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)

Between July, 1988 and November, 2002, 108 patients underwent total cavopulmonary connection (TCPC) at Kobe Children's Hospital. The primary malformation was univentricular heart in 40 tricuspid atresia in 21, mitral atresia in 16, and other complex cardiac defects in the remaining 31. Fenestrated TCPC, staged TCPC, and off-pump TCPC were performed in 39, 26, and 15 high risk patients, respectively. Nitric oxide inhalation was administered in 46 patients. The mean follow-up period was 4.3 years (range, 1 month to 14 years). There were 10 early deaths due to low cardiac output syndrome in 4, thrombosis in 3, tracheal bleeding in 2, and disseminated intravascular coagulation in 1. There were 5 late deaths due to congestive heart failure in 2 patients, arrhythmia in 1, cerebral infarction in 1, and subarachnoid hemorrhage in 1. Late complications included arrhythmia in 17 patients, systemic desaturation caused by abnormal systemic venous channels in 10, pleural or pericardial effusion in 3, chylothorax in 1, and aortic valve incompetence in 1.
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PMID:[Long-term results after the total cavopulmonary connection]. 1270 Nov 91

This prospective study was designed to investigate D-dimer concentrations in clinically healthy dogs, clinically ill dogs without thromboembolic disease (TE), and dogs with TE. The goals of this study were to determine whether the coagulation cascade is activated in nonembolic metabolic and inflammatory conditions and whether differentiation from TE is possible. Group 1 consisted of 30 clinically healthy dogs presented for routine care. Group 2 consisted of 67 clinically ill dogs without TE. This group was subdivided into the following categories: postoperative surgical procedures, congestive heart failure, renal failure, hepatic disease, and neoplastic disease. Group 3 consisted of 20 dogs diagnosed with TE. A CBC and a measurement of prothrombin time (PT), activated partial thromboplastin time (PTT), fibrinogen degradation product (FDP) concentration, and plasma D-dimer concentration was performed on dogs in all groups. D-dimer concentrations were highest in dogs with TE; next highest was the hepatic disease group. Only these 2 groups had median D-dimer concentrations markedly different from clinically healthy dogs. The frequency of platelet abnormalities was markedly greater for the TE and neoplastic disease groups. The sensitivity of D-dimer concentrations >500 ng/mL for predicting TE was 100%; however, the specificity of D-dimer for TE at that concentration was 70%. The specificity of D-dimer concentrations >1,000 ng/mL to predict TE was 94% (sensitivity, 80%), and the specificity of D-dimer concentrations >2,000 ng/mL was 98.5% (sensitivity, 36%). FDPs were not high in any TE patient; thus, they may be an insensitive indicator of thromboembolism, with or without overt disseminated intravascular coagulation (DIC).
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PMID:The utility of plasma D-dimer to identify thromboembolic disease in dogs. 1465 10

We report a case of maternal mortality in a 34-year-old multipara who presented at the 35th week of gestation with severe hypoglycaemia. She had no history of diabetes mellitus. This episode was a prelude to catastrophic and refractory congestive cardiac failure due to previously undiagnosed severe mitral stenosis. The rapid cardiovascular deterioration initially appeared to be consistent with amniotic fluid embolism. She also developed deranged liver function with disseminated intravascular coagulation, which mimicked acute fatty liver of pregnancy. The problems of diagnosis and management are discussed. Unfortunately the patient died before mitral valvular commissurotomy could be effected.
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PMID:Severe mitral stenosis in a parturient with congestive cardiac failure and hypoglycaemia. 1532 Dec 12

In the present study, we investigated the relationship between serum leukocyte cell-derived chemotaxin2 (LECT2) levels and liver function in patients with acute liver failure, and its use as a prognostic indicator. We studied six acute liver failure patients (two women, four men; 49.8 +/- 20.7 years old) admitted to our hospital in 2002. These patients had diagnoses of fulminant hepatitis due to acute liver failure (1) from congestive heart failure; (2) from portal venous gas, and (3) from postoperative disseminated intravascular coagulation (DIC). We measured serum LECT2, GOT, and GPT levels, the last two being inversely proportionate to the serum LECT2 levels. When the serum GPT levels peaked, the serum LECT2 levels were the lowest. When the liver function recovered, serum LECT2 levels increased. Three of four patients died due to liver failure, one to congestive heart failure. Maximum serum LECT2 levels among the expired group were significantly lower than those among the alive group (0.96 +/- 0.8 ng/mL vs 12.9 +/- 4.3 ng/mL). Serum LECT2 levels may be a prognostic indicator of recovery from liver failure. The present study suggests that in clinical medicine LECT2 participates in regeneration after injury of hepatocytes.
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PMID:Serum LECT2 level as a prognostic indicator in acute liver failure. 1556 Dec 49

An 84-year-old man was referred to the emergency department with severe dyspnea. Based on his physical findings, electrocardiogram, X-ray and echocardiographic findings, congestive heart failure was suspected and drip infusion of prophylactic heparin against intracardiac thrombosis was commenced together with dopamine, nitroglycerin and furosemide. Diuresis occurred and the pulmonary congestion ameliorated remarkably. Starting on the 20th hospital day, the platelet count was gradually reduced (from 256,000 to 55,000 /microl) and the fibrin degradation product concentration rose (27.6 microg/ml). However, prothrombin time was not prolonged (89%), the concentration of antithrombin III was low -normal (69%) and the fibrinogen concentration was high (650 mg/dl). Thus, heparin-induced thrombocytopenia (HIT), rather than disseminated intravascular coagulation (DIC), was suspected. Heparin was withdrawn on the 24th hospital day and replaced by nafamostat mesilate after which the platelet count was restored to 100,000 /microl. Enzyme-linked immunosorbent assay for HIT antibodies was positive. Unfortunately, the patient died from uncontrolled sepsis on the 29th hospital day. At autopsy, platelet-rich thrombi were found in the small pulmonary arteries and intestinal arteries. No evidence of DIC, such as fibrin-rich thrombosis, was observed. This is the first autopsy report of HIT in Japan.
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PMID:A case of heparin-induced thrombocytopenia with sepsis and congestive heart failure--first autopsy report on Japan--. 1556 10

A 69-year-old woman caught a cold resulting in nausea, vomiting, diarrhea and severe anorexia. Then she suffered progressively from dyspnea and leg edema, and finally became delirious. On admission severe hypoglycemia, hypothermia, marked tachycardia, generalized edema, mild jaundice and cachexy were noted. EKG showed atrial fibrillation. A chest X-ray, chest CT and echocardiography showed congestive heart failure. Therapeutic use of diuretics induced shock leading to serious liver dysfunction and disseminated intravascular coagulation. However, combined therapy by intravenous glucose, digitalis, diuretics, anti-fibrinolytic drug and hydrocortisone were effective. Addition of antithyroid therapy brought a further favorable outcome.
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PMID:Severe starvation hypoglycemia and congestive heart failure induced by thyroid crisis, with accidentally induced severe liver dysfunction and disseminated intravascular coagulation. 1580 13

We present a patient who visited emergency department owing to the skin manifestation of disseminated intravascular coagulation. Recent anterior myocardial infarction induced congestive heart failure and left ventricular thrombus, which were considered to be the cause of disseminated intravascular coagulation. Anticoagulant therapy with heparin and warfarin was used successfully to treat the disseminated intravascular coagulation and left ventricular thrombus.
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PMID:Severe disseminated intravascular coagulation caused by congestive heart failure and left ventricular thrombus. 1749 82

We describe a 26-year-old female patient, who had attempted suicide with Endosulfan, and who presented to the Emergency Department with status epilepticus. She subsequently developed hypotension refractory to inotropes, intravascular hemolysis, disseminated intravascular coagulation (DIC), metabolic acidosis and, finally, cardiac arrest and death. Endosulfan is a chlorinated insecticide that causes central nervous system hyperstimulation. It is absorbed from the gastrointestinal tract, skin, and respiratory tract, and leads to nausea, vomiting, paraesthesia, giddiness, convulsion, coma, respiratory failure, and congestive cardiac failure. Hepatic, renal and myocardial toxicity, agranulocytosis, aplastic anemia, cerebral edema, DIC, thrombocytopenia, and skin reaction also have been reported. Management includes decontamination of skin and gastrointestinal tract, supportive care including treatment of status epilepticus, dysrhythmias, and mechanical ventilation. Mortality and morbidity rates are very high and there is no specific antidote. Atropine and catecholamines should be avoided.
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PMID:Endosulfan poisoning with intravascular hemolysis. 1797 61

Venous thromboembolism (VTE) remains the most common preventable cause of in-hospital death and D-dimer (DD) is one of the essential diagnostic tools for it. Each risk factor for VTE can raise DD and they are numerous: 24 listed in 2008 European Guidelines. Acute coronary syndrome and stroke increase DD concentration, too. Thus, all three most important causes of cardiovascular death are capable of raising DD. Recent evidence suggests DD as a sensitive marker also for acute aortic dissection. Many other processes may raise DD concentration: atrial fibrillation, congestive heart failure, disseminated intravascular coagulation, etc. The adequate DD interpretation is additionally important due to the frequent usage of the test (probably millions of times a year in the world). Simple and concise classification is much easier to remember and such one is suggested.
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PMID:Pragmatic classification of the causes of high D-dimer. 1985 27

We report a very high risk case of reoperation for pseudoaneurysm after ascending aortic replacement for acute aortic dissection in a 78-year-old man with chronic renal failure and disseminated intravascular coagulation (DIC). Computed tomography 5 years after the 1st operation showed huge pseudoaneurysm originated from the distal anastomosis and the angiogram showed moderate aortic regurgitation. Hemodialysis and congestive heart failure associated with DIC complicated his general condition. Preoperative DIC score was 7 with D-dimer of 39.8 microg/ml. The patient underwent reoperation through night anterior thoracotomy. At 20 degrees C of urinary bladder temperature, we started re-median sternotomy and ablated the adhesion. When the pseudoaneurysm ruptured, we started hypothermic circulatory arrest with selective cerebral perfusion immediately. And Bentall operation and hemi-arch replacement were performed. Postoperative recovery required long period and he was transferred to another hospital at 3 months after the surgery. Postoperative data showed reduction of DIC score to 3.
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PMID:[Reoperation for postoperative pseudoaneurysm after repair for acute aortic dissection associated with disseminated intravascular coagulation and chronic renal failure]. 1989 70


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