Disseminated Intravascular Coagulation and Related Syndromes: A Clinical Review

Bick, Rodger L.

doi:10.1055/s-2007-1002793

Cited by 172 publications

(478 citation statements)

References 177 publications

(229 reference statements)

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“…69 The most important therapeutic concerns in the treatment of DIC in horses are elimination of the primary disease process and maintenance of adequate tissue perfusion.63,6437',80 Heparin may be therapeutic during DIC by inactivating thrombin, thereby preventing further conversion of fibrinogen to fibrin, reducing microthrombus formation, and decreasing the rate of intravascular coagulation and thrombosis.s2 Consequently, the consumption and biodegradation of coagulation factors and platelets is halted, allowing the liver to replenish coagulation factors and the hemorrhagic tendency to Low-dose heparin therapy (serum concentration 0.05 to 0.2 U of heparin/mL) has been as effective as high-dose therapy (serum concentration 0.2 to 0.4 U of heparin/mL) in the treatment of acute DIC in humans. 87 Controlled clinical trials to determine the value of heparin therapy in horses with DIC are lacking.…”

Section: Disseminated Intravascular Coagulationmentioning

confidence: 99%

Heparin: A Review of its Pharmacology and Therapeutic Use in Horses

Moore

Hinchcliff

1994

Veterinary Internal Medicne

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Heparin is used clinically in horses to treat hemostatic abnormalities associated with severe gastrointestinal disease, septicemia, and endotoxemia. The primary anticoagulant effect of heparin is through the suppression of thrombin-dependent amplification of the coagulation cascade, and inhibition of thrombin-mediated conversion of fibrinogen to fibrin. Heparin may be of benefit in preventing the complications associated with hypercoagulable states such as jugular vein thrombosis, laminitis, and organ failure. Heparin may also be beneficial in the prevention of intraabdominal adhesions after gastrointestinal surgery, and in amelioration of hernodynamic abnormalities associated with endotoxic shock. Because a sequential rise in serum unique compound with anticoagulant activity was ac-A cidentally discovered in 19 16 by McClean, a medical student, while he was attempting to identify a procoagulant in the liver.' The substance was named heparin because of its abundance in hepatic tissue.' In 1939, Brinkhous discovered that a plasma cofactor was necessary for the anticoagulant activity of h e~a r i n .~ Abildgaard named the cofactor antithrombin 111 (AT 111), and the specific mechanism of action of this cofactor was elucidated shortly thereafter. [4][5][6] Heparin is composed of a family of straight-chain, highly sulfated, anionic polysaccharides, specifically glycosaminoglycuronan sulfate esters, with molecular weights varying from 4,000 to 40,000 d.7-9 The structural unit of this complex molecule is a two hexose sugar that, in 8 to 15 repeating disaccharide subunits, forms a polymer of differing length^.^.' The structure of heparin is markedly heterogenous and varies with respect to the sequence and ratio of the different hexose units, the extent and type of sulfation, and the extent of N-a~etylation.~ The heterogeneity of heparin is not an artifact of preparation, but occurs because of the randomness of the biosynthetic process. lo Endogenous heparin is produced within mast cells of the lung, liver, and intestine.' ' Commercially-available heparin is derived from the mast cells of porcine intestinal mucosa and bovine lung."A small and distinct fraction of the heparin molecule is responsible for its anticoagulant effect. l 3 The active site of the heparin molecule contains a unique glucosamine unit with a specific pentasaccharide ~equence.'~.'~ This distinct fraction of the heparin molecule binds to AT 111, an endog-

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Section: Disseminated Intravascular Coagulationmentioning

confidence: 99%

Heparin: A Review of its Pharmacology and Therapeutic Use in Horses

Moore

Hinchcliff

1994

Veterinary Internal Medicne

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“…Disseminated intravascular coagulation (DIC) [1][2][3] is a frequent complication of inflammatory disease and trauma. Patients with this complication often have severe organ failure and are usually admitted to the intensive care unit (ICU).…”

Section: Introductionmentioning

confidence: 99%

Hemostatic markers and the sepsis‐related organ failure assessment score in patients with disseminated intravascular coagulation in an intensive care unit

et al. 2004

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We investigated the correlation between disseminated intravascular coagulation (DIC) score and hemostatic parameters and sepsis-related organ failure assessment (SOFA) score with clinical outcome of patients with DIC in an intensive care unit (ICU). The SOFA score was markedly elevated in patients with DIC relative to patients without DIC and significantly higher in non-survivors than in survivors. Abnormalities in almost all hemostatic parameters were significant in patients with DIC, but there was no significant difference in almost all hemostatic parameters between survivors and non-survivors. However, plasma antithrombin (AT) levels were significantly lower in non-survivors than in survivors. Soluble fibrin (SF) and tissue type plasminogen activator (tPA)-plasminogen activator inhibitor-I (PAI-I) complex correlated significantly with the SOFA score, whereas AT levels correlated significantly and negatively with the SOFA score. We conclude that the SOFA score is useful for predicting outcome in DIC patients in the ICU, and that hemostatic parameters, especially plasma AT levels, are also useful markers for organ failure and clinical outcome. Am.

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“…It can activate blood coagulation, leading to disseminated intravascular coagulation during sepsis, and it causes formation of endocardial vegetations during endocarditis (2,9,10). Tissue factor (TF), a single-chain protein, is the main physiological initiator of blood coagulation (22).…”

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confidence: 99%