1.4 ECT

Question 1

What is ect, and how does it work?

Answer 1

ECT, having been in clinical use since the late 1930s,

is the treatment for various psychiatric disorders and

involves artificially inducing a brief generalised tonic-clonic seizure.

The exact mechanism is still unclear,
although a common (and probably oversimplified)
view is that a tonic-clonic seizure ‘resets’
or ‘jumpstarts’ neuronal transmission

(in a similar way DC cardioversion does for the heart).

Question 2

What are the indications for ect?

Answer 2

• Depressive illness: failed medical therapy
• Mania: refractory cases
• Schizophrenia
• Parkinson’s disease
• Neuroleptic malignant syndrome
• Delirium

Question 3

How is it performed?

Answer 3

In the UK, it involves induction of general anaesthesia,
and usually partial muscle relaxation,

before inducing a generalised tonic-clonic seizure by
passing a brief current of 30–45 J

between two electrodes on either side
of the patient’s skull (bilateral ECT),

or more commonly over one side only
(unilateral) over 0.5–1.5 seconds.

Question 4

What are the main anaesthetic issues?

Answer 4

Remote site anaesthesia

1. • Unfamiliar environment and staff
2. • Potentially old/unfamiliar equipment
     (which may not have been checked recently)
3. • Inconsistent anaesthetic support (ODP)

Procedure

The overall aims of anaesthesia are

1. • To induce rapid onset, brief general anaesthesia,
     with partial muscle relaxation to reduce the
     risk of limb injury during convulsions
2. • To avoid raising the seizure threshold
     (which may make seizures harder to
     induce and/or shorter in duration,
     which in turn may make the ECT less effective)
3. • To minimise physiological effects of ECT

Question 5

Look at the ECG strip provided and explain the mechanism

Answer 5

This is because of the autonomic surges that happen at the onset and
maintenance of ECT, which is described below.
only parasympathetic symptoms are shown in the ECG.

Question 6

What are the main physiological
effects?

Answer 6

A. Cardiac

1. • Initial parasympathetic discharge,
     lasting 10–20 seconds;
     bradycardia, hypotension, and asystole may occur.
2. • Followed by sympathetic surge,
     leading to increased heart rate,
     blood pressure, and myocardial oxygen demand.

3 * Potential for myocardial ischaemia or infarction,
especially in those with preexisting LV impairment
or coronary artery disease.

Plasma adrenaline and
noradrenaline levels at 1 minute exceed baseline by 15 and 3 times, respectively

B. Cerebral

• Increased cerebral O2 consumption, blood flow, and ICP
  cerebral blood flow, which may increase more than fivefold
• Post-procedure cognitive deficits are common:
  post-ictal confusion, drowsiness,
  retrograde and anterograde amnesia commonly occur.

C. Other

• Raised intraocular and intragastric pressure
  are not thought to be clinically significant.
• Dental damage, tongue/lip lacerations may
  occur due to jaw clenching.
• Headache and myalgia.
• Fractures are rare now,
  due to widespread use of muscle relaxants.

Question 7

What are the key points in preoperative patient assessment?

Answer 7

1. • Often poor historians with multiple comorbidities (IHD, COPD, etc)
2. • No absolute contraindications exist,
     but most anaesthetists would
     consider an MI or CVA within the previous 3 months,
     or raised ICP, to
     place the patient at high risk of
     further cardiac or cerebral events
3. • Drug therapy may have anaesthetic implications (lithium, MAOI, etc)
4. • Patients may not have followed fasting instructions
5. • All patients should ideally be investigated and optimised as for any
     procedure; however, if ECT is deemed semi-urgent, the risks of delay
     must again be balanced against the benefits of optimising comorbidities

Question 8

How would you conduct your anaesthetic?

Induction

Answer 8

1. • Check patient, full monitoring, appropriate assistance and equipment as
     per AAGBI
2. • Intravenous access and pre-oxygenation
3. • Induction agent:
     ‘minimal sleep dose’,
     to minimise effects on raising seizure threshold.
     Methohexital used to be commonly employed but is no
     longer available;

propofol is a common choice;

etomidate reduces seizure threshold but affects adrenal hormone synthesis

4. • Short-acting opioids
     may allow dose of induction agent
     to be reduced and blunt haemodynamic responses
5. • Muscle relaxants:
     suxamethonium 0.5 mg/kg commonly used. If
     contraindicated, consider mivacurium
     (or rocuronium followed by sugammadex if available)

Question 9

How would you conduct your anaesthetic?

Maintenance

Answer 9

Maintenance

• Airway management:
  manual airway maintenance using a face mask is
  usually sufficient,

unless specific aspiration risks warrant intubation

• Bite block/mouthguard to prevent damage to the teeth or tongue
• Gentle hyperventilation after induction—
  causing hypocapnia—helps reduce seizure threshold
• Volatile not usually required,
  but further boluses of induction agent may
  be needed to maintain anaesthesia if repeated
  current bursts are required to induce a seizure
• Have glycopyrrolate and atropine on hand
  to treat parasympathetic surge;
  consider short-acting β-blocker at induction

(e.g. esmolol, labetalol) in patients at risk of myocardial ischaemia

Question 10

How would you conduct your anaesthetic?

Emergence

Answer 10

1. • Once seizure terminates,
     ventilation can be supported manually until
     anaesthesia and muscle relaxation start to
     wear off and spontaneous ventilation resumes
2. • Keep oxygen applied, and transfer to recovery
3. • Monitor standards and recovery facilities
     same as in a normal
     postoperative care unit
4. • Anticipate post-op confusion/agitation

Question 11

if severe bradycardia occurred,
how would you treat it?

Answer 11

1. • Check monitoring still attached
2. • Feel for pulse
3. • Give atropine 3 mg stat bolus (followed by 10–20 mL flush!)
4. • Commence CPR and put out crash call if no pulse palpable
5. • Document on anaesthetic chart and
     consider prophylactic glycopyrrolate next time

Question 12

What drug therapy may
influence your anaesthetic?

Answer 12

Lithium

SSRis

MAois

Question 13

Lithium

Answer 13

1. • Used mainly in bipolar disorder
2. • Decreases the central and peripheral neurotransmitters
     and may prolong depolarising neuromuscular blockade
3. • May cause nephrogenic diabetes insipidus
4. • Has a narrow therapeutic index and signs develop at > 2.0 mmol/L.
5. Signs of toxicity include
   lethargy or restlessness initially;
   then tremor,
   ataxia,
   weakness and muscle twitching,
   hypokalaemia,
   arrhythmias,
   renal failure,
   convulsions,
   and coma

Question 14

SSRIs

Answer 14

• May cause SIADH: low [Na+]

Question 15

MAOIs

Answer 15

MAOIs

1. • Potential for hypertensive crisis if used with sympathomimetics (mainly
     indirectly acting, i.e. metaraminol, ephedrine)
2. • Caution with opioids
     (unpredictable effects with pethidine;
     morphine and fentanyl thought to be safe)
3. • Irreversibly inhibit MAO,
     so consider stopping 2 to 3 weeks preprocedure
     if concerned about anaesthetic interactions

Question 16

Technique

Answer 16

a shock of about 850 mA is delivered across the cerebral hemispheres by
a stimulator that delivers a pulsatile square wave discharge. Pulses of 1.25 ms at
26 Hz are delivered for up to 5 seconds. Unilateral ECT is sometimes performed on
the non-dominant hemisphere with the aim of minimizing post-procedure cognitive
dysfunction. Memory impairment is substantially reduced with this technique.

Question 17

The Bolam principle,

Answer 17

which has underpinned the law relating
to medical negligence since 1957, followed from a case in which a patient suffered a
dislocated hip as the result of an unmodified convulsion during a session of ECT.

Question 18

Complications:

Answer 18

cardiac arrhythmias and hypertension. The risk of skeletal and tissue
damage, for example to the tongue, is minimized by ‘modifying’ the convulsion with
a small dose of suxamethonium. This attenuates the force of the muscle contraction
on the skeletal system. Post-procedure disorientation, memory impairment and
cognitive dysfunction occur in around 50% of patients and may persist for some
weeks. Patients often undergo a ‘course’ of ECT, typically twice-weekly sessions for
3 to 4 weeks depending on response, and so the cerebral effects are likely to be
cumulative.

not be used in patients who have suffered a recent cerebrovascular or
myocardial event (within 3 months), who have a CNS mass lesion or have raised
intracranial pressure.

Question 19

The Mental Capacity Act:

Answer 19

a patient is said to have capacity if

(1) they are able to understand the information that is imparted to them,

(2) are able to retain that information,

(3) are able to weigh up the information before arriving at a decision,

(4) are able to communicate that decision (not necessarily verbally).

Although patients who require ECT may have mental health issues which do not allow them to fulfill those criteria, that cannot be assumed to be the case, and so a proper
assessment of capacity is mandatory.

The involvement of an advocate is recommended
but is not a legal requirement. Advanced directives made at a time when the
patient did have capacity should not normally be overridden, although this is not