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

The possible association between acute respiratory failure and disseminated intravascular coagulation was examined in eight patients with severe acute respiratory failure--a condition characterized by tachypnea, right to left intrapulmonary shunting of blood greater than 30 per cent of cardiac output, increased pulmonary artery pressure with low or normal pulmonary artery wedge pressure and roentgenologic interstitial pulmonary edema. Treatment consisted of mechanical ventilation with positive end expiratory pressure sufficient to minimize intrapulmonary shunting. There was no abnormality in platelet concentration fibrin split product concentration, fibrinogen concentration, prothrombin time or activated partial thromboplastin time during the period of most severe respiratory failure in any patient. However, mean platelet concentration fell to 90,000+/-9,000 per cubic millimeter, less than 0.001, and mean fibrin split product levels rose to 60+/-10 micrograms per milliliter, p less than 0.05, the fourth day after the onset of acute respiratory failure. No significant change occurred in other coagulation parameters. Disseminated intravascular coagulation developed in none of the patients nor was there any correlation between coagulation abnormalities and severity of acute respiratory failure that would suggest a cause and effect relationship.
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PMID:Acute respiratory failure and intravascular coagulation. 78 44

Shock continues to be associated with a high mortality rate primarily because of delays in diagnosis and therapy. To diagnose shock early, and thereby increase the chances of reversal before there is extensive deterioration of vital organs, one should look for any decrease in pulse pressure, urine output, urine sodium concentration, alertness or any increase in urine osmolarity, tachypnea or tachycardia. Systolic hypotension, oliguria, metabolic acidosis and a cold clammy skin are late signs of shock. The pathophysiology of early hypovolemic shock includes hyperventilation, vasoconstriction, cardiac stimulation, fluid shifts into the vascular system and platelet aggregation. Late shock is characterized by lysosomal breakdown, subsequent release of kinins (especially bradykinin), impaired cell metabolism and organ function, fluid shifts out of the vascular system because of capillary endothelial damage and intravascular coagulation. The primary cause of shock should not be neglected in favor of treating signs, symptoms, and laboratory data. The resuscitation from the shock process itself involves correction of pathophysiologic changes, based on objective trends and responses rather than isolated measurements. A suggested outline of therapies in order of their use includes: 1) correction of the primary problem; 2) ventilation and oxygen; 3) fluid-loading: 4) inotropic agents; 5) correction of acid-based and electrolyte abnormalities; 6) steroids ("physiologic" or "pharmacologic" doses); 7) vasopressors (especially in elderly, severely hypotensive patients); 8) vasodilators (if excess vasoconstriction); 9) diuretics (if oliguric in spite of the above), and 10) heparin (if DIC). The most common errors are 1) late diagnosis; 2) inadequate control of the primary problems; 3) inadequate fluid loading; 4) delayed ventilator assistance, and 5) excessive reliance on and use if vasopressors and diuretics.
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PMID:Shock in the emergency department. 79 60

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

We report a patient with urinary sepsis who, during intravenous urography with iodinated contrast (70 mg Na, Ca diatrizoate and meglumine) developed dyspnea, tachypnea, sinus tachycardia and moderate hypoxemia (pO2: 72 with FiO2 of 0.21). She subsequently developed adult respiratory distress syndrome (ARDS) with refractory hypoxemia (pO2: 40 mmHg with FiO2 of 0.5) and disseminated intravascular coagulation (DIC) (prothrombin index: 5%, platelets: 20,000/mm3, APTT: 102/37 min, FDP: 80 ng/ml, and fibrinogen: 120 mg %). The patient required mechanical ventilation and treatment with inotropic drugs, antibiotics, corticosteroids, plasma, platelets and erythrocytes. The outcome was favorable, and she could be discharged from the Reanimation Service 7 days after admission. In severe systemic reactions to iodinated contrasts (SRIC), ARDS and DIC are common. In our patient, the close temporal association between the administration of iodinated contrast and the development of the clinical picture made us suspect their possible causal relation. A higher predisposition to SRIC in patients with sepsis has been reported. We review the SRIC in which the anesthesiologist may play a role for reanimation.
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PMID:[Respiratory distress in adults and disseminated intravascular coagulation after administration of iodinated contrast]. 238 76

Three patients with respiratory failure resulting from miliary tuberculosis had a characteristic clinical presentation that included a long history of a prominent cough, dyspnea, weight loss, tachycardia, tachypnea, pulmonary adventitious sounds, and hepatomegaly. Hematologic investigation showed a normal white cell count with marked left shift in the morphology of white cells in all three patients, and evidence of disseminated intravascular coagulation in one patient. In only one patient was the initial sputum positive for acid-fast bacilli; in the others, invasive diagnostic procedures including lumbar puncture, bone marrow trephine, and open-lung biopsy were necessary for diagnosis. Miliary tuberculosis should be suspected in patients with adult respiratory distress syndrome of unknown etiology. Simple diagnostic procedures such as sputum, bronchial brushings, and urine examination should be followed by bone marrow trephine, liver biopsy, transbronchial lung biopsy, and lumbar puncture if physical signs of meningitis are present.
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PMID:Adult respiratory distress syndrome associated with miliary tuberculosis. 396 42

The process of adaptation for extrauterine life can be easily disturbed by respiratory insufficiency. The surfactant deficiency as well as anatomical and physiological immaturity of a newborn can be considered as etiological factors in some diseases, such as respiratory distress syndrome (RDS), transient tachypnoea (TT) syndrome, segmental atelectasis or pneumonia complicated by atelectasis. The widespread used method of treatment is based on mechanical increase of difference between alveolar and atmospheric pressure. So-called constant distending pressure (CDP) increases functional residual capacity (FRC), keeps alveoli open and finally increases oxygenation of arterial blood. During 3 years period continuous positive airway pressure by nasal route (n-CPAP) was used as only one method in 26 newborns. The newborns were treated because of RDS (15 cases) and pneumonia with atelectasis (11 cases). n-CPAP was starting with pressure 8 cm H2O (0.8 kPa) and FIO2 0.5, if atelectasis with severe dyspnea, hypoxia and forced hyperventilation were found. This method was very well tolerated. 22 newborns treated for 2-7 days--survived, 4 small-for-date babies--died. The most common cause of death was septicaemia complicated by disseminated intravascular coagulation. The moderate hyperbilirubinemia, oliguria with tissue oedema was observed in many cases. The light nostril decubitus were only complications. No pneumothorax was detected. We found n-CPAP as a simple, safe method in treatment of atelectasis in newborns.
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PMID:[Continuous positive pressure respiration by nasal route (n-CPAP) as a preferred treatment method in various types of acute respiratory insufficiency in newborn infants]. 637 92

A 44-year-old Spanish woman travelled in Kenya without doing correct malarial prophylaxis. Upon her return to Spain, she suffered from Plasmodium falciparum malaria. She was initially treated with chloroquine for three days, but her state worsened and she was admitted to our intensive care unit. On admission, parasitaemia was 22%. She had hyperpyrexia, obtundation, hypotension, tachycardia, tachypnoea, jaundice, digestive haemorrhage, petechiae in her soles, oliguria with elevation of serum uraemia and creatinine, anaemia, thrombocytopaenia, hypoproteinaemia, hyponatraemia, hypocalcaemia, metabolic acidosis and parameters of disseminated intravascular coagulation. She was given quinine, sulfadoxine-pyrimethamine and clindamycin. An exchange transfusion was performed, during which an acute pulmonary oedema appeared, initially with high pulmonary artery wedge pressure. She required mechanical ventilation for 16 days and haemodialysis for 11 days. She remained in coma and had seizures which required diazepam, phenitoin and thiopentone. She received a total amount of 22 units of packed erythrocytes, 55 of platelets and 15 of plasma. After the first week, she had nosocomial infection due to Escherichia coli, Staphylococcus and Pseudomonas aeruginosa and was treated with the corresponding antibiotics. She cured completely. This case report gives us the possibility of discussing on frequent problems in the prevention and treatment of malaria, and on the treatment of severe, life-threatening malaria in the setting of the intensive care unit.
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PMID:[Multiple organ failure in Plasmodium falciparum malaria]. 853 25

Systemic inflammatory response syndrome (SIRS) is characterized by body temperature abnormalities, tachypnea or hyperventilation, tachycardia, and leukocytosis or leukopenia. Although it is typically associated with a serious infection and referred to as sepsis, SIRS can stem from noninfectious causes, as well. We report the cases of four patients with toxic serum levels of salicylate (33.5 to 67.6 mg/dL) and SIRS, and we discuss mechanisms responsible for SIRS. Our patients showed temperature disturbances (35.5 degrees C to 39.8 degrees C), noncardiogenic pulmonary edema, and mixed acid base disturbances. Other abnormalities included coagulopathy (disseminated intravascular coagulation), encephalopathy, and hypotension. All four patients recovered from SIRS, probably due to early recognition and treatment; only one patient did not survive the hospitalization. Chronic salicylate toxicity should be considered as a cause of SIRS in the absence of a source of infection, since survival appears to be dependent on prompt diagnosis and management.
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PMID:Systemic inflammatory response syndrome caused by chronic salicylate intoxication. 863 72

This study was undertaken to correlate the clinical features and pathologic changes noted during the initial and later stages of fatal typhoid illness. Five cases who died during the initial stage of the illness (< 2 weeks from onset) had altered mental status, tachypnea, and tachycardia. Three had shock and elevation of serum creatinine values. Autopsies of all five revealed hyperplastic Peyer's patches, features of adult respiratory distress syndrome, and megakaryocytosis. Five other cases died during the later stage of the illness (> or = 2 weeks after onset). They had a left shift in peripheral blood leukocyte count. Autopsies revealed deep ileal ulcerations with or without perforation and peritonitis and intercurrent pneumonia. Three of them had disseminated intravascular coagulation. Further studies are warranted to understand the mediators of shock and tissue injuries during the initial period of the illness.
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PMID:Comparison of clinical features and pathologic findings in fatal cases of typhoid fever during the initial and later stages of the disease. 918 May 95

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


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