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

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

A survey is given on disturbances in tissue homeostasis induced by hypovolemic shock conditions. Fluid shifts taking place between the extra- and intravascular fluid compartments are important early compensatory responses following hypovolemia. Usually the supply-to-demand ratio of oxygen in most tissues can however, not be kept up if the hypovolemic insult is severe due to deterioration of the microcirculation. Cellular hypoxia will ensue and may with time affect the integrity of the cells. Cellular functional disturbances occur earlier and are more pronounced in peripheral non-vital tissues such as e.g. skeletal muscle than in central organs, the blood flow of which is more favoured during shock. Anaerobically produced cellular metabolites as well as intracellular components released from hypoxically injured cells in peripheral tissues may be of importance for the initiation of decompensatory reactions. Cellular components reaching the central circulation may induce direct effects on organs or systemic effects due to activation of the cascade systems. Thereby reactions leading to severe complications such as adult respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC) and multiple organ failure may be started. The aim of shock treatment should be to reverse as rapidly and as efficiently as possible the pathophysiological disturbances induced by a shock state. If the cellular hypoxic insult can be limited then the incidence of systemic complications in the post-shock period will also be reduced.
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PMID:Pathophysiology of shock-induced disturbances in tissue homeostasis. 390 99

Therapeutic measures for acute pancreatitis depend on the severity of the disease and its complications. Since complications of acute pancreatitis may develop at any time, patients should be admitted to an intensive care unit for assessment (and frequent reassessment) of the severity of the disease and the development of complications. Basic therapy should include relief of pain, total fasting, nasogastric suction, parenteral replacement of fluids, electrolytes, albumin and blood, and antibiotics. Hyperglycaemia should be corrected and heparin should be given in cases of disseminated intravascular coagulation. In renal insufficiency, peritoneal dialysis is important, and in respiratory complications, humidified oxygen or artificial ventilation including positive and expiratory pressure therapy should be applied. Although the effect of peritoneal dialysis has been proven only in animal experiments and in retrospective studies in man, it is recommended in severe cases for shock therapy and for correction of electrolyte imbalance when ascites is present, even before anuria occurs. Conservative treatment measures in chronic pancreatitis are limited to the management of pain and of exocrine and endocrine pancreatic insufficiency.
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PMID:Acute and chronic pancreatitis. An update on management. 608 59

Central venous plasma concentrations of thromboxane B2 (TXB2) the stable metabolite of the vasoconstrictor platelet aggregator thromboxane A2, were measured in 12 patients with septic shock. In 8 patients dying with septic shock the concentration of plasma TXB2 (912 +/- 250 pg/ml) was ten times higher than that in 4 survivors of septic shock (92 +/- 25 pg/ml) and 6 controls (91 +/- 18 pg/ml). Prothrombin time and partial thromboplastin time were significantly prolonged in nonsurvivors compared with survivors. Similarly, the alveolar-arterial oxygen gradient was significantly raised in nonsurvivors (233 +/- 39 mm Hg) compared with survivors (112 +/- 47 mm Hg). This study demonstrates that the metabolism of arachidonic acid to thromboxanes is increased in patients dying of septic shock and this raises the possibility that thromboxanes may be involved in the disseminated intravascular coagulation and respiratory distress syndrome associated with severe sepsis.
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PMID:Plasma thromboxane concentrations are raised in patients dying with septic shock. 612 85

To study the haemodynamic, cellular and humoral changes seen during septicemia-endotoxinemia a relatively large animal is needed. Pigs are satisfactory in size but have a tendency to develop malignant hyperthermia reaction to stress situations and certain anaesthetic agents. This problem was solved using a screening test of halothane exposure. When later used for experiments, the nonresponding pigs developed the typical hypokinetic low-flow state after endotoxin challenge seen in the advanced stage of septicemia in man. Decreased number of circulating leucocytes and platelets, increased tissue thromboplastin production in monocytes, and a significant coagulation disorder (DIC) were observed. Release of oxygen radicals and lysosomal enzymes from leucocytes could be estimated. Endotoxin levels in plasma were easily measured. This pig model of controlled endotoxinemia correlates well with some important haemodynamic, cellular and humoral reactions observed during human in vivo observations and in vitro studies. This model may thus be a valuable tool in clinical research of endotoxinemia and septicemia.
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PMID:Controlled endotoxinemia in pigs. A suitable model for in vivo studies of some haemodynamic, humoral and cellular reactions. 653 28

A clinicopathological correlation of the lungs on 68 cases dying from burns was carried out. The patients were divided into two main groups. Those in which the burns were the main cause of death (30 cases) and the others that had other serious underlying pathology as well as burns (38 cases). The cases were analysed sequentially in order that the evolution of the pulmonary changes could be studied. Note was made of the level of inspired oxygen received by the patient. The pulmonary changes were similar in both cases. In the first 48 h there was congestion of the alveolar walls, capillary proliferation, interstitial and intra-alveolar oedema and intra-alveolar haemorrhage. 'Giant endothelial cells' appeared at 24 h. After 48 h there were many of these structures along with intravascular microthrombi denoting disseminated intravascular coagulation. Pneumonia and septicaemia were common findings after 48 h. In some of the septicaemic patients there was basophilic staining both in the blood vessel wall as well as inside the lumen. Hyaline membranes were uncommon, being found in only four cases. Similarly interstitial and intra-alveolar fibrosis were uncommon. Interstitial fibrosis was present in only 8/30 cases where burns were the main cause of death, and in some of these there were other causes for the fibrosis. No correlation was found between the presence of hyaline membranes, interstitial fibrosis and the percentage or duration of oxygen therapy. These findings once again question the validity of the concept of oxygen toxicity in man.
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PMID:The lung parenchyma in burns. 687 85

The infusion of ascitic fluid from the peritoneal cavity into the central venous circulation may relieve massive intractible ascites, and improve renal function when hepatorenal syndrome is present. preoperative preparation of these patients includes investigation of hepatic, renal, pulmonary, cardiac and neurological function, correction of electrolyte and coagulation abnormalities, restoration of normal fluid balance and the provision of supplemental vitamins and calories. Premedication is achieved with an oral benzodiazepine or an intramuscular injection of a narcotic agent. General anaesthesia is provided by thiopentone, suxamethonium, nitrous oxide, oxygen, pancuronium and a narcotic, with intermittent positive pressure ventilation. Close monitoring of cardiac, respiratory and renal function is imperative perioperatively. Postoperatively, supervision in an Intensive Care Unit is advised as complications such as cardiac failure, septicaemia and disseminated intravascular coagulation may occur.
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PMID:The anaesthetic and perioperative management of the patient undergoing insertion of a peritoneo-venous shunt. 710 37

A severe shock is produced in 18 mongrel dogs by standardized bone trauma and haemorrhagic shock. Impairment of microcirculation is demonstrated by acidosis, reduced oxygen uptake and disseminated intravascular coagulation (DIC). Further, a specific increase in pulmonary vascular resistance--independent of the reduction in blood flow--is evoked, concomitantly with the occurrence of microthrombi, oedema and haemorrhage in lung tissue. Pretreatment with heparin inhibits disseminated intravascular coagulation and reduces impairment of microcirculation and the consecutive damage of intestinal organs. However increase of pulmonary vascular resistance is unchanged and pulmonary haemorrhage is pronounced. Therefore heparin pretreatment enhances pulmonary histologic impairment after trauma and haemorrhagic shock.
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PMID:[Pretreatment with heparin in experimental trauma and haemorrhagic shock]. 712 76

The renal venous thrombosis is mostly produced by severe dehydration. The following, however, are also predisposing factors: infections, birth traumata, paranephritic processes, lack of oxygen, diabetes of the mother and cyanotic heart defects. The diagnosis is correctly made by means of the palpable flank tumor, the macrohematuria, together with the urogram and sonography. The most urgent therapeutic measure is the balancing of the water and electrolyte deficit to eliminate the dehydration, i.e. the existing oliguria or anuria. The therapy is primarily always conservative. In the event of a consumption coagulopathy, a therapeutical attempt can be undertaken with heparin but if this is unsuccessful, an immediate nephrectomy must be performed. A further nephrectomy will be necessary if hypertony persistent infection and renal atrophy occur. Two infants with renal venous thrombosis were used for this study on the causes and diagnosis of, and the therapy for the illness.
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PMID:[Renal venous thrombosis in the newborn (author's transl)]. 746 39

A 71 year-old man with adult onset Still's disease was admitted to our hospital because of fever, sore throat, myalgia and macular nonpruritic salmon pink eruption. He was treated with prednisolone, 40 mg daily and these symptoms disappeared. When the dose of prednisolone was reduced to 30 mg daily, he began to notice fever. 5 days later he developed adult respiratory distress syndrome (ARDS). The dose of prednisolone was increased to 50 mg daily and oxygen administration was started. All symptoms began to improve immediately and the dose of prednisolone was decreased to 40 mg daily. 10 days later he noticed fever and skin rash. Laboratory investigation showed platelet counts of 69,000/mm3, a ferritin of 37,000 ng/ml, and increased fibrinogen degradation product, indicating increased activity of adult onset Still's disease associated with disseminated intravascular coagulation (DIC). The dose of prednisolone was again increased to 60 mg daily, and 100 mg of nafamostat mesilate was administrated intravenously. All above symptoms associated with adult onset Still's disease and DIC disappeared. The dose of prednisolone was gradually decreased and the clinical course was uneventful with daily administration of 10 mg of prednisolone. Although there are a couple of case report which described the association of adult onset Still's disease with either ARDS or DIC, the association of adult onset Still's disease with both ARDS and DIC have not been reported yet.
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PMID:[A case of adult onset Still's disease complicated with adult respiratory distress syndrome and disseminated intravascular coagulation]. 755 55


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