FRCA Notes

Electroconvulsive Therapy

This topic appeared as a CRQ in 2024, with questions on 'the goals of anaesthesia' poorly answered although the physiological/autonomic changes were well known.

Resources

  • The mechanism through which ECT works remains unclear
  • However, it remains an effective treatment option for refractory depression, mania and schizophrenia
  • These are relative contraindications as they may be adversely affected by the physiological changes during ECT, e.g.
    • Cardiac disease owing to the high parasympathetic then sympathetic outflow
    • SOL, aneurysms, globe rupture or ICH owing to the raised ICP and IOP during the procedure
    • MSK disease e.g. fractures, osteoporosis due to the risk of muscle contraction
Respiratory Cardiovascular Neurological Renal
Acute respiratory infection Uncontrolled heart failure SOL (or any cause of ↑ ICP) Unstable major trauma
VTE not anticoagulated Unprotected cerebral aneurysm Untreated phaeochromocytoma
MI within 3 months Retinal detachment or globe rupture
Stroke within 1 month Cochlear implant Severe osteoporosis

  • Acute phase is performed 2 - 3x/week until lack of improvement (usually 3 - 4 weeks)
  • Maintenance therapy no longer recommended

  • An electrical current is applied to the brain via transcutaneous electrodes
  • It induces therapeutic generalised seizures lasting 10 - 120s
  • This should be accompanied by characteristic EEG seizure activity lasting 25 - 50s

  • Inefficacy may result from either missed or prolonged seizures

Electrode placement

  • Unilateral electrode positioning over the non-dominant hemisphere → reduces memory loss
  • Bilateral electrode positioning → more rapid clinical effects

Missed seizures

  • 22% of ECT treatments
  • Either no seizure is generated, or it lasts <15s
  • Causes include:
    • Inadequate or prematurely terminated stimulus
    • Hypercarbia
    • Effects of medication
    • Dehydration
    • Excess anaesthetic

Prolonged (tardive) seizures

  • Either lasting >120s or return of seizures/status epilepticus post-procedure
  • Most commonly seen when pre-treatment with theophylline is used
  • Management is supportive with agents to terminate the seizure

Cardiovascular

  • There is a biphasic cardiovascular response resulting from generalised autonomic nervous system activation
  1. Immediate, direct stimulation of vagal parasympathetic outflow lasting 10 - 15s
    • Leads to:
      • Transient bradycardia ± (rarely) asystole
      • Hypotension
    • Premedication with an anticholinergic agent is often used to attenuate this

  2. A more prominent, catecholamine-mediated sympathetic response lasting up to 5mins
    • Peaks 3 - 5 minutes after therapy
    • Leads to:
      • Tachycardia ± tachyarrhythmias: there is a ≥20% rise in HR
      • Hypertension: there is a 30 - 40% increase in systolic BP

    • This increases myocardial oxygen demand, which may be further compromised by:
      • Hyperventilation-induced hypocapnia and vasoconstriction
      • High tissue oxygen demand from seizures reducing oxygen supply
    • There may be LV dysfunction which persists up to 6hrs post-ECT, even in patients without cardiovascular disease

Neurological

  • There is a marked albeit transient increase in CBF, CMRO2 and ICP due to the seizure
  • Transient rises in IOP and gastric pressure are not usually clinically significant
  • Post-procedurally this may manifest as dizziness, confusion, agitation or headaches

  • Other features include short-term memory loss (50%) lasting up to six months
    • Reduced by using unilateral electrode over non-dominant hemisphere
  • Non-memory cognitive dysfunctions remain intact

  • Serious intracranial effects include TIA, ICH and cortical blindness

Perioperative management of the patient undergoing ECT


  • Routine pre-assessment and examination
  • Investigations as clinically indicated
  • Patients with PPMs and ICDs may need temporary deactivation or modification of functions prior to ECT
  • Patients with cerebral aneurysms need appropriate attenuation of cardiovascular responses lest there be rupture
  • Concurrent psychiatric medications should be noted:
Drug Side-effect or anaesthetic interaction
Benzodiazepines Avoid due to anticonvulsant effect
TCAs e.g. amitriptyline Proconvulsant
Hypertensive crisis with indirect sympathomimetics
SSRIs e.g. fluoxetine Reduce seizure threshold so associated with prolonged seizure
Associated with SIADH
Potential serotonin syndrome with tramadol
MAO-I e.g. phenelzine, tranylcypromine
(irreversible MAO-I)		 Increase seizure threshold
Hypertensive crisis with direct or indirect sympathomimetics
If on irreversible agent, transfer to a RIMA if possible (takes 2 months)
Lithium Reduces seizure threshold
Ensure level 0.4 - 1.0mmol/L
SNRIs e.g. duloxetine, venlafaxine Reduce seizure threshold
Hypertension
Neuroleptics Low dose - proconvulsant
High dose - increase seizure threshold

Capacity and consent

  • Patients under S3 MHA:
    • Can be given ECT without their consent if they lack capacity
    • Can refuse consent for ECT if they have capacity

  • The objectives of anaesthesia are to provide:
    • Rapid loss of consciousness
    • Muscle relaxation
    • Attenuation of hyper-dynamic cardiovascular responses
    • Minimal interference with seizure activity
    • Prompt recovery

  • Anaesthesia provided by an experienced anaesthetist
  • Ensure patient fasted and consented
  • Avoid sedative pre-medication
  • Ensure urination pre-procedure as incontinence is common
  • Standard AAGBI monitoring

Induction

  • Pre-oxygenate as standard
  • Choice of agents depends on patient's weight, previous responses and seizure threshold

  • Propofol is commonly used for induction, but no one agent has significant advantages over the others
  • Methohexital 1 - 1.5mg/kg was considered the gold standard for ECT owing to its short duration of action (4 - 7mins) and lack of effect on the seizure threshold/seizure length

  • Addition of short-acting opioids can reduce the dose of induction agent and improve seizure quality
  • E.g. Remifentanil 1μg/kg or alfentanil 10 - 25μg/kg

  • NMBA are used to prevent myalgia and MSK injury
  • Suxamethonium (0.5mg/kg) or short-acting non-depolarising agents e.g. mivacurium 0.15 - 2mg/kg are typically used

Airway management

  • Post-induction a bite block is inserted to protect the lips, teeth and tongue during seizure
  • Intubation generally not required unless high risk of gastric aspiration
  • Ventilation is maintained with a facemask
    • Hypocapnia lowers the seizure threshold, increasing the risk of prolonged or tardive seizures
    • Hypercapnoea increase the seizure threshold, increasing risk of missed seizures

Cardiovascular adjuncts

  • The sympathetic response can be attenuated using a variety of agents
  • Glycopyrrolate (100 - 300μg) is often used over atropine owing to its superior anti-sialagogue effects and lack of CNS effects

  • β-blockers are the most effective agents in controlling both HR and MAP
  • Short-acting agents such as esmolol or labetalol are preferred
    • Longer-acting agents may exacerbate the parasympathetic response
    • Esmolol is better at reducing peak systolic BP than labetalol
    • Labetalol may shorten seizure duration

  • Calcium channel blockers can also be effective
    • Nifedipine SL - may cause reflex tachycardia
    • Nicardipine
    • Diltiazem - may be associated with shorter seizure duration

  • Direct vasodilators e.g. GTN given shortly before the administration of ECT

  • Remifentanil is effective at reducing HR and BP, although using an infusion may not be available, suitable or practical for such short procedures

  • Standard recovery process is required
  • The majority of patients make uncomplicated recovery and can be discharged

  • Common post-operative issues include:
    • Confusion
    • Agitation
    • Amnesia
    • Headache
    • Dramatic emergence phenomenon requiring midazolam