Clinical History.
The dog was first brought in by the owner for respiratory distress. Stridor was evident on inspiration, visual examination revealed an intra-oral mass occluding the glottis and palpation of the neck revealed a mass present in the caudal oropharyngeal area over the larynx, dorsal to the trachea and about 5 cms in diameter. Exopthalamus was also noted. There were no other clinical symptoms. The owner reported that the dog had become increasingly more dyspnoeic over the last 2 months. A general anaesthetic for radiography and a biopsy was arranged for the following morning, the owner having been warned of the risks of general anaesthesia and having signed a consent form.

Pre-anaesthetic examination.
Blood samples were taken for both biochemistry and haematology profiles, the results of which were unremarkable. See anaesthetic record sheet. A clinical examination revealed temperature of 38 C, heart rate of 100 per min and respiration rate of 20. There were no apparent abnormalities of the cardiovascular or respiratory system, other than the mass. The dog was kept overnight in an oxygen cage in the intensive care unit (ICU) and starved from 10 pm with access to water until 8 am. The dog was given a class 3 anaesthetic risk, ie a patient with severe systemic disease that is not incapacitating.

Premedication.
Premedication consisted only of 0.37 mg atropine sulphate (Phoenix) given by intra- muscular route 30 minutes prior to induction. After premedication the dog was monitored constantly until induction.

Induction.
As difficulty of intubation was expected, due to the occlusion of the glottis, equipment was available for a tracheotomy and also an endoscope for assistance with intubation. Five minutes pre-oxygenisation was given via a mask before induction. The dog was quite calm prior to and during induction. A 20 g intravenous catheter was placed aseptically into the right cephalic vein. A smooth induction was achieved using 74 mg propofol (Diprivan, Zeneca) given slowly through the catheter. Intubation was performed successfully using a 6.5 mm cuffed endotracheal tube. Correct placing of the ET tube was carried out by palpating the thoracic inlet area with one hand whilst moving the tube in and out slightly in order to feel where the uninflated cuff was positioned. Correct inflation of the cuff was achieved by one person slowly inflating the cuff and listening by the mouth whilst a second person closed the valve on the circuit (which had been connected to the tube and 2 L oxygen turned on) and very gently squeezing the resevoir bag until no sounds of gas passing round the cuff could be heard and pressure was felt squeezing the bag. The dog had been connected to a circle circuit with oxygen flow of 2 L per min which was reduced to 1 L after 20 minutes. Isoflurane was used as the maintenance agent with initial settings of 2%, being reduced to 1% after 35 mins. An infusion of lactated ringers was started at a rate of 10ml/kg/hr. An area just distal to the stopper pad on the palmar surface of the left foreleg was clipped, conducting gel applied and a Doppler sensor attached with tape. A cuff was applied to the left proximal foreleg in order to measure blood pressure (BP). 0.465 mg of oxymorphone (Numorphan, Du Pont) was given by intravenous route.

Radiography.
The dog was radiographed which showed a mass consistent in size and position as described in the clinical examination. A biopsy was then taken through an incision in the right lateral neck.

Maintenance of anaesthesia.
For a detailed account of anaesthesia see attached anaesthetic record. Duration of anaesthesia was 60 minutes. General anaesthesia was unremarkable until 30 minutes into anaesthesia when a haemorrhage occurred at the incision site and the carotid artery was ligated. The systolic BP went up from 115 to 280 mm Hg. At this point the dog was connected to an ECG and within 1 minute premature ventricular contractions (PVC's) started intermittently. They then began to occur in ventricular bigeminy (every second complex was a PVC) and after a further 30 seconds were occurring in strings of 10 followed by one or two normal complexes. At this time a bolus of 9.3 mg of lidocaine (Abbott) was given by intravenous route. This had no effect and a further repeat bolus was given 1 minute later. At this time the isoflurane was reduced to 1%. See above right, where the PVCs can just be seen on the monitor. The PVC's then became intermittent again and a further 9.3 mg was given 10 minutes later, just before the cessation of anaesthesia. The systolic BP remained around 250 mm Hg and heart rate around 150 per minute. Little blood loss had occurred.

Recovery from anaesthesia.
Five minutes after cessation of isoflurane the larynx was swabbed, the oxygen had remained on and the ET tube was removed with the cuff partially inflated, and when the dog was in sternal recumbency. The dog initially seemed to have difficulty breathing and the tongue was extended and a pulse oximeter attached. The readings showed 72% (hypoxaemia) and an oxygen mask applied was immediately. The dog, at this time, became uncontrollable and disorientated, despite now being able to breath easily. It was impossible to maintain the oxygen mask over the face and the dog was taken straight through to the ICU where an intravenous bolus of 2.4 mg of diazepam (Elkins-Sinn) was given. This calmed the animal enough for telemetry pads to be attached whilst oxygen was administered and then the dog was put into an oxygen cage with the Doppler still attached. See the picture above, taken 15 minutes after being put in the oxygen cage. An hour later the dog was still showing signs of dyspnoea and had a systolic BP of 220 mm Hg, which was still high. The telemetry monitor showed that although the PVC's had stopped the T waves were large.

Post-operative progress.
Two hours after recovery the telemetry started showing abnormal traces and a cardiologist was called to interpret the trace. His recommendation was that the dog be monitored at all times, but that treatment was not necessary at this time. The dog remained in an oxygen cage for 48 hours, by which time the ECG trace had returned to normal and the dog was showing less dyspnoea than when it was first admitted. It was sent home the following day after being out for exercise and not showing any signs of dyspnoea. The owners were advised to restrict the dog to lead exercise and return in 3 days and 10 days for suture removal and biopsy results. It was not clear at this stage whether a tumour was present or whether the mass was in fact an aneurysm. If the results showed a tumour the dog would have radiotherapy as it was not possible to remove any more tissue. As this case was conducted in the University of Georgia, USA I was no longer present when the biopsy results came back.

Discussion.
The protocol for this general anaesthetic was discussed prior to induction and drugs were chosen to suit the animal's condition at the time of surgery. Possible complications were also discussed and provision made for dealing with these, ie the tracheotomy site was prepared and all equipment ready to use. This is very important as quick action needs to be taken and time is wasted making decisions after the crisis has occurred. The animal's life may also be at risk if necessary equipment is not at hand. However, this anaesthetic also proved that no matter how much planning takes place emergencies can always happen unexpectedly despite all possible precautions, ie the anaesthetic implications of ligating the carotid artery, which was also not expected. Only atropine was given as premedication, as there was concern that any sedative would cause further respiratory distress before an airway was secured. Atropine is an anticholinergic drug which was given to inhibit secretion of saliva and protect against bradycardia. Anticholinergics are standardly included in pre- medications in the University of Georgia, but other views held are that it should only be given if necessary, ie for bradycardia or if surgery might provoke a vagal response. Respiratory depression was also the reason that the oxymorphone was not given until after the dog was intubated, as although oxymorphone is ten times stronger than morphine, but has less effect as a depressant on the respiratory system, there is still some depression.

Oxymorphone can also be given quickly by intravenous route and has an onset time of about 3 minutes. When anaesthetising any dyspnoeic or very sick animal oxygen should always be given prior to induction so that the tissues are saturated, to cover the period of intubation when hypoxia can easily occur.

Propofol was used as the induction agent as recovery from this drug is rapid, which is very important when any surgery or problems with the upper respiratory tract are involved. This is because the swallow reflex and cough reflex need to present as soon as possible when consciousness returns, to avoid any aspiration or obstruction of the airway. Propofol would also be the choice of induction agent for otherwise healthy brachycephalic breeds, who anatomically have a predisposition for upper airway obstruction on recovery.

Correct placement of the ET tube is very important, and palpation of the cuff within the thoracic inlet ensures that the tube does not pass down into one bronchus which would be detrimental to the animal and would also mean difficulty in maintaining anaesthesia. Correct inflation of the cuff is also important, as it has to be inflated enough to provide a seal to stop wastage of gas and pollution by gases escaping into the theatre. Over inflation of the cuff can cause damage to the tissues with serious implications due to the nature of the site. The correct size of ET tube should, of course, be selected to suit the animal. The tube in this instance was placed correctly but could have been trimmed shorter, as the end of the tube should be by the nostrils, in order to keep the amount of mechanical dead space as small as possible. In this case the tube extended 5 cms beyond the nostrils. See the picture above, taken just prior to extubation.

A circle circuit with the valve opened slightly was used to maintain anaesthesia. The advantage of this is to save money on gases and maintenance agents. Also, if intermittent positive pressure ventilation (IPPV) is needed, and no ventilator available, it is easier to do this on a circle than a semi-closed circuit such as the Bains. The subject of whether nitrous oxide should be used in a circle system is controversial. In this country, generally, there is concern that nitrous oxide will build up within the system to harmful levels and that it should not be used unless inspired oxygen levels can be measured. However, in the US it is used frequently, as after extensive monitoring at the University of Georgia they found that using 1L of oxygen and 1 L nitrous oxide to be quite safe to use with the valve partially open, but would not recommend any higher percentage of nitrous oxide to be used without monitoring devices. Isoflurane was used as the maintenance agent, as it does not sensitise the myocardium to catecholamines which can lead to PVC's, (as halothane does). So it was an advantage that isoflurane was used in this case as, although the dog suffered severe PVC's, it probably would have been more of a problem if halothane had been used. Recovery from isoflurane is faster than halothane as less is retained in the body for metabolism, which was also needed in this case for reasons previously explained. The disadvantage usually with isoflurane is that it lowers blood pressure more than halothane, (when used at the correct dosage). However, in this case this was a distinct advantage as hypertension was a problem. Propofol also has less of an effect on sensitising the myocardium than, say, thiopentone so again this was another advantage of using propofol. It was not known if hypertension existed prior to anaesthesia, as it was not measured, although exopthalmus was noted during the clinical examination.

The hypertension was thought to be partly the cause of the extreme hyperactivity of the dog after extubation, however it was decided not to use acepromazine to sedate the dog and reduce the blood pressure, as it was unclear at this time as to the cause of the hypertension and how long it might last and the concern was that if the BP were to return to normal suddenly the added effect of the acepromazine might take the BP too low too quickly for the body to compensate. This is why diazepam was selected, although in healthy dogs it can actually increase excitement. However, the dog did become calmer and less dyspnoeic. Excitement with struggling or distress in an already dyspnoeic animal can easily lead to death and should always be avoided if possible or treated with drugs. In this case dyspnoea and hypoxia were the main concern on extubation and all monitoring other than the telemetry and visual observation was suspended for one hour to allow the dog's oxygen status to improve.

The other important feature of this general anaesthesia were the PVC's which started to occur 30 minutes after induction when the carotid artery was ligated which affected the baroreceptors present in the artery. PVC's can also be caused by anaesthetic drugs, hypoxia, interfering with certain tumours or organs, such as the pancreas, which then release catecholamines, inadequate depth of anaesthesia leading to stimulation of the sympathetic nervous system, hypoventilation and pulmonary and myocardial contusions caused by trauma to the chest. All of the above sensitise the myocardium to the effects of catecholamines, which can result in PVC's occurring. PVC's should be treated with drugs if the cause is not attributed to hypoxia or inadequate depth of anaesthesia, (both of which can be corrected by appropriate actions), if changing from halothane which sensitises the heart to isoflurane (which does not) has no effect, if the PVC's occur in conjunction with low BP or occur more than two in a row. The drug of choice is lidocaine which can be given at 1 to 2 mg per kg as a bolus or as an infusion. In this case 3 boluses were used to control the PVC's and an infusion was not necessary. The isoflurane was turned down to 1% after administration of lidocaine, as it is an anaesthetic and can affect the depth of anaesthesia (more usually when using an infusion). However, it was important to monitor the heart post-operatively to ensure that they did not recur. Telemetry was used for this purpose as it has several advantages over normal ECG monitoring. Firstly it is impractical to have ECG electrodes connected to a conscious animal for obvious reasons of disconnection problems. Telemetry involves putting electrode pads on the animal and plugging them into a small transmitter box, which fits into a pouch and tied round the animal. The ECG trace is radio transmitted and picked up by an aerial in the ceiling and the trace is displayed on a central monitor visible from anywhere in the ICU. Up to 8 animals can be displayed at one time. Two hours into the post-operative period the ECG trace showed several irregularities and the consultant cardiologist was called. The large T waves were attributed to myocardial hypoxia and, on examination of the other abnormalities, it was stated that interference with, or ligation of the carotid artery will often cause the hypertension, PVC's and other abnor- malities seen on the ECG trace. Stimulation of the vagal nerve is also involved. This is of importance for the anaesthetist to be warned in advance by the surgeon of any surgery which will interfere with the carotid artery or which will involve ligation of the artery. Fossum, Small Animal Surgery, Mosby 1997 recommends ligation of the carotid artery during a maxillectomy, but there is no mention of the possible anaesthetic implications associated with this procedure. Human literature states that even temporary occlusion of the carotid artery can cause permanent brain damage due to lack of oxygen. This hypoxia (shown by the pulse oximeter and large T wave) may have been the cause of the disorientation displayed by the dog after extubation. As to whether permanent brain damage occurs in animals when the carotid artery is ligated, animals may not show this as readily as humans or owners may notice changes in the behaviour of the animal but not relate it to the anaesthesia, and therefore not mention it. The chemoreceptors and baroreceptors are also involved in the oxygen/carbon dioxide homeostasis of the body and it would be difficult to tell whether, in this case, the hypoxia was caused by the reaction to the ligation or the original upper respiratory obstruction. At the time that the hypertension started the dog's temperature also rose and finished a little higher than prior to induction. Respiration remained constant, apart from a period of panting which is common after administration of oxymorphone, with a good tidal volume and it was not judged necessary to ventilate the dog. Lactated Ringers (Hartmann's) is the preferred intra-operative crystalloid to use and was infused at the correct rate. Post-operative analgesics were withheld due to concern over any respiratory depression being detrimental. This is a view that widely differs within the veterinary profession. It is understandable to have concern about opioids and their sedative and repressive effect, but injectible carprofen (a NSAID) could possibly have been used, as it is considered safe to use peri-operatively, due to it's lack of inhibition of the body's prostaglandin production which plays a role in renal function and protection of the gut lining. Although this procedure would not seem to be one of the most painful surgeries it would be considered unacceptable to withdraw analgesia if this procedure were carried out on a human. Carprofen is still relatively new in the US and is not yet often used peri-operatively.

Overall, this was a complicated general anaesthetic which was well planned and managed, which demonstrated the usefulness of monitoring devices for identifying complications.  

References:
Veterinary Anaesthesia, Hall & Clarke, 9th Ed, 1991
Manual of Anaesthesia, BSAVA 1992
Small Animal Surgery, T Fossum. Mosby 1997
Prof C Trim, Head of Sm & L An Anaes, University of Georgia, US. Aug 99
BSAVA Congress Anaesthesia Lectures, C Trim. 1999