ELECTROCONVULSIVE

THERAPY
1. AIMAN FARHAN BIN AZADDIN (046708)
2. NUR IFFAH BT KAMARUDDIN (046530)
3. ASNI BAHIRAH BT ABD GHANI (046602)
4. HANISAH BT SAZALI (047004)
5. NUR LIYATI BT GHANI (046563)
INTRODUCTION, INDICATION
AND CONTRAINDICATION OF
ECT
AIMAN FARHAN BIN AZADDIN
BHAL17046708
 INTRODUCTION

ECT is a treatment that involves sending an electrical impulse

through the brain, causing a brief surge of electrical activity within
the brain (seizure).
It was invented in Italy in the late 1930s.
Originally introduced to treat schizophrenia.
Currently, mainly being used in major depressive disorder besides
schizoaffective disorder, catatonia, neuroleptic malignant syndrome,
and bipolar disorder.

https://www.sciencedirect.com/science/article/abs/pii/S1569258200800288
 INTRODUCTION

ECT is generally reserved for:

1. patients who have failed to respond to pharmacotherapy.
2. have adverse reactions to standard pharmacotherapy.
3. as well as those with severe symptoms such as
• Suicidality
• Psychosis
• grave functional impairment
• a need for a rapid and definitive response.

Kaplan and Sadock’s Concise Textbook of Clinical Psychiatry 3rd edition

INDICATION OF ECT
 1. MAJOR DEPRESSIVE DISORDER
 The most common indication, for which it
is the fastest and most effective.

 Controlled studies = 70% of patients who

fail to respond to antidepressant
medications may respond positively to
ECT.

 Effective for depression in both major

depressive disorder and bipolar I
disorder.
Kaplan and Sadock’s Concise Textbook of Clinical Psychiatry 3rd edition
 2. ACUTE MANIC EPISODES
 ECT = lithium in treatment acute manic episodes.

generally limited to situations with specific contraindications to all

available pharmacological approaches.

ECT should not be used for a patient who is receiving lithium

lithium can lower the seizure threshold
cause a prolonged seizure.

Kaplan and Sadock’s Concise Textbook of Clinical Psychiatry 3rd edition

 3. SCHIZOPHRENIA
Effective for acute symptoms of schizophrenia (not for chronic).

Patients with schizophrenia who have marked

 positive symptoms
catatonia
affective symptoms
are considered most likely to respond to ECT.

 The efficacy of ECT = antipsychotics, but improvement may occur

faster.
Kaplan and Sadock’s Concise Textbook of Clinical Psychiatry 3rd edition
SUMMARY
 CONTRAINDICATION OF ECT

There is no absolute contraindications, only situations with

increased risk or increase need of monitoring.

1. Pregnancy
2. Patients with space-occupying central nervous system lesions
3. Patients with recent myocardial infarctions
4. Patients with hypertension
5. Pheochromocytoma

Kaplan and Sadock’s Concise Textbook of Clinical Psychiatry 3rd edition

CONTRAINDICATION OF ECT

MOH Pyschiatric and Mental Health Services Operational Policy 2011

 REFERENCE
1. Kaplan and Sadock’s Concise Textbook of Clinical Psychiatry 3rd
edition.
2. MOH Pyschiatric and Mental Health Services Operational Policy
2011
3. https://www.sciencedirect.com/science/article/abs/pii/S156925820
0800288
ELECTROCONVULSIVE
THERAPY(ECT)
PRE AND POST ECT
ELECTRODE PLACEMENT

BY: NUR IFFAH BINTI KAMARUDIN

 PREPARATION FOR ECT
• Indication verified
• No contraindications
• Vital signs(temperature ,blood pressure ,pulse rate, patient should be
kept fasting after midnight to reduce the risk of aspiration)
• Investigations(FBC, BUSE, FBS, Chest X-ray, ECG)
• Consent
• Anesthetist opinion

MOH Psychiatry Operational Policy

 CONSENT
According to Section 77(1) M.H.A. 2001, follows:
-By the patient himself if he is capable of giving consent as assessed by a psychiatrist, or
-By his guardian in the case of a minor or a relative in the case of an adult, if the patient is incapable
of giving consent, or
-By 2 psychiatrists, one of whom shall be the attending psychiatrist, if there is no guardian or
relative of the patient immediately available or traceable and the patient himself is incapable of
giving consent.

Under Section 77 (3) of M.H.A 2001 in cases of emergency, consent by

o By the guardian or relative of the patient or
o By 2 medical officers or registered medical practitioners, one of whom shall preferably be a
psychiatrist, if there is no guardian or relative of the patient immediately available or traceable.

MOH Psychiatry Operational Policy

 PRE TREATMENT EVALUATION
• Pre treatment evaluation should include standard physical, neurological, and pre
anaesthesia examinations and a complete medical history.
• PRE ECT investigations:
• FBC, BUSE, FBS
• Chest X-ray
• ECG
• A dental examination to assess the state of patients' dentition is advisable for elderly
patients and patients who have had inadequate dental care.
• X-ray of the spine is needed if other evidence of a spinal disorder is seen.
• Computed tomog­raphy (CT) or magnetic resonance imaging (MRI) should be performed
if a clinician suspects the presence of a seizure dis­order or a space-occupying lesion.
• no lon­ger consider SOL to be an absolute contraindication to ECT, but should be
performed only by experts.

2015 Kaplan & Sadocks

 CONCOMITANT MEDICATION
• Patients' ongoing medica­tions should be assessed for possible interactions with
the induc­tion of a seizure, for effects (both positive and negative) on the seizure
threshold, and for drug interactions with the medications used during ECT.
• Tricyclic and tetracyclic drugs, monoamine oxidase inhibitors, and antipsychotics
is generally considered acceptable.
• Drug that should be withdrawn
• Benzodiazepines : anticonvulsant activity;
• Lithium: increased postictal delirium and can prolong seizure activity;
• clozapine (Clozaril) and bupropion (Wellbutrin): development of late-appearing seizures.
• Contraindicated
• Lidocaine (Xylocaine): increases the seizure threshold
• Theophyl­line (Theo-Dur): increases the dura­tion of seizures.
• Reserpine (Serpasil): compromise of the respira­tory and cardiovascular systems during ECT.

2015 Kaplan & Sadocks

 PREMEDICATIONS

• Patients should not be given anything orally for 6 hours before treatment.
• Patient's mouth should be checked for dentures and other foreign objects
• Intra­venous (IV) line should be established.
• A bite block is inserted in the mouth just before the treatment is administered to
protect the patient's teeth and tongue during the seizure.
• 1 00 percent oxygen is administered at a rate of 5 L a minute during the
procedure until spontaneous respiration returns except for the brief interval of
electrical stimulation.
• Emergency equipment for establishing an airway should be immediately
available in case it is needed.

2015 Kaplan & Sadocks

 MUSCARINIC ANTICHOLINERGIC DRUGS
• administered before ECT to minimize oral and respiratory secretions and to block
bradycardias and asystoles
• unless the resting heart rate > 90 beats a minute.
• The most commonly used drug is atropine
• 0.3 to 0.6 mg intramuscularly (IM) or subcutaneously (SC) 30 to 60 minutes
before the anesthetic
• 0.4 to 1 .0 mg IV 2 or 3 minutes before the anesthetic.
• Option: glycopyrrolate (Robinul) (0.2 to 0.4 mg IM, IV, or SC),
• less likely to cross the BBB and cause cognitive dysfunc­tion and nausea,
• HOWEVER less cardiovas­cular protective activity

2015 Kaplan & Sadocks

 ANESTHESIA
• Administration of ECT requires general anaesthesia and oxygenation.
• Methohexital (Brevital) (0.75 to 1 .0 mg/kg IV bolus)
• shorter duration of action
• lower association with postictal arrhythmias
• Four alternatives:
• Etomidate (amidate) 0.15 to 0.3 mg/kg IV: for elderly patients
• Ketamine (ketalar) 6 to 10 mg/kg IM: its use is limited(association of psychotic symptoms)
• Alfentanil (alfenta) 2 to 9 mg/kg IV: co administered with barbiturates, increased incidence
of nausea.
• Propofol (diprivan) 0.5 to 3.5 mg/kg IV: less useful because of strong anticonvulsant Reduce
threshold of
properties. seizure

2015 Kaplan & Sadocks

 MUSCLE RELAXANTS
• to minimize the risk of bone fractures and other injuries resulting from motor activity during the
seizure.
• to produce profound relaxation of the muscles, not necessarily to para­lyze them
• unless patient has a history of osteoporosis or spinal injury or has a pacemaker(at risk for injury)
• Succinyl­choline (Anectine) 0.5 to 1 mg/kg as an IV bolus or drip.
• its action is marked by the presence of muscle fasciculations(depolarization agent).
• disappearance of fasciculation/absence of muscle contractions=maximal muscle relaxation.
• Tubocurarine (3 mg IV) : to prevent myoclonus and increases in potassium and muscle
enzyme(problem in patients with musculoskeletal or car­diac disease).
• Blood pressure cuff :To monitor the duration of the convulsion, may be inflated at the ankle to a
pressure in excess of the systolic pressure before infusion of the muscle relaxant
• observation of relatively innocuous seizure activity in the foot muscles.
• Patient known history of pseudocholinesterase deficiency: give atracurium (Tracrium) (0 . 5 to 1
mg/kg IV) or curare(as in this patient, metabolism of succinylcholine is disrupted, and prolonged
apnea may necessitate emergency airway management).

2015 Kaplan & Sadocks

 ELECTRODE PLACEMENT
• Bilateral ECT ( Both Sides)
• Temporal position 4cm above
midline joining lateral canthus
of eye to external acoustic
meatus.
• Unilateral ECT (Non Dominant
Hemisphere)
• Both electrodes are placed on the same
side (usually right side )
• 1st Electrode is placed at the temporal
position as for Bilateral E.C.T above
• 2nd Electrode is placed at an arc 18 cm from
first electrode over the parietal region.
MOH Psychiatry Operational Policy
 DOSE OF CURRENT DURING ECT TREATMENT

• Starting dose is 25- 50 mC=Seizure threshold

• Bilateral ECT : up to 2.5 times the seizure threshold in case of
emergency treatment.
• Unilateral ECT
• 4 times the seizure threshold
• up to 6 to 8 times the seizure threshold.

MOH Psychiatry Operational Policy

 NUMBER AND SPACING OF TREATMENTS

• ECT treatments are usually administered two to three times a week;

• twice-weekly treatments are associated with less mem­ory impairment
• Treatment should continue until the patient achieves what is considered the
maximal therapeutic response.
• Further treatment does not yield therapeutic benefit, but increases severity &
duration of adverse effect
• The point of maximal improvement, when patient fails to continue to improve
after two consecutive treatments.
• If is not improving after 6 to 10 sessions: do bilateral placement and high-
density treatment (three times the seizure threshold), before ECT is aban­doned.

2015 Kaplan & Sadocks

 POST ECT
• There shall be a dedicated recovery area manned by trained staff
• BP, PULSE, SPO2, R.R should be assessed
• 20 Mins for Unilateral
• 40 Mins for Bilateral
• Supervision by an adult for 24 hours
• Not to drive for 24 hours

MOH Psychiatry Operational Policy

 CONTINUATION AND MAINTENANCE ECT

• Continuation ECT is indicated in certain patients to prevent relapse of

depressive episode after the completion of a course of ECT.
• M-ECT is a course that begins after the end of C-ECT and is intended
to prevent recurrence of an episode (a new episode).
• Indications:
• rapid relapse after initial ECT,
• severe symptoms,
• psychotic symptoms,
• the inability to tolerate medications.

MOH Psychiatry Operational Policy

2015 Kaplan & Sadocks
 REFERENCES

• MOH Psychiatry Operational Policy

• 2015 Kaplan & Sadocks
PROCEDURE
BY: ASNI BAHIRAH (046602)
1. Consent and explain the procedure and
complication of ECT

2. Patients should not be given anything orally for

6 hours before treatment

3. Pre-ECT investigations
• FBC, BUSE, FBS, Chest X-ray, ECG

4. Pre-ECT vital signs monitoring

• Temperature, Blood Pressure, Pulse Rate
5. Establish an intravenous (IV) line

6. Muscarinic Anticholinergic Drugs

• eg. Atropine

7. Anaesthesia
• Short acting anesthetic i.e Propofol : 0.75 – 2.5 mg/ kg

8. Muscle relaxants
• After the onset of the anaesthetic effect, usually within a minute
• Scoline (suxamethonium) : 0.5 – 1mg/kg
9. 100 percent oxygen is administered at a rate of 5 L a
minute during the procedure until spontaneous
respiration returns.
• Except for the brief interval of electrical stimulation

10.Emergency equipment for establishing an airway should

be immediately available in case it is needed.
11.Just before the procedure, the patient's mouth should be
checked for dentures and other foreign objects

12. Bite block is inserted in the mouth just

before the treatment
• protect the patient's teeth and tongue
during the seizure.

13.Electrode placement – bilateral or

unilateral
 • Starting dose is 25- 50 mC=Seizure threshold
• Bilateral ECT : up to 2.5 times the seizure threshold in case
14. Induced seizure of emergency treatment.
• Unilateral ECT
• 4 times the seizure threshold
• up to 6 to 8 times the seizure threshold.
1. Tonic phase
• The first behavioral sign of the seizure is often a plantar extension, which lasts
10 to 20 seconds
• high-frequency, sharp EEG activity on which a higher frequency muscle artifact
may be superimposed

2. Clonic phase
• Rhythmic (i.e., clonic) contractions that decrease in frequency and finally
disappear.
• bursts of polyspike activity occur simultaneously with the muscular contractions
but usually persist for at least a few seconds after the clonic movements stop.
Monitoring
• The physician should be able to observe either some evidence of tonic-clonic
movements or electrophysiological evidence of seizure activity from the EEG or
electromyogram (EMG)
• For a seizure to be effective in the course of ECT, it should last at least 25 seconds.

Failure to Induce Seizures.

• up to four attempts at seizure induction can be tried during a course of treatment.
• The onset of seizure activity is sometimes delayed as long as 20 to 40 seconds after the
stimulus administration.
• If a stimulus fails to result in a seizure,
• the contact between the electrodes and the skin should be checked
• intensity of the stimulus should be increased by 25 to 1 00 percent.
• the clinician can also change the anesthetic agent to minimize increases in the seizure threshold
caused by the anesthetic.
• additional procedures to lower the seizure threshold include hyperventilation and administration
of 500 to 2,000 mg IV of caffeine sodium benzoate 5 to 1 0 minutes before the stimulus.
Prolonged and Tardive Seizures.
• seizures lasting more than 180 seconds and status epilepticus can be terminated
either with
• additional doses of the barbiturate anesthetic agent or
• IV diazepam (Valium) ( 5 to 1 0 mg).
• Management of such complications should be accompanied by intubation,
because the oral airway is insufficient to maintain adequate ventilation over an
extended apneic period.
• Tardive seizures-that is, additional seizures appearing some time after the ECT
treatment-may develop in patients with preexisting seizure disorders.
• Rarely, ECT precipitates the development of an epileptic disorder in patients.
Such situations should be managed clinically as if they were pure epileptic
disorders.
15. Post-ECT nursing care
• There shall be a dedicated recovery area manned by trained staff
• BP, PULSE, SPO2; R.R.
• 20 Mins for Unilateral
• 40 Mins for Bilateral
• Supervision by an adult x 24 hours
• Not to drive X 24 hours
REFERENCE
• MOH Psychiatry Operational Policy page 112
• 2015 Kaplan & Sadocks
 ELECTROCONVULSIVE
THERAPY

PREPARED BY: HANISAH BINTI SAZALI 047004

Learning outcomes:
Physiological changes during ECT
Electrophysiology in ECT
• In ECT, seizures are triggered in normal neurons by application through
the scalp of pulses of current, under conditions that are carefully
controlled to create a seizure of a articular duration over the entire
brain.
• The qualities of the electricity used in ECT can be described by Ohm’s
Law: E=IR or I=E/R;
• E: voltage
• I: current
• R: resistance
• Resistance or Impedance in this case of ECT, both electrode’s contact
with the body and the nature of the bodily tissues are the major
determinants of resistance.
• The skull has a high impedance while the brain has low impedance.
• Because scalp tissues are much better conductors of electricity than
bone, only 20% of the applied charge actually enters the skull to excite
neurons.
Electrophysiology in
ECT
• The induction of a bilateral generalised seizure is
necessary for both the beneficial and the
adverse effects of ECT.
• After generalised seizure, the
electroencephalogram (EEG) shows about 60 to
90 seconds of postictal suppression.
• This period is followed by the appearance of
high-voltage delta and theta waves and a return
of the EEG to pre-seizure appearance in about 30
minutes
Neurophysiological effects of ECT
• Positron emission tomography (PET) studies of both cerebral blood flow, use of glucose and
oxygen, and permeability of the blood brain barrier increase.
• After the seizure, blood flow and glucose metabolism are decreased, perhaps more markedly in
the frontal lobes.
• After 1 to 2 months following a session of ECT, EEG record a large increase in slow-wave activity
located at the prefrontal cortex in patients who responded well to the ECT.
• Effective forms of ECT resulted in increased delta power in prefrontal regions, and this change
was associated with the magnitude of symptomatic improvement. (Sackeim et al.,1996)
• High intensity, bilateral stimulation produced the best response while low intensity, unilateral
stimulation showed the weakest response.
• ECT affects the cellular mechanism of memory and mood regulation and raises the seizure
threshold.
Neurochemical changes during ECT
• Virtually, every neurotransmitter system is affected by ECT but a
series of ECT sessions results in downregulation of postsynaptic
B-adrenergic receptors.
• The effects of ECT on serotonergic neurons remain controversial.
• Various research studies have reported an increase in
postsynaptic serotonin receptors, no change in serotonin
receptors and a change in the presynaptic regulation of
serotonin release.
• ECT has also been reported to effect changes in the muscarinic,
cholinergic and dopaminergic neuronal systems.
• ECT has been reported to affect the coupling of G-proteins to
receptors, the activity of adenylyl cyclase and phospholipase C
and the regulation of calcium entry into the neurons.
Cardiovascular system changes
• Beginning with the electrical stimulus, there is an initial parasympathetic discharge lasting 10–15
seconds. This can result in bradycardia, hypotension, or even asystole.
• A more prominent sympathetic response follows during which time cardiac arrhythmias
occasionally occur.
• Systolic arterial pressure may increase by 30–40% and heart rate may increase by 20% or more,
generally peaking at 3–5 mins.
• Simultaneously, seizure activity increases tissue oxygen consumption, potentially reducing
myocardial oxygen supply.
• Myocardial ischaemia and infarction can therefore occur, particularly with pre-existing disease.

https://academic.oup.com/bjaed/article/10/6/192/299664
References
• Sackeim HA, Luber B, Katzman GP, Moeller JR, Prudic J, Devanand DP, Nobler MS. The effects of
electroconvulsive therapy on quantitative electroencephalograms. Relationship to clinical
outcome. Arch Gen Psychiatry. 1996 Sep;53(9):814-24.
• https://academic.oup.com/bjaed/article/10/6/192/299664
POSSIBLE SIDE
EFFECTS
LIYATI GHANI (046563)
 Kaplan & Sadock’s Shorter Oxford Textbook Of Psychiatry

Headache
Short-term effects.
Confusion
• Marked confusion may occur in up
• Loss of memory for events shortly
to 10% of patients within 30
before the treatment (retrograde
minutes of the seizure
• amnesia),
Can be treated with barbiturates
• Impaired retention of information
and benzodiazepines.
acquired soon after the treatment
(anterograde amnesia).
Delirium CENTRAL NERVOUS
• Occur shortly after the seizure
while the patient is coming out of SYSTEM EFFECTS
anesthesia. Long-term effects.
• The delirium characteristically
clears within days or a few weeks • Loss of memories for personal
at the longest. remote events (retrograde
amnesia for remote events) or
Memory loss autobiographical memory loss.
• 75% of all patients given ECT say
that the memory impairment is the
worst adverse effect.
• Follow-up data  almost all
patients are back to their cognitive
baselines after 6 months
 • The mortality rate with ECT is about 0.002
percent per treatment and 0.01 percent
for each patient.

MORTALITY • ECT death is usually from cardiovascular

complications and is most likely to occur
in patients whose cardiac status is already
compromised.

• Death occurs usually due to ventricular

fibrillation or myocardial infarction.
(Benbow and Waite, 2013)
 OTHER
COMPLICATION

Fractures
• Occur in the early days of ECT.
• With routine use of muscle relaxants, fractures of long bones or vertebrae should not occur.

Muscle soreness
• Often results from the effects of muscle depolarization by succinylcholine and is most likely to be
particularly troublesome after the first session in a series.
• Can be treated with mild analgesics, including nonsteroidal anti-inflammatory drugs (NSAIDs).

Nausea and vomiting

• Nausea and vomiting can be prevented by treatment with antiemetics at the time of ECT
• (e.g., metoclopramide [Reglan], 10 mg IV, or prochlorperazine [Compazine], 10 mg IV;
• Ondansetron [Zofran] is an acceptable alternative if adverse effects preclude use of dopamine receptor
antagonists).
REFERENCES