This document discusses anaesthesia for electroconvulsive therapy (ECT). It describes ECT as the artificial induction of a grand mal seizure through electrical stimulation of the brain to treat severe mental illnesses. It notes the common indications for ECT and outlines the anaesthetic considerations and techniques used to control physiological responses and complications during the procedure, including preoxygenation, induction agents like methohexital or propofol, and muscle relaxants like succinylcholine to prevent injury during seizures. Risks associated with ECT like increased intracranial pressure, blood pressure changes, and memory loss are also summarized.
Overview of anaesthesia's role in Electroconvulsive Therapy presented by Dr. Kundan Kishor Ghimire.
ECT is an artificial induction of seizures for mental health treatment; involves bilateral/unilateral electrical application. Mechanism of ECT and monitoring requirements; seizure duration and intensity are critical for success.
No absolute contraindications for ECT; relative contraindications include recent myocardial infarction and cerebrovascular events.
Physiological responses include increased intracranial pressure, altered blood flow, contraindications, and multiple side effects.
Anaesthetics are essential for ECT; control heart changes, ensure muscle relaxation, and manage premedication and induction.
Citations from key literature on anaesthesia in ECT, highlighting critical resources for further study.
ELECTROCONVULSIVE THERAPY
• Definition
•Artificial induction of a grandmal seizure(tonic
phase 10-15s, clonic phase;30-60s)
• Through the application of electrical current to the
brain
• Stimulus applied through electrodes which are
placed bilaterally in the fronto-temporal region or
unilaterally on the non dominant side.
3.
• Indications
• TheNational Institute of Clinical Excellence (NICE) UK Guidelines (1) recommend that
ECT be considered for patients who are suffering from:
1. Acute, life threatening depression (high suicide risk or very poor fluid and/or
fluid intake)
2. Drug resistant depression
3. Acute catatonia (where first line treatment with intramuscular
benzodiazepines has failed to produce improvement).
4. Mania, where treatment has failed to alleviate the condition, or is limited by
side effects
•TREATMENT
• Most patientsrequire between 6 and 10 treatments,
performed on a twice a week basis.
• usually administered bilaterally;
• electrodes are placed over the poles of the temporal
lobes.
• unilaterally to the non-dominant hemisphere if there
are concerns over post-ictal confusion.
6.
• EEG monitoring:initially localised seizure, which
becomes a generalised tonic-clonic seizure
within 5-10 seconds.
• seizure should ideally last for more than 15sec
and less than 120sec.
• A seizure longer than 120sec is classified as
“prolonged” and pharmacological agents may
need to be administered to terminate the
seizure
7.
• Contraindication
• Absolutecontraindications • None
• Relative contraindications
• Myocardial infraction within the last 3 months or
unstable angina
• Cerebrovascular event in the last 3 months
• Raised intracranial pressure or untreated cerebral
aneurysm
• Unstable major fracture or cervical spine injury
• Pheochromocytoma
• Uncontrolled cardiac failure or severe valvular
disease
• Deep venous thrombosis.
8.
PHYSIOLOGICAL RESPONSE TOECT
• Central Nervous System
• Increase in intracranial pressure
• Increased regional cerebral blood flow,
cerebral oxygen consumption, and glucose
utilization.
• Increase in blood-brain barrier permeability.
• Headache, confusion, and transient memory
loss are common in the immediate post-
treatment period.
9.
• Cardiovascular System
•Initial brief parasympathetic response: lasts for 10-
15seconds, bradycardia, hypotension or even
• Sustained sympathetic response, peaking at 3-5
minutes, associated with release of catecholamines, a
rise in systolic blood pressure (30-40%), and a rise in
heart rate (more than 20%)
• Increased myocardial oxygen consumption.
10.
• Other Effects•
• Increase in intraocular pressure
• Increase in intragastric pressure
• Nausea
• Myalgia and feeling of general ill-ease
• Damage to crowns, veneers, bridges, implants
or intraosseous denture supports
• Oral cavity damage to tongue and gums
11.
• anaesthetic requirementsfor ECT
• control of haemodynamic changes and
complications,
• amnesia and muscle relaxation.
• Anaesthesia is brief due to the short nature
the procedure.
• rapid, return of consciousness and full
orientation is desirable.
13.
• History andPhysical examination
• Detailed medical history and a thorough
phyisical examination
• History of psychotropic medications:
antipsychotics, mood stabilizers antidepressant
and anxiolytics.
• Investigations
• Full blood count, urea and electrolyte
• Other additional test:
14.
• Premedication
• Forparasympathetic stimulation
• Anticholinergic agents:
• Glycopyrrolate 0.01mg/kg IM 3 min prior the
scheduled surgery or IV just beore injecting the
induction agents
• For sympathetic stimulation:
• Beta blocker: Esmolol(1-2mg/kg), labetolol(0.05-
0.4mg/kg)
15.
• Pre-oxygenation
• 100%oxygen at a rate of 15–20 breaths/min,
beginning approximately 1 min before the
induction.
• continued until the resumption of spontaneous
breathing.
• Prior Hyperventilation reduce the seizure
threshold and enhance the seizure duration
16.
• Induction agents
•short-acting induction agent.
• most induction agents (barbiturates, etomidate,
benzodiazepines, and propofol) have
properties, small doses must be used.
• Seizure threshold is increased and seizure duration
is decreased by all of these agents.
• methohexital, 0.5–1 mg/kg, is most commonly
employed.
• Propofol, 1–1.5 mg/kg,
17.
• Muscle Relaxants
•Used to reduce the risk of injury
• Neuromuscular blockade is required from the
of electrical stimulation until the end of the
seizure.
• succinylcholine (0.25–0.5 mg/kg).
• . Controlled mask ventilation, using a self-inflating
bag device or an anesthesia circle system, is
required until spontaneous respirations resume.
18.
• References:
• Morganand Mikhails 6th edition
• Indian journal of Anaesthesia. 2017 may:61(5):373-380
#4 2. Drug resistant depression (failure to respond to two medications given at adequate dose for adequate period of time) or where treatment is limited by unacceptable side effects. It may also be appropriate to consider initiation of ECT early if a patient has shown good response previously, or it is known that they only respond to ECT.
#10 The above effects predispose to cardiac dysrhythmias, myocardial ischemia and infarction (especially with pre-existing cardiac dysfunction).
#14 For the presence of IHD, cardiac disaese, severe valvular heart disease, COPD, GERD
#15 Calcium channel blockers and alpha 2 agonists can also be used. Clonidine and dexmedetomidine (1 mcg/kg over 10 min before induction of anaesthesia) control blood pressure without affecting seizure duration.
#16 Hyperventilation just prior to application of the electrical stimulus reduce the seizure threshold and enhance the seizure duration
#17 An ideal induction agent: short half-life with rapid onset and recovery, maintain haemodynamic stability and have no interference with seizure duration or seizure threshold.
induction agents such as methohexital, propofol and etomidate are combined with a short acting, highly potent opioids, such as alfentanil (10–25 mcg/kg) or remifentanil (1 mcg/kg) but not fentanyl, to increase seizure duration
#18 Non-depolarising agents such as atracurium (0.3-0.5mg/kg), mivacurium ((0.08-0.2mg/kg) or rocuronium (0.3- 0.6mg/kg), can be used safely, though sufficient time must be allowed for the onset of the drug, and airway management must be anticipated while waiting for the effects to wear off.