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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

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

A rapidly growing haemangioendothelial sarcoma of the liver in a twenty-two year old woman was treated by liver transplantation. Disseminated intravascular coagulation resulted in massive blood loss during surgery, and contributed to the death of the patient from respiratory failure on the fourth post-operative day, despite continuous post-operative intermittent positive-pressure ventilation. Other factors leading to her respiratory failure are discussed. There was no evidence of dysfunction in the transplanted liver.
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PMID:Respiratory failure after liver transplantation. 110 48

The sick neonate may develop spontaneous or catheter-related thromboses, which must in part reflect poor regulation of the formation and activities of the coagulation enzyme, thrombin. We hypothesized that the balance between the generation and inhibition of thrombin may differ in sick neonates compared with healthy neonates. Fifty neonates with respiratory failure requiring mechanical ventilation and 40 healthy neonates were studied on d 1 of life. All neonates had normal coagulation screening tests and a platelet count greater than 150 x 10(9)/L. Plasma pools from neonates with similar gestational age (GA), birth weight, and health status were prepared. Eight plasma pools from 40 healthy neonates of GA 30-38 wk were compared with six plasma pools from 30 sick neonates of GA 30-38 wk. An additional four plasma pools prepared from 20 sick neonates of GA less than 30 wk were studied. Thrombin generation was measured by amidolysis of a chromogenic substrate, S2238, after defibrination, contact activation, and recalcification of the test plasmas. The contributions of antithrombin III, heparin cofactor II, and alpha 2-macroglobulin as inhibitors of 125I-thrombin were quantitated by SDS-PAGE followed by autoradiography and densitometry. Thrombin generation was similar for both healthy and sick neonates of GA 30-38 wk. However, the inhibition of thrombin was impaired in plasma from sick neonates of GA 30-38 wk compared with plasma from healthy neonates of GA 30-38 wk (4.37 +/- 0.22 versus 5.21 +/- 0.21 nmol; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thrombin inhibition is impaired in plasma of sick neonates. 137 86

We describe a case of multiorgan failure after intravesical bacillus Carmette-Guern (BCG) immunotherapy for bladder cancer. A 58-year-old man with superficial transitional cell carcinoma of the bladder was initially treated by transurethral resection and intravenous chemotherapy, and then administered 11 sessions of BCG intravesically. He was administered BCG intravesically after cystoscopic examination. The next day he complained of nausea and malaise. He became hypotensive. The symptom progressed with multiorgan failure, disseminated intravascular coagulation and respiratory failure. The patient gradually improved with administration of antibiotics and corticosteroid, and hemodialysis, without antituberculous antibiotics. Intravesical instillation of BCG should not be carried out immediately after cystoscopic examination.
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PMID:[Multiorgan failure following intravesical bacillus Calmette-Guerin administration: a case report]. 141 61

The clinical features of 22 postoperative multiple organ failure (MOF) patients, comprised of 8 with arterial disease (A-MOF) and 14 with gastrointestinal cancer (G-MOF), were investigated. Differences in the operative time, blood loss, and mortality were not significant. The initial organ impaired was the lungs in 78.6% of G-MOF patients and the heart or kidneys in all A-MOF patients. Infection developed in over 80% of both groups. In many A-MOF patients, the pneumonia or septicemia developed secondary to organ failure, while intraabdominal infection triggered respiratory failure in many G-MOF patients. Our organisms in infected specimens and their antibiotic sensitivities was valuable for the early administration of effective antibiotics. Upper gastrointestinal tract bleeding was important in the prognosis of both groups and occurred more frequently in A-MOF than in G-MOF patients. Consumption coagulopathy in A-MOF patients and DIC induced by infection in G-MOF patients mainly caused such bleeding. Preoperative administration of heparin was effective in improving coagulopathy. Furthermore, measurement of intramural pH with tonometer in the stomach and gastric irrigation with oxygenated perfluorochemicals were effective in the prediction and prevention of gastrointestinal bleeding.
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PMID:[The comparison of postoperative multiple organ failure with arterial disease to that with gastrointestinal cancer]. 143 3

A 62-year-old man was admitted because of paresis of the legs and a bleeding tendency. He was diagnosed as metastatic bone cancer with disseminated intravascular coagulation (DIC). In spite of treatment, his general condition progressively deteriorated and he died of respiratory failure 13 days later. Autopsy revealed a carcinoma in adenoma in the rectum. Although the depth of cancer invasion was confined to the submucosal layer, disseminated carcinomatosis of the bone marrow and tumor emboli in blood vessels of the lung were present.
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PMID:Disseminated carcinomatosis of bone marrow from submucosal carcinoma in adenoma of the rectum. 147 66

We had a sixty-five year old male patient who suddenly complained of dyspnea and fever with pulmonary tuberculosis, severe respiratory failure, disseminated intravascular coagulation (DIC) and intractable bilateral pneumothoraces. From the first hospital day severe hypoxemia which did not respond to conventional oxygen therapy developed with a diffuse ill-defined reticulo-nodular shadow in the plain chest x-ray film. On the 2nd hospital day mechanical ventilation with 2cmH2O PEEP was introduced. Antituberculous agents as well as corticosteroids were started suspecting acute interstitial pneumonia with pulmonary tuberculosis and adult respiratory distress syndrome (ARDS). Medication was followed by the treatment of Gabexate mesilate and heparin against DIC on laboratory data. Though clinical findings and pulmonary infiltrate on chest x-ray film transiently improved, right pneumothorax occurred suddenly on the 6th day followed with left pneumothorax on the 36th day. Tube drainage of both pleural spaces and repeated instillation of thrombin-rich oxycel cotton via bronchofiberscope failed to stop air leakage. He ultimately expired on 49th hospital day. At postmortem lung had multiple bilateral bulla several of which ruptured to the pleural site and caseating necrotic area containing bacilli positively stained with Ziehl-Nielsen stain in the bilateral upper lobe. No typical caseating necrotic lesion, however, was found in the other lung tissue. Therefore, it seemed to show a chronic phase of diffuse alveolar damage (DAD).
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PMID:[A case of pulmonary tuberculosis associated with severe respiratory failure, DIC and intractable bilateral pneumothoraces]. 148 64

Blood rheologic properties and homeostasis system were comprehensively examined in 23 patients with fibrous-cavernous pulmonary tuberculosis and 58 patients with various chronic nonspecific pulmonary diseases complicated by respiratory failure. The patients were found to have signs of erythrocyte edema, their more rapid depletion, lower resistance and higher aggregation which was accompanied by increased hematocrit and normal erythrocyte count. The thromboelastograms showed that all all phases of blood coagulation were shortened and fibrinolysis was deeply depressed. There was an increase in activated partial thromboplastin and thrombin time, a reduction in the values of the prothrombin indices and antithrombin III activity and higher heparin levels. The fibrinogen level was either normal or reduced despite an increase in other acute phase reactants, followed by the appearance of large amounts of blocked fibrinogen in the blood. Analysis of the findings enabled one to regard a combination of the above changes as signs of the latent DIC syndrome. Determination of fibrin and fibrinogen degradation products in a deep and long-term inhibition of fibrinolysis loses its diagnostic significance.
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PMID:[Status of the hemostatic system in patients with chronic lung diseases]. 175 60

The infant or child who presents to the Emergency Department with bacterial meningitis may have nonspecific vague symptoms with few signs of serious illness. However, the disease is often rapidly progressive and life-threatening, and may be associated with respiratory failure, circulatory failure, increased intracranial pressure, disseminated intravascular coagulation, or convulsions, any of which may lead to a fatal outcome. It is important for the triage technician in an Emergency Department to cautiously inspect each young patient who presents with illness, carefully considering whether the presenting syndrome of symptoms and signs might be consistent with early meningitis. If the young patient is triaged in a nonemergent category, then periodic assessments of the patients waiting to be seen may ensure that, when the infant or child with an obscure presentation develops evidence suggesting this diagnosis, the triage technician will promptly notify the appropriate definitive care providers who assume responsibility for immediate definitive evaluation and stabilization. Changes in delivery of lifesaving care to the life-threatened child are being impacted by current advances in the understanding of the biochemical basis of disease at the cellular and subcellular levels. Endotoxin release into the blood causes increased production of kinins, which results in vasodilatation and increased vascular permeability. Members of the leukotriene family may also enhance vascular permeability as well as produce augmented leukocyte aggregation to vascular endothelium, vasoconstriction, and bronchoconstriction. Endotoxin activates the complement cascade and induces platelets to form reversible aggregates that may be trapped in the pulmonary microcirculation; and endotoxemia-activated platelets release serotonin, which may be associated with pulmonary hypertension. Now that we have antibiotics that are effective against organisms whose degradation produces endotoxin, there is interest in lessening the host inflammatory response to endotoxin through use of dexamethasone as an anti-inflammatory agent. Clinical trials have revealed that patients who received dexamethasone became afebrile earlier and were less likely to acquire deafness after bacterial meningitis. Because administration of antibiotics is the current specific medical therapy for this life-threatening microbial invasion, it is reasonable to continue to strive to shorten the interval between recognition of disease and specific therapy. However, new studies suggest that consequences of the complex host inflammatory response (at the cellular and subcellular level) to microbial invasion and endotoxin release from bacterial degradation are increasingly important in determining survival or severity of morbidity. Therapeutic intervention with specific antibiotics and steroid anti-inflammatory agents for modulating host responses enhances outcome.
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PMID:Emergency department stabilization of pediatric patients with bacterial meningitis. Current advances. 189 92


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