Electroconvulsive Therapy

Article Author:
Irim Salik
Article Editor:
Raman Marwaha
Updated:
3/13/2019 6:02:33 PM
PubMed Link:
Electroconvulsive Therapy

Introduction

In a patient under intravenous sedation or general anesthesia, electroconvulsive therapy (ECT) uses an electric current to create a generalized cerebral seizure. Although it is primarily utilized to treat patients with severe depression, patients with schizophrenia, schizoaffective disorder, catatonia, neuroleptic malignant syndrome, and bipolar disorder may also benefit. However, the practice has a stigma attached to it due to misinformation regarding procedural methodology. 

Anatomy

There are various pathophysiologic changes in brain regions found in patients with severe depression. These include reduced activity and volumetric reductions in the dorsal areas of the frontal lobes. Areas of the ventral and orbital frontal cortex have altered processing of emotional stimuli.[1] In addition to the frontal lobe, functional alterations and volumetric reductions are apparent in the hippocampus, parahippocampal gyri, and amygdala.[2] The hypothalamic-pituitary-adrenal (HPA) axis becomes hypersensitive to stressors, exhibits chronically elevated levels of stress hormones and impaired feedback regulation. [3] The mesocorticolimbic dopamine system, as well as the HPA axis, are activated in patients with stress. Dopamine function is thought to be impaired in patients with depression, causing impairment in essential functions including concentration, motivation, and pleasure.[4] The antidepressive effects of ECT reflect changes in the systems mentioned above.

Indications

ECT is indicated in patients with treatment-resistant depression or severe major depression that impairs activities of daily living. The definition of treatment-resistant depression is depression that is unresponsive to multiple antidepressant medication trials.[5] There are also suggestions for ECT as a treatment for suicidality, severe psychosis, food refusal secondary to depression, and catatonia.[6][7] Bipolar depressive and manic patients can also receive treatment with ECT.[8] ECT may have a safer profile than antidepressants or antipsychotics in debilitated, elderly, pregnant and breastfeeding patients. Suicidal ideation is rapidly relieved by ECT, and complete resolution was seen in 38% of patients after one week, 61% of patients after two weeks and in 81% of patients with completion of ECT.[9] ECT is also recommended for patients that have exhibited a favorable response to ECT previously. 

Contraindications

The resultant seizure from ECT can cause transient increases in blood pressure, myocardial oxygen consumption, heart rate, and intracranial pressure. Care is necessary for patients with cardiovascular, pulmonary, or central nervous system compromise. A pheochromocytoma and elevated intracranial pressure with mass effect are absolute contraindications to ECT. Relative contraindications include elevated intracranial pressure without mass effect, cardiovascular conduction defects, high-risk pregnancies, aortic and cerebral aneurysms.[10]

Equipment

ECT treatment and recovery areas should include the standard American Society of Anesthesiologists (ASA) monitors. A stethoscope, blood pressure monitor, electrocardiography (EKG) monitor, pulse oximeter, suction apparatus, and an oxygen delivery system should be present. Anesthetic induction supplies and medication should be available along with ventilatory and resuscitation equipment. A nasal cannula or face mask to provide supplemental oxygen, bag valve mask, nerve stimulator to assess neuromuscular blockade, electromyograph (EMG), electroencephalography (EEG) leads, and multiple blood pressure cuffs should be available.

Personnel

ECT is administered by a team that typically includes an anesthesiologist, a psychiatrist and a nurse. 

Preparation

A complete history and physical examination may expose significant risk factors including cardiac ischemia or arrhythmia, heart failure, or intracranial pathology.[11] History should also include the use of herbal medications such as Ginkgo biloba, ginseng, St. John's wort, valerian, and kava, all of which may interfere with ECT. There is a risk of status epilepticus in patients on theophylline.[12] Short-acting intravenous beta blockers may reduce ECT related hypertension and tachycardia, but may also shorten seizure duration and reduce ECT efficacy.  Cardiac medications including aspirin, statins, antihypertensive agents, antianginal medications, and clopidogrel should be continued the day of the procedure. Serum glucose levels require checking both preoperatively and in the recovery room, as ECT treatments can raise blood glucose levels. Although ECT appears to be safe in a patient with a defibrillator, detection mode should be turned off during the procedure and equipment for external defibrillation should be available at the patient’s bedside. In pregnant patients, noninvasive fetal monitoring is the recommendation after 14 to 16 weeks and a nonstress test with a tocometer after 24 weeks.

ECT utilizes general anesthesia. Anesthetic induction medications used include barbiturates such as thiopental and methohexital and nonbarbiturate agents such as propofol and etomidate. Seizure-induced by ECT should last longer than 30 seconds. Methohexital is the most commonly used induction agent due to its quick onset, effectiveness, low cost, and minimal effect on seizure duration. Propofol and thiopental have been shown to reduce seizure duration. Etomidate has correlations with myoclonus and increased seizure duration.

Technique

ECT is commonly performed in a dedicated suite, a post-anesthesia care unit, or an ambulatory surgery site, most frequently on an outpatient basis. Patients with severe debilitation including substantial medical or psychiatric illness may start on an inpatient basis and transition to an outpatient basis as needed. Patients should be appropriately nil per os (NPO) for the procedure, which includes no light meal for six hours, no full-fat meal for eight hours, and no clear liquids for two hours before anesthesia.

Vital signs, including blood oxygen saturation, ECG and EEG activity are recorded continuously. EMG is recorded on the right foot to measure the motor component of seizure activity. A nerve stimulator is utilized to monitor succinylcholine, a depolarizing muscle relaxant used to reduce tonic-clonic contractions during the procedure. As an alternative to EMG, a blood pressure cuff is inflated on the patient’s ankle to prevent succinylcholine from entering the foot, allowing a visual monitor of seizure activity with measurement of tonic-clonic contractions. Following intravenous induction, a bite block is placed to protect the patient’s tongue and teeth. The beginning and termination of a cerebral seizure is monitored via EEG, recorded from right and left frontal and mastoid positions. Seizure induction is via two electrodes placed bitemporally or a right unilateral electrode; both of which allow electrical current to pass into the scalp.[13] A 2017 meta-analysis of numerous randomized trials of 792 patients specifically compared moderate dose bilateral ECT with high dose right unilateral ECT, and remission was comparable.[14] Right unilateral ECT is utilized preferentially to minimize retrograde amnesia.

The ECT stimulus is either a brief pulse (0.5 to 2.0 milliseconds) or ultra-brief pulse (less than 0.5 milliseconds) waveform. While the brief pulse is considered standard, the ultra-brief is considered more tolerable.[15] Electricity dose affects efficacy, the speed of response, and adverse cognitive effects. Seizure threshold is established via trial and error via incrementally higher doses of current during the primary treatment session.[16][17] Following initial dose calculation, the dose at subsequent ECT sessions for bilateral ECT is 1.5 to 2 times seizure threshold, and for right unilateral is six times the seizure threshold. During a course of ECT treatment, the seizure threshold commonly increases as the patient develops tolerance.

As with any other procedure, the goal of the anesthesiologist during ECT is to facilitate a safe and pain-free experience for the patient.[18] Preoxygenation of the patient via nasal cannula or face mask is followed by anesthetic induction and paralysis. Administration of an anticholinergic medication before ECT may prevent arrhythmias such as bradycardia or asystole and excessive oral secretions. To induce cerebral vasoconstriction via hypocarbia, the patient is often hyperventilated via bag valve mask before delivery of the electrical stimulus to increase seizure intensity.[19]The gold standard for induction of anesthesia is methohexital, given at 0.75 to 1 mg/kg.[18] Methohexital is preferred to propofol because a meta-analysis of two randomized trials revealed that seizure duration was shorter with propofol.[20] Skeletal muscle relaxation during ECT is integral to minimize a motor seizure and avoid musculoskeletal injury. The depolarizing neuromuscular relaxant succinylcholine is used at 0.75 to 1 mg/kg with an elimination half-life of 41 seconds.[21][22]  In cases where succinylcholine is contraindicated including neuromuscular disease or injury, burn injury, pseudocholinesterase deficiency or hyperkalemia, nondepolarizing neuromuscular relaxants are the preferred option.[5]

Once the patient is rendered unconscious, administration of a muscle relaxant follows, along with bag valve mask ventilation with 100 percent oxygen. A nerve stimulator is utilized to determine the adequacy of muscle relaxation along with the clinical assessment of plantar reflexes and fasciculations in the calves and left foot. An inflated blood pressure cuff prevents muscle relaxant from entering the right foot. Muscle relaxants do not prevent masseter muscle contraction from the electrical pulse, requiring placement of a bite block for lingual and tooth protection.

Although most therapeutic ECT seizures last from 15 to 70 seconds, EEG recording lasts about 25 percent longer than the motor seizure.[23] Seizures lasting less than 15 seconds may not be clinically effective, while prolonged seizures may cause cognitive impairment. A missed or short seizure should have a follow-up with a short period of hyperventilation and restimulation with a higher electrical current. If a patient is experiencing a prolonged seizure greater than two minutes, an induction agent such as propofol or methohexital is either given at a half dose or a benzodiazepine, to suppress seizure activity and avoid neurologic injury. In a patient with numerous missed seizures,[24][12] anesthetic induction agents such as etomidate or ketamine may be useful as they exhibit less anticonvulsant effects as compared to methohexital. While caffeine had been previously administered to prolong seizures, it is no longer the recommendation due to its uncertain safety profile for this purpose.

In pregnant patients receiving ECT,[25][26] hyperventilation should be avoided as it can reduce placental blood flow causing fetal hypoxia. Minimization of NPO time and adequate intravenous fluid hydration is essential to avoid dehydration and premature uterine contractions. In a female with a gestational age greater than 20 weeks, left lateral uterine displacement is essential to optimize maternal venous return and maintain optimal uterine blood flow. In pregnancies greater than 24 weeks gestation considered viable, fetal heart rate and uterine activity should undergo continuous monitoring 30 minutes before and after each treatment by an obstetrician that can manage obstetric and neonatal emergencies. Because pregnant patients are at higher risk for aspiration pneumonitis due to their full stomach status, anticholinergic drugs that reduce lower esophageal sphincter tone should be avoided, as they can increase reflux.[27][25][28]  In this case, a nonparticulate antacid such as sodium citrate is safer for aspiration prophylaxis.

Complications

Bilateral or bitemporal ECT causes more cognitive impairment than unilateral ECT, although this effect is transient. A meta-analysis of 1415 depressed patients treated with ECT revealed that global cognition, verbal memory, and autobiographical memory were worse with bilateral treatment three days after treatment.[29]

According to the American Psychiatric Association, patients receiving ECT are at higher risk if they show evidence of unstable or severe cardiovascular disease, a space-occupying intracranial lesion with evidence of elevated intracranial pressure, history of an acute cerebral hemorrhage or stroke, an unstable vascular aneurysm, severe pulmonary disease, or qualify as American Society of Anesthesiologists (ASA) Class 4 or 5.

Physiologically, during the tonic phase of the seizure, a 15- to 20-second parasympathetic discharge occurs, which can lead to bradyarrhythmias including premature atrial and ventricular contractions, atrioventricular block, and asystole. Patients with subconvulsive seizures are at higher risk for asystole.[30] Paradoxically, patients with heart block or underlying arrhythmias are less likely to develop asystole. The clonic phase of the seizure correlates with a catecholamine surge that causes tachycardia and hypertension, which lasts temporally with seizure duration.[31] Hypertension and tachycardia resolve within 10 to 20 minutes of the seizure, although some patients exhibit persistent hypertension that requires medical intervention.

Although patients with cardiac disease at baseline are at higher risk following treatment, ejection fraction can decrease following ECT in healthy patients as well.[32] In a study of 53 adults undergoing ECT, seven developed new global left ventricular (LV) systolic dysfunction and eight developed regional wall motion abnormalities. [33] Of these patients, there were no adverse outcomes in patients with LV dysfunction. In a prospective cohort study of 100 subjects undergoing ECT, increased cardiac troponin levels were present in eight patients, with only two having other evidence of myocardial ischemia or infarction. [34] Cerebral blood flow and intracranial pressure both increase with ECT therapy. Clinically, patients may exhibit confusion, delirium, disorientation and memory loss. ECT is classified as a low-risk procedure by the AHA-ACC guidelines because it is well tolerated, and demonstrates only transient hemodynamic lability and low mortality rate. [35][36][37]

Clinical Significance

ECT is a relatively safe and low-risk procedure that is helpful in the treatment of depression, suicidality, severe psychosis, food refusal secondary to depression, and catatonia. It requires interprofessional care coordination among anesthesiologists, psychiatrists, and nurses. Most patients require several sessions to see a durable effect. The stigma associated with ECT is largely due to the lack of anesthesia with early treatments resulting in significant injury and severe memory loss.  The antidepressant effect is seen relatively quickly and may last up to a few years. Overall, the mortality rate is very low with ECT administered in a controlled setting, but it continues to cause mild memory loss in the long term. ECT is commonly utilized in pregnant patients and the elderly due to the avoidance of psychotropic medication side effects. Although its mechanism of action is multifactorial, ECT causes changes in cerebral blood flow and regional metabolism. 

Enhancing Healthcare Team Outcomes

Today ECT is now frequently used to treat a variety of mental health disorders besides depression. The procedure is relatively safe, and does work. However, the delivery of ECT requires a multidisciplinary team that includes a nurse, anesthesiologist, psychiatrist and a neurologist. The benefits of ECT are seen after several sessions and the results are durable. The key is to educate the patient and family about ECT because the procedure has been associated with many false and illogical beliefs. The antidepressant effect is seen relatively quickly and may last up to a few years. Overall, the mortality rate is very low with ECT administered in a controlled setting, but it continues to cause mild memory loss in the long term. ECT is commonly utilized in pregnant patients and the elderly due to the avoidance of psychotropic medication side effects. Although its mechanism of action is multifactorial, ECT causes changes in cerebral blood flow and regional metabolism. Most patients who undergo ECT have a beneficial response without any adverse sequelae. [38](Level V)


References

[1] Mayberg HS,Lewis PJ,Regenold W,Wagner HN Jr, Paralimbic hypoperfusion in unipolar depression. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 1994 Jun;     [PubMed PMID: 8195877]
[2] Botteron KN,Raichle ME,Drevets WC,Heath AC,Todd RD, Volumetric reduction in left subgenual prefrontal cortex in early onset depression. Biological psychiatry. 2002 Feb 15;     [PubMed PMID: 11958786]
[3] de Kwaasteniet B,Ruhe E,Caan M,Rive M,Olabarriaga S,Groefsema M,Heesink L,van Wingen G,Denys D, Relation between structural and functional connectivity in major depressive disorder. Biological psychiatry. 2013 Jul 1;     [PubMed PMID: 23399372]
[4] Rigucci S,Serafini G,Pompili M,Kotzalidis GD,Tatarelli R, Anatomical and functional correlates in major depressive disorder: the contribution of neuroimaging studies. The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry. 2010 Mar;     [PubMed PMID: 19670087]
[5] The Practice of ECT: Recommendations for Treatment, Training and Privileging. Convulsive therapy. 1990 Jun;     [PubMed PMID: 11659302]
[6] Husain MM,Rush AJ,Fink M,Knapp R,Petrides G,Rummans T,Biggs MM,O'Connor K,Rasmussen K,Litle M,Zhao W,Bernstein HJ,Smith G,Mueller M,McClintock SM,Bailine SH,Kellner CH, Speed of response and remission in major depressive disorder with acute electroconvulsive therapy (ECT): a Consortium for Research in ECT (CORE) report. The Journal of clinical psychiatry. 2004 Apr;     [PubMed PMID: 15119910]
[7] Kellner CH,Knapp R,Husain MM,Rasmussen K,Sampson S,Cullum M,McClintock SM,Tobias KG,Martino C,Mueller M,Bailine SH,Fink M,Petrides G, Bifrontal, bitemporal and right unilateral electrode placement in ECT: randomised trial. The British journal of psychiatry : the journal of mental science. 2010 Mar;     [PubMed PMID: 20194546]
[8] Fink M, Indications for the use of ECT. Psychopharmacology bulletin. 1994;     [PubMed PMID: 7878176]
[9] Kellner CH,Fink M,Knapp R,Petrides G,Husain M,Rummans T,Mueller M,Bernstein H,Rasmussen K,O'connor K,Smith G,Rush AJ,Biggs M,McClintock S,Bailine S,Malur C, Relief of expressed suicidal intent by ECT: a consortium for research in ECT study. The American journal of psychiatry. 2005 May;     [PubMed PMID: 15863801]
[10] Taylor S, Electroconvulsive therapy: a review of history, patient selection, technique, and medication management. Southern medical journal. 2007 May;     [PubMed PMID: 17534086]
[11] Tess AV,Smetana GW, Medical evaluation of patients undergoing electroconvulsive therapy. The New England journal of medicine. 2009 Apr 2;     [PubMed PMID: 19339723]
[12] Devanand DP,Decina P,Sackeim HA,Prudic J, Status epilepticus following ECT in a patient receiving theophylline. Journal of clinical psychopharmacology. 1988 Apr;     [PubMed PMID: 3372714]
[13] Bjølseth TM,Engedal K,Benth JŠ,Dybedal GS,Gaarden TL,Tanum L, Clinical efficacy of formula-based bifrontal versus right unilateral electroconvulsive therapy (ECT) in the treatment of major depression among elderly patients: a pragmatic, randomized, assessor-blinded, controlled trial. Journal of affective disorders. 2015 Apr 1;     [PubMed PMID: 25590761]
[14] Kolshus E,Jelovac A,McLoughlin DM, Bitemporal v. high-dose right unilateral electroconvulsive therapy for depression: a systematic review and meta-analysis of randomized controlled trials. Psychological medicine. 2017 Feb;     [PubMed PMID: 27780482]
[15] Sienaert P,Spaans HP,Kellner CH, Pulse Width in Electroconvulsive Therapy: How Brief Is Brief? The journal of ECT. 2018 Jun;     [PubMed PMID: 29489561]
[16] Petrides G,Fink M, The     [PubMed PMID: 8872401]
[17] Petrides G,Braga RJ,Fink M,Mueller M,Knapp R,Husain M,Rummans T,Bailine S,Malur C,O'Connor K,Kellner C, Seizure threshold in a large sample: implications for stimulus dosing strategies in bilateral electroconvulsive therapy: a report from CORE. The journal of ECT. 2009 Dec;     [PubMed PMID: 19972637]
[18] Bryson EO,Aloysi AS,Farber KG,Kellner CH, Individualized Anesthetic Management for Patients Undergoing Electroconvulsive Therapy: A Review of Current Practice. Anesthesia and analgesia. 2017 Jun;     [PubMed PMID: 28277323]
[19] Bergsholm P,Gran L,Bleie H, Seizure duration in unilateral electroconvulsive therapy. The effect of hypocapnia induced by hyperventilation and the effect of ventilation with oxygen. Acta psychiatrica Scandinavica. 1984 Feb;     [PubMed PMID: 6422704]
[20] Lihua P,Su M,Ke W,Ziemann-Gimmel P, Different regimens of intravenous sedatives or hypnotics for electroconvulsive therapy (ECT) in adult patients with depression. The Cochrane database of systematic reviews. 2014 Apr 11;     [PubMed PMID: 24723301]
[21] Bryson EO,Kellner CH,Li EH,Aloysi AS,Majeske M, Extreme variability in succinylcholine dose for muscle relaxation in electroconvulsive therapy. Australasian psychiatry : bulletin of Royal Australian and New Zealand College of Psychiatrists. 2018 Aug;     [PubMed PMID: 29504412]
[22] Torda TA,Graham GG,Warwick NR,Donohue P, Pharmacokinetics and pharmacodynamics of suxamethonium. Anaesthesia and intensive care. 1997 Jun;     [PubMed PMID: 9209610]
[23] Mayur PM,Gangadhar BN,Janakiramaiah N,Subbakrishna DK, Motor seizure monitoring during electroconvulsive therapy. The British journal of psychiatry : the journal of mental science. 1999 Mar;     [PubMed PMID: 10448455]
[24] Datto C,Rai AK,Ilivicky HJ,Caroff SN, Augmentation of seizure induction in electroconvulsive therapy: a clinical reappraisal. The journal of ECT. 2002 Sep;     [PubMed PMID: 12394529]
[25] Miller LJ, Use of electroconvulsive therapy during pregnancy. Hospital     [PubMed PMID: 8045538]
[26] Rabheru K, The use of electroconvulsive therapy in special patient populations. Canadian journal of psychiatry. Revue canadienne de psychiatrie. 2001 Oct;     [PubMed PMID: 11692973]
[27] Yonkers KA,Wisner KL,Stowe Z,Leibenluft E,Cohen L,Miller L,Manber R,Viguera A,Suppes T,Altshuler L, Management of bipolar disorder during pregnancy and the postpartum period. The American journal of psychiatry. 2004 Apr;     [PubMed PMID: 15056503]
[28] Anderson EL,Reti IM, ECT in pregnancy: a review of the literature from 1941 to 2007. Psychosomatic medicine. 2009 Feb;     [PubMed PMID: 19073751]
[29] Semkovska M,Keane D,Babalola O,McLoughlin DM, Unilateral brief-pulse electroconvulsive therapy and cognition: effects of electrode placement, stimulus dosage and time. Journal of psychiatric research. 2011 Jun;     [PubMed PMID: 21109254]
[30] Kaufman KR, Asystole with electroconvulsive therapy. Journal of internal medicine. 1994 Mar;     [PubMed PMID: 8120525]
[31] Larson G,Swartz C,Abrams R, Duration of ECT-induced tachycardia as a measure of seizure length. The American journal of psychiatry. 1984 Oct;     [PubMed PMID: 6486265]
[32] Fuenmayor AJ,el Fakih Y,Moreno J,Fuenmayor AM, Effects of electroconvulsive therapy on cardiac function in patients without heart disease. Cardiology. 1997 May-Jun;     [PubMed PMID: 9129846]
[33] McCully RB,Karon BL,Rummans TA,Black JL,Andreen KM,Oh JK,Seward JB,Tajik AJ, Frequency of left ventricular dysfunction after electroconvulsive therapy. The American journal of cardiology. 2003 May 1;     [PubMed PMID: 12714169]
[34] Duma A,Pal S,Johnston J,Helwani MA,Bhat A,Gill B,Rosenkvist J,Cartmill C,Brown F,Miller JP,Scott MG,Sanchez-Conde F,Jarvis M,Farber NB,Zorumski CF,Conway C,Nagele P, High-sensitivity Cardiac Troponin Elevation after Electroconvulsive Therapy: A Prospective, Observational Cohort Study. Anesthesiology. 2017 Apr;     [PubMed PMID: 28166110]
[35] Zielinski RJ,Roose SP,Devanand DP,Woodring S,Sackeim HA, Cardiovascular complications of ECT in depressed patients with cardiac disease. The American journal of psychiatry. 1993 Jun;     [PubMed PMID: 8494067]
[36] Rice EH,Sombrotto LB,Markowitz JC,Leon AC, Cardiovascular morbidity in high-risk patients during ECT. The American journal of psychiatry. 1994 Nov;     [PubMed PMID: 7943453]
[37] Abrams R, The mortality rate with ECT. Convulsive therapy. 1997 Sep;     [PubMed PMID: 9342128]
[38] Benson NM,Seiner SJ,Bolton P,Fitzmaurice G,Meisner RC,Pierce C,Busch AB, Acute Phase Treatment Outcomes of Electroconvulsive Therapy in Adolescents and Young Adults. The journal of ECT. 2018 Dec 18     [PubMed PMID: 30562200]