The cardiopulmonary and anesthetic effects of isoflurane and propofol were determined in 10 healthy, adult Hispaniolan Amazon parrots (Amazona ventralis). Anesthesia was induced and maintained with isoflurane in oxygen for 30 minutes. Cardiopulmonary parameters including heart rate, respiratory rate, relative arterial oxygen hemoglobin saturation (SpO₂), and esophageal temperature were recorded at 1, 2, 3, 4, 5, 10, 15, 20, 25, and 30 minutes. End-tidal CO₂ (EtCO₂) concentrations and inspired and expired end-tidal isoflurane concentrations were recorded continuously. Before the study continued, birds were allowed to recover from isoflurane anesthesia for at least 2 hours. In a second trial, anesthesia was induced by intravenous administration of propofol (5 mg/kg) and maintained for 30 minutes by constant rate infusion of propofol (1 mg/kg per min IV). No supplemental oxygen was provided. Cardiopulmonary parameters and EtCO₂ concentrations were recorded as in the isoflurane trial. Induction times with propofol (51 ± 40 sec; mean ± SD) and isoflurane (58 ± 15 sec) were rapid and not significantly different. No significant changes in heart rates and SpO₂ values over time were seen with isoflurane anesthesia, but the respiratory rate decreased significantly from 41 ± 17 breaths/min at 1 minute to 25 ± 15 breaths/min at 10 minutes following induction. A significant decrease in respiratory rate was noted only at 2 (26 ± 10 breaths/min) and 3 (29 ± 12 breaths/min) minutes following induction with propofol. A significant increase in EtCO₂ concentrations was recorded at 3 (37% ± 4%) minutes and thereafter with propofol anesthesia. No significant change in heart rate was observed over time. The SpO₂ values significantly decreased below 90% at 2 minutes after induction with propofol and remained significantly decreased for the remainder of the anesthetic event. No significant differences in partial pressure of oxygen (P_aO₂) values were observed over time. SpO₂ values were significantly higher with isoflurane compared with propofol at any given time during anesthesia. No significant differences in EtCO₂ concentrations and heart rates were observed between groups throughout the study. Propofol recovery times (15.4 ± 15.2 min) were prolonged when compared with isoflurane (4.6 ± 1.6 min), and 6 birds had agitated recoveries from propofol anesthesia. A constant rate infusion of propofol at 1 mg/kg per minute resulted in a light anesthesic plane in 8 Hispaniolan Amazon parrots (Amazona ventralis) and a surgical plane in 2 birds. Supplemental oxygen is recommended during propofol anesthesia. Propofol can be useful for brief, noninvasive procedures or as an induction agent to facilitate endotracheal intubation prior to inhalational anesthesia.

We compared a radioimmunoassay and an enzymatic method to measure plasma bile acid concentrations of chickens and 5 psittacine genera. The 2 assays compared well with r² values ranging from 0.77 to 0.92. The radioimmunoassay was linear to 50 μmol/L, and the enzymatic method, to 200 μmol/L. When measured by the enzymatic method, bile acid concentrations were decreased in the presence of hemolysis and falsely increased in the presence of lipemia and high concentrations of lactate dehydrogenase. Results for both assays showed only small changes when samples were stored at −20°C and −70°C; however, storage at 4°C resulted in decreases in bile acid concentrations that were greater than 50% after 4 days. An advantage of the enzymatic method is that it can be performed more quickly than the radioimmunoassay and without the special procedures and guidelines applying to use of radioisotopes. However, the radioimmunoassay requires lower sample volumes (50 μl of plasma) than the enzymatic method (up to 400 μl unless the assay has been specifically adapted) and is not affected by hemolysis, lipemia, or elevated LDH concentrations. Others have found both assays to have adequate precision and accuracy. Therefore, the advantages and disadvantages of each should be weighed when selecting assay method. Clinicians should use assay-specific reference ranges as well as the same laboratory for paired determinations from the same patient.

Ten African white-backed vultures (Gyps africanus), 3 lappet-faced vultures (Torgos tracheliotus), and 6 marabou storks (Leptoptilos crumeniferus) were routinely treated for gastrointestinal parasitism with fenbendazole administered in the feed at dosages of 47–60 mg/kg for 3 days. Subsequently, all birds became depressed and anorectic. Results of hematologic testing of severely affected birds revealed profound leukopenia. Six white-backed vultures, 1 lappet-faced vulture, and 1 marabou stork died. Gross necropsy findings were minimal other than enlarged livers and spleens. On histologic examination, severe necrotizing enteritis, bacterial hepatitis, and evidence of septicemia were found. The clinical signs and necropsy findings in these birds were consistent with fenbendazole toxicosis. Fenbendazole at published doses can cause immunosuppression and secondary septicemia in some birds. Therefore, benzimidazole anthelmintics should be used with caution in certain avian species, and appropriate, broad-spectrum antibiotic therapy is indicated in suspected cases of benzimidazole toxicosis.

An umbrella cockatoo (Cacatua alba) of unknown age was examined because of a 6-month history of gradually worsening ataxia and intention tremors. Results of diagnostic tests were unremarkable, and the bird was euthanized after no improvement with empirical therapy. At necropsy, a large, poorly-defined mass was found in the cerebellum. The mass was identified as medulloblastoma, a type of primitive neuroectodermal tumor.

A 7-year-old male eclectus parrot (Eclectus roratus) was presented for evaluation of acute onset of dyspnea, tachypnea, and lethargy. Proventricular dilatation was observed on survey radiographs. Contrast fluoroscopic examination revealed decreased gastrointestinal motility and retention of contrast material in the proventriculus. Despite supportive care, the bird died. At necropsy, a tubular diverticulum of the ventriculus extended orad into the proventriculus. This diverticulum caused almost complete obstruction of proventricular outflow. No inflammation, infectious organisms, or neoplasia were associated with the lesion. The cause of the ventricular diverticulum in this parrot is unknown.