Electroconvulsive Therapy (ECT) ARNEL BANAGA SALGADO, Ed.D., D. Sc., MAT (Psych) Assistant Professor, RAKCON, RAKMHSU Mobile: 050 799 3803 E-mail: [email protected]

Electroconvulsive Therapy (ECT)

ARNEL BANAGA SALGADO, Ed.D., D. Sc., MAT (Psych)Assistant Professor, RAKCON, RAKMHSUMobile: 050 799 3803E-mail: [email protected]

www.arnelsalgado.com

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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

Learning Objectives


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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 was based upon a theory of opposition beween epilepsy and schizophrenia.

(Drawing by Renato Sabattini, PhD)


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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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(Reproduced with permission from: Somatics, LLC)

Thymatron™ System IV - Integrated ECT Instrument


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Electrical Stimulus Brief-pulse square-wave ACVoltage approx. 200V (based upon 220 Ω

impedance)Current 0.9AFrequency 30 - 70HzPulsewidth 0.5 - 2 msecDuration 0.1 - 8 secCharge 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 of neuronal population which

is: Paroxysmal Synchronous Repetitive

Post-ictal suppression follows seizure Inhibitory interneurons GABA (as detected by MRS)


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Modern (Modified) ECT1. 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, Beta-blockers, 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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References1. Abrams R. Electroconvulsive Therapy, 3rd Edition. New York: Oxford University Press, 1997.2. Rasmussen KG et al. Electroconvulsive therapy and newer modalities for the treatment of

medication-retractory mental illness. Mayo Clin Proc. 2002; 77:552-556.3. Fink M. Meduna and the origins of convulsive therapy. Am J Psychiatry. 1984; 141:1034-1041.4. Gagne GG et al. Efficacy of continuation ECT and antidepressant drugs compared to long-term

antidepressants alone in depressed patients. Am J Psychiatry. 2000; 157:1960-1965.5. Sackheim HA et al. Continuation pharmacotherapy in the prevention of relapse following

electroconvulsive therapy: A randomized controlled trial. JAMA. 2001; 285:1299-1307.6. Sackheim HA et al. Effects of stimulus intensity and electrode placement on the efficacy and

cognitive effects of electroconvulsive therapy. NEJM. 1993; 328:839-846.7. Bailine SH et al. Comparison of bifrontal and bitemporal ECT for major depression. Am J Psychiatry.

2000; 157:121-123.8. Letemendia FJJ et al. Therapeutic advantage of bifrontal electrode placement in ECT. Psychological

Medicine. 1993; 23:349-360.9. Lawson JS et al. Electrode placement in ECT:cognitive effects. Psychological Medicine. 1990; 20:335-

344.

10. Mayberg HS et al. Deep brain stimulation for treatment-resistant depression. Neuron. 2005 Mar 3; 45:651-60. (DBS study)

11. Newman ME et al. Neurochemical mechanisms of action of ECT: evidence from in vivo studies.The Journal of ECT. 1998; 14(3):153-171.

12. 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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Documents

Electroconvulsive Therapy (ECT) ARNEL BANAGA SALGADO, Ed.D., D. Sc., MAT (Psych) Assistant Professor, RAKCON, RAKMHSU Mobile: 050 799 3803 E-mail: [email protected]