Comparison between dexmedetomidine and acepromazine in combination with methadone for premedication in brachycephalic dogs undergoing surgery for brachycephalic obstructive airway syndrome.

OBJECTIVE: To compare dexmedetomidine with acepromazine for premedication combined with methadone in dogs undergoing brachycephalic obstructive airway syndrome (BOAS) surgery. STUDY DESIGN: Randomized, blinded clinical study. ANIMALS: A group of 40 dogs weighing mean (± standard deviation) 10.5 ± 6 kg, aged 2.6 ± 1.9 years. METHODS: Dogs received either acepromazine 20 µg kg-1 (group A) or dexmedetomidine 2 µg kg-1 (group D) intramuscularly with methadone 0.3 mg kg-1. Anaesthesia was induced with propofol and maintained with sevoflurane. Sedation (0-18), induction (0-6) and recovery (0-5) qualities were scored. Propofol dose, hypotension incidence, mechanical ventilation requirement, extubation time, additional sedation, oxygen supplementation, regurgitation and emergency intubation following premedication or during recovery were recorded. Data were analysed using t tests, Mann-Whitney U or Chi-square tests. RESULTS: Group A dogs were less sedated [median (range): 1.5 (0-12)] than group D [5 (1-18)] (p = 0.021) and required more propofol [3.5 (1-7) versus 2.4 (1-8) mg kg-1; p = 0.018]. Induction scores [group A: 5 (4-5); group D 5 (3-5)] (p = 0.989), recovery scores [group A 5 (4-5); group D 5(3-5)](p = 0.738) and anaesthesia duration [group A:93 (50-170); group D 96 (54-263) minutes] (p = 0.758) were similar between groups. Time to extubation was longer in group A 12.5 (3-35) versus group D 5.5 (0-15) minutes; (p = 0.005). During recovery, two dogs required emergency intubation (p > 0.99) and five dogs required additional sedation (p > 0.99). Oxygen supplementation was required in 16 and 12 dogs in group A and D, respectively (p = 0.167); no dogs in group A and one dog in group D regurgitated (p = 0.311). CONCLUSIONS AND CLINICAL RELEVANCE: Dexmedetomidine 2 µg kg-1 produces more sedation but similar recovery quality to acepromazine 20 µg kg-1 combined with methadone in dogs undergoing BOAS surgery.

Prolongation of the Time Window From Traumatic Limb Amputation to Replantation From 6 to 33 Hours Using Ex Vivo Limb Perfusion.

INTRODUCTION: Continuous extracorporeal perfusion (ECP), or machine perfusion, holds promise for prolonged skeletal muscle preservation in limb ischemia-reperfusion injury. This study aimed to extend the amputation-to-replantation time window from currently 6 hours to 33 hours using a 24-hour ECP approach. MATERIALS AND METHODS: Six large white pigs underwent surgical forelimb amputation under general anesthesia. After amputation, limbs were kept for 9 hours at room temperature and then perfused by 24-hour ECP with a modified histidine-tryptophan-ketoglutarate (HTK) solution. After ECP, limbs were orthotopically replanted and perfused in vivo for 12 hours. Clinical data, blood, and tissue samples were collected and analyzed. RESULTS: All 6 forelimbs could be successfully replanted and in vivo reperfused for 12 hours after 9 hours of room temperature ischemia followed by 24 hours ECP. Adequate limb perfusion was observed after replantation as shown by thermography and laser Doppler imaging. All pigs survived without severe organ failure, and no significant increase in inflammatory cytokines was found. Macroscopy and histology showed marked interstitial muscular edema of the limbs, whereas myofiber necrosis was not evident, implying the preservation of muscular integrity. CONCLUSIONS: The use of a 24-hour ECP has successfully extended limb preservation to 33 hours. The modified histidine-tryptophan-ketoglutarate perfusate demonstrated its ability for muscle protection. This innovative approach not only facilitates limb replantation after combat injuries, surmounting geographical barriers, but also broadens the prospects for well-matched limb allotransplants across countries and continents.

Iatrogenic cerebral arterial gas embolism from flushing of the arterial line in two calves.

BACKGROUND: Measurement of invasive blood pressure as reflection of blood flow and tissue perfusion is often carried out in animals during general anesthesia. Intravascular cannulation offers the potential for gas to directly enter the circulation and lead to arterial gas embolism. Cerebral arterial gas embolism may cause a spectrum of adverse effects ranging from very mild symptoms to severe neurological injury and death. Although several experimental models of arterial gas embolism have been published, there are no known published reports of accidental iatrogenic cerebral arterial gas embolism from flushing of an arterial line in animals. CASE PRESENTATION: A 7-day-old Red Holstein-Friesian calf (No. 1) and a 28-day-old Holstein-Friesian calf (No. 2) underwent hot iron disbudding and sham disbudding, respectively, under sedation and cornual nerve anesthesia. Invasive arterial blood pressure was measured throughout the procedure and at regular intervals during the day. Before disbudding, a sudden and severe increase of blood pressure was observed following flushing of the arterial line. Excitation, hyperextension of the limbs and rapid severe horizontal nystagmus appeared shortly thereafter. Over the following minutes, symptoms ameliorated and blood pressure normalized in both cases. Prompt diagnosis was missed in calf 1; supportive fluid therapy was provided. Severe deterioration of neurologic status occurred in the following 24 h and culminated with stupor. The calf was euthanized for ethical reasons and the histological examination revealed extensive cerebral injury. Treatment of calf 2 consisted of supportive fluid and oxygen therapy; furosemide (1 mg/kg IV) was injected twice. Calf 2 appeared clinically normal after 2 h and showed no neurologic sequelae on a 3-month-follow up period. CONCLUSIONS: There are no known reports of cerebral arterial gas embolism following flushing of the auricular arterial line in calves. The injection of a small amount of air at high pressure in a peripheral artery may lead to a significant cerebral insult. The clinical presentation is non-specific and can favour misdiagnosis and delay of therapy.