Oxford Handbook of Anaesthesia (3 edn)
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Psychiatric disorders
Some form of psychiatric illness is present in about 10% of the UK population at any time. The commonest psychiatric disorder is depression. Most psychiatric patients are well controlled most of the time. Many patients are on long-term drug therapy which should be continued perioperatively where possible.
Major psychiatric illness affects about 1% of the population. It carries a significant risk of self-harm or suicide. Alcohol and drug misuse is common among the psychiatric population. The stress of hospitalisation for surgery may exacerbate coexisting psychiatric problems.
The anaesthetic implications of psychiatric illness are as follows:
Where the capacity of the patient to give consent is impaired (e.g. dementia, mania, psychosis).
Where the psychiatric illness itself also causes physical illness (e.g. anorexia nervosa).
Where the psychiatric medication may interact with anaesthetic drugs and techniques (e.g. antidepressants).
Consent
Most patients can give consent normally (see p. 18). In England and Wales, the Mental Capacity Act (2005) and in Scotland the Adults with Incapacity Act (2000) clarify capacity and consent issues. Patients who are detained under the Mental Health Act (1983) may only be compelled to accept psychiatric treatment under the terms of the Act.
Anxiety
Anxiety in the anaesthetic room is extremely common and usually best managed with explanation, reassurance, oral premedication, or IV sedation (e.g. midazolam 2mg IV) titrated to effect. Anxiety disorder may be acute or chronic (symptoms are similar) or occur as part of other disorders (e.g. depression). Extreme agitation may make cannulation difficult. Patients may hyperventilate and have high levels of circulating catecholamines.
Dementia
Dementia refers to irreversible global deterioration in higher mental functioning. Fifty percent of cases are due to Alzheimer's disease.
Prevalence: 1% aged 65–74 rising to 10% aged >75, and 25% aged >85yr. Slightly more common in women.
Mean life expectancy is ∼7yr from diagnosis.
Patients may be unable to give informed consent: an incapacity form should be completed by the consultant responsible.
Patients are usually confused and may be agitated (occasionally violent) or profoundly withdrawn.
Patients with early or mild dementia are increasingly being treated with antidementia drugs. Donepezil, rivastigmine, and galantamine are all anticholinesterases, which may prolong the action of suxamethonium and partially antagonise the effects of non-depolarising neuromuscular-blocking drugs.
Regional anaesthesia may still be desirable if significant comorbidity: ketamine (e.g. 5–20mg IV) may facilitate this and preserves airway reflexes and BP (titrate to effect). (Midazolam may cause disinhibition, which may paradoxically worsen agitation.)
Patients with dementia may be at increased risk of post-operative cognitive dysfunction (POCD).
Anorexia nervosa is a chronic, severe, multisystem disorder which carries the highest morbidity and mortality rate of any psychiatric disorder. Up to 20% of patients may die prematurely.
Anorexia (abnormal body image with deliberate weight loss through food restriction) is present in 0.3% of young women, and is more common in teenagers. Bulimia nervosa (uncontrolled binge eating and purging) is more common (∼1%). In both disorders patients are about 90% female.
Typically anorexics are 25% below their ideal weight (bulimics may be normal or even overweight). A diagnostic criterion is BMI <17.5.
Many patients have psychiatric comorbidity such as depression, anxiety, and obsessive-compulsive disorder.
Misuse of laxatives, emetics, diuretics, and other substances to increase weight loss is common. Patients are evasive about their behaviour. A well-documented history (e.g. from the GP) is valuable.
Clinical features are those of malnutrition and starvation: cachexia, hair loss, amenorrhoea, and osteoporosis. Immunocompetence is usually preserved until >50% of normal body weight is lost. Endocrine derangements cause amenorrhoea and impaired thyroid function and glycaemic control, and may mimic panhypopituitarism.
CVS: significant bradycardia and hypotension are common (e.g. systolic BP <100mmHg). ECG changes may be present in up to 80% of patients (AV block; ST depression; T wave inversion and prolonged QT (associated with significant risk of sudden death)). Arrhythmias are common. Myocardial impairment may occur. Patients are at risk of cardiac failure if overfilled intraoperatively.
RS: prolonged starvation causes loss of lung elasticity. Airway pressures may be high.
Renal: GFR is reduced. Two-thirds of patients have proteinuria. Excessive losses of Na+, K+, Cl–, and H+ from the stomach result in hypochloraemic metabolic alkalosis and hypokalaemia. Severe hypokalaemia is uncommon but should be corrected with caution preoperatively. Hypocalcaemia may accompany hypokalaemia.
GI: anorexics and bulimics may have paradoxically delayed gastric emptying. Fasting is not a reliable way of ensuring an empty stomach.
Anaesthetic management: patients need more laboratory tests than their age alone would suggest. Check FBC, U&Es, LFTs, glucose, Ca2+, Mg2+, phosphate, and ECG. Rehydrate patient preoperatively and correct any abnormal electrolyte levels, but refeeding is dangerous and should not be attempted. Rapid sequence induction is recommended. Hypokalaemia and hypocalcaemia may potentiate neuromuscular blockade. Patients are prone to hypothermia. Patients should be positioned carefully because of their risks of pressure necrosis and nerve palsies.
Hypoalbuminaemia may cause elevated levels of unbound drugs in the plasma; and drug metabolism and elimination may be slowed. Avoid hyperventilation (this exacerbates hypokalaemia). Avoid large infusions, which may precipitate pulmonary oedema.
Reversal of neuromuscular blockade with neostigmine may provoke rhythm instability. Always use a nerve stimulator and consider allowing the block to wear off spontaneously.
Alcohol4
Alcohol use is common and causes problems as a result of both acute intoxication and the health effects of chronic consumption. Ask all adults about alcohol consumption, although their answers may be unreliable.
Acute alcohol intoxication causes problems with consent. Non-emergency surgery should be avoided. If surgery is unavoidable, ensure adequate rehydration with careful attention to electrolyte and glucose disturbances. Give IV B-vitamins (e.g. Pabrinex® slow IV bd for 7d).
Acute intoxication may cause vomiting, hypoglycaemia, and delayed gastric emptying. Rapid sequence induction is advised.
Patients with acute alcohol ingestion are partially anaesthetised and reduced concentrations of volatile agents may be required.
Chronic alcohol excess induces tolerance to general anaesthetics and is associated with a two- to five-fold increase in postoperative complications.
Alcoholic cardiomyopathy is characterised by a dilated, hypokinetic LV and decreased EF. Patients may present with congestive cardiac failure and oedema, exacerbated by low serum albumin. Consider echocardiogram.
Alcoholic liver disease: the earliest form is reversible fatty liver progressing to alcoholic hepatitis (abdominal pain, weight loss, jaundice, fever) and later cirrhosis (jaundice, ascites, portal hypertension, hepatic failure). Correct clotting abnormalities preoperatively. Transfuse appropriately if required. Patients with liver failure require intensive care if surgery is planned (see also p. 144).
Ketoacidosis may present after binge drinking in association with vomiting and fasting. Blood alcohol levels may already have normalised.
Anticipate alcohol withdrawal symptoms. Most patients can tolerate 24–48h abstinence perioperatively. Do not complicate management by attempting alcohol withdrawal perioperatively.
Seizures are most commonly seen 6–48h after cessation of drinking, typically tonic-clonic. Several fits over a period of a few days are common. Low K+ and Mg2+ predispose. Seizures may be preceded by disorientation and agitation (delirium tremens). Treat with benzodiazepines, e.g. diazepam 10mg IV, repeated as required.
Antidepressant drugs
The aetiology of depression is complex and multifactorial. The monoamine theory of depression postulates that depression is caused by functional deficiency of serotonin and noradrenaline in the CNS. Manipulation of CNS monoamines remains the most successful pharmacological approach to depression. Several families of drugs have this effect.
Tricyclic antidepressants (TCA)
Formerly the mainstay of treatment of depressive illness, TCAs have largely been superseded by SSRIs (fewer side effects and safer in overdose). They may be used in the treatment of other problems, e.g. chronic pain. They need to be given for 2–4wk to become effective.
TCAs block reuptake of monoamines (e.g. serotonin, noradrenaline) from the synaptic cleft by competing for a transport protein.
Most have atropine-like side effects: dry mouth, blurred vision, urinary retention, and constipation. Other common side effects are sedation and postural hypotension.
They are strongly bound to plasma proteins, and their effects may be enhanced by competing drugs (e.g. aspirin, warfarin, digoxin).
In overdose, TCAs are extremely toxic, producing agitation, delirium, respiratory depression, and coma. Cardiac arrhythmias with prolongation of the QT interval are frequent. There is no specific antidote and treatment is supportive, although intensive care may be required. Alkalinisation of plasma reduces the amount of free drug.
It is not necessary (and may be harmful) to withdraw TCAs perioperatively.
Increased sensitivity to catecholamines may result in hypertension and arrhythmias following administration of sympathomimetic drugs (adrenaline, noradrenaline). Indirect sympathomimetics (e.g. ephedrine, metaraminol) should be avoided (see p. 284).
Ventricular arrhythmias may occur with high concentrations of volatile agents, especially halothane.
TCAs may delay gastric emptying.
Anticholinergic drugs (e.g. atropine) which cross the blood–brain barrier may precipitate postoperative confusion.
Tramadol increases risk of CNS toxicity.
St John's wort (Hypericum perforatum)1
Extract of the plant contains several alkaloids which are similar in structure to tricyclic antidepressant drugs.
Useful and safe as monotherapy in mild depressive illness.
May induce certain cytochrome P450 enzymes, thereby enhancing the metabolism of many drugs, including warfarin, digoxin, theophylline, ciclosporin, tacrolimus, HIV protease inhibitors, and oral contraceptive drugs.
May interact with other drugs, e.g. SSRIs, to cause serotonin syndrome (see p. 283).
Selective serotonin reuptake inhibitors (SSRIs)
SSRIs are the most commonly prescribed antidepressants worldwide, and are increasingly being prescribed for other conditions (e.g. panic disorder, obsessive-compulsive disorder). They are highly specific inhibitors of presynaptic reuptake of serotonin from the synaptic cleft and are much less toxic in overdose than TCAs.
Common side effects affect the GI tract (nausea, vomiting, diarrhoea, upper GI bleeding) and the CNS (insomnia, agitation, tremor, headache, sexual dysfunction). Cardiovascular side effects are rare (occasional reports of bradycardia).
In patients with pre-existing ischaemic heart disease, SSRIs may precipitate coronary vasoconstriction.
SIADH has been described with the use of SSRIs, especially in the elderly, and may present with hyponatraemia ( p. 186).
High doses of SSRIs may impair platelet aggregation, and cause prolonged bleeding times.
Serotonin syndrome2,3, is a toxic crisis resulting from increased synaptic levels of serotonin in the brainstem and spinal cord due to overdose of SSRIs, or a combination of other drugs affecting serotonin (especially TCAs, MAOIs, pethidine, and tramadol). It presents as alteration in behaviour (agitation, confusion), motor activity (rigidity, myoclonus, hyperreflexia), and autonomic instability (pyrexia, tachycardia, diarrhoea, unstable BP). It may progress to seizures, oculogyric crises, DIC, rhabdomyolysis, myoglobinuria, acute renal failure, arrhythmia, coma, and death. It may mimic the neuroleptic malignant syndrome ( p. 287). The patient is likely to require intensive care. Treatment is mainly supportive, and the episode usually lasts <24hr.
SSRIs inhibit cytochrome P450 enzymes, which may prolong or enhance the activity of other drugs, notably warfarin, theophylline, phenytoin, carbamazepine, tolbutamide, benzodiazepines (diazepam, midazolam), type 1c antiarrhythmics (e.g. flecainide), tricyclic antidepressants, and some NSAIDs.
Anaesthesia for patients on SSRI
Abrupt withdrawal of SSRIs can precipitate a withdrawal syndrome.
Check urea and electrolytes to exclude hyponatraemia, especially in the elderly.
A coagulation screen should be assessed and corrected if necessary.
Benzodiazepines should be used cautiously as their effects may be prolonged.
Pethidine, tramadol, pentazocine, and dextromethorphan should be avoided (see above).
Monoamine oxidase inhibitors (MAOIs)1
MAOIs are third-line antidepressants, used in refractory cases. The enzyme monoamine oxidase is present on mitochondrial membranes, where it deaminates (thereby inactivating) monoamine neurotransmitters in the cytoplasm. It has two isoenzymes, A and B.
MAOA preferentially metabolises serotonin, noradrenaline, and adrenaline, and predominates in the CNS. MAOB preferentially metabolises non-polar aromatic amines such as phenylethylamine and methylhistamine. It predominates in the liver, lungs, and non-neural cells; 75% of all MAO activity is due to MAOB.
Tyramine (a monoamine found in cheese and other foods) and dopamine are substrates for both A and B.
Indirect sympathomimetics, which are metabolised by MAO, may have greatly exaggerated effects. They may displace noradrenaline from neurotransmitter vesicles in such high amounts that a fatal hypertensive crisis may be precipitated.
Older drugs (tranylcypromine, phenelzine, isocarboxazid) bind covalently to the MAO enzyme and are non-selective for A and B. Regeneration of new enzyme takes 2–3wk.
Newer drugs are reversible, and selective for MAOA: known as reversible inhibitors of monoamine oxidase A (RIMA). Moclobemide is the only RIMA available in the UK.
Linezolid (antibacterial used against MRSA) is a non-selective but reversible MAOI: treat patients as if on a classical MAOI.
Selegiline is an MAOB inhibitor used in Parkinson's disease.
Methylene blue (methylthioninium chloride) has MAOI properties.
Preoperative withdrawal
If the patient is taking tranylcypromine, phenelzine, or isocarboxazid, ideally it must be stopped at least 2wk prior to surgery to be of benefit. This may provoke drastic relapses in symptoms and should not be done without consultation with a senior psychiatrist. If stopped for <2wk patients should be considered as still on MAOI.
If the patient is taking moclobemide, it can safely be omitted for 24hr preoperatively and restarted afterward.
It is not necessary to stop selegiline if taken in doses of <10mg/d. At this dose there is no reaction with sympathomimetics. Pethidine, however, should still be avoided.
Anaesthesia for a patient on MAOI
General anaesthesia can be provided with caution to patients who are taking an MAOI.
The most dangerous interactions are with indirect sympathomimetics and some opioids (especially pethidine, which is absolutely contraindicated with any MAOI).
Indirect sympathomimetics (ephedrine, metaraminol, amphetamine, cocaine, tyramine), which release stored noradrenaline from vesicles, may precipitate potentially fatal hypertensive crises and are absolutely contraindicated with any MAOI.
Direct sympathomimetics (e.g. noradrenaline, adrenaline, phenylephrine, methoxamine, dopamine, dobutamine, isoprenaline) may have an exaggerated effect and should be used with caution.
Treat hypotension initially with IV fluid, then cautious doses of phenylephrine (e.g. 10–20µg).
Opioid drugs which have serotoninergic properties (including pethidine and dextromethorphan) may precipitate serotonin syndrome ( p. 283).
MAOIs can inhibit hepatic microsomal enzymes, prolonging the action of all opioids and enhancing their effect. This can be treated with naloxone.
Phenelzine decreases plasma cholinesterase levels and prolongs the action of suxamethonium. This is specific to phenelzine and is not typical of MAOIs.
Pancuronium releases stored noradrenaline and should be avoided.
Safe drugs: induction agents propofol, thiopental, and etomidate; non-depolarising neuromuscular blocking drugs (except pancuronium); volatile agents and nitrous oxide; NSAIDs; benzodiazepines.
Local anaesthetic drugs (except cocaine) are safe (caution if contain adrenaline). Axial and regional blocks are ideal; however, hypotension should be treated cautiously. Felypressin is a satisfactory alternative to adrenaline if a vasoconstrictor is required.
Anticholinergic drugs (atropine, glycopyrronium) are safe.
Morphine is the opioid of choice and should be titrated cautiously to effect. However, there is no direct evidence of problems with fentanyl, alfentanil, remifentanil, or sufentanil.
| Drugs to be avoided | Reason | Suitable alternative |
|---|---|---|
Pethidine, tramadol, dextromethorphan | Risk of serotonin syndrome | Morphine, fentanyl |
Ephedrine, metaraminol, cocaine | Hypertensive crises | Phenylephrine, noradrenaline |
Pancuronium | Releases stored noradrenaline | Vecuronium, atracurium |
Suxamethonium | Phenelzine only (decreased cholinesterase activity) | Mivacurium, rocuronium |
| Drugs to be avoided | Reason | Suitable alternative |
|---|---|---|
Pethidine, tramadol, dextromethorphan | Risk of serotonin syndrome | Morphine, fentanyl |
Ephedrine, metaraminol, cocaine | Hypertensive crises | Phenylephrine, noradrenaline |
Pancuronium | Releases stored noradrenaline | Vecuronium, atracurium |
Suxamethonium | Phenelzine only (decreased cholinesterase activity) | Mivacurium, rocuronium |
Antipsychotic drugs and lithium
Antipsychotic drugs
Antipsychotic drugs (formerly known as major tranquillisers or neuroleptics) include haloperidol, chlorpromazine, olanzapine, and risperidone, and are used in the treatment of schizophrenia and similar disorders. Their main action is antagonism at CNS dopamine (D2) receptors.
Most antagonise other receptors, including histamine (H1), serotonin (5HT2), acetylcholine (muscarinic), and A-adrenergic receptors.
Main side effects include sedation, extrapyramidal motor disturbances, and the development of tardive dyskinesia with chronic use. Other side effects include gynaecomastia, weight gain, postural hypotension, antimuscarinic effects, obstructive jaundice (uncommon), and agranulocytosis (rare but severe). Most are powerful antiemetics.
Many drugs prolong the QT interval, especially when combined with other drugs which may do the same (e.g. antidepressants).
Clozapine is associated with a risk of agranulocytosis.
Neuroleptic malignant syndrome1 is a rare idiosyncratic reaction to antipsychotic drugs which resembles malignant hyperthermia ( p. 270). Typical patients are young males. Features include hyperthermia, tachycardia, extrapyramidal dysfunction (rigidity, dystonia), and autonomic dysfunction (sweating, labile BP, salivation, urinary incontinence). CK and WCC are raised. Patients should be treated in ICU. Mortality is ∼20%.
Abrupt withdrawal of antipsychotic medication is dangerous.
Antipsychotic drugs potentiate sedative and hypotensive effects of anaesthetic agents (including opioids).
Lithium
Lithium is an inorganic ion used as a mood stabiliser in the treatment of bipolar affective disorder. It has a low therapeutic ratio, with optimal plasma concentration 0.4–1.0mmol/l.
Lithium mimics sodium in excitable tissues, being able to permeate voltage-gated ion channels, and accumulates inside cells, causing slight loss of intracellular potassium and partial depolarisation.
Chronic use causes weight gain, renal impairment, and hypothyroidism.
Lithium toxicity occurs at >1.5mmol/l and is exacerbated by hyponatraemia, diuretic therapy, and renal disease. Features include lethargy/restlessness, nausea/vomiting, thirst, tremor, polyuria, renal failure, ataxia, convulsions, coma, and death. Haemodialysis is effective.
Lithium potentiates both depolarising and non-depolarising neuromuscular blockade: nerve stimulator monitoring should be used.
Lithium may cause T wave flattening or inversion, but clinically important cardiovascular effects are rare.
NSAIDs should be used with caution (risk of exacerbating renal impairment and causing toxicity).
Sedation of agitated patients on the ward
Anaesthetists may be asked to help with sedation of agitated patients on general wards, and are more likely to be familiar with the effects of sedation than junior medical or surgical staff.
Patients are likely to be in an acute confusional state: exacerbated by pain, unfamiliar/threatening surroundings, and strangers. They may be disoriented, agitated, disinhibited, or violent, and may experience visual or auditory hallucinations.
When presentation is acute in a previously lucid patient, the cause is usually organic. Establishing and treating the cause may remove the need for sedation.
Exclude hypoglycaemia, hypoxia, pain, alcohol withdrawal, and full bladder.
Differential diagnosis includes infection (chest, urine, lines), drugs (cocaine, LSD, sedatives, analgesics), and metabolic derangement (e.g. hyponatraemia). Less frequently: head injury, stroke, acute psychiatric disorder (e.g. mania), acute porphyria.
Approach to the patient
Ensure the safety of yourself and other staff. A calm and reassuring approach will help the patient and any onlookers.
If physical restraint is necessary, ensure plenty of help is available (hospital security, porters, and even police) and discuss with psychiatrist.
Establish venous access if possible and bandage the cannula.
Aim to render patient calm and cooperative rather than unconscious.
Do not leave a sedated patient unattended.
Drug therapy
Haloperidol 5mg IV initially (reduce dose in elderly, e.g. 1mg). Repeat after 5min if no effect. Titrate to effect. Maximum dose: 18mg/24hr according to BNF, but higher doses are occasionally warranted.
Midazolam 1–2mg IV may also be useful (titrate to effect). May cause paradoxical disinhibition, especially in the elderly.
Alcohol withdrawal: give diazepam 5–10mg IV (or chlordiazepoxide 50mg PO) and repeat as required. Clomethiazole and IV alcohol are no longer advised.
Ketamine is useful in emergencies if patient is extremely violent or dangerous. Give 0.5–1mg/kg IV (or 5–10mg/kg IM).
Do not use propofol (too short acting), opioids (respiratory depression), or drugs you may be unfamiliar with.
In A&E, or where the history is unknown, further investigation (e.g. CT scan) may be appropriate. In this circumstance, rapid sequence induction of anaesthesia with full monitoring may be required.
Anaesthesia for drug-misusing patients
General considerations1
In the UK, around 10% of adults have used an illegal drug in the past year. Misuse of street drugs occurs in all socio-economic groups. Drug misuse causes the following specific problems:
Acute intoxication may impede informed consent. In addition the effects of the drug may counteract (stimulants) or enhance (sedatives) the effects of anaesthetic drugs. Consider drug misuse in all patients with a reduced conscious level, or requiring emergency surgery and anaesthesia.
Chronic drug misuse is associated with poor nutrition, medical and psychiatric comorbidity, and the presence of viral infections.
Intravenous drug users often have no accessible veins. IV drug misuse is associated with IV infective complications. HIV and viral hepatitis are commonest. Bacterial endocarditis is rare but serious, and associated with pulmonary abscesses, embolic phenomena from vegetations, and vasculitis.
Drugs in common use fall into four groups (see table). Combinations of drugs are common, often with alcohol.
| Drug | Clinical signs |
|---|---|
Cannabis | Tachycardia, abnormal affect (e.g. euphoria, anxiety, panic, or psychosis), poor memory, fatigue |
Stimulants: cocaine, amphetamines, ecstasy | Tachycardia, labile blood pressure, excitement, delirium, hallucinations, hyperreflexia, tremors, convulsions, mydriasis, sweating, hyperthermia, exhaustion, coma |
Hallucinogens: LSD, phencyclidine, ketamine | Sympathomimetic, weakly analgesic, altered judgement, hallucinations, toxic psychosis, dissociative anaesthesia |
Opioids: morphine, heroin, opium | Euphoria, respiratory depression, hypotension, bradycardia, constipation, pinpoint pupils, coma |
| Drug | Clinical signs |
|---|---|
Cannabis | Tachycardia, abnormal affect (e.g. euphoria, anxiety, panic, or psychosis), poor memory, fatigue |
Stimulants: cocaine, amphetamines, ecstasy | Tachycardia, labile blood pressure, excitement, delirium, hallucinations, hyperreflexia, tremors, convulsions, mydriasis, sweating, hyperthermia, exhaustion, coma |
Hallucinogens: LSD, phencyclidine, ketamine | Sympathomimetic, weakly analgesic, altered judgement, hallucinations, toxic psychosis, dissociative anaesthesia |
Opioids: morphine, heroin, opium | Euphoria, respiratory depression, hypotension, bradycardia, constipation, pinpoint pupils, coma |
Anaesthesia
Keep a high index of suspicion—especially in trauma.
Difficult venous access—IV drug users may be able to direct you to a patent vein. May need central venous cannulation or cut-down, or consider use of ultrasound for vein location. Consider inhalational induction.
Take full precautions against infection risk.
Plan postoperative analgesia with patient preoperatively (see below).
Do not attempt drug withdrawal perioperatively.
Opioids
Patients who misuse opioids should expect the same quality of analgesia as other patients. The commonest opioid misused is heroin. Recovering opioid users may be taking methadone.
If opioids are the only method of providing analgesia they should be administered in the same way as for normal patients, with doses titrated to effect (large doses may be required—see p. 1108 for a suitable dosing regime). Combinations of regional nerve blocks and NSAIDs may avoid the need for opioids.
Opioid-addicted surgical patients should be supported by specialist addiction services during the perioperative period (usually contactable via the local psychiatric services).
A small group of ‘ex-addicts’ may have fears about being prescribed opioids precipitating relapse. This should not become an obstacle to treating postoperative pain, but opioids should not be given without first obtaining consent.
Cocaine and crack cocaine
Cocaine is usually ‘sniffed’ in powder form. Free-base (‘crack’) cocaine is heat stable and can be smoked.
Cocaine toxicity is mediated by central and peripheral adrenergic stimulation. Presenting symptoms include tachycardia, hypertension, aortic dissection, arrhythmias, accelerated coronary artery disease, coronary spasm, infarction, and sudden death. Intracerebral vasospasm can lead to stroke, rigidity, hyperreflexia, and hyperthermia. Inhalation of cocaine can cause alveolar haemorrhage and pulmonary oedema.
Psychiatric symptoms range from elation and enhanced physical strength to full toxic paranoid psychosis.
Patients who need surgery following ingestion of cocaine may need intensive care while they are stabilised. Most of the life-threatening side effects of cocaine are due to vasospasm and can be reversed using combinations of vasodilators, antiarrhythmic agents, and A-/B-blockers titrated against effect using full invasive monitoring.
Combination local anaesthetic/vasoconstrictors (or any vasopressor) should be avoided. Tachycardia or hypertensive crisis may result. If vasopressors are required in theatre, use very small doses and titrate against response.
Intra-arterial injections of cocaine have lead to critical limb and organ ischaemia. Successful treatment has included regional plexus blockade, IV heparin, stellate ganglion block, intra-arterial vasodilators, urokinase, and early fasciotomy.
Ecstasy (3,4-methylenedioxymethamphetamine (MDMA))
Ecstasy is a stimulant drug related to amphetamine. It is usually taken in tablet form. Approximately 30 people die from taking ecstasy annually in the UK.
Hyperthermia (>39°C), disseminated intravascular coagulation, and dehydration are common features.
Excessive ADH release may also cause hyponatraemia leading to coma.
Carefully monitor fluid and electrolyte replacement.
Anaesthesia for electroconvulsive therapy (ECT)
Procedure | Electrically induced seizure |
Time | 5–10 min |
Pain | +/– |
Position | Supine |
Blood loss | Nil |
Practical technique | Short IV GA, FM only, bite block |
Procedure | Electrically induced seizure |
Time | 5–10 min |
Pain | +/– |
Position | Supine |
Blood loss | Nil |
Practical technique | Short IV GA, FM only, bite block |
General considerations
ECT is safe and effective in the treatment of severe depression unresponsive to drugs or where there is a high risk of suicide. ECT is commonly carried out in an isolated site: ensure skilled assistance and adequate resuscitation facilities. Anaesthetic equipment may be old or unfamiliar.
Physiological effects of ECT
During the seizure there is parasympathetic hyperactivity: bradycardia and hypotension, lasting about 15s, followed by a more prolonged (5min) sympathetic stimulation: tachycardia, hypertension, dysrhythmias, increased myocardial oxygen requirement.
CNS: increased ICP, CBF, and cerebral oxygen requirement.
Other: hypersalivation, increased intragastric pressure, increased intraocular pressure, occasionally incontinence.
Preoperative
A careful preoperative assessment (including investigations) should be undertaken, as for any general anaesthetic.
Consent is normally arranged by the psychiatrist responsible.
ECT is usually given several times weekly for several weeks: read the notes for documentation of previous problems.
Absolute contraindications: recent MI or CVA, phaeochromocytoma, intracranial mass lesion, intracranial or aortic aneurysm.
Relative contraindications: uncontrolled angina, congestive cardiac failure, severe osteoporosis, major bone fracture, glaucoma, retinal detachment. ECT in pregnancy is possible.
Avoid sedative premedication, which is anticonvulsant.
Glycopyrronium (0.1–0.3mg IV) may be used to reduce secretions and to counteract bradycardia. Consider antacids if history of reflux.
Perioperative
Efficacy of ECT is dependent on seizure quality as measured by EEG-derived variables such as the Postictal Suppression Index. However, there is no further benefit beyond about 1min.
Good technique provides short GA, muscle relaxation to lessen risk of trauma, attenuation of physiological effects, and rapid recovery.
Thorough preoxygenation is recommended.
Propofol, thiopental, etomidate, and ketamine (less suitable) may be used for induction. Propofol attenuates the sympathetic response but shortens the seizure more than the others. Etomidate shortens the seizure less but sympathetic response may be more pronounced. Inhalational sevoflurane is effective but takes longer. All general anaesthetics shorten the seizure in a dose-related fashion: use light doses.
Suxamethonium (0.5–1mg/kg) is given to ‘modify’ the seizure (reduce muscle power to prevent injury during seizure). Mivacurium (0.2mg/kg) may be used instead but will probably require reversal.
Insert a bite-block to prevent damage to the mouth and teeth.
Maintain the airway with a facemask and/or oral airway. Hand-ventilate the patient with oxygen until breathing resumes afterward.
The psychiatrist may titrate the magnitude of the stimulus to the length of seizure: be prepared to maintain anaesthetic with further boluses of induction agent if a second stimulus is required.
Sympathetic response may be attenuated with alfentanil (10µg/kg) or esmolol (e.g. 0.25mg/kg). Remifentanil, labetalol, sodium nitroprusside, and hydralazine have also been used.
Seizure augmentation: both caffeine and theophylline lower the seizure threshold and prolong the seizure. Moderate hyperventilation with bag and mask before the seizure is also effective.
If the seizure lasts longer than 120s it should be terminated, e.g. with diazepam 10mg IV or propofol titrated to response.
Postoperative
Post-ictal agitation, confusion, or aggression may occur in up to 10% of patients. They should be nursed in a calm environment and may occasionally require sedation (e.g. midazolam 1mg IV).
Headache and muscle pains are commonly reported and usually respond to simple analgesics.
Drowsiness and cognitive impairment are very common but typically resolve within a few hours.
No evidence of memory loss is demonstrable at 6 months. However, patients sometimes complain of memory loss for specific life events.
Other complications include nausea, exacerbation of ischaemic heart disease, fractures/dislocations, dental/oral injury, and laryngospasm.
ECT does not increase the risk of other types of seizure.
Overall mortality is about 1 per 80 000 treatments.
Further reading
Seller CA, Ravalia A (2003). Anaesthetic implications of anorexia nervosa. Anaesthesia, 58, 437–443.
Denner AM, Townley SA (2009). Anorexia nervosa: perioperative implications. Continuing Education in Anaesthesia, Critical Care and Pain, 9, 61–64.
Morris J, Twaddle S (2007). Anorexia nervosa. British Medical Journal, 334, 894–898.
Chapman R, Plaat F (2009). Alcohol and anaesthesia. Continuing Education in Anaesthesia, Critical Care and Pain, 9, 10–13.
Mills E, Montori VM, Wu P, et al. (2004). Interaction of St John's wort with conventional drugs:systematic review of clinical trials. British Medical Journal, 329, 27–30.
Chinniah S, French JLH, Levy D (2008). Serotonin and anaesthesia. Continuing Education in Anaesthesia, Critical Care and Pain, 8(2), 43–45.
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