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

Current management of hemorrhage in cirrhotic patients is disappointing, probably because it deals only with the portal hypertension, while the coagulation disorders are neglected. Some new suggestions can be made : 1) Hemorrhage originates in coagulation disorders. The mechanical lesion of the mucosa is only the opportunity for these disorders to become apparent. The lesion may be : infrequently, a ruptured esophageal varix or a gastroduodenal peptic ulcer ; a lesion of the cardia (hiatal hernia, reflux, esophagitis, minimal traumatic tears) ; a gastric anomaly (hemorrhagic gastritis, superficial ulcerations, petechiae) ; in some cases no mucosal lesion is apparent. 2) Any widespread liver disease results in lasting hypercoagulability which is responsible for : permanent lysis, consumption, DIC. The spleen is responsible for the functional alteration of the platelets. Splenectomy is followed by permanent recovery. 3) Changes involving the platelets are responsible for most hemorrhages. Thrombopenia and severe anomalies of platelet aggregation are common findings in liver cirrhosis. Further deterioration can be induced by acetylsalicylic acid, especially if it is absorbed after an immoderate ingestion of alcohol. Emergency treatment consists in platelet transfusions. 4) Stasis in the portal system may, however, result in permanent activation of coagulation. 5) Cirrhosis results in chronic hypercoagulability and severe platelet deterioration. Any stress involving coagulation mechanisms may therefore induce hemorrhage : infection, acetyl salicylic acid, respiratory distress, estrogens, massive transfusion. It is always dangerous to "feed" consumption or to restrain lysis. 6) Coagulation tests should be performed rapidly, in order to evaluate hypercoagulability, consumption, lysis, and evidence of DIC ; FDP can probably be responsible for inflammatory changes in the liver and spleen. 8) Coagulation disorders are permanent since the hepatic alterations are irreversible.
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PMID:[Hemorrhage in liver cirrhosis : new suggestions (author's transl)]. 627 81

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

The "shock lung" syndrome may occur in diabetic ketoacidosis in association with disseminated intravascular coagulation; occasionally it occurs alone after treatment of the ketoacidosis. Two patients developed pulmonary opacities with clinical features of acute respiratory distress such as are seen in the shock lung syndrome; in both, however, the findings suggested a different mechanism from that occurring in the syndrome. Hypoalbuminaemia was prominent, and it is postulated that a low plasma osmotic pressure caused by high volume crystalloid infusions may have precipitated the acute respiratory complications. Plasma osmotic pressure may be an important variable in patients given large volumes of crystalloid infusions; further studies are required to elucidate mechanisms of pulmonary oedema in such patients.
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PMID:Acute respiratory distress in diabetic ketoacidosis: possible contribution of low colloid osmotic pressure. 640 36

Automated microanalytic chromogenic coagulation assays allow serial monitoring of critically ill newborn infants. In this study 84 premature infants [26 healthy prematures and 58 neonates with idiopathic respiratory distress syndrome (IRDS)] were studied daily during the first week of life, to investigate the possible significance of hemostatic abnormalities in IRDS. In neonates with IRDS, coagulation factors II and X, antithrombin III (AT-III), plasminogen, and alpha 2-antiplasmin were significantly lower than control values. Recovery of the initially low AT-III levels was delayed relative to the other coagulation parameters measured. An AT-III less than or equal to 0.15 U/ml was present within the first 6 h of life in eight patients who developed IRDS, seven of whom died within 48 h. Autopsy of these neonates showed widespread fibrin deposition and hemorrhage in vital organs consistent with intravascular coagulation. These findings indicate that very low levels of AT-III are associated with disseminated intravascular coagulation in neonates with IRDS and suggest that a deficiency of AT-III is predictive of a poor outcome.
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PMID:Low antithrombin III levels in neonates with idiopathic respiratory distress syndrome: poor prognosis. 672 60

Four cases of acute respiratory distress syndrome due to miliary tuberculosis are reported. All four patients had tuberculin anergy; three developed disseminated intravascular coagulation. All were treated early with anti-tuberculous drugs. Three patients were intubated and ventilated with positive end expiratory pressure, but they died shortly afterwards. The fourth patient was treated with continuous positive airway pressure and corticosteroids and survived. In view of such reports, the possibility of tuberculosis should be considered systematically in all adult patients with unexplained acute respiratory distress syndrome. The extremely rapid course of the disease and the inconsistent results of standard examinations for tuberculosis justify an "aggressive" diagnostic approach. Extra-pulmonary biopsies, notably of the bone marrow, are very helpful.
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PMID:[A rare cause of acute respiratory distress syndrome in adults: acute disseminated pulmonary tuberculosis. Four cases (author's transl)]. 702 79

A case is presented in which a fatal acute respiratory distress syndrome, associated with disseminated intravascular coagulation, developed immediately after the insertion of a peritoneovenous shunt for management of refractory ascites. The absence of left-sided heart failure or fluid overload was established by (a) lack of diuresis from intravenous furosemide; (b) repeatedly normal pulmonary wedge pressures; and (c) autopsy findings. The nature of the toxic effect of this patient's ascites upon the alveolar membrane remains obscure.
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PMID:Acute respiratory distress syndrome after peritoneovenous shunt. 706 30

We report two cases of neonatal disseminated intravascular coagulation (DIC). One case is associated with placenta previa and respiratory distress, and the other shows hemorrhage with Gram-negative sepsis. In both cases, results of autopsy show microscopic confirmation of DIC in several body tissues. One pair of eyes demonstrates intraocular hemorrhages and intravascular fibrin in the choriocapillaris (a typical manifestation) and intravascular fibrin in the ciliary body vessels of one eye. In addition, the other pair of eyes shows involvement of iris vessels, a unique finding, as is intraretinal intravascular fibrin in one eye of the same patient.
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PMID:Disseminated intravascular coagulation in infancy and in the neonate. Ocular findings. 711 64

In a patient with gestational trophoblastic disease midtrimester abortion was induced by intravenous application of prostaglandin F2 alpha. After evacuation of the uterus the patient developed a severe acute respiratory distress syndrome (ARDS). This syndrome has been described as resulting from trophoblastic emboli, hemorrhage shock, gestational osmotic imbalance or disseminated intravascular coagulation. Also an indirect side effect of prostaglandin has to be discussed. Patients who develop acute pulmonary complications after evacuation of a molar pregnancy appear to be at extremely high risk for persistent trophoblastic disease. The paper details the management and follow-up of this patient.
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PMID:[Gestational trophoblastic emboli as possible cause of an acute respiratory distress syndrome (author's transl)]. 731 29

Twenty cases of hemothorax in newborns, including 4 of our own patients, are reviewed in detail. This unusual cause of acute respiratory distress within the neonatal period was observed in 14 males and 6 females. Most of the patients were fullterm newborns. As causal factors hemorrhagic disease of the newborn (vitamin K deficiency), disseminated intravascular coagulation, arteriovenous malformations and pleural/vascular rupture are considered. The time of occurrence of bleeding symptoms ranged from 1 to 28 days of life. Sixteen out of 20 patients survived without sequelae, but in 4 cases the outcome was lethal.
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PMID:Hemothorax in the newborn. 739 66

Fatal Mycoplasma pneumoniae infection in a 30-yr-old woman is described. After 9 days of symptoms, the patient developed severe respiratory distress, rapidly progressive pneumonia, cardiovascular collapse, and acute renal failure. Death occurred 24 h after hospital admission. Postmortem examination demonstrated a diffuse membranous laryngotracheobronchitis, massive bilateral pneumonia, disseminated intravascular coagulation with widespread renal involvement, and hemorrhagic necrosis of the adrenal glands. Mycoplasma pneumoniae was isolated from the trachea, lungs, kidney, and brain, indicating hematogenous dissemination of the organism from its portal of entry in the respiratory tract.
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PMID:Fulminant Mycoplasma pneumoniae infection. Report of a fatal case, and a review of the literature. 741 24


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