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

Four cases of intravascular coagulation associated with a state of acidosis in diabetics were observed in 57 patients with diabetic acidosis and 19 with lactic acidosis, in a series of 112 cases of consumption coagulopathy admitted to a department of medical resuscitation. In three cases the coagulopathy was found only on investigation; in one there were clinical and anatomic signs. The coagulopathy may be found either during the phase of recovery from ketoacidosis, or during the course of severe lactic acidosis, particularly during a recurrence of this form of acidosis. In spite of the unfavorable outcome in 3 of the 4 cases, the abnormal findings of coagulopathy reverted toward normal along with successful metabolic corrections. The factors responsible for consumption coagulopathy are acidosis, collapse, generalised systemic reactions and alterations of platelet function, of coagulation, of the balance between fibrin deposition and lysis and of lipid levels, all characteristic of diabetes. The clinical effects of this coagulopathy seldom become apparent but provide a possible explanation of some of the complications of diabetic ketoacidosis, particularly certain hemorrhagic or thrombotic events, as well as certain visceral complications, especially those affecting renal, pulmonary and cerebral areas.
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PMID:[Consumption coagulopathy and acidosis in the diabetic patient (author's transl)]. 82 99

Patients with classical heat stroke are different in many ways from those with exertional injury; contrasts included difference in demographic factors, prior general health, in-hospital complications and laboratory abnormalities (lactate, liver enzymes, pH, electrolytes). Severe hyperkalemia, acute renal failure, rhabdomyolysis and disseminated intravascular coagulation often dominate the course of patients with exertional heat stroke but are uncommon in those with classical heat stroke (Table 4). While lactic acidosis is the rule in exertional injury, it is somewhat unusual in patients with classical heat stroke and when above 3 mmoles/L predicts a poor outcome or death. In spite of the advanced age and multiple medical problems of the patients with classical heat stroke, careful attention to early and aggressive cooling and scrutiny for potential complications can result in salvage of most patients.
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PMID:Epidemic classical heat stroke: clinical characteristics and course of 28 patients. 707

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

A 34-year-old obese woman with human immunodeficiency virus (HIV) infection diagnosed a year earlier was seen because of nausea, vomiting, and intermittent diarrhea for 3 weeks. Her current medications included zidovudine. Physical examination revealed tachypnea and tender hepatomegaly. Computed tomography of the abdomen showed hepatomegaly with fatty infiltration. Liver enzymes were within normal range except for elevated lactate dehydrogenase (LDH). The serum bicarbonate value was low, with a lactate level three times normal. The tachypnea and dyspnea worsened as lactate concentrations rapidly increased to 15 times normal. Although her Po2 and cardiac index were initially adequate, the patient had acute respiratory failure. She died with multiorgan dysfunction, including hepatic failure, severe lactic acidemia, disseminated intravascular coagulation, and renal failure. Autopsy revealed hepatomegaly and massive steatosis. Physicians should consider lactic acidosis in patients taking zidovudine and having unexplained tachypnea, dyspnea, and low serum bicarbonate concentrations.
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PMID:Zidovudine-associated type B lactic acidosis and hepatic steatosis in an HIV-infected patient. 1021 65

Sepsis-associated purpura fulminans is defined as septicemia, shock, disseminated intravascular coagulation and circulatory failure leading to multiple organ dysfunction. 40-70% of patients with sepsis-associated purpura fulminans die. Early prognostic factors in adults have not been well delineated yet. Aim of our study was 1) to evaluate currently used scoring systems for meningococcal septicemia in the setting of sepsis-associated purpura fulminans and 2) to assess if other parameters are feasible as early prognostic factors. From 1.1 1994-31.12.1998 twelve patients (female: 7; mean age: 31 (21; 43) years) were studied. Six patients (50%) died within 2 hours and 7 days after admission despite standard intensive treatment. On admission non-survivors had a more pronounced degree of disseminated intravascular coagulation compared to survivors (platelet count 18000 (15000; 45000) G/l vs. 119.000 (111000; 152000) G/l, (p = 0.03); fibrinogen 67 (50; 108) mg/dl vs. 356 (234; 483) mg/dl, (p = 0.02); PTZ 28% (20%; 30%) vs. 44% (35%; 51%), (p = 0.05); aPTT 120 (120; 128) sec vs. 46 (44; 69) sec, (p = 0.001). Severity of lactic acidosis was significantly higher in non-survivors than in survivors (pH 7.08 (6.92; 7.21) vs. pH 7.4 (7.25; 7.4), (p = 0.02); lactate 13.5 (11; 15) mval/l vs. 6.0 (4.4; 6) mval/l, (p = 0.02); data presented as median (25-75% interquartile range). In our patients the Glasgow Meningococcal Septicemia Prognostic Score (GMSPS) and the Niklasson-Score failed to distinguish between survivors and non-survivors (GMSPS 7 (6; 11) vs 7.5 (7; 9) out of 15; predicted mortality according to Niklasson-Score 73% vs 88%). There was no difference in the APACHE II Score (22 (18.5, 24) vs 22 (20.25, 26)). The severity of disseminated intravascular coagulation assessed by routine laboratory parameters and the degree of lactic acidosis on admission were the strongest predictors of outcome in patients with sepsis-associated purpura fulminans. Scoring systems developed for patients with meningococcal septicemia are of limited value in the setting of sepsis-associated purpura fulminans.
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PMID:Sepsis-associated purpura fulminans in adults. 1125 35

We report the survival of a multiply injured patient with exanguinating haemorrhage and an arterial pH of 6.5, following a road vehicle crash. The previously healthy 38 years old male driver veered off the motorway and collided with a tree. The ambulance arrived at the scene 9 min after being called by an eyewitness and, following rapid extrication from the wreckage; the patient arrived in hospital 27 min later (with a GCS of 6), and was immediately intubated. The patient had suffered near-complete amputation of the left leg at upper femoral shaft level, along with multiple distal fractures and open wounds. He also sustained a head injury and closed displaced fractures of left radius and ulna. The patient received 2 l of crystalloids in the pre-hospital phase. Once in hospital the haemorrhage was controlled with a pressure dressing and intra-venous fluids were kept to a minimum until he was taken promptly to theatre. His initial arterial blood sample revealed a pH of 6.57, pCo(2) of 9.18 kPa, a pO(2) of 70.11 kPa and a base excess of -27.5 mmol l(-1). The co-oximeter Hb was 5.8 g dl(-1). Haemorrhage was controlled in theatre where he was transfused a total of 30 U of blood, 1 pack of platelets, 12 U of fresh frozen plasma, 3.5 l of crystalloids and 1.5 l of colloid. Sodium bicarbonate was administered three times. He subsequently remained ventilated in intensive care unit (ICU). Over the following week he survived sepsis, disseminated intravascular coagulation and myoglobinuria (with transient renal failure) attributable to rhabdomyolysis secondary to muscle necrosis. He later underwent diversion colostomy and disarticulating amputation of the left femur after several debridements. After 6 weeks on ICU he made an excellent recovery will full return of his mental abilities. In this case, the serial arterial blood samples obtained were reliable. The lactic acidosis observed was the result of profound tissue hypo-perfusion and its rate of clearance seems to have greater prognostic value than its peak or initial value. Several factors may have contributed to the patient's survival: rapid retrieval from the scene; early intubation with excellent subsequent oxygenation (thus avoiding the dangerous combination of hypoxia and acidosis with synergistic influence on cardiac depression) and limited initial fluid resuscitation in the emergency department with prompt surgical intervention and vigorous restoration of organ perfusion after surgical haemostasis. Immediate operative haemostasis, coupled with restricted fluid administration beforehand and vigorous restoration of organ perfusion afterwards is now replacing the old resuscitation paradigm. Perhaps this shift in practice has helped this patient to survive.
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PMID:Survival with an arterial pH of 6.57 following major trauma with exsanguinating haemorrhage associated with traumatic amputation. 1200 26

A 14-year-old girl was found to have a large, non-tender breast mass with anemia and thrombocytopenia. The diagnosis of an undifferentiated carcinoma of unknown primary was made after open breast biopsy of the mass with negative immunohistochemical studies for breast malignancies. Further evaluation showed extensive metastatic disease affecting the bone marrow, ribs, liver, and brain with magnetic resonance imaging evidence of carcinomatous meningitis. Despite 2 months of chemotherapy and intensive supportive care, the patient died of severe lactic acidosis and disseminated intravascular coagulation after exaggerated menstrual bleeding. The association of severe lactic acidosis and undifferentiated carcinoma of unknown primary in an adolescent has not been previously described.
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PMID:Severe lactic acidosis in a 14-year-old female with metastatic undifferentiated carcinoma of unknown primary. 1554 20

We report the athletic, the clinical, and the pathological details of a case of fatal rhabdomyolysis during training in a college football player with sickle cell trait (SCT) who collapsed minutes after running 16 successive sprints of 100 yd each. The player, 19 yr old, African American, was apparently healthy when he took the field for the conditioning run. No exertional heat illness was present. After collapsing on-field, the player soon went into coma and developed fulminant rhabdomyolysis, profound lactic acidosis, acute myoglobinuric renal failure, refractory hyperkalemia, and disseminated intravascular coagulation. Despite intensive care in the hospital, he died about 15 h after admission, likely from a hyperkalemic cardiac arrhythmia; the terminal rhythm was pulseless electrical activity. The forensic autopsy confirmed that the cause of death was acute exertional rhabdomyolysis associated with SCT. Counting this case, at least 15 college football players with SCT have died from complications of exertional sickling, as have younger football players and other athletes. In SCT, maximal, sustained exercise evokes four forces that can foster sickling: hypoxemia, acidosis, hyperthermia, and red cell dehydration. The setting, the clinical and laboratory features, and the clinicopathological correlation here suggest that the fulminant rhabdomyolysis and its fatal sequelae were from exertional sickling. These data suggest that screening and simple precautions for SCT may be warranted to prevent tragedies like this and enable all athletes with SCT to thrive in their sports.
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PMID:Sickle cell trait and fatal rhabdomyolysis in football training: a case study. 2001 Jan 36

A 41-year-old man with a history of hyperthyroidism had been treated with methimazole and propranolol for the past 2 months. He developed multiorgan dysfunction with acute liver failure, severe lactic acidosis, disseminated intravascular coagulation, heart failure and acute pulmonary edema with rapid deterioration of renal function. The patient had no history of alcoholism, drug abuse, blood transfusion, or exposure to hepatitis A, B, or C. Extrahepatic obstruction was ruled out with an abdominal ultrasonogram. Serologic studies and immunologic tests were negative. This case illustrates the sudden and abrupt deterioration of multiorgan dysfunction due to antithyroid drug administration and thyroid storm. The thyroid storm score of Burch and Wartofsky was 90/140. The multiorgan dysfunction was reversed by discontinuation of the methimazole and treat with hemodialysis, steroids, cholestyramine, nonselective beta-blocker, fresh frozen plasma infusion and supportive management in the intensive care unit. The patient was discharged from the hospital with normal coagulation parameters, renal and liver function tests.
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PMID:Multiorgan dysfunction accompanied with metimazole and thyroid storm. 2228 65

We describe a case of thyroid crisis with hypoglycemia, lactic acidosis, multiple organ failure, and disseminated intravascular coagulation--rare but severe complications of thyroid crisis. The patient was a 59-year-old Chinese woman who presented with evidence of heart failure and atrial fibrillation. Analysis of a blood sample yielded astonishing results: her blood glucose was 1.7 mmol/L, and lactate greater than 15 mmol/L with the arterial pH as 6.94. Liver enzymes (alanine aminotransferase, 1846 U/L; aspartate aminotransferase, 6242 U/L) and bilirubin elevated rapidly and dramatically. Prompt treatments such as mechanical ventilation, plasma exchange, and continuous venovenous hemofiltration were preformed, along with antithyroid medication. The patient finally survived after 3 weeks of intensive care. We herein discuss the possible mechanisms of these metabolic disorders in thyroid crisis and possible therapeutic measures that could be used to reduce mortality.
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PMID:Successful treatment of thyroid crisis accompanied by hypoglycemia, lactic acidosis, and multiple organ failure. 2238 56


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