Successful treatment of acute respiratory failure following hypertensive crisis in a dog with presumed pheochromocytoma or paraganglioma.

Background: Acute respiratory failure has been reported as one of the manifestations of hypertensive crisis in pheochromocytoma in human medicine. In dogs, no reports have been described as acute respiratory failure following hypertensive crisis. Here, we report the clinical presentation, course, and treatment of acute respiratory failure following the hypertensive crisis in a dog with presumed pheochromocytoma or paraganglioma. Case Description: A 12-year-old neutered male toy poodle was referred for the diagnostic evaluation of a right adrenal gland mass. The dog suddenly exhibited severe dyspnea with abnormal hypertension (systolic blood pressure >200 mmHg) 15 minutes after recovery from the anesthesia for the computed tomography (CT) examination. Pulmonary CT and ultrasonography findings suggested acute onset of severe pulmonary edema. Pulmonary edema was treated with mechanical ventilation (pressure-support ventilation with continuous positive airway pressure) and negative fluid balance after the administration of furosemide. Weaning from mechanical ventilation was successful 24 hours after the onset of respiratory failure. Finally, the dog was discharged 3 days after weaning from ventilation without complications. Conclusion: This report outlines a case of acute respiratory failure following a hypertensive crisis requiring mechanical ventilatory management in a dog. The onset and progression of pulmonary edema were extremely rapid. However, improvement in pulmonary edema was also rapid. Hemodynamic stability, in addition to prompt diagnosis and aggressive therapeutic intervention, including mechanical ventilation, may have contributed to the good prognosis of pulmonary edema following hypertensive crisis in a dog, which we attribute to a catecholamine storm.

Sparing effect of tramadol, lidocaine, dexmedetomidine and their combination on the minimum alveolar concentration of sevoflurane in dogs.

BACKGROUND: Problems associated with using inhalational anaesthesia are numerous in veterinary anaesthesia practice. Decreasing the amount of used inhalational anaesthetic agents and minimising of cardiorespiratory disorders are the standard goals of anaesthetists. OBJECTIVE: This experimental study was carried out to investigate the sparing effect of intravenous tramadol, lidocaine, dexmedetomidine and their combinations on the minimum alveolar concentration (MAC) of sevoflurane in healthy Beagle dogs. METHODS: This study was conducted on six beagle dogs. Sevoflurane MAC was determined by the tail clamp method on five separate occasions. The dogs received no treatment (control; CONT), tramadol (TRM: 1.5 mg kg-1 intravenously followed by 1.3 mg kg-1 h-1), lidocaine (LID: 2 mg kg-1 intravenously followed by 3 mg kg-1 h-1), dexmedetomidine (DEX: 2 µg kg-1 intravenously followed by 2 µg kg-1 h-1), and their combination (COMB), respectively. Cardiorespiratory variables were recorded every five minutes and immediately before the application of a noxious stimulus. RESULTS: The COMB treatment had the greatest sevoflurane MAC-sparing effect (67.4 ± 13.9%) compared with the other treatments (5.1 ± 25.3, 12.7 ± 14.3, and 40.3 ± 15.1% for TRM, LID, and DEX treatment, respectively). The cardiopulmonary variables remained within the clinically acceptable range following COMB treatment, although the mean arterial pressure was higher and accompanied by bradycardia. CONCLUSIONS: Tramadol-lidocaine-dexmedetomidine co-infusion produced a remarkable sevoflurane MAC-sparing effect in clinically healthy beagle dogs and could result in the alleviation of cardiorespiratory depression caused by sevoflurane. Cardiorespiratory variables should be monitored carefully to avoid undesirable side effects induced by dexmedetomidine.

Comparison of the anesthetic effects between 5 mg/kg of alfaxalone and 10 mg/kg of propofol administered intravenously in cats.

To compare the anesthetic effects after intravenous administration of alfaxalone or propofol without premedication, either alfaxalone (5 mg/kg) or propofol (10 mg/kg) was administered intravenously over 120 sec in 6 cats. Each cat received the alternate treatment at least a 7-day interval. Anesthetic effects (tolerance of intubation, behavior changes and neurodepressive score) and physiological parameters were evaluated. Both treatments produced a rapid loss of consciousness, no apnea, and physiological parameters were maintained within clinically acceptable ranges apart from transient hypoxemia. The degree of hypoxemia was greater after the propofol treatment compared with the alfaxalone treatment. During the recovery period, more adverse events (ataxia, muscular tremors) were observed after the alfaxalone treatment compared with the propofol treatment.

Unrecognized difficult airway management during anesthesia in two brachycephalic dogs with narrow cricoid cartilage.

Difficulty in airway management during anesthesia was noted in a 10-year-old, castrated, male Pekingese dog and a 13-year-old male French Bulldog. They showed strong resistance during tracheal tube insertion through the subglottic lumen. Therefore, the airway was secured by using a small endotracheal tube or supraglottic airway device. Computed tomography scan revealed a markedly narrower vertical dimension of the cricoid cartilage compared to that seen in common brachycephalic breeds. Posterior glottis was relatively more accessible for translaryngeal intubation in the present cases. Our findings showed that brachycephalic airway syndrome may be associated with narrow cricoid cartilage. To the best of our knowledge, this is the first clinical case report of airway management during anesthesia in dogs with narrow cricoid cartilage.

The anesthetic effects of intramuscular alfaxalone in dogs premedicated with low-dose medetomidine and/or butorphanol.

We aimed to evaluate the induction, anesthesia, and cardiorespiratory effects of intramuscular (IM) anesthetic protocol with alfaxalone following premedication with low-dose medetomidine, butorphanol, or a combination of both (medetomidine-butorphanol) in dogs. Six healthy beagles were administered 1, 2.5, or 5 mg/kg alfaxalone IM following premedication with low-dose medetomidine (5 µg/kg; MA-IM), butorphanol (0.3 mg/kg; BA-IM), or medetomidine-butorphanol (5 µg/kg and 0.3 mg/kg, respectively; MBA-IM). Each dog received 9 treatments with minimum 7-day washout period between treatments. Dogs were allowed to breath room air during anesthetic induction. We attempted endotracheal intubation after alfaxalone administration. Alfaxalone produced a dose-dependent anesthetic effect in each anesthetic protocol. Intubation was achieved in 4 out of 6 dogs that received MA-IM and BA-IM with 2.5 mg/kg alfaxalone and in all dogs that received MBA-IM with 1, 2.5, and 5 mg/kg alfaxalone. The median durations [minimum-maximum] of accepting intubation were 79 [0-89], 97 [84-120], and 117 [84-217] min, respectively. Hypotension (mean arterial blood pressure <60 mmHg) did not develop, but bradycardia (heart rate <60 beats/min) was observed in all dogs that received the MA-IM and MBA-IM protocols. Severe hypoxemia (percutaneous arterial oxygen saturation <90%) developed in 2 dogs that received MBA-IM with 5 mg/kg alfaxalone. We consider that the MA-IM and BA-IM protocols with ≥2.5 mg/kg alfaxalone and the MBA-IM protocol with 1-2.5 mg/kg alfaxalone could provide clinically useful and effective anesthesia without causing severe cardiorespiratory depression in healthy dogs.

ST segment depression and ventricular fibrillation in a dog after contrast agent administration.

An 11-year-old Toy Poodle underwent a computed tomography examination with contrast (iohexol) enhancement under anesthesia. Heart rate and R-wave amplitude on electrocardiogram (ECG) increased 2.5 min after iohexol administration, and end-tidal carbon dioxide decreased to 12 mmHg. A progressive ST segment depression was observed on ECG. Subsequently, the ECG waveform changed to ventricular fibrillation. However, spontaneous circulation returned following cardiopulmonary resuscitation. Myocardial ischemia or anaphylactic shock was suspected in the dog, which explains the ST segment depression observed on ECG. When performing radiological examinations with a contrast agent, the ECG waveform changes, such as an increase in heart rate, R-wave amplitude, or ST segment depression, should be carefully monitored. This might enable early detection of cardiac dysfunction and the ensuing cardiac arrest in dogs.

Surgical removal of cataract in an Asiatic black bear (Ursus thibetanus) by phacoemulsification and aspiration.

A twenty-year-old male Asiatic black bear (Ursus thibetanus) presented at the Rakuno Gakuen University Animal Medical Center with a 10-year history of bilateral blindness and cataracts. Surgical treatment of bilateral cataracts by extracapsular lensextraction using phacoemulsification and aspiration (PEA) was performed under general anesthesia. An anterior capsulectomy was performed using micro iris scissors and micro anterior lens capsule forceps. The cataract was removed with PEA using the two-handed technique. After surgery, systemic corticosteroids, anti-inflammatory drugs and antibiotics were administered. After cataract removal, the bear had recovered vision, and good quality vision has been maintained to date (15 months). PEA can be a safe and effective treatment for cataracts that impair vision in bears.

Cardiovascular effects of intravenous colforsin in normal and acute respiratory acidosis canine models: A dose-response study.

In acidosis, catecholamines are attenuated, and higher doses are often required to improve cardiovascular function. Colforsin activates adenylate cyclase in cardiomyocytes without beta-adrenoceptor. Here, six beagles were administered colforsin or dobutamine four times during eucapnia (partial pressure of arterial carbon dioxide 35-40 mm Hg; normal) and hypercapnia (ibid 90-110 mm Hg; acidosis) conditions. The latter was induced by CO2 inhalation. Anesthesia was induced with propofol and maintained with isoflurane. Cardiovascular function was measured by thermodilution and a Swan-Ganz catheter at baseline and 60 min after 0.3 µg/kg/min (low), 0.6 µg/kg/min (middle), and 1.2 µg/kg/min (high) colforsin administration. The median pH was 7.38 [range 7.33-7.42] and 7.01 [range 6.96-7.08] at baseline in the Normal and Acidosis conditions, respectively. Endogenous adrenaline and noradrenaline levels at baseline were significantly (P < 0.05) higher in the Acidosis than in the Normal condition. Colforsin induced cardiovascular effects similar to those caused by dobutamine. Colforsin increased cardiac output in the Normal condition (baseline: 3.9 ± 0.2 L/kg/m2 [mean ± standard error], low: 5.2 ± 0.4 L/kg/min2, middle: 7.0 ± 0.4 L/kg/m2, high: 9.4 ± 0.2 L/kg/m2; P < 0.001) and Acidosis condition (baseline: 6.1 ± 0.3 L/kg/m2, low: 6.2 ± 0.2 L/kg/m2, middle: 7.2 ± 0.2 L/kg/m2, high: 8.3 ± 0.2 L/kg/m2; P < 0.001). Colforsin significantly increased heart rate and decreased systemic vascular resistance compared to values at baseline. Both drugs increased pulmonary artery pressure, but colforsin (high: 13.3 ± 0.6 mmHg in Normal and 20.1 ± 0.2 mmHg in Acidosis) may have lower clinical impact on the pulmonary artery than dobutamine (high: 19.7 ± 0.6 in Normal and 26.7 ± 0.5 in Acidosis). Interaction between both drugs and experimental conditions was observed in terms of cardiovascular function, which were similarly attenuated with colforsin and dobutamine under acute respiratory acidosis.

Sedative and physiological effects of low-dose intramuscular alfaxalone in rabbits.

To evaluate sedative and physiological effects of low dose intramuscular (IM) alfaxalone, six healthy rabbits were administered single IM doses of alfaxalone at 1mg/kg (IM1), 2.5 mg/kg (IM2.5), or 5 mg/kg (IM5) with a minimum of 7-day washout period. Sedative effects were subjectively evaluated using a composite measure scoring system (maximum sedation score of 16) and pulse rate, respiratory rate, non-invasive blood pressure, and percutaneous oxygen-hemoglobin saturation were measured before and after IM alfaxalone. Loss of righting reflex (LRR) was achieved in all rabbits after IM2.5 and IM5 treatments but in only three rabbits after IM1 treatment. Median (interquartile range) times to LRR were 16 min (15-17), 6 min (6-6), and 4 min (4-4), and median durations of LRR were 0.5 min (0-7), 22.5 min (19-27), and 53 min (48-58) after IM1, IM2.5, and IM5 treatments, respectively. The duration of LRR after IM5 treatment was significantly longer than those after IM1and IM2.5 treatments (P<0.01). Median value of total sedation scores peaked at 10 min [score 3.5 (3-4)], from 10 min [score 13.5 (12-14)] to 15 min [score 13.5 (12-14)], and from 10 min [score 15 (12-15)] to 15 min [score 15 (14-15)] after IM1, IM2.5, and IM5 treatments, respectively. No rabbit showed circulatory depression and apnea although respiratory rate decreased after IM 2.5 and IM5 treatments. In conclusion, alfaxalone produced a dose-dependent sedative effect and a deep sedation was achieved by alfaxalone at 2.5 mg/kg IM in rabbits.

Effect of sevoflurane anesthesia on neuromuscular blockade produced by rocuronium infusion in dogs.

This study evaluated the effect of sevoflurane anesthesia on neuromuscular blockade with rocuronium in dogs. Six healthy beagle dogs were anesthetized four times with a minimum 14-day washout period. On each occasion, the dogs were administered 1.25-, 1.5-, 1.75-, or 2.0-fold of the individualized minimum alveolar concentration (MAC) of sevoflurane and received an infusion of rocuronium (0.5 mg/kg followed by 0.2 mg/kg/hr) for 120 min. Neuromuscular function was monitored with acceleromyography and train-of-four (TOF) stimulation of the left hind limb. Time to achieve TOF count 0 (onset time), time from the onset of neuromuscular blockade to the reappearance of TOF count 4 (blockade period), and time from the onset of rocuronium infusion to attaining a 70 or 90% TOF ratio (TOFR70 or TOFR90) were recorded. There were no significant differences in the onset time, blockade period, and plasma rocuronium concentration between the sevoflurane MAC multiples. The TOFR70 and TOFR90 were dose-dependently prolonged with the sevoflurane MAC multiples. There were significant differences in the TOFR70 and TOFR90 between the 1.25 sevoflurane MAC (median: 55 and 77.5 min, respectively) and 1.75 sevoflurane MAC (122.0 and 122.6 min; P=0.020 and P=0.020, respectively), 1.25 sevoflurane MAC and 2.0 sevoflurane MAC (126.0 and 131.4 min; P=0.020 and P=0.020), and 1.5 sevoflurane MAC (97.5 and 121.3 min) and 2.0 sevoflurane MAC (P=0.033 and P=0.032). In dogs, sevoflurane anesthesia produced dose-dependent prolongation of recovery from neuromuscular blockade produced by rocuronium.

Influence of sevoflurane anesthesia with mechanical ventilation and fluid-therapy on distribution of subcutaneously administered robenacoxib in dogs.

Robenacoxib is a novel nonsteroidal anti-inflammatory drug approved for dogs. The present study aimed to evaluate influences of sevoflurane anesthesia on the distribution of robenacoxib in dogs. Ten healthy beagle dogs (1 to 11 years old, 9.3 to 14.3 kg body weight, 6 males and 4 females) were subcutaneously administered robenacoxib (2 mg/kg) under conscious condition or sevoflurane anesthesia inhaled a 1.3-fold predetermined individual minimum alveolar concentration of sevoflurane at a 28-day interval. The dogs under sevoflurane anesthesia were also mechanically ventilated and received fluid-therapy. On each occasion, serum samples were collected from the dogs before and at 5, 15, 30, 60, 120, 180, and 240 min after the robenacoxib administration. Serum robenacoxib concentration was measured by a liquid chromatography-tandem mass spectrometry. Maximum serum concentration of robenacoxib (Cmax) was 2.2 µg/ml [range: 1.2-4.6] (median [range: minimum-maximum]) and time of Cmax (Tmax) was 90 min [range: 60-120] in the conscious dogs. In the sevoflurane-anesthetized dogs, the Cmax significantly declined (1.3 µg/ml [range: 0.8-1.4], P=0.008) and Tmax was delayed (120 min [range: 120-240], P=0.018) compared with those in the conscious dogs. The serum robenacoxib concentration at 240 min (C240) decreased to 0.5 µg/ml [range: 0.2-0.9] in the conscious dogs, while it remained higher in the sevoflurane-anesthetized dogs (1.0 µg/ml [range: 0.3-1.4], P=0.011). In conclusion, the anesthetic procedure with sevoflurane, mechanically ventilated, and received fluid-therapy might affect the pharmacokinetics of subcutaneously administered robenacoxib in dogs.

Anesthetic and cardiorespiratory effects of single-bolus intravenous alfaxalone with or without intramuscular xylazine-premedication in calves.

The anesthetic and cardiorespiratory effects of xylazine-alfaxalone combination were evaluated in calves. Six calves (age: 6-9 months old; weight: 114-310 kg) were anesthetized with intravenous alfaxalone 15 min after administration of intramuscular saline (0.5 ml/100 kg) or xylazine (0.1 mg/kg; 0.5 ml/100 kg of a 2% xylazine solution). Anesthesia induction was smooth and orotracheal intubation was achieved in all calves. The calves anesthetized with xylazine-alfaxalone required a smaller induction dose of alfaxalone (1.23 ± 0.17 mg/kg, P=0.010) and accepted endotracheal intubation for a significantly longer period (16.8 ± 7.2 min, P=0.022) than the calves anesthetized with alfaxalone alone (2.28 ± 0.65 mg/kg 7.3 ± 1.6 min). At 5 min after induction, tachycardia (heart rate: 166 ± 47 beats/min of heart rate), hypertension (mean arterial blood pressure: 147 ± 81 mmHg) and hypoxemia (partial pressure of arterial blood oxygen [PaO2]: 43 ± 10 mmHg) were observed in the calves anesthetized with alfaxalone alone, whereas hypoxemia (PaO2: 47 ± 7 mmHg) and mild hypercapnia (partial pressure of arterial blood carbon dioxide: 54 ± 5 mmHg) were observed in the calves anesthetized with xylazine-alfaxalone. Premedication with xylazine provided a sparing effect on the induction dose of alfaxalone and a prolongation of anesthetic effect. Oxygen supplementation should be considered to prevent hypoxemia during anesthesia.

Sedative effects of intramuscular alfaxalone administered to cats.

The sedative effects of intramuscular (IM) alfaxalone in 2-hydroxypropyl-beta-cyclodextrin (alfaxalone-HPCD) were evaluated in cats. The cats were treated with alfaxalone-HPCD in five occasions with a minimum 14-day interval between treatments: an IM injection of 1.0 mg/kg (IM1), 2.5 mg/kg (IM2.5), 5 mg/kg (IM5) or 10 mg/kg (IM10), or an intravenous injection of 5 mg/kg (IV5). The sedative effects were evaluated subjectively using a composite measurement scoring system (a maximum score of 16). Cardio-respiratory variables were measured non-invasively. The median sedation scores peaked at 10 min (score 9), 15 min (score 14), 10 min (score 16), 10 to 20 min (score 16) and 2 to 5 min (score 16) after the IM1, IM2.5, IM5, IM10 and IV5 treatments, respectively. The IM5 treatment produced longer lasting sedation, compared to the IV5 treatment. Durations of maintenance of lateral recumbency after the IM10 treatment (115 ± 22 min) were longer than those after the IM2.5 (40 ± 15 min), IM5 (76 ± 21 min) and IV5 treatments (50 ± 5 min). Cardio-respiratory variables remained within clinically acceptable ranges, except for each one cat that showed hypotension (<60 mmHg) after the IM10 and IV5 treatments. Tremors, ataxia and opisthotonus-like posture were observed during the early recovery period after the IM2.5, IM5, IM10 and IV5 treatments. In conclusion, IM alfaxalone-HPCD produced dose-dependent and clinically relevant sedative effect at 2.5 to 10 mg/kg in healthy cats. Hypotension may occur at higher IM doses of alfaxalone-HPCD.

The pharmacological effects of the anesthetic alfaxalone after intramuscular administration to dogs.

The pharmacological effects of the anesthetic alfaxalone were evaluated after intramuscular (IM) administration to 6 healthy beagle dogs. The dogs received three IM doses each of alfaxalone at increasing dose rates of 5 mg/kg (IM5), 7.5 mg/kg (IM7.5) and 10 mg/kg (IM10) every other day. Anesthetic effect was subjectively evaluated by using an ordinal scoring system to determine the degree of neuro-depression and the quality of anesthetic induction and recovery from anesthesia. Cardiorespiratory variables were measured using noninvasive methods. Alfaxalone administered IM produced dose-dependent neuro-depression and lateral recumbency (i.e., 36 ± 28 min, 87 ± 26 min and 115 ± 29 min after the IM5, IM7.5 and IM10 treatments, respectively). The endotracheal tube was tolerated in all dogs for 46 ± 20 and 58 ± 21 min after the IM7.5 and IM10 treatments, respectively. It was not possible to place endotracheal tubes in 5 of the 6 dogs after the IM5 treatment. Most cardiorespiratory variables remained within clinically acceptable ranges, but hypoxemia was observed by pulse oximetry for 5 to 10 min in 2 dogs receiving the IM10 treatment. Dose-dependent decreases in rectal temperature, respiratory rate and arterial blood pressure also occurred. The quality of recovery was considered satisfactory in all dogs receiving each treatment; all the dog exhibited transient muscular tremors and staggering gait. In conclusion, IM alfaxalone produced a dose-dependent anesthetic effect with relatively mild cardiorespiratory depression in dogs. However, hypoxemia may occur at higher IM doses of alfaxalone.