Haemostatic changes associated with fluid resuscitation in canine parvoviral enteritis

Abstract

The haemostatic status of dogs with canine parvovirus (CPV) enteritis, within 24 h of admission after initial fluid administration, has been described previously, but the haemostatic status at admission and after standard fluid resuscitation, as well as after initial fluid redistribution, has not been investigated previously. The objective of this study was to characterise the haemostatic status at admission and describe the effect of crystalloid fluid resuscitation on haemostatic variables in dogs with CPV enteritis. Twenty-seven client-owned, hospitalised dogs with confirmed natural CPV infection and 15 healthy age-matched controls were included in a prospective, observational clinical study. The volume of resuscitation fluid, haematocrit (HCT), platelet count, thromboelastography (TEG) variables, antithrombin (AT) activity, fibrinogen- and C-reactive protein (CRP) concentrations were measured in all dogs at admission, after fluid resuscitation and, in 10 dogs, after receiving an additional 3 hours of maintenance-rate crystalloid fluids. For the CPV group at admission, the median TEG reaction time (R) and maximum amplitude (MA) or clot strength, as well as the median HCT, fibrinogen and CRP concentrations, were significantly increased compared to the controls. After fluid resuscitation, median R was significantly shorter, MA significantly increased and HCT and AT activity significantly decreased compared to admission values. The haemostatic variables remained unchanged after 3 h of maintenance-rate crystalloid therapy. The increased clot strength present in dogs with CPV enteritis at admission was exacerbated after fluid resuscitation and persisted for hours after large-volume crystalloid fluid administration.

Mean Platelet Volume and Platelet Volume Distribution Width in Canine Parvoviral Enteritis

“…Larger platelets have been shown to have more exposed fibrinogen receptors than smaller ones indicating a greater degree of activation and therefore an elevated risk of thrombus formation (51,52). Increased fibrinogen concentration, secondary to the marked host inflammatory response, has been reported in dogs with CPV enteritis (53). In another study investigating the presence of hypercoagulability in dogs with CPV enteritis, there was a high prevalence of clinical thrombosis or phlebitis in these cases (54).…”

Intravenous Fluid Administration and the Coagulation System

“…Despite the paucity of clinical veterinary studies to draw upon in this area, one observational study in dogs with parvoviral enteritis compared TEG changes in dogs that received bolus fluid therapy (median, 26.5 mL/kg) to those that received a smaller amount (median, 10 mL/kg) (56). Dogs that received bolus therapy showed relative hypercoagulability, but also likely had more severe disease.…”

“…Resuscitation corresponded with a lower median HCT and higher platelet concentration from admission values for both groups, with a decreased AT activity in the group that received a larger volume of LRS. In both groups, the fibrinogen concentration was above the assay detection limit (700 mg/dL), raising the question of the role of fibrinogen in maintaining ex vivo coagulation competency in animals with severe inflammation that are aggressively resuscitated (56).…”

Coagulation Abnormalities in Dogs with Parvoviral Enteritis

“…Systemic inflammation and a reduction in antithrombin III (AT III) activity induce a state of hypercoagulability that, when associated with blood stasis and vascular endothelial damage, may lead to thrombosis and/or disseminated intravascular coagulation (DIC), worsening the prognosis. The AT III activity decrease is secondary to the loss of gastrointestinal wall integrity, severe diarrhea, and endotoxin-mediated activation of coagulation [ 2 , 6 , 7 ]. Two previous studies have evidenced coagulation disorders in dogs with CPE by using thromboelastography (TEG) and standard coagulation parameters [ 6 , 7 ].…”

“…The AT III activity decrease is secondary to the loss of gastrointestinal wall integrity, severe diarrhea, and endotoxin-mediated activation of coagulation [ 2 , 6 , 7 ]. Two previous studies have evidenced coagulation disorders in dogs with CPE by using thromboelastography (TEG) and standard coagulation parameters [ 6 , 7 ]. Thromboelastography is a viscoelastic test used to assess global hemostasis by measuring clot formation, clot strength, and fibrinolysis [ 8 , 9 , 10 ].…”