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

Dyspnea, back pain, edema, and cyanosis developed suddenly in a 23-year-old woman during the last trimester of her first pregnancy. Although she had been noticed to have the enlarged heart and exertional shortness of breath to a slight degree, she had been apparently in good condition without any significant heart murmurs. Clinically, recurrent episodes of disseminated intravascular coagulation, including pulmonary thrombosis, were thought to be superimposed to Eisenmenger syndrome associated with toxemia of pregnancy. Anticoagulant and fibrinolytic treatments were tried, but their effectiveness was limited by hemorrhagic diathesis. She died of respiratory and circulatory failure after delivery of a moribund baby. Autopsy revealed Eisenmenger complex (a defect in the membranous portion of the interventricular septum and pulmonary vascular disease) and many fresh hemmorrhages in both lungs with a lot of new and organized thrombi. Fresh thrombi were also seen in the heart, the pancreas and the kidneys. The high peripartal mortality in Eisenmenger syndrome could be attributed to pulmonary thrombosis, which may be related to DIC, as well as to peripartal changes in circulatory function.
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PMID:An autopsied case of Eisenmenger syndrome complicated by recurrent thromboembolic phenomena in postpartal period. 13 43

The concept of shock is discussed emphazising the microcirculatory disturbance implied with the resulting failure in tissular perfussion and its consequences (hypoxia, acidosis, enzymatic damage, metabolic changes). Its causes are outlined (cardiogenic, hypovolemic, septic, neurogenic, anaphylactic, endocrine); its phases, vasoconstriction, precapillary dilatiation and pooling, disseminated intravascular coagulation and hemorrhages following hypocoagulability due to an excessive consumption of factors and the fundamental elements of the clinical picture. Treatment is analyzed outstanding the necessity of an adequate and urgent correction of the disturbance in volume, stressing the importance of supplying about 400 ml. x m-2 during the first hour and the necessary monitoring of central venous pressure as the best index to control perfussed fluids. Indications for electrolytic solutions are given, including blood, platelets, plasms, albumin, dextran and manitol. The fact that respiratory failure following "shock lung" is stressed as the main cause of death and the different procedures of management are described (ventilation, intubation, oxygen therapy, tracheostomy, mechanical ventilation and use of respirators, specially the Bird type). Vasodilator drugs are described together with their indications; also, contraindications of vasoconstrictive drugs. Several complications, such as disseminated intravascular coagulation, acute adrenal failure, acute renal failure and arrhythmia are mentioned together with basic elements for prevention and treatment. Emphasis is placed on the serial control of several elementsusing a special counter in their outline: sensory, respiration including type, rythm and rate, cyanosis, central venous pressure, pulse, color of the skin, capillary filling, temperature, arterial pressure, diuresis, weight, and hydration. A careful hydrous balance is stressed. It is handled in the same counter
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PMID:[Treatment of acute circulatory failure (shock) in childhood]. 105 88

Rabbits were given polyclonal anti-tissue factor (TF) immunoglobulin G (IgG) before an injection of endotoxin to test the hypothesis that TF triggers disseminated intravascular coagulation (DIC) after endotoxin. The rabbits had been prepared with cortisone to develop DIC after one injection of endotoxin. Anti-TF IgG substantially reduced the falls in fibrinogen, factors V and VIII, and platelets noted in control rabbits given preimmune IgG before endotoxin. At autopsy 24 hours later, fibrin was present in glomerular capillaries of 4 of 5 control rabbits, but in none of 11 rabbits given anti-TF IgG. DIC was also induced in a second group of rabbits by the infusion, over 4 hours, of 1 microgram/kg of purified, reconstituted rabbit brain TF. This resulted in striking falls in plasma fibrinogen, factors V, and VIII that were diminished, but not prevented by prior treatment with anti-TF IgG. Circulating activated factor VII, induced by either TF infusion or endotoxin, could not be detected after DIC. Mean plasma extrinsic pathway inhibitor (EPI) activity did not fall significantly after endotoxin, and only to about 65% of the preinfusion after infusion of TF. Thus, DIC induced by both agents proceeded despite nearly normal plasma EPI levels. Because EPI neutralizes factor VIIa/TF in vitro only after a short lag period, the DIC that persisted for up to 6 hours after injection of endotoxin suggests that TF activity continued to be generated during this period on cells to which the circulating blood was exposed. All animals given endotoxin became ill with cyanosis, tachypnea, cold ears, and diarrhea, regardless of whether they had received anti-TF IgG to attenuate DIC. Infusion of TF caused some animals to die acutely with pulmonary arterial thromboses, but surviving animals did not appear ill. The findings support the hypothesis that exposure of blood to TF triggers DIC after endotoxin, but is not important for the pathogenesis of endotoxin-induced shock.
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PMID:Disseminated intravascular coagulation in rabbits induced by administration of endotoxin or tissue factor: effect of anti-tissue factor antibodies and measurement of plasma extrinsic pathway inhibitor activity. 231 59

A previously healthy 19-year-old woman had a febrile illness with hypotension, progressive cyanosis, and an evolving petechial rash. Despite aggressive therapy in the face of shock and disseminated intravascular coagulation, the patient suffered a cardiac arrest and could not be resuscitated. Haemophilus influenzae type b was cultured from the blood and echovirus 30 from the cerebrospinal fluid post mortem. Fulminant H influenzae type b infection in an immunocompetent adult is rare but should be recognized as a possible cause of the Waterhouse-Friderichsen syndrome.
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PMID:Waterhouse-Friderichsen syndrome caused by Haemophilus influenzae type b in an immunocompetent young adult. 259 28

Amniotic fluid embolism is a catastrophic event of the intra- and early postpartum period which may also be seen with cesarean delivery and during abortions. Presenting symptomatology includes respiratory distress with cyanosis, shock, and possibly tonic-clonic seizures. DIC frequently occurs. The pathogenesis may include entry of amniotic fluid through lacerations or ruptures of the uterus or cervix, through endocervical veins and through abnormal uteroplacental sites, such as with placental abruption, placenta previa, or placenta accreta. Amniotic fluid probably causes cardiovascular-respiratory symptoms by pulmonary vascular obstruction and through a vasoactive substance causing pulmonary vascular constriction. The lethality of amniotic fluid may be enhanced by a high particulate content or meconium staining. The diagnosis of amniotic fluid embolism may be made ante mortem by demonstrating amniotic fluid debris in central blood samples or expectorated sputum. Postmortem diagnosis often requires meticulous examination of the pulmonary microvasculature with the utilization of special stains. Treatment is directed towards symptoms of shock, arterial hypoxemia, and DIC. Acute renal failure may complicate the picture after shock. If the patient survives the embolic and coagulative problems, recovery is usually complete without long-term sequelae.
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PMID:Amniotic fluid embolism. Three case reports with a review of the literature. 402 76

Seven cases of DIC with cutaneous manifestations which permitted us to make the diagnosis. Etiopathogenic references are cited and the dermatological literature pointing out especially the cutaneous lesions with their clinical characteristics: ecchymoses which usually evolve to necrosis, bullae, petechiae, hematomas, cyanosis and bleeding at injection sites, and histological: Fibrinous thrombosis of the vessels of the dermis, with hemorrhages, necrosis and dermoepidermic bullae, with slight or no inflammation . In some of these cases the dermatological lesions antedated the characteristic laboratory data.
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PMID:[Cutaneous manifestations of disseminated intravascular coagulation syndrome. Apropos of 7 cases]. 637 31

The case of a 72-year-old man with cutaneous cholesterol emboli in association with disseminated intravascular coagulation (D.I.C.) is described. Favouring the crystal cholesterol emboli hypothesis are the livedo reticularis and purpura in the lower extremities, palpable pulses, arterioles containing cholesterol clefts. Favouring the hypothesis of D.I.C. are the purpuric lesions on the ears and nose, acral cyanosis and haemorrhagic bullae on the hands, intravascular fibrinous thrombi, hemostatic abnormalities and the efficacy of heparin. Two pathogenic hypotheses are discussed: 1) "spontaneous" crystal cholesterol emboli have started a D.I.C. following the release of thromboplastic substances; 2) a D.I.C. with its secondary fibrinolysis has provoked a dissolution of the thrombosis which covered the atheromatous plaques and started cholesterol crystal emboli.
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PMID:[Association of disseminated intravascular coagulation and cutaneous crystal cholesterol emboli (author's transl)]. 731 94

A study based on clinical analysis was conducted regarding the 125 episodes in the elderly 112 patients of sepsis who were 70 (average 83.8 +/- 7.5) years old at Nagoyashi-Koseiin Geriatric Hospital from 1985 through 1994. 1) The backgrounds of the elderly patients with sepsis were as follows: bedridden (72.8%), urinary catheter in place (61.2%), central venous catheter in place (48.8%), and prior antibiotic use (40.8%). All patients had an underlying disease. 2) Organisms isolated were Escherichia coli (21.2%), Staphylococcus aureus (18.4%); Coagulase-negative staphylococci (CNS) (17.4%) and Candida albicans (6.1%). Chronologically, the quantity of gram-positive cocci increased while that of gram-negative bacilli decreased. As the age of the patients increased, the frequency of infections by Methicillin-resistant Staphylococcus aureus (MRSA), E. coli, and/or multiple bacteria increased, while that of infections by CNS and gram-negative bacilli excluding E. coli decreased. 3) The primary infected sites were the urinary tract system (24.8%), central venous catheter (21.6%) and unknown (31.2%). 4) The primary clinical observations were fever exceeding 38.0 degrees C (88.0%), tachycardia (60.8%), shivering (44.0%) and cyanosis (32.8%). 5) Complications were multiple organ failure (33.6%), septic shock (26.4%) and disseminated intravascular coagulation (22.4%). 6) The prognosis indicated that 65.6% were survivors, and 34.4% were nonsurvivors. At the onset of sepsis, weight, blood pressure, serum albumin, and total cholesterol in the nonsurvivors were significantly lower than those in the survivors, whereas heart rate, GOT, LDH, and BUN in the nonsurvivors were significantly higher than those in the survivors.
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PMID:[Study on sepsis in the elderly at Nagoyashi-Koseiin Geriatric Hospital]. 749 17

Spontaneous aortic thrombosis in the neonate is a rare entity with a high mortality rate. The present patient, who was diagnosed after showing haematuria and cyanosis, underwent aortic thrombectomy with a Fogarty catheter through a left thoracotomy, but died of sepsis, disseminated intravascular coagulation and multiple organ failure. Autopsy revealed multiple residual thrombi in the main branches of the abdominal aorta and necrosis of the abdominal organs despite a patent thoracoabdominal aorta. In patients with no blood flow in the main branches of the abdominal aorta on preoperative examination, removal of thrombi, including those in the main branches of the abdominal aorta, might be performed in a single, early and aggressive procedure.
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PMID:Spontaneous aortic thrombosis in a neonate with multiple thrombi in the main branches of the abdominal aorta. 760 11

The maternal mortality rate associated with eclampsia ranges from 100 to 6000 per 100,000, and the perinatal mortality rate ranges from 150 to 400 per 1000. Both eclampsia and its preceding condition, pregnancy-induced hypertension, occur in varying degrees in different parts of India. The warning signs of imminent eclampsia are 1) systolic blood pressure of 160 mmHg or more on two occasions six hours apart when the patient is on bed rest; 2) proteinuria of 5 g or more in 24 hours or 3 + or more by semiquantitative assay; 3) oliguria or anuria; 4) cerebral or visual disturbances; 5) pulmonary edema or cyanosis; and 6) epigastric/right hypochondriac pain, impaired liver function, and thrombocytopenia and coagulation disorders. Eclampsia is classified as the acute fulminating type, which can occur without warning, and the insidious type. Most cases (61%) show onset of eclampsia during the prenatal period. Treatment of eclampsia involves 1) control of convulsions (through an injection of magnesium sulphate or diazepam or the intravenous administration of phenytoin); 2) correction of hypoxia and acidosis; 3) a gradual lowering of blood pressure with hydralazine hydrochloride, nifedipine, atenolol, labetalol, oxprenolol, or metoprolol); and 4) steps to effect delivery. Diagnosis of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) requires a complete blood count, blood film for platelet count and red blood cell fragmentation, and a coagulation screen for diagnosis of disseminated intravascular coagulation. Efforts to induce delivery in cases of prenatal eclampsia can take place 12-24 hours after convulsions have stopped. There is no reason to prolong pregnancy in the interests of the fetus, and in some cases Cesarean section may be required. Adequate prenatal care should allow the identification of almost every potential case of eclampsia and allow the prompt treatment of pre-eclampsia or termination of pregnancy when necessary. Medical staff must receive proper training to diagnose pre-eclampsia and treat the condition.
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PMID:Eclampsia. 765 39


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