The advantages of injectable anesthetics include ease of administration, rapid induction, low cost and availability. Disadvantages include the fact that recovery is often dependent on organ metabolism, potentially difficult reversal of medications in emergency situations, prolonged and sometimes traumatic recovery periods, muscle necrosis at injection sites and lack of adequate muscle relaxation with some medications.
This must be used intravenously, and hence a jugular, medial metatarsal or brachial vein catheter needs to be placed. It produces profound apnoea and is rarely used as an induction / anesthetic agent in birds.
Ketamine and ketamine combinations
When used alone this produces inadequate anesthesia and recoveries are often traumatic with the patient flapping wildly (doses of 20-50mg / kg are quoted). In addition, due to the high doses required, the duration of anesthesia may be prolonged, leading to poor recovery rates, potential hypothermia and hypoglycaemia.
Combining ketamine with other injectable anesthetic agents allows reduction of the dose of ketamine and can therefore allow faster recovery times. Diazepam at a dose of 1-1.5 mg / kg allows the dose of ketamine to be reduced to 20-40mg / kg or midazolam at a dose of 0.5-1.5mg / kg allows the ketamine dose to be reduced to 10mg / kg. These two tranquillisers help with muscle relaxation and sedation, and reduce flapping on recovery as well as shortening recovery time.
Ketamine may also be combined with xylazine at 1-2.2 mg / kg, which can reduce the dose of ketamine to 5-10mg / kg. Coles (1997) has recommended a dosage of 20 mg / kg ketamine and 4 mg / kg xylazine, intramuscularly, and finds that this gives 10-20 min of anesthesia with full recovery in 1-2 hours. It should however be avoided for pigeons and doves and for all wading birds.
Medetomidine (60-85 μg / kg) can reduce the ketamine dose to 5mg / kg. However slightly higher doses of 10mg / kg ketamine and 100-150 μg / kg medetomidine may be required for full surgical anesthesia in some species such as waterfowl and owls.
Again the use of these a2 agonist drugs reduces the ketamine dosage appreciably and so improves recovery rates, whilst enhancing levels of sedation and analgesia. Xylazine has the side effect of inducing respiratory and cardiac suppression and so has become less popular and should be used with caution in debilitated patients. It may be reversed with yohimbine at 0.1mg / kg intravenously, but this may not fully reverse its effects. Medetomidine may be reversed fully with atipamezole (administer the same volume as medetomidine given) and does not seem to produce such profound side effects making this a very useful injectable anesthetic. It can still have cardiopulmonary depressive effects and may compromise blood flow to the kidneys, risking renal damage. Sun conures have been noted to be particularly intolerant of ketamine-oc2 agonist combinations.
The above combined medications are generally given intramuscularly and induction will take on average 5-10 min. Complete recovery may take 2-4 hours or more unless reversible agents are used.
Midazolam (Hypnovel®) may be used on its own as a sedative in many species, and of course as an anticonvulsant. Doses for sedation in geese and swans have been quoted as 2mg / kg intramuscularly.
Extending and maintaining anesthesia
It is always advisable if using injectable anesthetics that the avian patient is intubated and oxygen supplied, or at least that it is available on standby. This also allows for anesthesia to be extended from the 15-20 minutes provided by many injectable agents, by introducing low levels of isoflurane (0.5-1%) if the surgical procedure is likely to be prolonged.
Alternatively, anesthesia may be induced directly using an inhalational agent via a face mask. It may be necessary with some species with long bills to adapt face masks from juice or water bottles, although the majority of birds of prey and parrots have short enough beaks to fit inside standard face masks.
This has been used in avian anesthesia. It has good analgesic properties, but accumulates in large hollow viscous organs. There is some thought that it may therefore accumulate in the air sacs and may prolong anesthetic recovery times. Recent evidence disputes this as air sacs have a means of venting gases. Some species of bird have subcutaneous air pockets, such as many diving birds (e.g. gannets and pelicans), and these can rupture following gas accumulation: its use in these species should therefore be avoided.
Nitrous oxide cannot be utilised on its own for anesthesia, and halothane or isoflurane is required to allow a surgical plane to be reached. It should not exceed 50% of fresh gas flow, and should not be used for avian anesthetics if respiratory disease is suspected. As with mammalian anesthesia, the nitrous oxide supply must be discontinued some 5-10 min prior to the end of anesthesia to minimise diffusion hypoxia.
Halothane is now rarely used for birds and is not licensed for use in the UK. One of the reasons is that halothane is partly metabolised by the liver and, as many sick avian patients have some degree of hepatic function impairment, this can place the patient at some risk. Recovery is often extended and cardiac arrest often occurs at the same time as respiratory arrest giving little response time in an emergency. Halothane also depresses the responsiveness of the bird’s intrapulmonary chemoreceptors (IPCs) to carbon dioxide. This is important as the intrapulmonary chemoreceptors only respond to increasing carbon dioxide levels in the anesthetised bird and not to hypoxia. Hence birds anesthetised with halothane are less able to adjust ventilation in response to changes in carbon dioxide levels.
This is the anesthetic of choice for the avian patient. Induction may be achieved by face mask on 4-5% concentration, being turned down to 1.25-2% for maintenance, preferably delivered via an endotracheal tube. Maintaining the patient using a face mask requires an extra 25-30% increase in gas concentration.
The advantages of this agent include its low blood solubility, which allows rapid changes in anesthetic depth to occur. At sedative or light anesthesia levels the adverse cardiopulmonary effects are minimal. It does not require liver metabolism for recovery to occur. Hence it is a useful anesthetic for sick avian cases. Cardiovascular arrest tends not occur at the same time as respiratory arrest, as happens with halothane, so giving some time for resuscitation.
Sevoflurane produces a quicker recovery time than isoflurane, but otherwise seems to have the same safety margins and anesthetic effects as isoflurane, although it is not licensed for use in birds in the UK. It often requires higher induction percentages than isoflurane (5-6% compared with 3-4%). This is due to its much lower blood solubility (blood:gas coefficient 0.68), which leads to rapid recovery rates once supply of the anesthetic is discontinued. Maintenance levels average at 3%. It is minimally metabolised in the body (<1%) and, like isoflurane, seems not to produce cardiac dysrhythmias. Its high cost currently restricts its use, however its quicker revival rate may make it the gaseous anesthetic of choice for avian patients in the future.