Putative postanaesthetic pulmonary oedema in a horse

Abstract

A two-year-ten-month colt was referred for investigation and surgical treatment of cryptorchidism. Preanaesthetic clinical examination revealed no abnormalities and no relevant history was reported. The patient was anaesthetised with a total intravenous anaesthesia technique, both testicles were identified after induction, and a bilateral open castration was performed in the recovery box. Surgery, anaesthesia and recovery were uneventful. However, in the first hour postrecovery, clinical signs compatible with pulmonary oedema developed. Following arterial blood sampling and airway endoscopy, a low-grade pulmonary oedema was suspected and alleged to have occurred following transient laryngeal spasm. The patient was treated symptomatically and received supportive care. Two days after the surgery, the clinical signs were resolved, and the patient was discharged.

Mortality and morbidity in equine anaesthesia

“…Reports of pulmonary oedema are accumulating (Jones et al 1988;Abrahamsen et al 1990;Dixon et al 1993;Kollias-Baker et al 1993;Shaw et al 1995;Ball and Trim 1996;Tute et al 1996;Tidwell et al 2002;Borer 2005;Senior 2005;Holbrook et al 2007;Pellegrini-Masini et al 2009;Kaartinen et al 2010;Veres-Ny eki et al 2011;Melis et al 2014;Merlin et al 2019). Respiratory complications are described in CEPEF as fatal in 12 out of 35,978 horses; some 4% of the fatalities, and presumably included pulmonary oedema, but not exclusively.…”

“…Pulmonary oedema develops for a number of reasons, including UAO (Abrahamsen et al 1990;Dixon et al 1993;Kollias-Baker et al 1993;Ball and Trim 1996;Tute et al 1996;Borer 2005;Senior 2005;Kaartinen et al 2010;Merlin et al 2019), microembolism (Jones et al 1988), drug-associated capillary leakage (Shaw et al 1995), venous air embolism (Holbrook et al 2007;Pellegrini-Masini et al 2009) and mechanical causes (Tidwell et al 2002). Re-expansion injury and anaphylaxis, which increases vascular permeability (Ball and Trim 1996;Kaartinen et al 2010), have been considered likely to contribute.…”

“…Upper airway obstruction due to bilateral laryngeal paralysis after extubation in horses without pre-existing signs (Abrahamsen et al 1990;Dixon et al 1993;Bidwell et al 2007) were associated with nerve damage due to neck extension, laryngeal nerve ischaemia (Abrahamsen et al 1990), tissue oedema due to surgical manipulation, laryngeal oedema and spasm or functional airway collapse (Dixon et al 1993;Tute et al 1996;Merlin et al 2019). Pre-existing left laryngeal hemiplegia, large body mass, prolonged anaesthesia, hyperextension of the neck, hypotension, hypoventilation and hypoxaemia were named as risk factors for UAO (Southwood et al 2003).…”