Introduction to ECT
History
Indications
Practicalities
Side Effects
Anaesthesia for ECT
Patient factors –Hx/ Exam / Ix
Venue / Equipment
Conduct
Induction / Muscle relaxation
Recovery
It is a treatment for severe mental illness in
which brief application of electrical stimulus
is used to produce genaralized seizure.
ECT induces a generalized, tonic–clonic
epileptic seizure, yet despite being first
described in 1937 the exact mechanism of
action remains elusive.
1934 Von Meduna –Insulin
induced seizures for
schizophrenia
1937 Cerletti and bini–
Electric shock induced
seizures
For almost 30 year it was
used without anaesthesia.
Safer (Mortality 2-5 : 100
000)
Life threatening illness
Sever depression-if drug tt fail or is not tolerated.
Bipolar disorder-manic or depressed phase.
Acute or catatonic schizophrenia.
Refusal of food / fluids
Depressive delusions / hallucinations
Prolonged / severe manic episode
Treatment resistance
Depression
Mania
Schizophrenia (4
th
line treatment)
Patient choice
An electrical current applied transcutaneous
to brain via two electrode positioned either
bilaterally or unilaterally.
BILATERAL ECT-used more commonly and
preferred when speed of clinical recovery
take priority.
UNILATERAL ECT-performed on nondominant
hemisphere.
-it performed twice weekly until lack of
further improvement( on average 3-4 week)
Genaralizedseizure for 30-60s in duration
are required for therapeutic effect.
-To short(<10s) or to long(>120s) may
reduce clinical efficacy.
-Amount of current deliverdis more
important than length of seizure.
-Almost 75-90% ptexhibit dramatic and
sustained improvement.
-Transient neurological deficit but permanent
neurological deficit is rare.
Initial parasympathetic discharge(15 s )
-Coincident with tonic phase
-Bradicardia<30 bpm
-Transient asystole
-Sustained sympathetic discharge(1-3min)
-Coicidentwith clonicphase
-Tachycardia
-Hypertension
-dysarrythmiasand T wave abnormalities.
CNS-
Initial vasoconstriction.
Sustained increase in cerebral blood flow.
Increase cerebral metabolism.
Increase intracranial HTN.
TIA,intracranialhaemorrhage,cortical
blindness.
Cognitveadverse effects-disorientation,
impaired attention, Short term memory
loss.
-Intraocular and intragastricpressure rises.
Unmodified ECT-Incidence of fracture and
dislocation( now rare).
-Headache ,myalgia.
-Drowsiness,weakness, nausea , anorexia.
-Increased salivation.
-Dental damage and oral cavity laceration.
Procedure should be provided at remote site.
Anaesthesia should be provided by
experienced anaesthetist.
Appropriate resuscitation equipment drugs
must be immediately available.
-Trained assistance and recovery facilities
must be available.
To provide ultra brief, light general
anaesthesia with moderate degree of
musle relaxation.
Minimizing aforementioned physiological
and physical effect.
Avoiding drug having anticonvulsant
properties.
Balance b/w to provide adequte
anaesthesia without affecting efficacy of
ECT.
Gold standard.
Methylbarbiturate.
White powder with 6% anhydrous sodium
carbonate.
Induction similar to STP.
Less cvsand respiratory depression than STP.
Recovery within 3-4 min after single dose.
S/E-
-Pain on injection.
-causes convulsion in epileptic pt.
-incidence of involuntary movement, hiccup
and laryngospasm.
Adequate no. of trained personnel.
Should be Fully equipped
O2 until awake and maintaining Saturation.
Written instructions
ECT is safe and effective if appropriately
administered.
-Anaestheticsmust be aware of not only
physiological response to ECT and how to
modify this, but also understand the
anaestheticfactors that may influence the
efficacy of ECT.