Gene/Protein Disease Symptom Drug Enzyme Compound
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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 clinical course and radiographs of 30 patients with fat embolism syndrome were reviewed. In all cases the classic triad of neurologic dysfunction, respiratory insufficiency, and petechiae were present. Three responses to embolized fat were noted. The hyperacute response was seen in two patients with paradoxical embolization of fat to the systemic circulation. A "classic response" was noted in 18 patients with transient respiratory compromise and variable radiographic findings. The two deaths in the group responding in the classical manner were attributed to massive pulmonary emboli. The third response, noted in ten patients, consisted of a chest radiograph compatible with pulmonary edema in the clinical setting of the adult respiratory distress syndrome. In this group the degree of respiratory dysfunction and pulmonary damage correlated with the development of disseminated intravascular coagulation. Pathologic correlations are presented and the mechanisms by which embolic fat produces tissue damage are discussed.
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PMID:The three syndromes of fat embolism: pulmonary manifestations. 45 28

Patients with leukaemia, on anticoagulant therapy, or with disseminated intravascular coagulation may develop occult pulmonary haemorrhage; it will mimic pulmonary oedema, pulmonary hemosiderosis or opportunistic infections. It can be diagnosed by bronchopulmonary lavage. The radiographic changes are described and the differential diagnosis discussed in a series of 12 such patients.
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PMID:Radiographic aspects of occult pulmonary haemorrhage. 63 50

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

Five patients who had injected intravenous (i.v.) phenmetrazine or methamphetamine developed marked prostration resembling septic shock, disseminated intravascular coagulation, rhabdomyolysis with myoglobinuria, and azotemia. Soon after injection, four noted chills, fever, sweats, nausea, and abdominal cramps. Within hours, they developed vomiting, myalgias, paresthesias, headache, and orthostasis. Cardiorespiratory arrest, accelerated bleeding, and noncardiac pulmonary edema were observed in one patient. From 4 to 11 litres of saline were required in the first 24 h to maintain blood pressure and urine output, suggesting that shock resulted from massive loss of intravascular volume into necrotic muscle. Recognition of this syndrome and treatment by aggressive volume replacement led to the recovery of all five patients.
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PMID:Rhabdomyolysis and shock after intravenous amphetamine administration. 84 98

Fibrinogen content was determined for each of 50 units of citrate-dextrose-phosphate (CPD)-preserved whole blood, packed red blood cells reconstituted with 250 ml. of saline, and packed red cells reconstituted with 250 ml. of purified plasma protein fraction (PPF). The total protein and albumin were measured, by electrophoresis, on each of 10 units of the three varieties of blood. The fibrinogen content of the two types of reconstituted cells was significantly lower than that of whole blood. Although the total protein/albumin content of whole blood and PPF-reconstituted red cells was similar, saline-reconstituted cells were markedly deficient in both total protein and albumin. Low fibrinogen and platelet levels subsequent to transfusion with reconstituted packed red cells can lead to an erroneous diagnosis of disseminated intravascular coagulation. Administration of large quantities of saline-reconstituted packed cells could be an etiologic factor in postoperative interstitial pulmonary edema.
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PMID:Fibrinogen and albumin deficiencies associated with packed red blood cell transfusions. 109 Feb 9

The "shock lung syndrome," whenever associated with trauma, is probably in part the consequence of fat emboli, though aspiration, disseminated intravascular coagulation, microatelectasis, pulmonary edema, and hemorrhage due to other lung insults may be important in the etiology of many cases. When lung injury is due to fat emboli, there is an interval between the time of trauma and the onset of clinical symptoms and chest radiographic findings. The radiographic picture is that of a diffuse alveolar and interstitial lung density. In severe cases marked respiratory embarrassment requires the use of both oxygen therapy and mechanical respirators for survival.
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PMID:The fat embolism syndrome. 111 52

Patients with shock lung syndrome were identified as those who developed acute respiratory failure after a profound episode of hypotension secondary to hemorrhagic, gram-negative, or endotoxic shock. In this study, each of the 10 patients with shock lung syndrome received methylprednisolone sodium succinate, 30 mg. per kilogram, intravenously every 6 hours for 48 hours. In addition, all patients were supported with mechanical ventilation, with or without positive end-expiratory pressure (PEEP). Arterial oxygenation improved markedly, and pulmonary edema resolved in all patients. Nine were discharged from the hospital and one died subsequently of disseminated intravascular coagulation. This study demonstrated a significant improvement in mortality rate with repeated pharmacologic doses of methylprednisolone compared to previously reported mortality rates of 60 to 90 per cent in patients with shock lung syndrome treated without repeated pharmacologic doses of steroid therapy.
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PMID:Methylprednisolone. Pharmacologic doses in shock lung syndrome. 126 66

This review describes the properties and side effects of Hyskon and the implications for the patient and anaesthetist during hysteroscopy. The amount of Hyskon absorbed is dependent on the injection pressure, the extent of tissue trauma, the seal of the hysteroscope around the cervix, and the duration of infusion. The mechanism of pulmonary oedema after absorbtion of Hyskon is fluid overload, and not injury to pulmonary capillary endothelium. The haematological effects are primarily due to haemodilution. However, case reports suggest that Dextran 70 may cause a syndrome resembling disseminated intravascular coagulation. The allergic response to Hyskon consists of both an anaphylactic and an anaphylactoid component. It is recommended that hysteroscopy with Hyskon be limited to 45 min, and that all possible measures be taken to minimize tissue trauma and bleeding. The volume of Hyskon should be limited to less than 500 ml, since pulmonary oedema and coagulopathy have been described with even lesser amounts. The cumulative volume of Hyskon should be monitored frequently and the patient should be closely monitored for signs of impending pulmonary oedema.
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PMID:Anaesthetic implications of 32% Dextran-70 (Hyskon) during hysteroscopy: hysteroscopy syndrome. 128 May 35

It is well known that pulmonary influx of neutrophils is involved in lung injury in patients with adult respiratory distress syndrome (ARDS). Neutrophils are major contributors to the self-defence mechanism, however, adverse effects of neutrophils have also been recognized. Recently, we found that a highly toxic substance, 9, 10-epoxy-12-octadecenoate (leukotoxin) is biosynthesized by human neutrophils. This study was designed to investigate whether or not leukotoxin participates in lung injury in ARDS and coagulation abnormality which is often associated with ARDS. Intravenous injection of leukotoxin (100 mumol/kg) caused acute edematous lung injury, which was evidenced by increased lung weight, albumin concentrations, and angiotensin converting enzyme activities in lung lavages. Pulmonary capillary endothelial damage and pulmonary edema were observed by electron microscopy. Moreover, considerable amounts of leukotoxin were detected in lung lavage fluid of rats exposed to pure oxygen for 60 h and patients with ARDS. An increased number of neutrophils and albumin concentrations were also observed in these lavage fluids. Intravenous injection of leukotoxin (100 mumol/kg) induced coagulation abnormalities such as disseminated intravascular coagulation. Increased levels of plasma leukotoxin were detected in ARDS patients with coagulation abnormalities. These results suggest that leukotoxin biosynthesized by neutrophils is an important contributor to lung injury in ARDS and associated coagulation abnormalities.
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PMID:[ARDS and leukotoxin]. 185 3

Increased pulmonary vascular resistance (PVR) and microvascular hyperpermeability resulting in lung edema and arterial hypoxemia are mainstays in the development of adult respiratory distress syndrome (ARDS). The proposed pathophysiologic mechanisms include activation of complement and polymorphonuclear leukocytes secreting lysosomal enzymes, toxic oxygen metabolites (TOM) and eicosanoids. Platelets and coagulation factors are also involved, and in the most severe cases even monocytes are activated as reflected in release of thromboplastin. The latter may elicit disseminated intravascular coagulation (DIC). Under physiologic conditions lung blood flow is diverted from poorly to better oxygenated areas by way of hypoxic pulmonary vasoconstriction (HPV), thereby counteracting a decrease in arterial oxygenation. Many vasoactive substances have been proposed and again refuted as possible mediators of HPV. In this study we have focused on the following: histamine, catecholamines, arachidonates, calcium, phosphoinositides and TOM as well as endothelium-derived relaxing and constricting factors. Whether HPV is present in ARDS and whether it is advantageous or not seems to depend on the stage and extent of disease. We discuss possible interactions between HPV and ARDS mediators and between HPV and various vasoactive agents tested for therapeutic effects. Out of the abundance of mediators released, prostacyclin, prostaglandin E1, activated complement and platelet activating factor have been shown explicitly to inhibit HPV whereas others are suspected of doing so. In therapeutical use, prostacyclin has proved to reduce PVR and at the same time enhance cardiac output and oxygen delivery. In mild to moderate ARDS, improvement of arterial oxygenation has also been obtained employing almitrine bismesylate, a potentiator of HPV. Experimentally, adenosine effectively reduces increments in PVR and microvascular permeability with modest effects on systemic circulation. However, further investigations are warranted to decide whether adenosine or more specific blockers as, for instance, monoclonal antibodies against tumor necrosis factor should be integrated in ARDS therapy in the future.
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PMID:Hypoxic pulmonary vasoconstriction in the adult respiratory distress syndrome. 192 27


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