Electroconvulsive Therapy (ECT)

Report
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Electroconvulsive Therapy
(ECT)
ARNEL BANAGA SALGADO, Ed.D., D. Sc., MAT (Psych)
Assistant Professor, RAKCON, RAKMHSU
Mobile: 050 799 3803
E-mail: [email protected]
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Learning Objectives
1. Define ECT
2. Describe the possible mechanisms of action of
ECT
3. State the indications, contraindications and
adverse effects of ECT
4. Apply the steps of nursing care to clients
receiving ECT
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(Pre-)History of Convulsive Therapies
 1933
– Manfred Sakel develops insulin coma
therapy (Insulin-shock behandlung) – treated
opioid dependent pt’s first, later schizophrenia.
 Txs were occasionally, but not always,
accompanied by seizures.
 (Sakel later claimed to have invented
convulsive therapy, but this is disputed)
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History of Convulsive Therapies
 1934
– Ladislas Meduna induces seizures
using SC camphor in oil initially and later,
IV Metrazol (pentylenetetrazol,
pentamethylenetetrazol):
 Tx
(Drawing
by Renato Sabattini, PhD)
was based upon a theory of
opposition
beween epilepsy and schizophrenia.
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History of Convulsive Therapies

1938 – Ugo Cerletti and Lucio Bini induce seizures in Rome
using electrical stimuli

1940 – Renato Almansi and David Impasto administer ECT at
Columbus Hospital in NYC. Lothar Kalinowsky starts giving ECT
at Psychiatric Institute

1940 - A.E. Bennett uses curare for muscle relaxation with
Metrazol convulsive therapy

1952 – Holmberg uses succinylcholine as a muscle relaxant
with ECT
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(Image provided courtesy of Renato Sabattini, PhD)
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Thymatron™ System IV - Integrated ECT Instrument
(Reproduced with permission from: Somatics, LLC)
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Electrical Stimulus
 Brief-pulse
square-wave AC
 Voltage approx. 200V (based upon 220 Ω
impedance)
 Current 0.9A
 Frequency 30 - 70Hz
 Pulsewidth 0.5 - 2 msec
 Duration 0.1 - 8 sec
 Charge 25 - 504mC (5 - 99J)
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How does it work?
 Seizure
- 15 to 180 sec (by EEG)
 Low-dose RUL ECT - Less effective clinically
despite adequate seizure duration
 Down-regulation of beta receptors
 Up-regulation of 5HT2 receptors
 GABA (anti-convulsant theory of ECT)
 BDNF (reversal of hippocampal atrophy)
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Anticonvulsant theory of ECT
 Increasing
seizure threshold during a
course of ECT is associated with clinical
response
 Hypothesis:
linked anticonvulsant and
antidepressant response to ECT
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ECT induced seizure
 Discharge
is:



Paroxysmal
Synchronous
Repetitive
 Post-ictal


of neuronal population which
suppression follows seizure
Inhibitory interneurons
GABA (as detected by MRS)
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Modern (Modified) ECT
1.
General anesthesia (propofol 1mg/kg, etomidate
0.15mg/kg, methohexital 1mg/kg)
2.
Muscle relaxant (succinylcholine 1mg/kg, mivacurium
0.15mg/kg)
3.
Anticholinergic (glycopyrrolate 0.2mg, atropine 0.4mg)
4.
Oxygen/ventilation by mask
5.
Continuous cardiac and EEG monitoring
6.
(Other pre- and post-medications as indicated – NTG, Betablockers, promethazine, ketorolac, midazolam, sumatriptan,
sodium amytal)
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(Fink M. Electroshock revisited. American Scientist. March-April 2000.)
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Indications for ECT
 Treatment-refractory
conditions
 Severe or life-threatening psychiatric
illness
 Most often used for the treatment of
medication-resistant depression (MDD)
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Diagnostic Indications
 MDD
 BPAD
 Psychosis
(Schizophrenia)
 Catatonia
 NMS
 PD
 Delirium
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Reasons to consider ECT first
 Severe
sucidality
 Catatonia/NMS
 Patient preference (usually previous ECT)
 Pregnancy and severe psychiatric illness
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Patient categories:
 Healthy
young adults
 Pregnant
 Medical complicated - stable
 Elderly
 Adolescents
 Children
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Risks/Side Effects
 Common:
transient confusion, headache,
nausea, myalgia, retrograde and anterograde
amnesia
 Uncommon: cardiac arrest, unstable
arrhythmias, ischemia, severe hypertension or
hypotension, stroke, prolonged apnea,
aspiration, laryngospasm, prolonged seizures
(status), fractures, malignant hyperthermia
 Death: 1:80,000 Txs (1:10,000 patients)
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Conditions of increased risk
 Increased
ICP (mass)
 Unstable angina
 Recent MI
 Recent stroke
 Pheochromocytoma
 Retinal detachment
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Medications and ECT
 Anticonvulsants
- taper and d/c or reduce
(except in the case of seizure disorder)
 Stimulants - taper and d/c
 D/C Lithium 36-48 hrs prior to Tx
 Trazodone -d/c
 Others (SSRI’s, TCA’s, MAOI's, anti-PD ) - consider
dose reduction or d/c
 Neuroleptics - may be synergistic
 Reserpine, chlopromazine - adverse effects
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ECT and Medications, cont.
 Beneficial
•
•
•
•
•
medications (Give before Tx)
Anti-HTN (other than diuretics)
Anti-GERD/reflux (not Carafate, Mylanta, etc.)
Pulmonary (brochodilators)
Glaucoma meds
Neuroleptics/Antipsychotics – Haldol, Clozapine,
Risperdal – may be beneficial in combination with ECT
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Consent
 Informed
consent - adequate mental capacity,
understand procedure, risks, side effects,
benefits, alternatives
 Printed consent form
 Surrogate consent – Guardian, POA, NOK if
patient is incapacitated - two licensed
physicians concur (SC Adult Health Care
Consent Act – SC Code of Laws Title 44, Chapter
66)
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Electrode Placement
 Bilateral
(BL) - most common, most effective, most
cognitive dysfunction
 Right unilateral (RUL) - less cognitive effect, may be
less clinically effective
 Bifrontal (BF) – may be as effective as BL with less
cognitive effect
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Bilateral
RUL
Bifrontal
Source: Rasmussen KG et al. Mayo Clin Proc. 2002:77:552-556
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Electrode Placement, BL vs. RUL
 Response
rates:
 Low-dose RUL - 17%
 High-dose RUL - 43%
 Low-dose BL - 65%
 High-dose BL - 63%
Source: Sackheim HA et al. NEJM. 1993; 328:839-846.
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Course of ECT
 Index
course 6 - 8 Txs
 2 -5 Txs per week
 Tx until improvement plateaus
 Continuation/Maintenance ECT
 Prophylactic medication
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ECT Instructions/Orders
 Void
on call to ECT in AM
 NPO after MN
 Hold BZ after 9pm
 Hold all current medications the morning of ECT
except
•
•
•
•
Anti-HTN (other than diuretics)
Anti-GERD/reflux (not Carafate, Mylanta, etc.)
Pulmonary (brochodilators)
Glaucoma meds
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Alternatives to ECT
 Pharmacologic
Tx - TCA, MAOI, SSRI, venlafaxine,
Atypical Neuroleptic, Lamictal
 Psychotherapy - CBT
 VNS (Vagus Nerve Stimulation - FDA approved)
 rTMS (repetitive Transcranial Magnetic
Stimulation - experimental)
 Neurosurgery –(experimental)
OSCE Checklist (ANC 2 @ 2013)
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References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Abrams R. Electroconvulsive Therapy, 3rd Edition. New York: Oxford University Press, 1997.
Rasmussen KG et al. Electroconvulsive therapy and newer modalities for the treatment of medicationretractory mental illness. Mayo Clin Proc. 2002; 77:552-556.
Fink M. Meduna and the origins of convulsive therapy. Am J Psychiatry. 1984; 141:1034-1041.
Gagne GG et al. Efficacy of continuation ECT and antidepressant drugs compared to long-term
antidepressants alone in depressed patients. Am J Psychiatry. 2000; 157:1960-1965.
Sackheim HA et al. Continuation pharmacotherapy in the prevention of relapse following
electroconvulsive therapy: A randomized controlled trial. JAMA. 2001; 285:1299-1307.
Sackheim HA et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive
effects of electroconvulsive therapy. NEJM. 1993; 328:839-846.
Bailine SH et al. Comparison of bifrontal and bitemporal ECT for major depression. Am J Psychiatry. 2000;
157:121-123.
Letemendia FJJ et al. Therapeutic advantage of bifrontal electrode placement in ECT. Psychological
Medicine. 1993; 23:349-360.
Lawson JS et al. Electrode placement in ECT:cognitive effects. Psychological Medicine. 1990; 20:335-344.
Mayberg HS et al. Deep brain stimulation for treatment-resistant depression. Neuron. 2005 Mar 3; 45:65160. (DBS study)
Newman ME et al. Neurochemical mechanisms of action of ECT: evidence from in vivo studies.The
Journal of ECT. 1998; 14(3):153-171.
Duman RS and Vaidya VA. Molecular and cellular actions of chronic electroconvulsive seizures. Journal
of ECT. 1998; 14(3):181-193.
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