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39 Notes on sedation and general anaesthesia

Shailen Jasani, with, Simon Ripoll

General Considerations

Successful management of the emergency patient frequently requires the use of sedative and anaesthetic drugs. However, it is in the emergency setting that the inherent risks and adverse effects of these drugs on patient physiology assume an increased significance and this should never be underestimated.

Clinical Tip

Where the patient’s condition allows, every effort should be made to delay anaesthesia until the patient is stabilized.
Cautious and extremely careful use of agents and techniques with which the clinician is personally familiar is more important than the choice of any particular agent.

Potential risks of sedation and anaesthesia

Clinical Tip

Before commencing sedation or anaesthesia, the patient should be assessed in the context of how the major body systems are likely to cope with the adverse effects of the drugs employed, and also in turn how the course of anaesthesia is likely to be influenced by the patient’s condition. Potential problems should be anticipated and prepared for in advance.

See Tables 39.1 and 39.2.

Table 39.1 Potential adverse effects of anaesthesia on body systems

Body system Adverse effects
Cardiovascular
Hypotension
Reversal of peripheral vasoconstriction which the patient may be relying on to maintain perfusion of vital organs
Bradycardia or tachycardia
Cardiac dysrhythmia
Respiratory
Reduced ventilation or apnoea
Ventilation/perfusion mismatch
Hypoxia
Hypercapnia
Respiratory acidosis
Nervous
Direct central nervous system suppression
Raised intracranial pressure
Reduced cerebral or spinal perfusion
Renal Reduced renal perfusion
Hepatic Reduced hepatic perfusion
Gastrointestinal Increased risk of regurgitation and subsequent aspiration
Temperature Hypothermia

Table 39.2 Potential effects of patient condition on the course of anaesthesia

Patient condition Effect on anaesthesia
Cardiovascular compromise (e.g. hypovolaemia)
Risk of overdose (e.g. due to reduced volume of drug distribution, delayed response to intravenous injection)
Reduced cardiac output increases rate of inhalation anaesthetic uptake resulting in more rapid inhalation induction
Reduced hepatic and renal perfusion reduces metabolism and elimination of drugs
Respiratory compromise Reduced ventilation results in slower onset of inhalation anaesthesia and a slowed response to altered inhalation anaesthetic concentration
Central nervous system disease Reduced level of consciousness increases sensitivity to all sedatives and anaesthetic agents
Renal disease Reduced renal elimination of drugs, prolonging duration of effect
Hepatic disease Reduced hepatic metabolism of anaesthetic drugs, prolonging duration of effect
Hypoalbuminaemia Increases nonprotein-bound, active concentration of many drugs, increasing sensitivity to these drugs

Hypothermia

Body temperature is likely to fall progressively in proportion to the duration of anaesthesia and may result in widespread detrimental effects, for example:

Hypoventilation
Hypoxaemia
Cardiac dysrhythmias
Central nervous system dysfunction
Slowed drug metabolism, potentiating or prolonging sedative and anaesthetic effects.

Maximizing patient safety prior to sedation and anaesthesia

The fundamental goal is to ensure adequate oxygen delivery to the vital organs.

By ensuring vital organ perfusion
Correct blood pressure
Correct hypovolaemia (± correct dehydration)
Normalize heart rate
Correct malignant or premalignant dysrhythmia
By ensuring adequate blood oxygenation
Restore blood oxygen-carrying capacity (correct packed cell volume/haemoglobin content)
Improve ventilation (e.g. drain pleural fluid, relieve pneumothorax, treat pulmonary oedema)
In addition
Reduce intracranial pressure if suspected to be elevated
Control seizures
Correct hypoglycaemia
Treat acute renal failure, improve urine output in oliguria/anuria, correct azotaemia
Correct any clinically significant electrolyte abnormality

Is general anaesthesia necessary?

Depending on the intended investigation or procedure, important questions to consider may be:

Can general anaesthesia be avoided while still providing sufficient restraint and insensibility to pain to accomplish the task?
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Will appropriate analgesia, with or without additional sedation, be sufficiently effective?
Could local anaesthesia be utilized in combination with sedation to perform a painful procedure?
Or in fact, is general anaesthesia the safest option?

Maximizing patient safety during general anaesthesia

1 Select the most appropriate induction method.
2 Establish good venous access.
3 Do anything you can do without anaesthesia beforehand to minimize anaesthetic time (e.g. pre-clip surgical site).
4 Have all equipment and drugs well prepared (anticipate problems) (Table 39.3).
5 Preoxygenate via a facemask or flow-by oxygen until ready to intubate.
6 Adopt a calm, quiet approach – relaxing the patient minimizes the dose of anaesthetic required.
7 Take preinduction readings of vital parameters.
8 Attach the required monitoring equipment pre-induction if the patient allows it.
9 Intravenous fluids. Unless the patient’s condition contraindicates it, run isotonic crystalloid fluids at surgical rates (typically 10 ml/kg/hr) as induction commences to offset any potential drop in blood pressure. The type and rate of fluids employed subsequently under anaesthesia in general will be based on that already instituted for stabilization (see Ch. 4). To what extent these rates are modified for anaesthesia depends on:
(a) Cardiovascular status at induction
(b) Packed cell volume, albumin and electrolyte levels
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(c) Expected on-going pathological fluid losses (bleeding, body cavity effusions or gut sequestration)
(d) Intraoperative blood loss.
10 Calculate the approximate expected dose of anaesthetic agent required – be conservative. Consider using an intravenous sedative pre-induction to minimize the intravenous anaesthetic dose (e.g. diazepam). Dose in increments until the desired effect is reached (usually to allow smooth intubation), allowing plenty of time between doses if the patient is cardiovascularly unstable. More rapid administration may be justified if patent airway or intermittent positive pressure ventilation (IPPV) is a priority.
11 Ensure smooth intubation. Use local anaesthetic spray in cats in a timely fashion and allow it time to work.
12 Perform an airway, breathing, circulation (ABC) check immediately on intubation and be prepared to implement IPPV:
(a) Airway = check correct intubation and secure the tube in place
(b) Breathing = confirm breathing through tube (chest movement produces bag movement) or give a breath if no breath observed (bag movement produces chest movement)
(c) Circulation = check pulse.
13 Use a balanced anaesthetic technique for the maintenance of anaesthesia: use nitrous oxide in the gas mixture if it is safe to do so, timely opioid analgesia bolus or constant rate infusion (local anaesthetic techniques, muscle relaxants if familiar with their use). Minimize anaesthetic concentrations at all times.

Table 39.3 Being prepared for anaesthesia of critical patients

Anaesthetic aspect Equipment
Intubation
Laryngoscope
Range of ET tubes – include several much smaller tubes where potential for unexpectedly narrow airway exists (e.g. upper airway obstruction)
Tube tie
Local anaesthetic spray for cats
Complications of intubation
Face mask
Alternative narrow endotracheal oxygen delivery device: long narrow bore tube such as urinary catheter which can be adapted to connect to oxygen supply
ET tube stylets/wire to act as guide and thread tube over in event of partial obstruction of nasopharynx
Suction apparatus
Emergency tracheotomy kit
Oxygen administration and ventilation Appropriate breathing circuit: if continuous IPPV anticipated, use T-piece for <10 kg, use Bain or Circle for >10 kg
Monitoring Pulse oximeter, ECG, blood pressure monitor, capnograph, thermometer or temperature probe, glucometer
Intravenous fluids
Include those that might be required later or in event of patient deterioration: crystalloids, colloids, Oxyglobin®, appropriate blood products as indicated and as available
Fluid administration equipment, preferably including infusion pumps
Temperature control
Preventing heat loss: blanket, bubble wrap, heat and moisture exchanger on circuit (Thermovent®), warm ambient temperature of room
Heat sources if appropriate: warm air blanket, warm water bed, ‘hot hands’
Emergency drugs Atropine, adrenaline (epinephrine), lidocaine (only indicated if there is continuous ECG monitoring to characterize nature of cardiac dysrhythmia)

ECG, electrocardiograph; ET, endotracheal; IPPV, intermittent positive pressure ventilation.

Clinical Tip

Because anaesthetic drugs cause cardiorespiratory depression in a dose-dependent manner, it is important to try to minimize the dose used. Anaesthetic administration can be minimized by the rational use of additional drugs which contribute to the anaesthetic state, without producing significant cardiorespiratory effects of their own.
The anaesthetic state consists of unconsciousness, analgesia and muscle relaxation. The provision of effective analgesia using opioids and, where possible, local anaesthesia in particular can go a long way to reducing anaesthetic dosage.
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14 Control temperature (see Table 39.3). Rebreathing circuits (circle systems) recycle exhaled breath (minus carbon dioxide) and so help to retain warmth and moisture.
15 Monitor appropriately (see below).
16 Ensure that intensive patient monitoring and support continue through the recovery as well.

Patient monitoring during general anaesthesia

Under anaesthesia, the following questions should constantly be asked:

Is there adequate circulation and perfusion?
Is the patient adequately oxygenated?
Is there adequate ventilation to get rid of carbon dioxide from the body?
Is there adequate kidney function to ensure other waste products are removed from the body?

The emphasis should be on continuous monitoring of physical examination parameters, ideally by a member of staff dedicated to this purpose:

Pulse rate and quality – ideally access to a central (femoral) and peripheral (distal limb, tongue) pulse. This should be supplemented by heart auscultation by stethoscope or oesophageal stethoscope
Respiratory rate and quality – observation of chest and reservoir bag movement
Capillary refill time and mucous membrane colour
Core temperature and the temperature of the extremities
Eye position, palpebral reflex, pupil size, jaw tone.

Clinical Tip

Recording of measurements every 5 minutes is to be encouraged, primarily to focus the mind and alert the recorder to important trends in vital parameters over time.

Clinical Tip

Monitoring such as pulse oximetry, blood pressure measurement, capnography and electrocardiography should be used as available. There are two golden rules with monitoring:

1 When in doubt, always look at the patient and rely on your own senses.
2 Do not rely on what just one monitor is telling you; always consider it in the context of all the other information you have available – from the patient, from other monitors, and from what is being done to the patient (surgery, drugs, fluids, anaesthetic, etc.).

Sedative and Anaesthetic Drugs

Benzodiazepines

These are especially useful for sedation or calming in emergency patients when combined with an opioid; if possible, give the opioid first and allow time for it to take effect.

Minimal cardiovascular or respiratory effects at standard doses.
Can be given i.v., showing an obvious effect within less than 1 minute.
Diazepam is poorly absorbed following i.m. administration; use midazolam.
Either drug can be combined with a low dose of ketamine to provide more profound sedation without undue cardiovascular compromise.

Clinical Tip

A combination of benzodiazepine, opioid and low dose ketamine may provide particularly effective sedation without needing to use a high dose of any of the individual drugs.
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Opioids

Clinical Tip

Opioids have an important role to play in the anaesthetic management of the emergency patient, and as a general rule they should be utilized whenever possible.
It should be remembered, however, that what is an acceptable dose for analgesia in the conscious patient may sometimes represent overdose if given in the anaesthetized patient.

See Chapter 5.

Medetomidine and dexmedetomidine

Potent agonists at alpha2-adrenoceptors in the brain and spinal cord.
Cause profound and predictable sedation as well as good analgesia.
Use with caution in the emergency patient because of marked physiological effects.
Cause widespread peripheral vasoconstriction and significant bradycardia; also cause a reduction in cardiac output, although perfusion of vital organs is considered to be well preserved.
Very low doses of medetomidine (1–2 µg/kg) have very much reduced side effects, while still contributing to effective sedation in combination with other drugs:
Combines well with opioids
Higher doses of opioids or addition of small doses of benzodiazepine can improve sedation whilst allowing the medetomidine dose to remain low
Combination with low dose ketamine can provide good sedation whilst offsetting bradycardia to some extent.

Contraindications for use

Absolute contraindications

Any form of shock
Severe hypotensive state
Bradycardia or pathophysiological tachycardia
Cardiac dysrhythmia
Significant respiratory compromise.
Relative contraindications

Potential to seizure
Raised intracranial pressure (bradycardia)
Unstable diabetic patients (hyperglycaemic effects)

Acepromazine

Anxiolytic agent.
Combines effectively with opioids to produce good sedation.
Arterial hypotensive effects unhelpful in many emergency patients and cannot be pharmacologically reversed.
Lacks significant direct respiratory depressant effects; can be useful in calming certain patients in respiratory distress (e.g. upper respiratory tract obstruction, rib injury).
History of seizures is not a contraindication for judicious use.

Ketamine

Minimal cardiovascular and respiratory effects at lower doses.
Can contribute to sedation or general anaesthesia, and is also an effective analgesic (see Ch. 5).
Should almost always be combined with another agent (benzodiazepine, medetomidine or acepromazine); addition of an opioid helps to produce smooth sedation whilst adding to analgesia.

Contraindications

May increase heart rate which is unhelpful in certain patients, e.g. cats with hypertrophic cardiomyopathy; any patient with cardiac disease where increased myocardial oxygen demand would be detrimental.
May increase intracranial pressure and is potentially pro-convulsant, therefore avoid in head trauma and seizuring patients.
Ketamine is excreted primarily unchanged by the kidneys in cats, therefore use judiciously if there is severe renal dysfunction; primary hepatic metabolism in dogs.

Propofol

Rapid-acting; can be used as both a sedative and anaesthetic.
Causes dose-related hypotension and respiratory depression so use judiciously.
Can be titrated to effect and slow, incremental dosing should always be employed:
Failure to do this in the shocked or severely hypotensive patient can easily prove fatal
Cardiovascular-sparing sedative agents should be used whenever possible to minimize the dose of propofol in animals with cardiovascular compromise; combination of opioid and benzodiazepine often ideal
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If sedation only is required, small sub-anaesthetic doses of propofol can be used to ‘top up’ a diazepam/opioid combination.
Tendency to cause apnoea at induction (particularly in dogs); easily rectified by IPPV following intubation but allowance must be made for the possibility of delayed or difficult intubation:
Preoxygenate
Administer propofol slowly
Use good premedication to minimize propofol dose.

Alfaxalone

Good alternative to propofol in many situations; can also be used as both a sedative and general anaesthetic.
Also produces dose-dependent hypotension and respiratory depression at higher doses.
Use of cardiovascular-sparing premedication is recommended to minimize the total dose of alfaxalone used.
Best administered in increments allowing 15–20 s between boluses; given in this way, it appears to be less likely to produce apnoea than propofol:
May be the intravenous agent of choice in respiratory compromised patients
Low doses of alfaxalone, titrated to effect, are useful in head trauma where apnoea and consequent hypercapnia is particularly undesirable.

See Tables 39.4 and 39.5 for information on drugs used for sedation and anaesthesia; see Table 5.1 for information regarding opioids.

Table 39.4 Information for drugs used for sedation and general anaesthesia

image

Table 39.5 Reversal agents for sedatives

Drug Reversing agent Dose and route
Medetomidine, dexmedetomidine Atipamezole
5× dose in mg/kg of medetomidine (same volume) in dogs
Usually given at 2.5× dose in mg/kg of medetomidine (half volume) in cats, but repeat the dose if sedation poorly reversed
Licensed for i.m. use, but use i.v. in an emanergency
Full (pure) opioid Naloxone
0.01–0.1 mg/kg slow i.v. to effect, i.m.
Short duration of action (20–60 minutes) due to rapid metabolism therefore repeat doses may be required
Diazepam, midazolam Flumazenil
0.01 mg/kg rapid i.v
Onset of action 1–2 minutes
Short duration of action (60 minutes)

Sedative combinations

These may allow a reduced dose of each drug to be used, thus reducing the potential for side-effects (Box 39.1).

BOX 39.1 Sedative combinations for emergency patients

Very unstable patient, low pain

Butorphanol 0.2–0.3 mg/kg i.v. followed 5–10 minutes later by diazepam/midazolam 0.2 mg/kg i.v.

Unstable patient, high pain

Substitute butorphanol with morphine/methadone 0.1–1.0 mg/kg (dogs) or 0.1–0.5 mg/kg (cats) i.v. or i.m.; use buprenorphine 0.02 mg/kg i.v. or i.m. if no full opioid

Critical but stable, and not sedated enough or likely to be sedated enough with above combinations

ADD acepromazine 0.005–0.01 mg/kg i.v.
OR medetomidine 1–2 µg/kg i.v.
OR ketamine 2–3 mg/kg i.v.
Choice depending on patient condition, temperament

Critical but stable, and temperament suggests more predictable sedation required

Leave out diazepam/midazolam, go straight for a triple combination of opioid (as above) + ketamine + acepromazine OR medetomidine – choice depending on patient condition. Medetomidine combinations will usually give the most profound sedation and should be used with care

Lively or aggressive patient with potential critical illness or unpredictable response to sedatives

Go for medetomidine 3–5 µg/kg + appropriate opioid at above doses i.v. or i.m. Medetomidine can always be topped up if there is not enough sedation

Primary clinical problem is respiratory compromise

Acepromazine 0.01 mg/kg i.v. + butorphanol 0.1 mg/kg i.v.
Acepromazine 0.01 mg/kg i.v. + ketamine 2–3 mg/kg i.v.
Diazepam/midazolam 0.2 mg/kg i.v. + ketamine 2–3 mg/kg i.v.
Acepromazine + diazepam/midazolam + ketamine at same doses if smoother sedation required

Additional notes

Medetomidine doses may need to be up to two times higher in cats
All combinations can be mixed in one syringe, except diazepam which must be given separately
These doses are a guide only, based on personal experience. They are deliberately intended to be for the emergency patient with critical illness, and so are deliberately conservative ‘starter’ doses, on the grounds that it is better to top up poor sedation as required, rather than to risk destabilization of a patient
In patients with the potential for severe respiratory compromise, general anaesthesia and intubation may be safer than any of these sedative combinations

Inhalation Anaesthesia

Induction

Induction with inhalant agents is generally less desirable in critical patients.
Especially avoid it where it is important to establish a secure airway rapidly, e.g. respiratory compromise, risk of airway obstruction, high risk of regurgitation and aspiration of stomach contents.
May be the induction technique of choice in paediatric, especially neonatal and juvenile, animals.

Maintenance

Drugs of choice in most critical patients.
Depth of anaesthesia readily controlled; cardiorespiratory depressant effects readily reversible because the anaesthetic can be rapidly removed from the body via the lungs.
Greatest clinical familiarity.
Dose-related arterial hypotension and respiratory depression can be minimized by supplemental sedation and analgesia using cardiovascular-sparing drugs, in particular opioids.
Sevoflurane is the most rapidly responsive form of anaesthesia of the commonly available agents and is the author’s preferred agent in the emergency patient.
Nitrous oxide can be used to reduce the concentration of inhalant and so help to reduce the cardiorespiratory depressant effects of these agents:
Avoid if arterial saturation of haemoglobin with oxygen (SpO2) less than 95%
Will rapidly diffuse into any abnormal air-filled spaces in the body; avoid in pneumothorax, gastric dilation and gastrointestinal obstruction in particular.

Considerations in Specific Disorders

Caesarean section

Anaesthetic considerations for dam

Increased risk of regurgitation/vomiting due to pressure from gravid uterus and not being starved.
Anaesthetic doses must be calculated according to estimated non-pregnant weight.
Inhalation induction more rapid but overdose more likely.
Displacement of diaphragm by gravid uterus interferes with ventilation.
Positioning in dorsal recumbency may cause hypotension due to compression of the caudal vena cava by the gravid uterus.
Intraoperative and postoperative pain.

Anaesthetic considerations for neonates

Periods of hypotension or vasoconstriction may reduce placental blood flow.
Anaesthetics cross the placenta and cause neonatal depression.
Potential for hypothermia.
Smooth, rapid recovery of dam required for optimum nursing of neonates.
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Example anaesthetic protocol

Premedication:
Pethidine (1–2 mg/kg i.m.)
Pre-clip ventral abdomen and perform initial surgical scrub
Preoxygenate
Induction: Propofol
Maintenance: Isoflurane in oxygen/nitrous oxide mixture (discontinue nitrous oxide prior to removal of foetuses to avoid potential diffusional hypoxia when they start to breathe)
Intravenous fluids: Isotonic crystalloid at 10 ml/kg/hr
Analgesia:
Lidocaine (diluted with saline) infiltrated into abdominal midline prior to final scrub and at time of laparotomy closure
Carprofen or meloxicam i.v. following delivery
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Intractable blood loss: surgery for ruptured splenic haemangiosarcoma

Anaesthesia may interfere with compensatory mechanisms for hypovolaemia and cause hypoperfusion of vital organs (brain, heart, lungs).
Appropriate fluid resuscitation and possible abdominal counterpressure are essential preoperatively (see Ch. 29) and increase the margin of safety for anaesthesia.
Packed red blood cell transfusion if indicated; Oxyglobin® may be used but small bag size so may not be practical for big dogs.
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Example anaesthetic protocol

Premedication:
Full opioid (e.g. morphine 0.3 mg/kg slow i.v.)
Pre-clip ventral abdomen and perform initial surgical scrub
Induction:
Preoxygenate
Diazepam 0.2 mg/kg i.v.
Propofol or alfaxalone i.v.
Maintenance: Inhalant anaesthesia in 100% oxygen
Intravenous fluids: Isotonic crystalloid at 10–20 ml/kg/hr ± synthetic colloid (5 ml/kg boluses or appropriate infusion) as necessary
Analgesia:
Full opioid premedication, intra- and postoperatively
Carprofen or meloxicam only when cardiovascular status is completely stable

Diaphragmatic rupture

Anaesthesia only indicated following adequate and sustained patient stabilization (see Ch. 28).

Example anaesthetic protocol

Premedication: Midazolam 0.2 mg/kg, ketamine 2 mg/kg and acepromazine 0.01 mg/kg i.v.
Induction:
Preoxygenate
Attach pulse oximeter if available
Propofol i.v.
Lidocaine spray on larynx (cats)
Commence IPPV as quickly as possible
Maintain initially in sternal recumbency with chest raised above abdomen while the anaesthesia is stabilized and good oxygenation confirmed
Clip in lateral and dorsolateral recumbency with the chest raised above the abdomen
Breathing circuit: Must allow manual IPPV (e.g. modified Ayres T-piece for smaller patients)
Maintenance:
Inhalant anaesthesia in 100% oxygen
Continuous manual IPPV throughout surgery until the diaphragm is repaired and air drained from thoracic cavity
Intravenous fluids: Isotonic crystalloid at 10 ml/kg/hr
Analgesia:
Full opioid immediately after induction i.v. or i.m.; topped up as necessary
Carprofen or meloxicam after induction if the cardiovascular status is stable

Gastric dilatation and volvulus syndrome

Anaesthesia is only indicated following adequate patient stabilization with fluid therapy and gastric decompression (see Ch. 29).

Anaesthetic considerations

Compression of the caudal vena cava is likely to be worse in dorsal recumbency exacerbating reduced venous return to the heart and depressing cardiac output; gastric decompression is essential before induction.
Aggressive fluid therapy must be continued during anaesthesia.
Cardiac dysrhythmia may exist before induction and exacerbate hypoperfusion; anaesthetic agents may sensitize the myocardium to dysrhythmogenic molecules with a risk of deterioration into malignant and potentially fatal rhythm disturbances. Minimize risk by using high inspired oxygen concentrations, preventing hypoventilation with IPPV, and minimizing anaesthetic doses. Monitor and treat if indicated (see Ch. 12).

Example anaesthetic protocol

Premedication: Methadone 0.3 mg/kg slow i.v. (avoid morphine as more emetic)
Induction:
Preoxygenate
Aggressive intravenous crystalloids as indicated (10–40 ml/kg/hr)
Attach ECG electrodes prior to induction
Diazepam 0.2 mg/kg i.v.
Alfaxalone or propofol i.v. 30 seconds later
Maintenance: Isoflurane in 100% oxygen
Analgesia:
Methadone continued regularly
Carprofen or meloxicam only when the cardiovascular status is completely stable; also delay administration depending on the severity of gastrointestinal compromise

Traumatic brain injury

Only anaesthetize in exceptional circumstances.
Anaesthetics directly suppress central nervous system activity, therefore there is a particular risk in any patient with significant, symptomatic brain pathology.
Avoid ketamine.
Inhalant anaesthetics tend to elevate intracranial pressure; use with extreme caution; consider propofol infusion instead.
Try to avoid the patient being in a relatively head-down position or continuous pressure over the jugular veins as this may worsen intracranial hypertension.