SummaryThis case report describes venous air embolism as a complication of stifle joint arthroscopy in a 16‐year‐old French Saddle Pony. Carbon dioxide was used to achieve joint distension during the procedure and accidentally entered the vasculature, causing the embolism. The diagnosis was based on a sudden onset of laboured breathing, tachycardia and dropping end‐tidal carbon dioxide (PE'CO2) and was confirmed by arterial blood gas analysis showing hypercapnia and large PE'CO2—arterial partial pressure of carbon dioxide (PaCO2) difference. This complication was treated by increasing the fraction of inspired oxygen (FIO2) and immediate ceasing of further gas insufflation. The horse suffered no further complications. To our knowledge, this is the first publication reporting this complication during arthroscopy in a horse. Awareness of this complication should be raised between veterinarians performing arthroscopies when using gas as the distending agent. A high index of suspicion and early recognition of the embolism can improve chances for full and unremarkable recoveries.
The aim of this prospective, randomized, nonblinded, controlled clinical trial was to compare mean arterial blood pressure (MAP) and heart rate (HR) during an intravenous bolus of three different balanced isotonic crystalloid solutions in euvolemic, anesthetized dogs with hypotension. Thirty healthy dogs (American Society of Anesthesiologists Physical Status I–II) weighing at least 15 kg that presented for elective orthopedic or dental surgical procedures at the Ryan Veterinary Hospital for Small Animals of the University of Pennsylvania were included in this study. Anesthetized hypotensive patients (defined as a MAP ≤ 65 mmHg), were administered an infusion of Lactated Ringer’s solution (LRS), Plasma-Lyte (PLYTE) or Canadian Plasma-Lyte (PLYTECA), selected at random. The infusion was administered over 15 min via a volumetric fluid pump. Differences in oscillometric MAP and HR between time points and across treatments were evaluated by mANOVA. Intravenous isotonic crystalloid infusions over 15 min did not significantly change MAP or HR in hypotensive dogs under general anesthesia. Neither LRS, PLYTE nor PLYTECA exacerbated hypotension or caused tachycardia.
OBJECTIVE:To evaluate the incidence of tranexamic acid (TXA)-induced nausea and vomiting after the prophylactic use of 2 antiemetics, ondansetron and maropitant, compared with saline.DESIGN:Prospective, blinded, placebo-controlled, randomized, crossover study.SETTING:University research facility.ANIMALS:Eight adult, purpose-bred Beagles.INTERVENTION:Dogs received 3 treatments on 3 occasions with a 3-week washout period. Either maropitant (1 mg/kg), ondansetron (0.2 mg/kg), or saline solution was given intravenously in equal volumes, followed 10 minutes later by 50 mg/kg IV TXA. A blinded observer evaluated the dogs for signs of vomiting and nausea for 30 minutes. The severity of nausea was assessed with a visual analog scale (VAS) and recorded at baseline before TXA, and at the end of 3 observational periods: 0-5, 5-15, and 15-30 minutes after TXA. A generalized linear mixed effect model was used to assess for group and period effects. Statistical significance was set at P < 0.05 .MEASUREMENTS AND MAIN RESULTS:None of the dogs vomited after maropitant. Emesis occurred in 5 out of 8 dogs (62.5%), a median (range) of 1 time (1-2) after ondansetron and 1 time (1-3) after saline. There was a significant effect on vomiting of maropitant against saline (P < 0.0001) but not for ondansetron against saline (P = 0.53). The highest nausea VASs were recorded during the first 5 minutes after TXA with a significant reduction of VAS variability in the maropitant group (P = 0.003). The effect of maropitant and ondansetron against saline on the severity of nausea was not statistically significant (P = 0.069).CONCLUSION:The neurokinin 1 receptor antagonist maropitant at the dose used, administered IV 10 minutes before 50 mg/kg TXA, was effective in preventing vomiting compared with ondansetron and placebo. Our results support the prophylactic IV administration of maropitant in dogs that are scheduled to receive TXA.
Anaesthetic drugs are commonly used during the evaluation of laryngeal function in dogs. The aim of this review was to systematically analyse the literature describing the effects of anaesthetic drugs and doxapram on laryngeal motion in dogs and to determine which drug regime provides the best conditions for laryngeal examination. PubMed, Google Scholar, and EMBASE databases were used for the literature search up to November 2019. Relevant search terms included laryngeal motion, anaesthetic drugs and dogs. Studies were scored based on their level of evidence (LoE), according to the Oxford Centre for Evidence-based Medicine, and the quality was assessed using the risk-of-bias tool and SIGN-checklist. In healthy dogs, premedication before laryngeal examination provided better examination conditions and maintained overall adequate laryngeal motion in 83% of the studies. No difference in laryngeal motion between induction drugs was found in 73% of the studies but the effects in dogs with laryngeal paralysis remain largely unknown. Doxapram increased laryngeal motion in healthy dogs without serious side effects, but intubation was necessary for some dogs with laryngeal paralysis. Methodological characteristics varied considerably between studies, including the technique and timing of evaluation, number of assessors, study design, drug dose, combinations, route and speed of administration.
In people, the antifibrinolytic drug tranexamic acid reduces bleeding and the need for blood products with both normal and exaggerated fibrinolysis without increasing the number of thromboembolic events. In dogs, in addition to prevention and treatment of bleeding, higher doses of tranexamic acid can be used to induce vomiting. The objective of this study was to evaluate the effect of a high dose of tranexamic acid on the coagulation of healthy Beagle dogs. A prospective trial was conducted in eight healthy Beagles receiving tranexamic acid for a concurrent trial evaluating different antiemetics. Rotational thromboelastometry (ROTEM) analysis (EXTEM, APTEM, FIBTEM, INTEM) was performed before and 30 minutes after intravenous administration of 50 mg/kg tranexamic acid. ROTEM parameters before and after tranexamic acid administration and between EXTEM and APTEM were compared with Wilcoxon matched pairs signed rank test and data is presented as median (range). After tranexamic acid administration, FIBTEM clotting time became significantly shorter (p=0.03) from 37 s (28-124 s) to 33 s (27-40 s) and INTEM clot formation time significantly decreased (p=0.02) from 82 s (47132 s) to 60 s (43-107 s). After tranexamic acid APTEM MCF was significantly weaker (p=0.01) with 45 mm (30-63 mm) than EXTEM MCF with 55 mm (43-69 mm) and than APTEM MCF before tranexamic acid with 55 mm (43-69 mm) (p=0.02). All other analysed parameters including maximum lysis did not change after administration of tranexamic acid. The administration of 50 mg/kg intravenous tranexamic acid resulted in small changes in ROTEM profiles without inducing a hypercoagulable clot. In conclusion, tranexamic acid can safely be administered to healthy dogs with normal coagulation profiles. As an additional finding, APTEM parameters measured in the current study do not support the use of this test in dogs.
Cerebral cortical laminar necrosis (CLN) is a consequence of severe hypoxic, ischemic, or hypoglycemic events. In humans, these cortical lesions show characteristic linear T1-weighted (T1W) hyperintensity in the late subacute stage. Limited information reporting magnetic resonance imaging (MRI) findings in dogs affected by CLN is available. A 3-year-old Belgian Shepherd dog was referred 8 days after sudden onset of blindness after general anesthesia. Neurological examination showed central blindness and mild ataxia. Three-Tesla MRI examination of the brain revealed bilateral asymmetrical areas of T2-weighted hyperintensity within the occipital, parietal, temporal, and frontal cortex, involving gray and white matter. Furthermore, linear T1W-hyperintense lesions were found in the cerebral cortex of the same areas and showed heterogeneous contrast enhancement. Perfusion-weighted images revealed hyperperfusion in the affected regions. Lesions were compatible with subacute CLN with corresponding edema suspected to be secondary to anesthesia-related brain hypoxia. Three-Tesla MRI enabled identification of the laminar pattern of the cortical lesions.