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ANESTHESIA FOR ELECTROCONVULSIVE THERAPY

Husong Li, M.D., Ph.D. Assistant Professor Department of Anesthesiology University of Texas Medical Branch Galveston, Texas

ELECTROCONVULSIVE THERAPY

INTRODUCTION TO ELECTROCONVULSIVE THERAPY


Electroconvulsive therapy (ECT) is a treatment for severe mental illness in which a brief application of electrical stimulus is used to produce a generalized seizure

MENTAL HEALTH CARE PRE-1930S

Cerletti and Bini (1934): ECT


Initially done without muscle blocker or anesthetic

INTRODUCTION TO ECT
ECT

has changed substantially during the past decades. The use of general anesthesia has promoted the interest in ECT (Ottoson 1962) ECT become more complex, more precise, and safer procedure (mortality 1/1000 early to 3-4/100,000 now)

INTRODUCTION TO ECT
Generalized

seizures for 30-60 seconds in duration are required for therapeutic effects 75-90% of patients exhibit a dramatic and sustained improvement Transient neurological dysfunction does occur but permanent neuronal injury is questionable

TREATMENT PROTOCOL FOR ECT

Generalized seizure can be induced by adjusting waveform, frequency, duration of electrical stimuli. Seizure should last at least 30-60 seconds in duration Good therapeutic effect is generally not achieved until 400-700 seizure seconds Treatments are usually given every other days unto 12 sessions Treatment endpoints are based on clinical experience and evaluation

INDICATIONS FOR ECT


Severe

depression: if drug treatment fails or is not tolerated ( i.e. elderly with Parkinson's disease ) Bipolar disorder: manic or depressed phase Acute or Catatonic Schizophrenia Patient is severely withdrawn or starving: effects seen in days rather than weeks Depression in pregnancy: with acute mania

CONTRAINDICATIONS TO ECT
ABSOLUTE

RELATIVE

CV Recent MI < 3 months; Severe angina, CHF Aneurysm of major vessel Pheochromocytoma CNS Cerebral tumor or aneurysm Recent CVA <1 month Respiratory System Severe respiratory failure

Pregnancy Thyrotoxicosis Cardiac dysrhythmias Glaucoma Retinal detachment

PHYSIOLOGIC EFFECTS OF ECT-INDUCED SEIZURES

Initial Parasympathetic Discharge (15 seconds) Bradycardia: marked Bradycardia <30 bpm or transient asystole Increased secretion Increased intragastric and intraocular pressure

Sustained Sympathetic Discharge (1-3 min) Tachycardia Hypertension Dysrhythmias and Twave abnormalities CNS: increased CBF, ICP, O2 consumption

ADVERSE EFFECTS TO ECT


Muscle

contractions: can result in fractures and dislocations; prevented by small doses of muscle relaxants Injury to teeth, tongue or lips: stimulus causes intense contraction of the masseter muscles and forceful movement of the jaw; use a bite block Electrical injury to the staff or patient

ADVERSE EFFECTS TO ECT


Postictal

Headache (45%) and muscle

ache Short-term memory loss and cognitive deficits Difficult relationship with patients: frightened; withdrawn; suspicious; uncooperative Anesthesia related problem: i.e. air way issue (more pt with OSA); aspiration Line infection and sepsis

TREATMENT PROTOCOL

Premedicate Glycopyrrolate and Beta blocker ? Patient not intubated Bite block Cuff leg to monitor seizure activity EEG and EMG Length of seizure: 30 sec to 1 min.

ECT DEVICE

EEG ACTIVITY

EEG Seizure Activity

EEG Seizure Termination

PRE-ECT EVALUATION
Regular

anesthesia pre-op evaluation: Esp. airway, CV, CNS Psychotropic medication should be stopped before ECT (antidepressants, benzodiazepine, lithium) for 7 days? Pre-ECT sedation: hydroxyzine or promethazine 25-50 mg, droperidol 2.5-5 mg (promote seizure) Pain medication prior to ECT

ANESTHETIC AGENTS SELECTION


To leave the patient unaware of (amnesia) frightening sensations, particularly muscle paralysis and feelings of suffocation and the image of a light flash that may accompany the beginning of the stimulus, without obstructing the seizure (McCleave & Blackmore, 1975) PRINCIPLE: To provide ultra-brief, light general anesthesia with moderate degree of muscular relaxation (APA, 1990, 2001)
OBJECTIVE:

INDUCTION AGENTS
An ideal agent: rapid unconsciousness, painless on injection, no hemodynamic effects, no anticonvulsant properties, rapid recovery, and inexpensive (APA1990,

2001; Folk et al, 2000) Brevital Sodium : 0.5-1 mg/kg thiopental: 2-4 mg/kg ketamine: 0.5-2 mg/kg propofol: 1.5-3 mg/kg etomidate: 0.15-0.3 mg/kg

MUSCLE RELAXANTS
Succinylcholine:

0.3-1.5 mg/kg. Atracurium, 0.3-0.5 mg/kg (Hickey et al, 1987) Mivacurium, 0.15-0.2 mg/kg (Kelly & Brull, 1994) Rocuronium, 0.45-0.6 mg/kg (Motamed et al, 1997)

ADJUNCTIVE AGENTS

Caffeine 0.25-1.5 gm IV Flumazenil: 0.2-1 mg IV (benzodiazepine antagonist) Benzodiazepine: Valium 5-10 mg IV (status epilepticus) Anticholinergics: atropine 0.4-0.8 mg IV or glycopyrrolate 0.2-0.4 mg IV Beta blockers: Labetalol and Esmolol Nitroglycerine Antihypertensives: Labetalol, Trimethaphan, Nicardipine

POST-ECT RECOVERY
Headache:
N/V:

Up to 45 % (Devanand
(Gomez 1975;

et al. 1995; Freeman and Kendell 1980) Sackeim et al. 1987d)

1.4% - 23%

Muscle

ache Post-ECT confusion

SUGGESTED REGIME
Preoperative Evaluation Fasting Preoperative Medications
IV placement

Monitors EKG, SpO2 Blood Pressure

SUGGESTED REGIMEINDUCTION

Preoxygenation Inform MD and RN for the readiness of induction Methohexital or others /Succinylcholine Hyperventilate until fasciculation completed Insertion of bite block or part of oral airway for tooth protection Ascertain the muscle relaxation with stimulator ECT

SUGGESTED REGIME
Emergence Hyperventilate with 100% O2 until normal vital signs obtained, then slow assisted breaths until spontaneous ventilation resumes. Turn patient on side and transport to PACU Drugs ready to use Atropine or glycopyrrolate, esmolol or labetalol, ephedrine, phenylephrine Equipment ready to use Laryngoscopes, ETT, stylet, airways, suction, defibrillator, alternative airway devices

BURST SUPRESSION THERAPY (BST)


Induction Intubation Hyperventilation Emergence Recovery

SEVOFLURANE BST