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Isoflurane is the anesthetic of choice for most avian anesthetic procedures. However, inhalation anesthesia is not always
available in field situations involving wild birds, although small portable inhalation anesthesia units are available. Certain
surgical procedures, such as tracheal resection, may warrant the use of injectable anesthesia regardless of whether or not an
anesthesia machine is available [1]. Anesthetic gases can escape from the bird during surgical procedures that disrupt air sacs,
or the extension of air sacs into pneumatic bones, and thereby expose staff to anesthetic gases. Advantages of injectable
anesthetic agents include rapid administration, low cost, and minimal equipment. Some anesthetic agents can be reversed, an
important advantage when working in field situations. Injectable anesthetics are frequently used in large, long legged birds,
such as ratites, when physical restraint is impossible or dangerous. Injectable anesthetics used in birds include barbiturates,
chloral hydrate, alpha chloralose, phenothiazines, dissociatives, alpha-2 adrenergic agonists, alphaxalone/alphadolone and
propofol [2]. Some of these anesthetics, such as barbiturates, chloral hydrate, alpha chloralose and alphaxalone/alphadolone,
are no longer recommended and will not be discussed here.
The greatest disadvantage of injectable anesthetics is individual and species variation relative to drug dose and response to a
specific drug. Elimination of an injected drug depends on distribution, biotransformation and excretion. While we recognize
species differences within domestic animals and tailor drug and dose accordingly, we nonetheless tend to treat all birds as if
they belonged to one genus or species; as if, for instance, the pigeon is the same as an ostrich when in fact these two birds are
as phylogenetically different from each other as the horse is from the cat. Pharmacokinetic studies of antimicrobial drugs in
different species of birds have shown that kinetics vary significantly between species and even between birds of the same
order such as cockatiels and Amazon parrots (both Psittaformes). Therefore data collected on an injectable anesthetic using a
pigeon may not be directly transferable to another species of bird. Nevertheless, information collected on one avian species is
likely to be better for extrapolation to another avian species than are data from mammalian species.
It is important that the overall clinical condition of the bird be considered during selection of an anesthetic protocol. Precise
body weight in grams is essential for accurate dosing. When using injectable anesthetics for birds it is difficult to maintain a
surgical plane of anesthesia. The risk of cardiopulmonary depression is high and warrants careful monitoring during an
anesthetic procedure. Orotracheal intubation of the anesthetized patient allows for supplemental oxygen and positive pressure
ventilation if needed. A ventilation rate of 2 breaths per minute assists the spontaneously ventilating bird. When birds are
apneic, the ventilatory rate should be 10 - 15 breaths per minute. In the bird, both inspiration and expiration require skeletal
muscle activity and most anesthetics depress muscular activity, thus reducing air flow rate and oxygen exchange. Assisted or
controlled ventilation ensures air flow and improves gas exchange at the level of the parabronchus and air capillaries.
Intubation provides a patent airway that permits easy control of ventilation in emergency situations. Nevertheless, intubation
is not recommended in very small birds because dried mucus may obstruct very narrow endotracheal tubes and the
endotracheal tube may increase resistance to airflow because of a significant decrease in tracheal diameter.
It is recommended to calculate and prepare doses of standard emergency and supportive drugs such as epinephrine,
doxapram, lidocaine, and atropine before inducing anesthesia. The small size of many avian patients requires accurate dosing
of very small volumes or dilution of standard concentrations. Having these drugs prepared and in labeled syringes saves time
and anxiety in critical situations.
Rapid anesthetic recoveries are best for birds. Birds appear very disoriented during recovery and tend to flap their wings and
twist their head and neck. Holding the patient in a light towel wrap or rolling the bird into a loose newspaper "burrito"
provides mild restraint to prevent chaotic body movements. Keeping the bird in a warm, quiet, dark place also aids a smooth
recovery.
Injection Sites
In most birds, intramuscular injections are best given in the pectoral muscles. In flightless birds, such as ratites, pectoral
muscle mass is minimal, thus the thigh muscles are preferred. Subcutaneous injections are not advocated because uptake of
anesthetic is slowed, but if selected the recommended site is the inguinal region. Intravenous sites for injection or
catheterization include the right jugular vein, brachial vein, or the medial metatarsal vein. Intraosseous catheters are useful
when venous access is difficult, as occurs with hypotensive birds or very small birds. Intraosseous catheters can be placed in
the proximal ulna or the cranial tibiotarsus. Uptake of the drug is comparable to intravenous injection of the drug [3].
Local Anesthetics
The toxicity of lidocaine is similar for birds as it is for mammals and it has been reported to cause seizures and cardiac arrest
[4]. Toxicity can be prevented by using appropriate concentrations and volumes. Lidocaine (1 - 2 mg/kg) can be used as a
local anesthetic or to treat ventricular arrhythmias [4], and the maximal dose is 4 mg/kg. For the small avian patient this often
requires that the stock concentration of lidocaine (2%; 20 mg/ml) be diluted. Because of reluctance to use local anesthetics in
birds, information regarding long-acting local anesthetics, such as bupivacaine, is sparse. Topical benzocaine has been used
for local analgesia during repair of minor wounds in small birds [5]. A 1:1 mixture of bupivacaine and dimethyl sulfoxide
(DMSO) was applied to amputated chicken beaks immediately after amputation and feed intake was improved [6]. Intra-
articular bupivacaine, at a dosage of 3 mg in 0.3 ml saline, was reported to be effective for treating arthritic pain in chickens
[7].
Benzodiazepines
Diazepam and midazolam can reduce anxiety during anesthetic induction and recovery. These sedatives work best if given
10 - 20 min prior to further manipulations. The birds behavior does not often reflect pre-anesthetic sedation, but birds appear
to struggle less during restraint. High doses of midazolam produced sufficient sedation in geese to facilitate restraint for
diagnostic procedures [8]. This is highly advantageous with dangerous birds such as large raptors, and long-legged birds such
as cranes and ratites. The sedative effect of these drugs is evident during recovery which is slow and smooth. No studies have
been done to determine the duration of effect for diazepam or midazolam. The benzodiazepines provide muscle relaxation
when used in conjunction with ketamine and reduce the level of isoflurane needed for anesthesia [9]. Flumazenil
administered IV, helps to reverse benzodiazepine-induced sedation and restores alertness as long as enough time has passed
so that additional anesthetic agents are no longer effective.
Dissociatives
Ketamine is rarely used alone because it is associated with poor muscle relaxation, muscle tremors, myotonic contractions,
opisthotonus and rough recoveries [1, 10-12]. The dose of ketamine depends on body weight, and its dosing follows the
principles of allometric scaling so that large birds (>1 Kg) respond to 10 - 20 mg/kg whereas small birds (< 50 grams) require
much higher doses, e.g. 70 - 80 mg/kg. Additionally, there is inter-species variability in the response to ketamine. For
example, ketamine causes salivation, excitation and convulsions when given to vultures but these signs are rare in other birds
[12]. When effective, anesthesia occurs within 5 - 10 min of intramuscular injection and may last 5 - 20 min depending on the
dose and size of the bird. Recovery from ketamine, until the bird can perch or stand, can take 40 - 100 min, depending on
dose, body temperature, metabolic health, and size of the bird. It is recommended that ketamine not be used alone and be
combined with benzodiazepines or alpha2-adrenergic agonists to improve relaxation and depth of anesthesia.
Alpha2-adrenergic agonists
Xylazine, detomidine and medetomidine are usually used in combination with ketamine. The alpha-2-adrenergic agonists
provide muscle relaxation, analgesia and sedation which smoothes induction and recovery. The greatest advantage of this
group of drugs is the availability of specific antagonists to reverse the effects, allowing for smooth and rapid recovery.
Atipamezole is recommended to reverse medetomidine and detomidine, and will also reverse the effects of xylazine.
Yohimbine has been used in raptors and psittacines to reverse the effects of xylazine, both alone or in combination with
ketamine [14-16]. Similar results were noted when tolazoline was used in turkey vultures to shorten xylazine plus ketamine
anesthesia [17]. When reversing an alpha2-adrenergic agonist used in combination with ketamine, reversal must be timed so
as to avoid the bird recovering under the effects of ketamine alone as this can result in a rough recovery.
Alpha2-adrenergic agonist drugs are not recommended as single anesthetic or immobilization agents for birds. In pigeons and
Amazon parrots, high doses of medetomidine had a sedative effect but did not immobilize the birds [18]. Xylazine
administered alone causes respiratory depression, excitation, convulsions and prolonged recovery [12]. All alpha2-adrenergic
agonists have profound cardiopulmonary effects. Xylazine and medetomidine cause decreases in HR, RR, blood pH,
hypoxemia, and hypercarbia [4,12,14,18]. The arrythmogenic effects of the alpha2-adrenergic agonists can lead to
cardiovascular instability and, when coupled with hypoventilation and hypercarbia, can have an irreversible, fatal effect.
Alpha2-adrenergic agonist drugs are a poor choice of anesthetic, alone or in combination, when a bird is highly stressed.
General excitement can effectively over-ride the sedative effects of alpha2-adrenergic agonists, although the mechanism for
this effect is not clear. Therefore, when using alpha2-adrenergic agonist drugs, approach the bird quietly, inject the drug and
place the bird back into a familiar, quiet and dimly lit enclosure while waiting for the drug to take effect. The induction
period is 5 - 10 min, depending on dose and size of the bird. Ratites, raptors and long-billed birds can have a hood placed
over the head for calming when a dark cage is not available.
Xylazine plus ketamine combinations have been evaluated in several avian species. Blood pressure becomes elevated, heart
rate is decreased, and hypoxemia, hypoventilation, and hypercapnia occur [19-20].
An anesthetic combination consisting of medetomidine, midazolam and ketamine was evaluated and found to be unsafe for
use in ducks [21] as it caused bradycardia, primarily attributed to the medetomidine [21,22]. Medetomidine also decreases
respiratory rate. Apnea followed by a fatal decrease in heart rate and blood pressure was documented in four of twelve ducks
receiving medetomidine [21]. Atipamezole and flumazenil were given intravenously to reverse medetomidine and
midazolam, respectively, and the ducks rapidly regained consciousness and voluntary movement [21].
Propofol
Propofol is an intravenously administered anesthetic with rapid onset, smooth induction, short duration of effect, and smooth,
rapid recovery. Intravenous catheters are highly recommended for its administration because the drug must be given slowly
for induction and often given repeatedly to maintain anesthesia. A maximum of 2 mg/kg bolus every 30 seconds is
recommended for induction, after which 0.5 - 1.0 mg/kg/min is used to maintain surgical anesthesia [1,23]. In a study using
ducks, propofol was given as an initial IV bolus and was constantly bolused at 1 - 4 mg/kg every 5 min to maintain a light
plane of anesthesia [21]. In studies that monitored cardiopulmonary responses to propofol, mean arterial pressure (MAP)
decreased significantly [1,23]. A short period of apnea following induction is a consistent finding [21,22,24] and respiratory
depression can occur during induction and maintenance with propofol [23, 24]. Cardiac arrhythmias including ventricular
premature contractions and ventricular tachycardia, were common in chickens and profound bradycardia was noted in ducks
after the initial bolus of propofol [21,23]. Propofol has a narrow margin of safety in birds and supplemental oxygen and
respiratory assistance must be provided to counteract apnea, hypoventilation and hypoxemia [21,23-25].
Anticholinergics
The use of anticholinergics for birds is controversial. Indeed, atropine and glycopyrrolate are effective for the treatment of
vagally induced bradycardia [26]. Some argue, however, that they cause respiratory secretions to become more viscous and
thus more likely to plug narrow endotracheal tubes [27]. Others [28] recommend anticholinergics for their ability to reduce
respiratory mucus production and prevent formation of mucus plugs in small endotracheal tubes [4]. The oculocardiac reflex
has been reported in a cockatiel and suggests that treatment with an anticholinergic prior to or during ocular surgery may
prevent this reflex which is thought to be caused by ocular manipulation resulting in cardiac dysrhythmias [29].
Analgesia
Opioids -
The early literature regarding the use of opioids in birds is confusing and contradictory. For example, one study used two
different strains of chickens to evaluate the analgesic effect of equal doses of morphine. Based on their response to a noxious
thermal stimulus, one strain had a hyperalgesic response while another strain had an analgesic response [36]. With many such
conflicting results in the literature, it was assumed that opioids were not effective analgesics for birds. More recently, the
physiological effects of opioids on birds have been documented using isoflurane-sparing techniques [37-39]. In these studies,
unpremedicated birds are anesthetized with isoflurane. The minimal anesthetic concentration (MAC) is determined in each
bird, after which each bird is injected with an analgesic and MAC is again determined. A significant reduction of MAC
indicates that the drug being tested has analgesic properties. Using this technique, the analgesic effects of butorphanol were
evaluated in cockatoos, African grey parrots, and Amazon parrots. Butorphanol at 1 mg/kg was found to be analgesic in
African gray parrots and cockatoos, but not Amazon parrots [38,39]. Following injection of butorphanol, heart rate, tidal
volume, and inspiratory and expiratory times were all significantly decreased [38,39]. A similar study compared mu and
kappa opioids in chickens and both drugs had isoflurane-sparing effects [37].
Recent studies evaluated the effects of butorphanol and buprenorphine in conscious parrots [40,41]. In African grey parrots,
butorphanol (1 - 2 mg/kg, IM) had an analgesic effect while large doses of buprenorphine had no significant analgesic effect
[41]. In Hispanolian parrots, higher doses of butorphanol (3 mg/kg) were needed to produce a similar analgesic effect (J.
Paul-Murphy, personal observation). Species variability in response to opioids does occur and caution is advised when
extrapolating butorphanol doses from one avian species to another. Fentanyl (0.02 mg/kg, IM), a synthetic mu agonist, was
tested in a similar fashion in cockatoos, and was found to have little analgesic effect; a higher dose (0.2 mg/kg, SQ) was
analgesic (S. Hoppes, unpublished data). This may be due to fentanyl binding both mu and kappa receptors when given at
high doses. An excitement phase was noted in several of the birds shortly after fentanyl was injected (S. Hoppes, unpublished
data). The duration of effect of all of these opioids has only been evaluated empirically and their duration of effect may be as
short as 2 - 4 hours.
Pharmacodynamic studies have demonstrated that pigeons have more kappa opioid receptors than mu opioid receptors [42].
This one piece of information in pigeons is used to explain why birds do not respond as do mammals to mu agonists like
morphine, buprenorphine and fentanyl, and why kappa opioids, such as butorphanol, may be more efficacious analgesic in
birds. Butorphanol is currently recommended for opioid analgesia in birds, and it can be given as a pre-operative and post-
operative analgesic. When butorphanol is used as an induction agent and pre-operative analgesic the concentration of
isoflurane needed for anesthesia will be reduced.
~100 - 240 mg/kg (12 - 30 Red-necked ostriches (Struthio camelus): to reverse Ostrowski
Diprenorphine
mg dose), IV etorphine; lead to a fast but violent recovery. [33]
Ostrowski
Glycopyrrolate 0.011 mg/kg, IV Ostriches (Struthio camelus): to treat bradycardia
[33]
Chickens: pharmacokinetic study with no assessment of
analgesic effects; shorter half-life than in dogs; low
bioavailability (F= 46.7% IM and 24.2% PO) compared to
25 mg/kg, IV Roder, et
Ibuprofen mammals. high pH in the crop may have precipitated the
50 mg/kg, IM, PO al. [44]
drug in the g.i. tract; unpredictable crop emptying and
decreased motility of the crop due to handling the birds
could have affected absorption.
Broiler Chickens: Acute toxicity! Exhibited
hyperexcitability, respiratory distress and death within 3
min; these central nervous system signs have not been
Roder, et
50 mg/kg, IV reported in other species; postulated that this may be a
al. [44]
nonpharmacological effect such as the displacement of
other albumin bound ions (Ca or Mg) that leads to acute
toxicity.
Chickens: pharmacokinetic study with no assessment of
analgesic effects; a large volume of distribution (suggesting
tissue retention by peripheral tissues and/or high binding to
plasma proteins with a slow return of the drug to the
blood); slow but sustained oral absorption, attributed to
Cristofol,
Indomethacin 2 mg/kg, IV, PO high pH and unpredictable emptying of the crop, lead to
et al. [45]
mean residence times that were five times larger with the
PO route than by IV administration; from the oral Cmax
range of 0.5 - 1.1 mg/ml observed, they inferred that this
was an effective anti-inflammatory dose based studies in
mammals.
Drug Dosage (Dose), Route Species / Remarks Reference
(K) 7.3 - 11.2 mg/kg (10 Mallard ducks: 20 min duration; transient hypertension,
Ketamine (K) /
mg dose) / (Me) 36.5 - 56.2 bradycardia, and apnea; decreased respiratory rate after
Medetomidine Machin
mg/kg (50mg dose) / (Mi) induction; resuscitation often required; survival risk;
(Me) / [21]
1.46 - 2.25 mg/kg (2 mg reversal with atipamezole, 0.25 mg, and flumazenil, 0.025
Midazolam (Mi)
dose), IV mg, IV
Ketamine (K) / (K) 10 - 25 mg/kg / (M) Pet Birds: (M) is short-acting & contraindicated when Wheler
Midazolam (M) 0.5 - 1.0 mg/kg, IM severe hepatic disease is present. [59]
Pigeons (Columbia livia): ketamine followed by repeated
doses of propofol provided ~ 3.5 min loss of muscle tone
(K) 20 mg/kg, IM / (P) and pedal reflexes for each dose of propofol. Increased Fitzgerald
Ketamine (K) /
4.1 - 8.6 mg/kg (to effect), heart rate and decreased respiration within first minute & Cooper
Propofol (P)
IV after propofol administration. Apnea occurred after 62% of [25]
the propofol incremental doses. Assisted ventilation was
necessary to revive the bird if the apnea was prolonged.
Budgerigars (Melopsittacus undulatus): no response to toe
Heaton
pinch within 5 min; anesthesia was effective for 45 + min
Ketamine (K) / (K) 40 mg/kg / (X) 10 and
2/14 birds died; one at 44 min and the other at 220 min
Xylazine (X) mg/kg, IM Brauth
after ketamine/xylazine administration. Reversal with
[16]
yohimbine.
(K) 50 mg/kg / (X) 4 Lumeij
Goshawks (Accipiter gentilis): lethal dose!
mg/kg, IM [20]
Great Horned Owl (Bubo virginianus): immobilization
noted within five min; transient apnea during initial 5 min;
(K) 15 mg/kg / (X) 0.15 normal ventilation returned after 10 min Advise caution in Raffe, et
mg/kg, IM using repeated doses due to an observed deterioration in al. [19]
cardiopulmonary stability. Supplemental oxygen improved
cardiopulmonary performance.
(K) 50 mg/kg / (X) 4 Pigeons: no satisfactory induction of anesthesia was Lumeij
mg/kg, IM observed at this dosage. [20]
Naltrexone (N) / (N) 3.0 mg/kg / (Y) 0.125 Ostrich (Struthio camelus): reversal of Raath, et al.
Yohimbine (Y) mg/kg, IV Carfentanil/xylazine mixture [31]
Drug Dosage (Dose), Route Species / Remarks Reference
10, 15, 20, or 40 mg/kg, Red Tailed Hawks: None of these doses induced a loss of Kreeger,
IM consciousness. et al. [13]
~1.1 - 1.3 mg/kg (150 mg Ostrich (Struthio camelus) (n=1): darted; marked excitation Ostrowski
Xylazine
dose), IM but no immobilization and the bird was unapproachable [33]
Xylazine (X) / (X) 1.06 - 2.03 mg/kg / (B) Ostriches & emus: produced a calming effect; drowsy and
Lin [30]
Butorphanol (B) 0.10 - 0.14 mg/kg, IM ataxic 10 - 15 min after injection
Rheas: higher dosages of xylazine/butorphanol needed to
produce a similar tranquilizing effect as seen in ostriches
(X) 2.26 - 2.75 mg/kg / (B)
and emus; maintained on isoflurane, 1 - 5%; midazolam Lin [30]
0.12 - 0.20 mg/kg, IM
(0.15 mg/kg, IV) or diazepam (0.33 mg/kg, IV)
administered post-op to smooth recovery
Xylazine (X) / Ratites: tranquilized with X/B; induced with Tz;
(X) 1.06 - 2.21 mg/kg / (B)
Butorphanol (B) / maintained with 1 - 3.5% isoflurane; bradycardia & apnea
0.10 - 0.55 mg/kg, IM / Lin [30]
Tiletamine- observed; diazepam (0.13 - 0.40 mg/kg, IV) administered
(Tz) 3.5 mg/kg, IV
zolazepam (Tz) post-op to smooth recovery
Cornick
Xylazine (X) / (X) 0.5 mg/kg, IM / (C) Ratites: Xylazine given prior to carfentanil. good induction and
Carfentanil (C) 0.15 mg/kg, IV allowing intubation; apnea, hypercapnia, IPPV needed; Jensen
[34]
Ostrich; used to reverse xylazine during a prolonged
Yohimbine 0.11 mg/kg, IM Lin [30]
recovery period
Red-tailed hawks (Buteo jamaicensis): optimal dosage to
significantly reduce standing times after 20 min anesthesia Degernes
0.10 mg/kg, IV
with a 4.4 mg/kg ketamine and 2.2 mg/kg xylazine without [14]
causing profound cardiovascular or respiratory responses
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