Diagnosis of disseminated intravascular coagulation in dogs admitted to an intensive care unit

Shane W. Bateman From the Departments of Clinical Studies (Bateman, Mathews, Abrams-Ogg), Pathobiology (Lumsden, Foster), and Biomedical Sciences (Johnstone), Ontario Veterinary College, University of Guelph, Guelph, ON, Canada NIG 2WI; and Department of Critical Care (Hillers), Hamilton Civic Hospitals, Hamilton General Division, 237 Barton St E, Hamilton, ON, Canada L8L 2X2.

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Karol A. Mathews From the Departments of Clinical Studies (Bateman, Mathews, Abrams-Ogg), Pathobiology (Lumsden, Foster), and Biomedical Sciences (Johnstone), Ontario Veterinary College, University of Guelph, Guelph, ON, Canada NIG 2WI; and Department of Critical Care (Hillers), Hamilton Civic Hospitals, Hamilton General Division, 237 Barton St E, Hamilton, ON, Canada L8L 2X2.

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Anthony C. G. Abrams-Ogg From the Departments of Clinical Studies (Bateman, Mathews, Abrams-Ogg), Pathobiology (Lumsden, Foster), and Biomedical Sciences (Johnstone), Ontario Veterinary College, University of Guelph, Guelph, ON, Canada NIG 2WI; and Department of Critical Care (Hillers), Hamilton Civic Hospitals, Hamilton General Division, 237 Barton St E, Hamilton, ON, Canada L8L 2X2.

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John H. Lumsden From the Departments of Clinical Studies (Bateman, Mathews, Abrams-Ogg), Pathobiology (Lumsden, Foster), and Biomedical Sciences (Johnstone), Ontario Veterinary College, University of Guelph, Guelph, ON, Canada NIG 2WI; and Department of Critical Care (Hillers), Hamilton Civic Hospitals, Hamilton General Division, 237 Barton St E, Hamilton, ON, Canada L8L 2X2.

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Ian B. Johnstone From the Departments of Clinical Studies (Bateman, Mathews, Abrams-Ogg), Pathobiology (Lumsden, Foster), and Biomedical Sciences (Johnstone), Ontario Veterinary College, University of Guelph, Guelph, ON, Canada NIG 2WI; and Department of Critical Care (Hillers), Hamilton Civic Hospitals, Hamilton General Division, 237 Barton St E, Hamilton, ON, Canada L8L 2X2.

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Thomas K. Hillers From the Departments of Clinical Studies (Bateman, Mathews, Abrams-Ogg), Pathobiology (Lumsden, Foster), and Biomedical Sciences (Johnstone), Ontario Veterinary College, University of Guelph, Guelph, ON, Canada NIG 2WI; and Department of Critical Care (Hillers), Hamilton Civic Hospitals, Hamilton General Division, 237 Barton St E, Hamilton, ON, Canada L8L 2X2.

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Robert A. Foster From the Departments of Clinical Studies (Bateman, Mathews, Abrams-Ogg), Pathobiology (Lumsden, Foster), and Biomedical Sciences (Johnstone), Ontario Veterinary College, University of Guelph, Guelph, ON, Canada NIG 2WI; and Department of Critical Care (Hillers), Hamilton Civic Hospitals, Hamilton General Division, 237 Barton St E, Hamilton, ON, Canada L8L 2X2.

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Objective

To describe and evaluate hemostatic function in critically ill dogs with clinical signs of diseases that predispose to disseminated intravascular coagulation (DIC).

Design

Prospective case series.

Animals

59 critically ill dogs (affected dogs) with clinical signs of diseases known to predispose to DIC and 52 clinically normal dogs (control dogs).

Procedure

Activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin clotting time (TCT), plasma fibrinogen concentration, serum concentration of fibrin and fibrinogen-related antigens (FRA), and plasma antithrombin III (AT III) activity were determined for all dogs. Results from affected dogs were compared with those of control dogs. In some affected dogs, postmortem tissue specimens were examined for evidence of microvascular thrombosis. A diagnosis of DIC was made by fulfilling at least 3 of the following criteria: 1) abnormal aPTT, PT, or TCT value, 2) low plasma fibrinogen concentration, 3) low plasma AT III activity, 4) high serum FRA concentration, or 5) low platelet count. To evaluate the severity of hemostatic dysfunction, 3 arbitrary categories (mild, moderate, and severe) were proposed.

Results

A diagnostic strategy based on moderate hemostatic dysfunction identified DIC in 16 of 59 (27.1%) affected dogs. The AT III activity was < 70% in 15 of 16 dogs with DIC. Microvascular thrombosis was observed in tissue specimens from 7 of 8 affected dogs. Serum FRA and plasma fibrinogen concena did not contribute in establishing a diagnosis of DIC.

Conclusions and Clinical Relevance

A diagnosis of DIC can be made when hemostatic dysfunction is moderate in dogs with clinical signs of diseases associated with DIC. (J Am Vet Med Assoc 1999;215:798–804).

Objective

To describe and evaluate hemostatic function in critically ill dogs with clinical signs of diseases that predispose to disseminated intravascular coagulation (DIC).

Design

Prospective case series.

Animals

59 critically ill dogs (affected dogs) with clinical signs of diseases known to predispose to DIC and 52 clinically normal dogs (control dogs).

Procedure

Activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin clotting time (TCT), plasma fibrinogen concentration, serum concentration of fibrin and fibrinogen-related antigens (FRA), and plasma antithrombin III (AT III) activity were determined for all dogs. Results from affected dogs were compared with those of control dogs. In some affected dogs, postmortem tissue specimens were examined for evidence of microvascular thrombosis. A diagnosis of DIC was made by fulfilling at least 3 of the following criteria: 1) abnormal aPTT, PT, or TCT value, 2) low plasma fibrinogen concentration, 3) low plasma AT III activity, 4) high serum FRA concentration, or 5) low platelet count. To evaluate the severity of hemostatic dysfunction, 3 arbitrary categories (mild, moderate, and severe) were proposed.

Results

A diagnostic strategy based on moderate hemostatic dysfunction identified DIC in 16 of 59 (27.1%) affected dogs. The AT III activity was < 70% in 15 of 16 dogs with DIC. Microvascular thrombosis was observed in tissue specimens from 7 of 8 affected dogs. Serum FRA and plasma fibrinogen concena did not contribute in establishing a diagnosis of DIC.

Conclusions and Clinical Relevance

A diagnosis of DIC can be made when hemostatic dysfunction is moderate in dogs with clinical signs of diseases associated with DIC. (J Am Vet Med Assoc 1999;215:798–804).

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