Use of propofol for induction and maintenance of anesthesia in a king penguin (Aptenodytes patagonicus) undergoing magnetic resonance imaging.
Key words: seizure, propofol, total intravenous anesthesia, TIVA, avian, king penguin, Aptenodytes patagonicus
A 9-year-old captive male king penguin (Aptenodytes patagonicus) weighing 13.5 kg was referred to the University of Melbourne Veterinary Hospital for magnetic resonance imaging (MRI) of the brain after it developed cluster seizures in the previous 48 hours. The penguin was part of a closed flock with no recent introductions, and it had been considered healthy and was fostering chicks before the onset of seizures. The penguin was fed a diet of salmon, whiting, and squid supplemented with a multivitamin twice weekly in the weeks leading up to the onset of seizures. The referring veterinarian collected blood samples for plasma biochemical analysis and measurement of a blood lead level, results of which were normal except for a marginally low blood glucose concentration (175 mg/dL; reference interval, 205-326 mg/[dL.sup.-1]).
Before transport to the hospital, the penguin was sedated with medetomidine (25 [micro]g/kg; Dornitor, Zoetis West Ryde, NSW, Australia) and diazepam (0.38 mg/kg; Pamlin, Ceva Animal Health, Glenorie, NSW, Australia) administered intramuscularly in the pectoral muscles. On arrival at the University of Melbourne Veterinary Hospital, the penguin's sedation level was assessed as adequate, as it was able to be handled and positioned for radiographs with light restraint using adhesive tape. Whole body screening radiographs were taken to rule out metal ingestion and confirm that the penguin could safely enter the MRI suite. No obvious metallic opacities were detected, and the osseous and pulmonary parenchymal structures and cardiohepatic silhouette appeared normal.
A 22-gauge catheter was placed in the left brachial vein to facilitate administration of intravenous drugs and lactated Ringer's solution (4.5 mL/kg per hour). General anesthesia was induced by administration of 50 mg of propofol (3.7 mg/kg; Provive 1%, Claris Lifesciences Australia, NSW, Australia) over approximately 120 seconds. A 6-mm internal-diameter cuffed silicon endotracheal tube was inserted and advanced approximately 5 cm into the trachea to the level just proximal to the median tracheal septum (based on radiographic measurements) and secured to the beak with adhesive tape. An adult rebreathing circuit was connected and manual ventilation was initiated immediately at a rate of 4-6 respirations per minute and peak inspiratory pressure of approximately 20 cm [H.sub.2]O. Physiologic monitoring was performed with a multiparameter monitor (SurgiVet Advisor Vital Signs Monitor V9203, Smiths Medical ASD, Inc, St Paul, MN, USA) and included lead II electrocardiograph and cloacal temperature. A separate oscillometric noninvasive blood pressure device (petMAP graphic, Ramsey Medical Inc, Tampa, FL, USA) was used with a size 8-cm cuff (cuff width approximately 40% of the circumference of the limb) placed around the right hind limb proximal to the tarsometatarsus joint. Pulse oximetry measurement was attempted; however, because of the positioning of the penguin required to perform the MRI scan, placing the pulse oximetry probe on the tongue was not possible and attempts to obtain readings from various locations on the wings and webbing of the feet were unsuccessful.
Anesthesia was maintained via a propofol constant rate infusion (CRI) (0.3 mg/kg per minute) started at 5 minutes after induction. Fifteen minutes after induction of anesthesia, the penguin was transferred into the MRI room and connected to an MRI-compatible anesthesia machine through an adult rebreathing circuit. Mechanical intermittent positive-pressure ventilation (Mallard Small Animal Ventilator Model 2800, Mallard Medical Inc, Redding, CA, USA) was started at a rate of 5 respirations per minute and a tidal volume corresponding to a peak inspiratory pressure of 18 cm [H.sub.2]O (tidal volume 14.8 mL/kg). A MRI-compatible multiparameter monitor (Medrad Veris MR Vital Signs Monitor, Medrad Inc, Warrendale, PA, USA) was used and included, in addition to the already-monitored physiologic parameters described, side-stream capnography allowing the measurement of end-tidal carbon dioxide (EtC[O.sub.2]). The first EtC[O.sub.2] reading obtained was 70 mmHg, and mechanical ventilation rate was increased until the EtC[O.sub.2] decreased. The EtC[O.sub.2] was then maintained between 46 and 53 mmHg for the remainder of the anesthetic period. Blood pressure continued to be monitored in between MRI scan sequences using the same oscillometric device as previously described. Throughout the anesthetic period the heart rate ranged from approximately 82 to 105 beats per minute (reference interval 140-150 beats per [minute.sup.2]) and mean arterial pressure (MAP) ranged from 68 to 142 mmHg.
At 5 minutes after induction, the propofol CRI was started at 0.3 mg/kg per minute. The penguin was maintained at an appropriate level of anesthesia for the first 30 minutes of the procedure. Two intravenous boluses of propofol (10 mg each) at 30 and 35 minutes postinduction were required because the patient was moving during positioning for the MRI. After that time, an appropriate anesthetic plane for imaging was maintained with the CRI alone. The propofol CRI was reduced periodically throughout anesthesia in response to increasing anesthetic depth (lack of palpebral response and decreasing heart rate from approximately 100 to 85 beats per minute) as follows after induction: 0.25 mg/kg per minute (70 minutes), 0.2 mg/kg per minute (85 minutes), 0.15 mg/kg per minute (100 minutes), and 0.1 mg/kg per minute (130 minutes).
The MRI scanning was performed, and precontrast images were obtained. At 110 minutes after induction, the penguin was given 1.3 mmol of gadodiamide contrast agent (2.6 mL IV, Omniscan, gadodiamide 2.5 mmol/5 mL, GE Healthcare Australia, NSW, Australia) and postcontrast images were acquired. No cardiopulmonary response to the contrast agent was detected by physiologic monitoring. The MRI images were reviewed by a veterinary radiologist and no macroscopic cause for the seizures could be identified.
At the completion of MRI image acquisition, the propofol CRI was discontinued (138 minutes after induction) and the penguin was transferred out of the MRI suite and placed back on the initial monitoring equipment. Fluid therapy with lactated Ringer's solution was continued in recovery, as was delivery of 100% oxygen and manual intermittent ventilation. The penguin regained spontaneous ventilation approximately 10 minutes after discontinuing the propofol CRI, and was extubated 15 minutes later as it had started lifting its head and moving its wings. The recovery was smooth and the patient did not show any excitement or adverse behavior and was returned to the captive colony uneventfully.
This report describes the successful use of a propofol-based total intravenous anesthetic (TIVA) protocol in a king penguin with a history of seizures. An underlying cause for the seizure activity was not identified on imaging, and the penguin was diagnosed with presumptive idiopathic epilepsy in the absence of evidence for other causes. Seizures present a diagnostic challenge in avian patients as there are multiple potential causes or underlying conditions leading to seizure activity such as nutritional deficiencies, trauma, atherosclerosis and brain infarction, neoplasia, metabolic disturbances, infectious processes, toxicoses, and idiopathic epilepsy. (3) In this case, many diagnoses had been excluded, and imaging of the brain was requested to determine if a structural or vascular intracranial lesion was present.
The Monroe-Kellie hypothesis asserts that the volumes of the brain, cerebrospinal fluid, and intracranial blood are constant if the skull is intact, and any change to the volume of one of these components results in an inverse change in the volume of one or both of the other two to prevent changes in intracranial pressure (ICP). (4) Cerebral blood flow (CBF) and cerebrospinal fluid provide buffers to increases in ICP by changing in response to each other. The primary source of energy for the brain is through aerobic metabolism, and CBF is critical to providing the brain with oxygen and nutrients. The cerebral vasculature is able to autoregulate delivery of blood to the brain and provide constant CBF, regardless of a range of changes in blood pressure. (5) For example, a sudden increase in arterial blood pressure triggers vasodilation followed by a series of responses to changes in tissue oxygen concentration and products of cerebral metabolism resulting in vasoconstriction to restore the balance between oxygen supply and demand and maintain CBF. (6) The CBF-metabolism coupling in the brain is also mediated by numerous chemical agents, including hydrogen ions ([H.sup.+]), partial pressure of oxygen (Pa[O.sub.2]) and C[O.sub.2], nitric oxide, carbon monoxide, oxygen-derived free radicals, and adenosines among many others. (6) Cerebral blood vessel diameter depends on tissue [H.sup.+] concentration, as acidosis causes dilation of cerebral blood vessels resulting in increased CBF. (6) Hypoxia causes vasodilation and increases CBF, although the extent of these changes is different in birds than in mammals. Arterial oxygen tension (Pa[O.sub.2]) below 60-70 nimHg in pekin ducks (Anas platyrhynchos domestica) results in an increase in CBF, unlike in humans where CBF is maintained until Pa[O.sub.2] falls to less than 50 mmHg. (6,7) Pulse oximetry was attempted, despite the unreliability of this method in birds due to differences in the absorption characteristics of oxygenated and deoxygenated hemoglobin in avian species, (8) but oximetry readings were not obtained consistently. Blood gas analysis was also not attempted, and we were unable to monitor oxygen concentration in this penguin. In the absence of oxygenation monitoring, changes in EtC[O.sub.2], heart rate, and blood pressure were used to assess the hemodynamic and physiologic status of the penguin during anesthesia. Birds respond differently to changes in partial pressure of C[O.sub.2] compared with mammals. In birds, like mammals, hypercapnia causes cerebral vessel vasodilation and subsequent increases in CBF. In contrast to mammals, however, hypocapnia in birds does not cause a decrease in CBF. This difference in response to hypocapnia between birds and mammals has been attributed to a difference in the oxygen binding affinity of avian blood. In particular, the oxygen hemoglobin dissociation curve is left-shifted in many penguins compared with mammals. (7,9)
Anesthesia protocols for patients with intracranial lesions need to provide hemodynamic stability, preserve cerebrovascular autoregulation, avoid increases in ICP, and facilitate a rapid recovery. (10,11) Inhalant anesthetic agents such as isoflurane can affect CBF and impair autoregulation. (12)
Conscious pigeons (Columba livia) are able to autoregulate CBF over a MAP range of approximately 50-190 mmHg. (13) Normal blood pressure ranges for king penguins have not been established, and normal MAP in king penguins possibly is as high as 200 mmHg, as seen in some avian species. (14) Invasive blood pressure measurement was not possible in this case; however, blood pressure trends were monitored with oscillometric monitoring. Autoregulation of CBF occurs in many avian and mammalian species, and it would be reasonable to expect that king penguins are able to autoregulate CBF within a similarly wide (but possibly higher) blood pressure range. Loss of autoregulation may lead to increased ICP, which can cause cerebral ischemia, cerebral edema, or cerebellar herniation. (5,12) Propofol TIVA maintains CBF autoregulation, and in humans, when combined with opioid CRI, can also reduce ICP. (10) While there is no specific evidence in birds regarding the effects of anesthetic agents on CBF or ICP, the evidence from humans and other species suggests this method of anesthesia may result in better outcomes for avian patients with intracranial lesions.
Propofol has been evaluated in many avian species and typically produces smooth and rapid induction of anesthesia when given intravenously. (15-20) The dose of propofol used here for induction (3.7 mg/kg) and to maintain anesthesia (0.1-0.3 mg/kg per minute) is lower than doses described in other avian species. (20) Previous studies evaluating CRI doses of propofol in birds have not included the use of premedication with sedatives such as opioids, benzodiazepines, or alpha-2 agonists. (15-19,21,22) The use of premedication in captive animals as part of a balanced anesthetic protocol is important as it can reduce stress and provide analgesia, and allows lower doses of induction and maintenance agents. (23) In this case, the penguin had been sedated with medetomidine (an alpha-2 agonist) and diazepam (a benzodiazepine) to facilitate safe transport to the hospital. The sedation from these drugs likely allowed a lower dose of propofol to induce and maintain anesthesia than has been previously reported in other avian species.
Propofol administration in birds has been associated with both increases and decreases in heart rate. In chickens, arrhythmias have been reported, although these may have been caused by hypoxemia, hypercapnia, or catecholamine release in response to stress. (15,17,18) In the penguin described here, we did not observe clinically significant changes in heart rate from baseline or any arrhythmia after administration of propofol. This was a captive penguin accustomed to receiving injections by hand, and this allowed administration of sedative agents before transport, thus reducing the stress experienced. In addition, medetomidine was used in the premedication, and this decreases perioperative concentrations of catecholamines and can reduce the incidence of arrhythmias during isoflurane anesthesia in some species. (24-26)
Significant increases in EtC[O.sub.2] have been reported in red-tailed hawks (Buteo jamaicensis), great-horned owls (Bubo virginianus), and Hispaniolan Amazon parrots (Amazona ventralis) when anesthetized with propofol CRI. (16,27) Respiratory depression and apnea are common side effects reported in birds anesthetized with propofol, and manual or mechanical ventilation has been recommended. (20) Vasoactivity in response to C[O.sub.2] levels influences CBF and, in many bird species, hypercapnia increases CBF while hypocapnia causes no net change to CBF. (28-31) To prevent severe hypercapnia and a subsequent increase in CBF, and hence elevation in ICP, manual intermittent positive-pressure ventilation was started immediately after induction and was continued (mechanically) until the recovery period. Normal partial pressure of C[O.sub.2] in arterial blood (PaC[O.sub.2]) in conscious king penguins is approximately 54 mmHg, and 67 mmHg in molting king penguins. (32) The EtC[O.sub.2] is used to estimate [P.sub.a]C[O.sub.2] in birds under anesthesia, although, as gas exchange in birds occurs in parabronchi via a cross-current mechanism of oxygen uptake and C[O.sub.2] release, EtC[O.sub.2] measured in expired air often lies between the partial pressure of C[O.sub.2] in venous and arterial blood and is therefore an overestimate of the true PaC[O.sub.2]. (33) Normocapnia (EtC[O.sub.2] between 43 and 56 mmHg) was achieved through mechanical ventilation during anesthesia in this case, which would have prevented potential increases in CBF and ICP and offered some protection against further brain injury.
Medetomidine and the D-rotary enantiomer dexmedetomidine also cause a decrease in respiratory rate in many avian species; however, this decrease does not always cause a corresponding increase in EtC[O.sub.2] as a consequence of the reduced rate of ventilation. (8,26) Medetomidine causes a reduction in ICP in anesthetized dogs and may be neuroprotective in animals where increasing ICP is of concern. (34) Elevated EtC[O.sub.2] after medetomidine administration has not been demonstrated in king penguins and the direct effects of decreasing ICP caused by medetomidine possibly may offset the potential increase in CBF caused by increased EtC[O.sub.2]. Atipamezole, the reversal agent for medetomidine, causes an extreme drop in cerebral perfusion pressure in dogs and its use in animals with increased ICP in this species is not advised. (34) In light of the effects of atipamezole seen in dogs, reversing the medetomidine in the king penguin would not have been advisable if an intracranial lesion or increased ICP had been suspected. This could have been a factor if the penguin experienced a prolonged recovery or demonstrated adverse effects attributable to medetomidine such as severe bradycardia or arrhythmias.
Propofol TIVA in birds has also been associated with excitable recovery phases, myoclonic activity, and head twitching. (15,16,22) In contrast, a report describing the use of propofol for induction and maintenance of anesthesia in ostriches (Struthio camelus) after intramuscular premedication with ketamine and medetomidine indicated recovery was smooth and uneventful. (35) Similarly in this case, the recovery of the penguin was rapid and smooth, with no evidence of muscle tremors or excitation. The observed quality of recovery could have resulted from the use of premedication (medetomidine and diazepam), allowing for reduced doses of propofol for induction and maintenance. In addition, some sedative effects of the medetomidine possibly persisted into the recovery phase and contributed to the excellent quality of recovery of this penguin.
In conclusion, propofol given intravenously produced a fast and smooth induction and recovery of anesthesia in this king penguin. Once the penguin was positioned and mechanical stimulation ceased, a stable plane of anesthesia was maintained by using a propofol CRI at a dosage of 0.1-0.3 mg/kg per minute with minimal cardiovascular side effects. The penguin was mechanically ventilated throughout anesthesia and rapidly regained spontaneous breathing after the propofol CRI was discontinued. When control of ventilation is possible, propofol TIVA may be a superior choice to inhalant agents for anesthesia of birds with potential intracranial lesions.
(1.) International Species Information System. Reference Ranges for Physiological Values in Captive Wildlife. Eagan, MN: International Species Information System; 2002.
(2.) Ponganis PJ, Kooyman GL. van Dam R, LeMaho Y. Physiological responses of king penguins during simulated diving to 136 m depth. J Exp Biol. 1999; 202(20):2819-2822.
(3.) Delk K. Clinical management of seizures in avian patients. J Exot Pet Med. 2012;21(2):132-139.
(4.) Shardlow E, Jackson A. Cerebral blood flow and intracranial pressure. Anaesth Int Care Med. 2011; 12(5):220-223.
(5.) Dagal A, Lam AM. Cerebral autoregulation and anesthesia. Curr Opin Anaesthesiol. 2009;22(5):547-552.
(6.) Bor-Seng-Shu E, Kita WS, Figueiredo EG, et al. Cerebral hemodynamics: concepts of clinical importance. Arq neuropsiquiatr. 2012;70(5):352-356.
(7.) Grubb B. Jones JH, Schmidt-Neilsen K. Avian cerebral blood flow: influence of the Bohr effect on oxygen supply. Am J Physiol. 1979;236(5):H744-H749.
(8.) Hawkins MG, Zehnder AM, Pascoe PJ. Cagebirds. In: West G. Heard D, Caulkett N, eds. Zoo Animal and Wildlife Immobilization and Anesthesia. 2nd ed. Ames, IA: John Wiley & Sons, Inc; 2014:399-433.
(9.) Meir JU, Ponganis PJ. High-affinity hemoglobin and blood oxygen saturation in diving emperor penguins. J Exp Biol. 2009;212(Pt 20):3330-3338.
(10.) Cole CD, Gottfried ON, Couldwell WT. Total intravenous anesthesia: advantages for intracranial surgery. Neurosurgery. 2007;61 (5 Suppl 2):369-378.
(11.) Miura Y, Kamiya K, Kanazawa K, et al. Superior recovery profiles of propofol-based regimen as compared to isoflurane-based regimen in patients undergoing craniotomy for primary brain tumor excision: a retrospective study. J Anesth. 2012;26(5): 721-727.
(12.) Greene SA. Anesthesia for patients with neurologic disease. Top Companion Anim Med. 2010;25(2):83-86.
(13.) Pavlov NA, Krivchenko Al. Cerebral blood flow during changes of the systemic arterial blood pressure in the pigeon Columba livia. J Evol Biochem Physiol. 1983; 19(3):245-250.
(14.) Zehnder AM, Hawkins MG, Pascoe PJ, Kass PH. Evaluation of indirect blood pressure monitoring in awake and anesthetized red-tailed hawks (Buteo jamaicensis): effects of cuff size, cuff placement, and monitoring equipment. Vet Anaesth Analg. 2009; 36(5):464-479.
(15.) Machin KL, Caulkett NA. Cardiopulmonary effects of propofol infusion in canvasback ducks (Aythya valisineria). J Avian Med Surg. 1999; 13(3): 167-172.
(16.) Hawkins MG, Wright BD, Pascoe PJ, et al. Pharmacokinetics and anesthetic and cardiopulmonary effects of propofol in red-tailed hawks (Buteo jamaicensis) and great horned owls (Bubo virginianus). Am J Vet Res. 2003;64(6):677-683.
(17.) Lukasik VM, Gentz EJ, Erb HN, et al. Cardiopulmonary effects of propofol anesthesia in chickens (Callus gallus domesticus). J Avian Med Surg. 1997; 11 (2):93-97.
(18.) Machin KL, Caulkett NA. Cardiopulmonary effects of propofol and a medetomidine-midazolam-ketamine combination in mallard ducks. Am J Vet Res. 1998;59(5):598 602.
(19.) Schumacher J, Citino SB, Hernandez K, et al. Cardiopulmonary and anesthetic effects of propofol in wild turkeys. Am J Vet Res. 1997;58(9): 1014-1017.
(20.) Gunkel C, Lafortune M. Current techniques in avian anesthesia. Semin Avian Exot Pet Med. 2005; 14(4):263 276.
(21.) Mama KR, Phillips LG, Pascoe PJ. Use of propofol for induction and maintenance of anesthesia in a barn owl (Tyto alba) undergoing tracheal resection. J Zoo Wildl Med. 1996;27(3):397-401.
(22.) Muller K, Holzapfel J, Brunnberg L. Total intravenous anaesthesia by boluses or by continuous rate infusion of propofol in mute swans (Cygnus olor). Vet Anaesth Analg. 2011;38(4):286-291.
(23.) Arnemo JM, Caulkett N. Stress. In: West G, Heard D, Caulkett N, eds. Zoo Animal and Wildlife Immobilization and Anesthesia. Ames, IA: Blackwell Publishing; 2007:103-109.
(24.) Vaisanen M, Raekallio M, Kuusela E, et al. Evaluation of the perioperative stress response in dogs administered medetomidine or acepromazine as part of the preanesthetic medication. Am J Vet Res. 2002;63(7):969-975.
(25.) Ishibashi M, Akiyoshi H, Iseri T, Ohashi F. Skin conductance reflects drug-induced changes in blood levels of cortisol, adrenaline and noradrenaline in dogs. J Vet MedSci. 2013;75(6):809-813.
(26.) Santangelo B, Ferrari D, Di Martino I, et al. Dexmedetomidine chemical restraint of two raptor species undergoing inhalation anaesthesia. Vet Res Commun. 2009;33(Supp] 1):S209-S211.
(27.) Langlois I. Harvey RC, Jones MP, Schumacher J. Cardiopulmonary and anesthetic effects of isoflurane and propofol in Hispaniolan Amazon parrots (Amazona ventralis). J Avian Med Surg. 2003;17(1): 4-10.
(28.) Matta BF, Lam AM, Strebel S, Mayberg TS. Cerebral pressure autoregulation and carbon dioxide reactivity during propofol-induced EEG suppression. Br J Anaesth. 1995;74(2):159-163.
(29.) Grubb B. Mills CD, Colacino JM. Schmidt-Neilsen K. Effect of arterial carbon dioxide on cerebral blood flow in ducks. Am J Physiol. 1977;232(6): H596-H601.
(30.) Faraci FM, Fedde MR. Regional circulatory responses to hypocapnia and hypercapnia in barheaded geese. Am J Physiol. 1986;250(3 Pt 2):R499-R504.
(31.) Stephenson R, Jones DR, Bryan RM Jr. Regional cerebral blood flow during submergence asphyxia in pekin duck. Am J Physiol. 1994;266(4 Pt 2):R1162-R1168.
(32.) Maxime V, Hassani S. Blood oxygen- and carbon dioxide-carrying properties in captive penguins: effects of moulting and inter-specific comparison. Comp Biochem Physiol A Mol Integr Physiol. 2014; 168:76-81.
(33.) Edling TM, Degernes LA, Flammer K, Horne WA. Capnographic monitoring of anesthetized African grey parrots receiving intermittent positive pressure ventilation. J Am Vet Med Assoc. 2001;219(12): 1714-1718.
(34.) Itamoto K, Nakaichi M, Okuda M, et al. Effects of medetomidine and atipamezole on cerebral perfusion pressure in dogs. J Anim Vet Adv. 2010;9(5): 913-919.
(35.) Langan JN, Ramsay EC, Blackford JT, Schumacher J. Cardiopulmonary and sedative effects of intramuscular medetomidine-ketamine and intravenous propofol in ostriches (Struthio camelus). J Avian Med Surg. 2000;14(1):2-7.
Sarah E. Bigby, BVSc (Hons), MVS, Jennifer E. Carter, DVM, Dipl ACVAA, Sebastien Bauquier, DVM, Dipl ACVAA, and Thierry Beths, DVM, PhD
From the Veterinary Hospital, Faculty of Veterinary and Agricultural Sciences, University of Melbourne, 250 Princes Highway, Werribee, Victoria, 3030, Australia.
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||Clinical Report|
|Author:||Bigby, Sarah E.; Carter, Jennifer E.; Bauquier, Sebastien; Beths, Thierry|
|Publication:||Journal of Avian Medicine and Surgery|
|Date:||Sep 1, 2016|
|Previous Article:||Blood biochemical values of wild scarlet macaw (Ara macao macao) nestlings and adults.|
|Next Article:||Right heart failure in an African penguin (Spheniscus demersus).|