Objective The aim of this study was to describe the coagulation status of traumatized dogs over the first 24 hours after admission. Study Design In 33 dogs presenting within 6 hours after trauma blood was sampled for rotational thromboelastometry (ROTEM), thrombocyte number and venous blood gas analysis at presentation and 6 and 24 hours thereafter. At each time point, dogs were defined as hypo-, normo- or hypercoagulable based on extrinsic, intrinsic and fibrinogen ROTEM profiles. Results Significantly more dogs (11/33) presented hypocoagulable compared with 6 hours (p = 0.046) and 24 hours (p = 0.008) thereafter and none presented hypercoagulable. Significantly more dogs were hypercoagulable (6/23, p = 0.014) and no dog was hypocoagulable at 24 hours compared with presentation. All evaluated ROTEM parameters except maximum lysis were significantly more hypocoagulable at presentation compared with 24 hours thereafter. Conclusion Hypocoagulability is more common in acutely traumatized dogs than previously described. Dogs were hypo- or normocoagulable at presentation and the coagulation status changed to normo- or hypercoagulability over the first 24 hours. Clotting times, clot formation and clot firmness but not clot lysis were significantly altered at presentation compared with 24 hours and fibrinogen concentration or function may play an important role in the dynamic change of coagulation state over time.

Objective The aim of this study was to determine the prevalence of acute traumatic coagulopathy (ATC) and identify associated clinical and laboratory parameters including rotational thromboelastometry. Study Design Dogs presenting within 6 hours after trauma were allocated to the ATC or non-ATC group based on thromboelastometry analysis (ex-tem S, in-tem S, fib-tem S). ATC was defined as ≥2 hypocoagulable parameters in 1 profile and ≥ 1 hypocoagulable parameter in an additional profile. Parameters used were ex-tem and in-tem clotting time (CT), clot formation time (CFT), maximum clot firmness (MCF), maximum lysis and fib-tem MCF. Clinical and laboratory parameters at presentation, animal trauma triage (ATT) score, transfusion requirement and outcome were compared. Logistic regression was used to identify independent factors associated with ATC. Results Eleven of 33 dogs presented with ATC and showed ex-tem CT and CFT prolongation and reduced MCF amplitude in all profiles (all p < 0.001). pH (p = 0.043) and potassium concentration (p = 0.022) were significantly lower and bleeding (p = 0.027) and plasma transfusions (p = 0.001) more common in dogs with ATC. Time after trauma (p = 0.040) and Animal Trauma Triage score (p = 0.038, including haematocrit as confounding factor) were associated with the presence of ATC. Conclusion Acute traumatic coagulopathy is more common in traumatized dogs than previously reported. Acute traumatic coagulopathy was associated with acidosis, Animal trauma triage score, time after trauma and higher transfusion needs. Coagulation abnormalities include ex-tem CT and CFT prolongations and decreased clot strength.

Case series summary In this report we describe the origin of protein loss and development of acute kidney injury after ibuprofen intoxication in two cats. Two 13-month-old neutered male domestic shorthair siblings were presented with acute kidney injury (AKI) and severe glomerular proteinuria following witnessed ibuprofen intoxication 3 days prior. Both cats presented with severe azotaemia (creatinine >900 µmol/l [>10 mg/dl]) and severe proteinuria (urine protein:creatinine [UPC] >20, normal <0.5). Urine protein electrophoresis upon presentation revealed mainly albumin and primary glomerular protein losses. The proteinuria and azotaemia resolved completely within 5 days of hospital treatment (8 days after ingestion). Urine protein electrophoresis, once the azotaemia and proteinuria resolved (UPC 0.11; normal <0.5), had a similar pattern to the one from admission. Both cats made a full recovery with supportive care. Relevance and novel information This is the first clinical report of AKI with nephrotic-range protein losses following ibuprofen intoxication in cats. We propose that this finding is due to idiosyncratic glomerular injury, as described in humans.