Post-anesthetic pulmonary edema in two horses.

CASE 1: A two-year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO(2): 3.7 kPa [28 mmHg]) and hypocapnia (PaCO(2): 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra-nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. CASE 2: An 11-year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4-hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO(2): 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood-gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.

The use of lingual venous blood to determine the acid-base and blood-gas status of dogs under anesthesia.

OBJECTIVE: To assess the suitability of lingual venous blood (LBG) as an alternative to arterial blood (ABG) samples in determining acid-base balance and blood-gas status in dogs anesthetized for elective procedures and with medetomidine and isoflurane administration under experimental conditions. STUDY DESIGN: Prospective, randomized clinical and experimental study. ANIMALS: Clinical population of 18 ASA I/II dogs for elective surgery and five healthy Beagles (3 females and 2 males) for the experimental study. METHODS: Blood sampling was simultaneously performed at dorsal pedal arterial and lingual venous sites, generating paired data. Two paired samples were collected from each dog in the clinical part and four from each dog in the experimental part (two during isoflurane anesthesia and two during isoflurane plus medetomidine). A modified Bland and Altman method was used to examine data from the clinical part and the experimental data were subjected to a paired sign's test following transformation where appropriate. RESULTS: The pH of LBG overestimated ABG, with limits of agreement of (-0.01, 0.02). The partial pressure of carbon dioxide (PCO(2)) of LBG overestimated ABG by 0.6 mmHg [0.1 kPa], with limits of agreement of (-3.5, 4.6) mmHg [-0.5, 0.6 kPa]. The partial pressure of oxygen (PO(2)) of LBG underestimated ABG by 86.3 mmHg [-11.5 kPa], with limits of agreement of (-199.8, 27.3) mmHg [-26.6, 3.6 kPa]. During medetomidine administration values for PO(2) (p = 0.03) and lactate (p = 0.03) were lower for LBG when compared with ABG. The LBG value of PO(2) was lower (p = 0.03) during medetomidine and isoflurane administration versus isoflurane alone. CONCLUSIONS AND CLINICAL RELEVANCE: The pH and PCO(2) of LBG samples provide clinically acceptable substitutes of ABG samples in the dog population studied. The wider limits of agreement for PO(2) render it less reliable as a substitute for ABG. The difference in PO(2) identified between LBG and ABG during medetomidine administration may not preclude the use of LBG as substitutes for ABG samples.

Sudden cardiac death associated with occult hypertrophic cardiomyopathy in a dog under anesthesia.

A 6-year-old, 3.0 kg, neutered female, Yorkshire terrier was referred for orthopedic surgery. Cardiac arrest followed unsuccessful treatment of bradycardia and systemic arterial hypotension under general anesthesia. Postmortem examination revealed hypertrophic cardiomyopathy. A possible relationship between treatment of bradycardia, systemic arterial hypotension, and sudden cardiac death is described.