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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 prognosis for a patient with a severe head injury is dependent not only upon the location and the degree of this trauma, but also upon additional complications. For example, disseminated intravascular coagulation (DIC) can occur because of the thromboplastic activity of the damaged brain tissue that enters the circulation. The complement (C) system is activated by certain enzymes that cleave the clotting factors. Therefore, after head injuries we searched for C activation because it could result in the adult respiratory distress syndrome (ARDS). Patients and methods. We had two groups of patients: (1) 23 with large destruction and (2) 13 with little destruction of the brain tissue. Eighteen patients in group 1 and 8 in group 2 had isolated brain trauma. Blood samples were taken--upon arrival at the hospital and then 1, 3, 7, 12, 24, and 48 h later; after that we took weekly blood samples up to the completion of their treatment in the intensive care unit. We measured the total hemolytic serum C activity (CH50), activation of alternative pathway hemolysis (APH50), cleavage products C3a and C3d, and total protein. Furthermore, we studied the coagulation parameters of the extrinsic (prothrombin time) and intrinsic (partial thromboplastin time) pathways and fibrinogen content. From the patients records we extracted clinical parameters such as neurological status, intracranial pressure, pathological details on computer tomography hemoglobin and arterial-alveolar oxygen difference. Results. Figure 1 shows the different reactions of the C system in both groups: while patients of group 1 suffered from a decrease in total and alternative hemolytic activity, the other group increases in both parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Complement activation following head and brain trauma]. 349 78

In spite of all the scientific and technical advances in recent years, shock that is not rapidly correctable with fluid can have a morbidity rate exceeding 80%. Consequently awareness of such precipitating factors as sepsis and early diagnosis and treatment are essential. Treatment should be rapid and should follow a previously outlined protocol. Such protocols should include correction of the precipitating problem and aggressive resuscitation to assure adequate ventilation and oxygenation of the blood and optimal oxygen delivery to the tissues. Fluid and blood should be given as needed until filling pressures begin to rise rapidly with further fluid infusion. With hemorrhagic shock in previously healthy individuals, a hemoglobin level of 10.0 g/dL is usually adequate. In older, septic, or cardiogenic shock patients, a hemoglobin level of 12.5 to 14.0 may be preferable. If an optimal preload does not increase cardiac output to normal or higher levels, inotropic agents should be used. If shock still persists, one must be sure that the arterial pH is not excessively high or low. Glucocorticoids may then be given in low dose (200 mg hydrocortisone) in case some degree of adrenal insufficiency is present. They can also be given in high doses (equivalent to 150 mg/kg hydrocortisone) early in septic shock primarily to prevent excess complement activation and to preserve membrane integrity. Vasopressors may occasionally be required if there is excessive vasodilation, especially if there is persistent hypotension in the presence of high-grade coronary or cerebral artery stenosis. Vasodilators may be used to try to correct myocardial ischemia (nitroglycerin), excessive preload (nitroglycerin), or excessive afterload (nitroprusside or hydralazine). Combinations of vasodilators and inotropic agents may be required in some patients with high systemic vascular resistance and persistently low cardiac outputs. Mechanical assist with IABP can be of great value in persistent cardiogenic shock. Diuretics may occasionally help prevent renal failure in patients who are persistently oliguric after blood flow and pressure are restored. Heparin is occasionally of value if DIC develops with no concomitant fibrinolysis. Antibiotics are important in septic shock and may also be important if persistent shock has reduced gastrointestinal mucosal integrity so that bacteria and bacterial products can enter the portal system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Science and shock: a clinical perspective. 389 56

Evidence of disseminated intravascular coagulation (DIC) was sought in New Zealand white rabbits infused with autologous, hemolyzed whole blood. Hemoglobinemia was induced in 17 rabbits by rapid intravenous injection of frozenthawed whole blood. Three dose regimens yielded mean peak plasma hemoglobin concentrations of 325, 615 and 860 mg/100 ml respectively (range 260 to 1050 mg/100 ml). Eleven control animals were infused with autologous, nonhemolyzed whole blood in similar doses. Rabbits were killed at either 15, 60, 120 or 180 minutes following infusion and multiple organ biopsies obtained immediately post-mortem. Coagulation studies demonstrated no significant alterations in prothrombin time, partial thromboplastin time, thrombin time or fibrinogen. Fibrin degradation products were not found. Histologic examination of lung, heart, liver, spleen and kidney revealed no fibrin deposition, thrombus formation or other abnormalities. We conclude from our study that induction of brief, experimental hemoglobinemia in New Zealand white rabbits, utilizing moderately large doses of autologous, hemolyzed whole blood, does not result in the development of DIC.
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PMID:Coagulation studies and correlative histology during experimental hemoglobinemia in rabbits. 481 1

Disseminated intravascular coagulation as indicated by glomerular capillary thrombosis was induced in unprepared virgin rats by the infusion of endotoxin. Dose-time curves revealed that the minimal amount necessary was 0.9 mg and the time required was 3 hours. A marked difference in susceptibility between the summer and winter seasons was observed, the animals being more sensitive in the former. The platelet count decreased in a dose-related manner; however, there was no difference between an infusion and injection regimen. There was no difference in platelet numbers between the animals who had fibrin deposits and those free of fibrin. Plasma hemoglobin increased by 500% in those animals who developed glomerular fibrin deposition and the hematocrit decreased less profoundly. The data demonstrate that unprepared virgin rats can be used as an experimental model for studying glomerular fibrin deposition, the hallmark of what is generally referred to as the generalized Shwartzman reaction, if endotoxin is continuously infused rather than injected.
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PMID:Endotoxin-induced disseminated intravascular coagulation in nonpregnant rats. A new experimental model. 493 96

Although many attempts have been made to demonstrate the existence of a shock-producing toxin, little success has been attained. Traumatic shock is generally believed to be caused by simple loss of blood. Evidence is presented that tissue trauma causes hemolysis. Although hemoglobin is harmless, the stroma of the broken red cells is a clotting stimulant which, in the presence of the slow capillary flow of hemorrhagic shock, sustains a continuing disseminated intravascular coagulation. This disseminated intravascular coagulation produces a clotting defect, morbidity and death. The condition is not responsive to intravenously administered fluids but is responsive to fibrinolysin therapy.
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PMID:Mechanism of traumatic shock. 644 68

The patient, a 76-year-old man, was referred with fever, large ecchymotic lesions and ulcerative laryngitis. Blood counts showed a hemoglobin of 11 g/100 ml, hematocrit of 31%, red blood cell count of 3.5 X 10(12)/1, white blood cell count of 6.8 X 10(9)/1 and platelet count of 16.0 X 10(9)/1. The differential count showed 17% neutrophils, 4% lymphocytes, 40% promyelocytes and 39% myeloblasts. The sternal marrow sample showed a marked hypercellularity. Of the cells, 80-85% were hypergranular promyelocytes, some of them showing bundles of Auer rods. No granulocytic maturation was observed. A few erythroblasts were present. A disseminated intravascular coagulation was observed (fibrinogen 0.85 g/l, factor V 18%, fibrin degradation products 640 mg/l). The serum creatinin was at 217 micromol/1 and the urea at 16.8 mmol/1. The treatment (daunorubicin, heparin, platelet transfusion) was unsuccessful and the patient died three days after entering hospital. The bone marrow karyotype by direct examination showed only normal metaphases (32 photographed). All the metaphases from the unstimulated blood 48-h culture (25 photographed) were clonal, showing the pattern 47,XY,del(11) (q23),t(15;17) (q24? q22?), +mar. The marker was '16 like' in size but its origin could not be determined (Figs. 1 and 2).
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PMID:Acute promyelocytic leukemia with (15;17) translocation and chromosome no. 11 deletion (q23). 696 Dec 74

Intravascular hemolysis and ultrastructure of erythrocytes from liver sinusoids were studied during and after infusion of Escherichia coli endotoxin in Labrador retriever dogs. Endotoxin infusion caused hemoconcentration, and induced disseminated intravascular coagulation (DIC), characterized by a rapid drop of platelet numbers, a gradual consumption of coagulation factors and activation of fibrinolysis. Advanced DIC and circulatory shock gradually developed, and the animals died after 7-15 h. Plasma hemoglobin concentrations did not rise for several hours, but late in the experimental period a significant intravascular hemolysis was constantly found. Circulating adenosine diphosphate (ADP) did not appear. During shock, liver biopsies revealed accumulation of erythrocytes often disintegrated within distended sinusoidal lumina. In advanced shock the fragmented erythrocyte seemed to form occlusive masses within the vessels. A fibrin-like material frequently appeared adjacent to the red cells. However, it did not have the periodicity characteristic for fibrin, and the ultrastructure of the material was very similar to that inside the erythrocytes. None of these changes were induced by saline infusion in control animals. The lack of fibrin formation and the late development of intravascular hemolysis indicate that red cell breakdown was of little importance for the initiation and progress of DIC.
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PMID:Intravascular hemolysis and ultrastructural changes of erythrocytes in lethal canine endotoxin shock. 699 9

Esophageal varices were injected with 5% sodium morrhuate and a solution containing thrombin, concentrated dextrose, and cephalothin sodium using the flexible gastroscope with balloon cuff modification. Hematologic and coagulating parameters were checked before and after the procedure to look for evidence of disseminated intravascular coagulation. No effect was noted on hematocrit, hemoglobin, platelet count, haptoglobin, prothrombin time, partial thromboplastin time, fibrinogen, fibrin split products, factor V, or factor VIII. Injection sclerotherapy with currently available solutions appears to have no effect on the systemic coagulation system.
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PMID:Absence of disseminated intravascular coagulation with endoscopic sclerosis of esophageal varices. 708 44

A group of values were prospectively analyzed in 24 infants under 3 months, of age, who showed over 3% fragmented RBC's with no history of blood transfusions. Results were compared with those obtained in group of 26 infants of the same age and less than 1% fragmented RBC's. These infants with over 3% fragmented cells were found to have a significant association with: sepsis, jaundice, crenated RBC's, low levels of hemoglobin, increased reticulocyte count, and low vitamin E levels. No relationship was found with weight at birth, feeding history and disseminated intravascular coagulation. No cases of hemangioma or cardiac diseases were found. These findings are commented.
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PMID:[Jaundice caused by microangiopathic hemolysis associated to septicemia in the newborn]. 739 25

In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin < 5 g/dl (0/12), < 8 g/dl (2/12); serum creatinine > 265 mumol/l (3/12); blood glucose < 2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH < 7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia > 5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia < 30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12), < 125 mmol/l (2/12); rhabdomyolysis with creatine kinase > 1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intensive care aspects in severe tropical malaria: clinical aspects, therapy and prognostic factors]. 777 Jul 59


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