss of multiple limbs. This study suggests that early diagnosis and surgical intervention in the form of compartment release and sympathectomy should be performed concurrently with the initial treatment of sepsis to minimize amputations in surviving patients.
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PMID:Surgical management of acute infectious purpura fulminans. 2123 23


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