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

Hypertension during pregnancy and its complications are the most important cause of maternal and foetal death and morbidity. The chronic primary hypertension can be differentiated from the dysgravidia by anamnestic, biological, clinical and technical investigations. However the diagnosis remains difficult and the renal needle biopsy can help to ascertain it. The pathogenesis of dysgravidia is still obscure: the placental ischemia leads to a slow disseminated intravascular coagulation state with renal injury, while a vascular hyperreactivity leads to an increase of the resistance, a relative hypovolemia and lowering of cardiac output. The treatment and remote prognosis of the hypertensive disease associated with the pregnancy are summarized. The antihypertensive drugs improve the maternal prognosis while jeopardize the foetal outcome.
Acta Cardiol 1977
PMID:[Hypertension and pregnancy]. 30 56

Standardized bone trauma by means of open osteotomy is performed on both hind legs of 16 out of 24 anaesthetised mongrels. During the following 6 hours the most important parameters of blood coagulation and the serum lipids are estimated at regular intervals. Subsequently in a number of the animals 50% of the total blood volume is withdrawn continuously over a period of one hour. All animals without the preceding trauma survive the hemorrhage. The animals in the trauma group die on the average 42 minutes after the beginning of the hemorrhage. The trauma causes an acute decrease in total platelet count (GTZ) to 40% of the pretraumatic value. During an initial phase of hypercoagulability there is a formation of reversible microaggregations containing platelets and fibrin, caused by an increased turnover of coagulation factors. Secondary fibrinolysis develops in the traumatised animals. A further increase in coagulation is caused by the following hemorrhage. In combination with decreased and inhibited fibrinolysis, a disseminated intravascular coagulation state is found and results in irreversible pulmonary microthrombosis. Massive pulmonary fat deposits cannot be found histologically in spite of an increase in serum triglycerid levels to 35% above the pretraumatic values. In dogs great amounts of fat are filtered by the glomeruli and are demonstrable in the tubular epithelium. Histological examinations show a marked disseminated pulmonary microthrombosis of platelets, fibrin and fat in those animals with trauma and hemorrhage. Only the accompanying hypovolemia produces the characteristic histologic changes of the so-called Pulmonary Microembolism Syndrome.
Basic Res Cardiol
PMID:[Pulmonary microembolism: pulmonary hemodynamics following trauma and hemorrhage (author's transl]. 119 Dec 8

The authors report a case of chronic dissection of the aorta discovered during the evaluation of disseminated intravascular coagulation. The first signs of bleeding occurred 4 years after the initial aortic trauma at the time of unclamping of the aorta during an aorto-coronary bypass. This case was characterised by the severity of coagulation abnormalities, the severe thrombocytopenia and that of platelet aggregation events.
Ann Cardiol Angeiol (Paris) 1991 Nov
PMID:[Disseminated intravascular coagulation and chronic aortic dissection]. 177

A 3-month-old male infant died of tricuspid valve nonbacterial thrombotic endocarditis complicating disseminated intravascular coagulation. The vegetations were so extensive as to cause tricuspid atresia and led to congestive right ventricular failure terminating in death. The diagnosis was made only at post mortem.
Int J Cardiol 1989 Mar
PMID:Endocarditis in an infant causing "tricuspid atresia". 270 18

Known variously as disseminated intravascular coagulation, defibrination consumption coagulopathy or, more simply, as defibrination, disseminated intravascular coagulation is a serious epiphenomenon that occurs most often as a complicating factor of an underlying disease process. Although frequently triggered by underlying disease such as infection or tumor, if not recognized and treated appropriately, disseminated intravascular coagulation alone may lead to the patient's death as a result of hemorrhage or thrombosis, or both, of vital organs. Frequently, it may only manifest itself as an abnormality of coagulation tests, causing no immediate problem for the patient, and potentially normalizing when the inciting cause is appropriately managed. The central process that marks disseminated intravascular coagulation is the generation of thrombin in the circulating blood by means of the activation of the coagulation mechanism, leading to the conversion of fibrinogen to fibrin, which, in turn, may lead to thrombosis mainly of the microcirculation. Because platelets and coagulation factors are consumed and fibrinolysis is enhanced during the coagulation process, hemorrhage may also ensue. Although disseminated intravascular coagulation is frequently encountered in medical and obstetric patients, the difficulty in diagnosis and controversy regarding optimal therapy are frustrating for both patient and physician. By understanding the pathophysiology of disseminated intravascular coagulation and combining clinical observation and laboratory data, one can arrive at the appropriate diagnosis. Therapy must be individualized, and assessment of the benefit versus risk ratio of intervention must be made. Early recognition of acute and life-threatening disseminated intravascular coagulation can be lifesaving with appropriate supportive measures.
J Am Coll Cardiol 1986 Dec
PMID:Disseminated intravascular coagulation. 353 68

Bleeding remains a serious problem in patients with ventricular assist pumping (VAP). Clinical and hemostatic laboratory data in 24 patients who could not be separated from cardiopulmonary bypass (CPB) at the conclusion of open heart surgery and who underwent VAP for 54 to 610 hours were analyzed. The most important variable that correlated with the occurrence of severe bleeding was the duration of CPB: 5.2 +/- 1.6 hours in 13 patients with excessive bleeding, vs 3.6 +/- 1.1 hours in 11 patients with "acceptable" levels of bleeding (p less than 0.01). Moderate thrombocytopenia occurred in all patients but did not appear to be a major contributing factor to excessive bleeding. Disseminated intravascular coagulation (DIC) occurred in 12 patients, 4 of whom were in cardiogenic shock. DIC also correlated with time on CPB: 5.2 +/- 1.7 hours for patients with DIC, vs 3.7 +/- 1.1 hours for patients without DIC (p less than 0.01). No correlation was noted between the duration of VAP and the occurrence of DIC or bleeding.
Am J Cardiol 1984 May 01
PMID:Hemostatic abnormalities associated with prolonged ventricular assist pumping: analysis of 24 patients. 671 36

Controversy exists regarding the effect of defibrination on spontaneous echo contrast and flow dynamics in left atrial appendage (LAA) in atrial fibrillation. We aimed to investigate the effect of batroxobin, which decreases plasma fibrinogen level, on the echo intensity of spontaneous echo contrast in LAA. In 36 patients with atrial fibrillation (duration 7 +/- 4 years), transesophageal echocardiography was performed at baseline and 24 hours after batroxobin administration (0.2 U/kg). At the orifice of the LAA, integrated backscatter of echo contrast and peak velocity of LAA emptying flow were measured. Plasma fibrinogen and whole blood viscosity were also measured. Fibrinogen and viscosity were significantly lower after batroxobin administration (96 +/-38 mg/dl and 4.35 +/- 0.56 cp) than those at baseline (320 +/- 61 mg/dl and 4.71 +/- 0.61 cp, both p <0.001). A significant positive correlation between changes in plasma fibrinogen and whole blood viscosity (r = 0.49, p = 0.002) was shown. The integrated backscatter significantly decreased from 14 +/- 3 to 12 +/- 3 decibels after batroxobin (p <0.001), and the changes in integrated backscatter and plasma fibrinogen was significantly correlated. Therefore, batroxobin administration improved blood rheology and decreased blood cell aggregation, which are effective in preventing left atrial thrombus formation.
Am J Cardiol 1999 Oct 01
PMID:Effect of batroxobin on spontaneous echo contrast and hemorheology in left atrial appendage in atrial fibrillation assessed by transesophageal echocardiograpy. 1051 80

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.
 ...
PMID:Sepsis-associated purpura fulminans in adults. 1125 35

Infectious endocarditis following cardiac surgery, particularly that caused by methicillin-resistant Staphylococcus, aureus is a rare and highly lethal complication. We report a case of a 2-year-old girl who developed methicillin-resistant S. aureus endocarditis and mediastinitis following the intracardiac repair of tetralogy of Fallot using Dacron patches. The patient enveloped severe bacteremia accompanied by disseminated intravascular coagulation and progressive enlargement of vegetation. Despite this condition, the patient was successfully treated by repair using double autogenous pericardial patches. Aggressive removal of foreign material and replacement with autogenous tissue resulted in a favorable outcome.
Pediatr Cardiol
PMID:Methicillin-resistant Staphylococcus aureus endocarditis following repair of tetralogy of Fallot. 1218 14

3,4-Methylenedioxymethamphetamine (MDMA, 'ecstasy') is an amphetamine synthetic analog widely used as an recreational drug. Acute and severe toxic effects following MDMA ingestion include hyperthermia, arrhythmias, rhabdomyolisis, disseminated intravascular coagulation, hepatotoxicity and even death. Recently, we treated a patient in whom hyperkalemia, in the absence of renal failure, aggravated the expected toxic complications of MDMA, becoming the immediate cause of his death.
Int J Cardiol 2004 Feb
PMID:Hyperkalemia in fatal MDMA ('ecstasy') toxicity. 1497 67


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