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

We identified 39 patients with acute cocaine intoxication and rhabdomyolysis over an 8-year period. Twenty-three of the patients (59%) demonstrated biochemical evidence for hepatic dysfunction. Sixteen of these patients had severe liver injury as defined by an alanine aminotransferase (ALT) of greater than 400 U/l (group A). Seven had an ALT between 36-399 U/l (group B) and 16 showed no evidence of liver injury (group C). In contrast to those with normal ALT, the clinical course of the group A patients was more often accompanied by profound hypotension (44 vs. 0%, p less than 0.025), disseminated intravascular coagulation (50 vs. 0%, p less than 0.005), hyperpyrexia (75 vs. 25%, p less than 0.025) and acute renal failure (81 vs. 0%, p less than 0.001). Seven of the group A patients expired (44%). Histologic examination of liver tissue obtained from post-mortem samples demonstrated extensive centrilobular and midzonal necrosis in three cases and panlobular necrosis in two others. A mild lymphocytic infiltrate with bile duct proliferation was present in each specimen. We conclude that cocaine intoxication can be accompanied by liver dysfunction which is most likely multifactorial; the presence of severe dysfunction identifies a patient with potentially significant morbidity and mortality.
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PMID:Hepatic dysfunction accompanying acute cocaine intoxication. 194 Feb 59

A veterinarian dealing with critical and trauma patients must be proficient with techniques for tracheostomy, thoracostomy tube placement for chest drainage, diagnostic peritoneal lavage, and autotransfusion. The utilization of these techniques may be life-saving in the critical patient. A tracheostomy is indicated in any patient with upper airway obstruction that cannot be managed with supplemental oxygen and/or orotracheal intubation. A tracheostomy tube with an inner cannula is preferred. Tracheostomy tubes should be cleaned at 3- to 4-h intervals, and methods should be employed to decrease thick tracheal secretions and to remove them from the trachea. A patient with a tracheostomy tube should be monitored continuously. A thoracostomy tube is indicated in any patient with large and/or continuous accumulation of air, blood, fluid, or chyle in the pleural space. The thoracostomy tube should be at least the same size as the patient's main stem bronchus. The thoracostomy tube is placed aseptically at the seventh intercostal space at the junction of the upper one third and lower two thirds of the lateral chest wall. Fluid or air may be removed from the chest intermittently with a three-way stopcock attached to the thoracostomy tube and a 60-ml syringe. If continuous drainage is needed, a continuous underwater seal and suction system should be used. Diagnostic abdominal paracentesis and peritoneal lavage are useful techniques in the determination of abdominal trauma, hollow viscus rupture, peritonitis, hepatic trauma, and urinary system trauma. When a multiholed catheter and lavage are used, the accuracy of detecting abdominal trauma is 95 per cent. When only needle paracentesis is used, the accuracy drops to 47 per cent. Abdominal lavage fluid can be analyzed for bacteria, whole blood, white blood cells, free bilirubin, creatinine, blood urea nitrogen, amylase, alkaline phosphatase, and alanine aminotransferase. Large volumes of whole blood recovered from abdominal or thoracic paracentesis can be reinfused into the patient if needed, providing it is not contaminated or markedly hemolyzed. The blood should be collected aseptically into blood bottles or bags. If the bleeding is ongoing or the blood only a few hours old, anticoagulants should be used. If the hemorrhage is several hours old, then clotting and defibrination has already occurred and the blood can be collected into "dry" bags or bottles. Before use, abdominal blood should be analyzed for urine, bile or fecal contamination. Blood collected from the thoracic cavity is much less likely to be contaminated. Autotransfused blood is administered through a standard blood administration set.
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PMID:Critical care surgical techniques. 268 82

Erythema multiforme major and disseminated intravascular coagulation developed in a dog 24 hours after exposure to a d-limonene-based insecticidal dip. Clinical signs included severe lethargy and weakness, ulceration of the oral mucosa, and erythematous serpiginous, annular, and arciform lesions on the head, trunk, and limbs. Clinicopathologic abnormalities included leukocytosis with neutrophilia, normocytic normochromic anemia, thrombocytopenia, prolongation of prothrombin and partial thromboplastin times, increased fibrin degradation products, hypoproteinemia, hyponatremia, hypochloremia, azotemia, high serum alanine aminotransferase and alkaline phosphatase activities, and high serum bilirubin concentration. Despite intensive supportive care, the dog developed severe intrathoracic and abdominal hemorrhage and died. Necropsy revealed severe diffuse epidermal necrosis and widespread hemorrhage within organs. Insecticidal dips containing d-limonene have the potential to induce various toxic effects, including, possibly, erythema multiforme major, and should be used cautiously.
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PMID:Erythema multiforme major and disseminated intravascular coagulation in a dog following application of a d-limonene-based insecticidal dip. 759 26

Experimental infection of three indigenous breeds of sheep in Nigeria, namely the West African Dwarf (WAD), Yankasa and Ouda resulted in fatal disease with the Zinga Rift Valley Fever virus. Infected sheep of the three breeds responded by pyrexia within 24 h of infection, that lasted 6 to 7 days, but peaked between day 2 and 4 post-infection. Viraemia coincided with pyrexia and peaked (10(9) PFU/ml) 3 days p.i. in Yankasa and WAD sheep, but with highest titre (10(7.5) PFU/ml) in Ouda sheep. Zinga Rift Valley Fever virus infection of sheep was characterised by hyperactivity, watery and mucoid nasal discharges, projectiles and bloody diarrhoea, external haemorrhage and clinical manifestations of nervous disorders. Viraemia was followed by low level of antibody development in all the infected sheep. Haemotological changes included a sharp fall in the PCV, Hb concentration and total RBC count during the course of the disease. These changes were most severe in the Yankasa, followed by WAD and Ouda breeds. There were thrombocytopaenia, prolongation of prothrombin and clotting times in all the infected sheep. There was also progressive leucopaenia associated with lymphopaenia. The total protein and albumin levels were depressed, but the globulin level rose from day 5 p.i. The changes in the serum biochemical constituents included sharp and progressive increase in the level of alanine aminotransferase and aspartate aminotransferase. The sodium level decreased gradually while that of potassium was initially stable but later increased until the infected animals died. There was a significant increase in the level of blood urea nitrogen from day 3 p.i. that continued until the infected animals died. Gross and microscopic examinations of the carcasses of the infected sheep showed significant lesions in many organs, including disseminated intravascular coagulation.
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PMID:Experimental infection of three Nigerian breeds of sheep with the Zinga strain of the Rift Valley Fever virus. 888 13

Clinical, clinico-pathological and serological studies were performed in sheep experimentally infected with Babesia ovis. Acute babesiosis occurred in all the lambs infested with adult Rhipicephalus bursa ticks and in one lamb infested with the larvae. The rate of parasitaemia and the degree of anaemia were not correlated. Decrease in the packed-cell volume ranged from 30 to 40%. Parasitized erythrocytes were not observed to block capillaries in the brain, which explained the absence of nervous symptoms in acute babesiosis. The kidneys were the most severely affected organs, exhibiting acute glomerulonephritis. The lesions observed were suggestive of vascular alteration and vascular stasis, leading to anoxia of the tissues. A disseminated intravascular coagulation (DIC) syndrome was recorded in sheep infected with babesiosis. A marked increase in the enzymes of the transaminase groups, mainly aspartate aminotransferase (AST), was observed. Enzymatic changes (increases in AST, alanine aminotransferase (ALT) and lactic dehydrogenase (LDH) and decreases in sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP) and malic enzyme (MEZ)), decreases in total proteins and albumin, and increases in urea and creatinine might reflect the degree of severity of the damage to the liver and kidney tissues. Most of the lambs (85%) that were infested with larvae, and all lambs infested with adult R. bursa ticks, reacted serologically to B. ovis antigen. The serological reactions following infestation with the larvae occurred much later than those following infestation with the adult stage. The lambs which were infested with larvae showed mild clinical reactions when challenged by infected R. bursa adults, as compared with the reactions to the challenge in naive control animals. The serological findings, in addition to the fact that one splenectomized lamb reacted to larval infestation with acute ovine babesiosis, show that the preimaginal stages of R. bursa can transmit B. ovis, usually causing a sub-clinical disease. It is suggested that infections derived from preimaginal ticks in the winter can preimmunize sheep for the subsequent more severe infections derived from adult ticks in the summer. Furthermore, in the absence of a reliable vaccine against B. ovis, grazing flocks in the enzootic regions should be exposed to the preimaginal stages during their activity period (October-February) before exposure to the adult ticks in spring and summer (April-July).
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PMID:Clinical, clinico-pathological and serological studies of Babesia ovis in experimentally infected sheep. 978 Aug 25

A twenty-year-old woman with anorexia nervosa (body mass index=11) suffered from severe liver dysfunction (aspartate aminotransferase 5,000 IU/l, alanine aminotransferase 3,980 IU/l, prothrombin time 32%), hypoglycemia (serum glucose 27 mg/dl), and pancreatic dysfunction (amylase 820 IU/l, lipase 558 IU/l). She fell into a depressive state with irritability, which was not improved by intravenous glucose. Despite treatment with plasmapheresis for the liver dysfunction, she subsequently developed pulmonary edema, acute renal failure, gastrointestinal bleeding, and disseminated intravascular coagulation. Hemodialysis, mechanical ventilation and drug therapy including prednisolone, prostaglandin E1, and branched-chain amino acid, improved her critical condition. In this case, malnutrition may have been the cause for the liver dysfunction and subsequent complications.
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PMID:Anorexia nervosa with severe liver dysfunction and subsequent critical complications. 1043 64

Use of hyperthermia in the treatment of cancer and viral infection has received renewed interest. However, the in vivo relationship between hyperthermia and direct versus indirect effects upon hemostasis are incompletely defined, although we do know that disseminated intravascular coagulation (DIC) is a common sequel to heat stroke. The purpose of the present study was to more precisely define the relationship between hyperthermia and derangements of hemostasis, thereby providing a guideline for the development of safe hyperthermia treatment regimens. The present investigation examined the in vivo effects of high-grade whole-body hyperthermia (WBH) (42.5 degrees C, 90 min) on hemostasis in a canine model. Induction of hyperthermia via extracorporeal circulation of heated blood (ECC-WBH) caused thrombocytopenia, increased plasma fibrin degradation products (FDPs), prolonged clotting times, increased serum liver enzymes, and evidence of spontaneous bleeding. However, when WBH was induced by peritoneal lavage (PL-WBH), transient thrombocytopenia was the only significant alteration. Temporal correlation between hemostatic alterations and elevations in serum alanine aminotransferase (ALT) levels in the ECC-WBH treatment group suggested that liver injury is responsible, at least in part, for the coagulopathy associated with high-grade hyperthermia and that in the absence of liver injury, identical degrees of hyperthermia cause only incidental decreases in platelet numbers.
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PMID:Alterations in hemostasis associated with hyperthermia in a canine model. 1091 78

The effect of urinary protein C inhibitor (uPCI) on disseminated intravascular coagulation (DIC) was investigated using an experimental DIC in rats. uPCI (0.5 and 1.0 mg/kg) was continuously administrated into the left femoral vein of the rats with lipopolysaccharide (50 mg/kg)-induced DIC. In all doses, uPCI significantly prevented the drastic changes in the parameters such as fibrinogen concentration, activated partial thromboplastin time (APTT), prothrombin time (PT), fibrin/fibrinogen degradation products (FDP) level, aspartate amino-transferase (AST) level and alanine aminotransferase (ALT) level. Furthermore, uPCI significantly inhibited the increase in the levels of plasma kallikrein and thrombin which act not only as the procoagulant proteases but also as the chemotactic factors to neutrophils and monocytes. These results show that uPCI may prevent hypercoagulation, the induction of secondary fibrinolysis and organ failure in the DIC model. Therefore, uPCI may be a useful agent for the clinical treatment of DIC.
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PMID:Effect of urinary protein C inhibitor on lipopolysaccharide-induced disseminated intravascular coagulation in rats. 1092 70

We compared urinary protein C inhibitor (uPCI) with low molecular weight heparin (LMWH) in terms of the effect on the pathophysiology of disseminated intravascular coagulation (DIC), such as hypercoagulation, induction of secondary fibrinolysis and organ failure, using lipopolysaccharide (LPS)-induced DIC in rats. The uPCI (0.5 and 1.0 mg/kg) administration significantly inhibited both the decrease in fibrinogen level and the increase in fibrin/fibrinogen degradation products (FDP) level, and the effects compared favorably with those of LMWH (100 and 200 IU/kg). Both uPCI (0.5 and 1.0 mg/kg) and a low dose of LMWH also inhibited the increases in the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), thrombin, and plasma kallikrein equally, but a high dose of LMWH did not inhibit the changes in those parameters. Furthermore, uPCI dose-dependently prevented the prolongation of activated partial thromboplastin time (APTT), while LMWH excessively prolonged APTT at a high dose. These results suggest that the preventive effect of uPCI on the pathophysiology of DIC compares favorably with that of LMWH, including the lack of a hemorrhagic reaction in contrast to LMWH.
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PMID:Urinary protein C inhibitor as a therapeutic agent to disseminated intravascular coagulation (DIC): a comparison with low molecular weight heparin in rats with lipopolysaccharide-induced DIC. 1099 2

We investigated the relationship between endothelin, a potent vasoconstrictor peptide, and the pathophysiology of disseminated intravascular coagulation (DIC), using two models of DIC. Experimental DIC was induced by sustained infusion of 50 mg/kg lipopolysaccharide (LPS), or 3.75 U/kg thromboplastin, for 4 h via the rat tail vein. The effect of administration of a non-selective endothelin receptor antagonist (TAK-044) (2, 10, or 50 mg/kg, from -0.5 to 4 h) on thromboplastin-induced DIC was not significant. However, LPS-induced elevation of alanine aminotransferase, creatinine and glomerular fibrin deposition was significantly suppressed by co-administration of TAK-044 in a dose-dependent manner, although no effect of TAK-044 was observed on the platelet count, fibrinogen concentration or the level of thrombin-antithrombin complex. Moreover, plasma levels of D-dimer, which reflect the grade of fibrinolysis of cross-linked fibrin, were significantly increased by co-administration of each dose of TAK-044 in the LPS-induced DIC model in rats. Our results suggest that vasoconstriction, as well as depressed fibrinolysis, contribute to severe organ dysfunction in LPS-induced, but not thromboplastin-induced, DIC, and that endothelin plays a role in the development of organ injury in LPS-induced DIC in rats.
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PMID:Relationship between endothelin and the pathophysiology of tissue factor-induced and lipopolysaccharide-induced disseminated intravascular coagulation in rats: a study examining the effect of an endothelin receptor antagonist. 1538 27


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