© Springer International Publishing Switzerland 2017Basavana G. Goudra and Preet Mohinder Singh (eds.)Out of Operating Room Anesthesia10.1007/978-3-319-39150-2_19
19. Anesthesia for Electroconvulsive Therapy
Department of Anesthesia and Perioperative Care, University of California, San Francisco, 521 Parnassus Ave, San Francisco, CA 94143, USA
Jonathan Z. Pan
Electroconvulsive therapy (ECT) is commonly used to treat major depression and other psychiatric disorders. Although the mechanism of action is not clear, ECT is safe and effective, if managed appropriately. A sufficient long seizure induced by lowest possible amplitude of current is most likely to produce optimal effect, yet with fewer side effects. ECT elicits significant physiological responses, including cardiovascular (e.g. hypertension and tachycardia) and central nervous system (e.g. increase of intracranial pressure and cerebral blood flow). Thus anesthesia preoperative evaluation should identify patients with higher risks, who should be consulted beforehand with proper plan of care. General anesthesia is usually planned for ECT procedure. Although different anesthetic regimens can be used, the goal is to minimize the anesthetic factors on the efficacy of ECT treatment, while maintaining adequate depth of anesthesia and ensuring patient’s safety. In many hospitals, ECT is often performed at remote sites; anesthesiologist should be aware and well prepared for escalation of care if emergency occurs.
KeywordsECTDepressionPsychiatric disorderSeizureGeneral anesthesiaNORA (non-operating room anesthesia)Adverse responseAnestheticPreoperative evaluationPatient safety
Electroconvulsive Therapy (ECT)
Electroconvulsive therapy (ECT) is used to treat psychiatric disorders after failure of pharmacologic medical management or as an emergent procedure in gravely debilitated patient populations . While a widely accepted definition of failed pharmacologic therapy or treatment resistance does not exist, a lack of clinical response, intolerance of side effects, and acute deterioration in the psychiatric condition are all reasons to consider the initiation of ECT. Indications for ECT include primarily unipolar and bipolar depression, mania, but also schizophrenia, schizoaffective disorders, mixed affective disorders, and catatonia [2, 3]. Further applications include depression secondary to neurological disorders such as multiple sclerosis and obsessive-compulsive disorder, although the efficacy in these contexts remains to be determined. Notably, clinical improvement can occur within several treatments and as such is important in gravely affected populations including acutely suicidal patients and the severely catatonic. Importantly, the American Psychiatric Association (APA) states “[ECT] should not be reserved for use only as a ‘last resort.’ Such practice may deprive patients of an effective treatment, delay response and prolong suffering” .
Cerletti and Bini first reported the use of ECT in humans in Rome in 1938 after numerous studies on electrical induction of seizures in dogs [4, 5]. The first patient was a male with schizophrenia and delusions. In this report, a bitemporal shock was applied to the patient, a seizure was induced, respirations ceased, he became cyanotic and tachycardic then 48 s later he emitted a deep sigh, his cyanosis diminished and heart rate began to normalize. The patient had a series of 11 treatments and was discharged in good condition and well-oriented. For approximately 30 years ECT was practiced in the US and abroad without general anesthesia and neuromuscular blockade, which are now incorporated into routine practice [6, 7]. The initial use of neuromuscular blockade occurred in 1951, and the utilization of the hypnotic barbiturate methohexital occurred in the early 1960s. Now, ECT is considered a low-risk procedure routinely performed under general anesthesia with a mortality rate that is similar to that of brief general anesthesia and is estimated to be between 0.01 and 0.1 % with a complication rate of 0.3 % .
Proposed Mechanisms of Action
The mechanism of action of ECT is currently unknown, however, hypotheses for the improvement in psychiatric disorders are via the following mechanisms: the release of neurotransmitters (specifically dopamine, serotonin, and GABA) during the induced seizure or reestablishment of neurotransmitter levels after seizure activity (i.e., recalibrating the thermostat); altered cerebral glucose metabolism and blood flow; modulation of the hypothalamic-pituitary-adrenal axis, changes in synaptic transmission and plasticity; and cell proliferation .
A shock is applied to one or both cerebral hemispheres to induce a seizure. Importantly, the seizure must be of sufficient duration (20–60 s) for optimal effects, with therapeutic benefit often apparent after a total of 400–700 s of seizure activity. This can occur after 2–3 weeks of treatment with 2–3 sessions of ECT per week . Short seizure duration, then, is a predictor of poor outcome. The psychiatrist determines the pattern, amplitude, and duration of the electrical impulse, yet the anesthetic plan may be the difference between a clinically significant seizure and a sub-optimal seizure. Changing from unilateral to bilateral electrode placement, increasing the stimulus intensity, or potentiating the seizure pharmacologically may facilitate the induction of seizures of an adequate length [10, 11]. A sufficiently long seizure, generated with the lowest possible amplitude of current has the best chance of fewer untoward side effects. Seizure duration is monitored by both electroencephalography and motor activity. A seizure longer than 120 s is classified as “prolonged” and the anesthesiologist should administer pharmacological agents to terminate the seizure.
Seizures are characterized by an initial tonic phase noted by bradycardia (and rarely asystole), premature atrial and ventricular contractions, hypotension, and salivation that occur secondary to activation of the parasympathetic autonomic system. This phase may last only 10–15 s, followed by a myoclonic phase lasting 30–60 s marked by sympathetic activation and associated tachycardia (HR >130 bpm), hypertension (SBP increases of 30–70 mmHg and diastolic BP increases of 10–50 mmHg), premature ventricular contractions, and rarely, ventricular tachycardia and changes in the electrocardiogram, including ST-segment depression and T-wave inversion. Transient atrial and ventricular tachyarrhythmias occur in 10 % of patients with known or suspected cardiovascular disease. ECT induced cardiovascular mortality has been reported as 0.03 %. Notably, tachycardia peaks 1–2 min after the electrical stimulus is applied, hypertension peaks 1–3 min later and may continue into emergence and the post-procedural period [7, 12].
Electrical stimulation produces large increases in cerebral blood flow and thus intracranial pressure (ICP) . It has been reported that after electrically induced seizures CBF increases ~300 % and cerebral metabolism increases ~200 %. Additionally, there is evidence of a temporary increase in the vascular permeability of the blood brain barrier. These effects should be considered in all patients presenting for ECT with cerebral aneurysms, arteriovenous malformations (AVMs), intracranial lesions/tumors, and those with increased intracranial pressure of unknown etiology. As such, there has been concern that those with increased ICP are at risk for herniation and even death. However, not all intracranial lesions are created equal. Small slow growing lesions without edema pose less risk when compared to a large, highly-vascularized, aggressive tumor with radiological or clinical evidence of edema and mass effect.
Intraocular pressure increases as a result of ECT and also secondary to the administration of succinylcholine . Care should be taken in those with increased intraocular pressures and patients at high-risk for retinal detachment. Glucose homeostasis is also affected and elevated blood glucose has been noted in patients after ECT, most likely as a function of the stress response. The clinical significance of this finding remains to be elucidated. Patients should hold oral hypoglycemics and short acting insulin on the day of the procedure and decrease their home long acting insulin in preparation for the procedure .
As with all anesthetics, pre-operative evaluation requires a focused history and physical to determine whether the patient is in an optimal state to proceed with brief general anesthesia, with attention to the cardiovascular, neurologic/cerebrovascular, and airway/pulmonary co-morbitities. Pre-operative evaluation may require consultation with cardiologists, neurologists, and other specialists to medically optimize a patient prior to this elective procedure and ascertain whether the potential benefits of treatment outweigh the risks. A 12-lead ECG should be done on all patients above the age of 60 .
According to the APA Task Force Report, there currently are no absolute contraindications to ECT. Strong relative contraindications include a known pheochromocytoma, recent myocardial infarction (<3 months) or stroke (<1 month), and increased intracerebral pressure of any cause. Other relative contraindications include angina, poorly controlled heart failure, severe valvular disease; aortic and cerebral aneurysms or other vascular malformations subject to rupture with increased blood pressure; bone fractures, severe osteoporosis; high risk pregnancy (for which an Obstetrics consult and fetal monitoring would be recommended); intraocular processes including glaucoma, and retinal detachment; and significant pulmonary disease including asthma/COPD. Thorough pre-procedural evaluation should be performed for all ASA IV patients, and ECT may be safer in the operating suite where the anesthesiologist would have access to more emergency equipment, medications, and resources in the event of life-threatening physiology .
Special Patient Populations
Patients with pacemakers/Automatic Implantable Cardioverter-Defibrillator (AICD)
Patients with pacemakers/AICDs can have ECT as the device is far from the field of electrical stimulation, thus only small amounts of electricity reach the device. One retrospective study noted that anesthesia proceeded uneventfully in patients with pacemakers receiving ECT and no pacemaker malfunctions were noted in 146 treatments. One should have a magnet accessible to disable AICD functionality and/or use the magnet to set a pacemaker to a fixed rate if necessary. Patients with severe heart disease should be medically optimized, if possible, prior to initiation of ECT. Electrolyte abnormalities should be corrected and hypertension well-controlled .
In 2001, the APA stated its support of ECT as an appropriate treatment modality in the pregnant patient as neglected psychiatric illness can have a negative impact on the fetus by affecting development, gestational age at the time of delivery, and birth weight . ECT is safe and effective for pregnant patients and some would argue that it is safer than pharmacologic agents . Most anesthetic agents and all induction agents are US FDA category B or C; methohexital, thiopental, etomidate, propofol, ketamine and sevoflurane can all be utilized in the pregnant woman. Only benzodiazepines have been categorized as category D (with positive evidence of risk to fetus, however potential benefits may outweigh potential risk), and cocaine is the only category X (contraindicated) anesthetic agent. Ideally, ECT should occur during the second and third trimesters as rapid organogenesis is occurring in the fetus during the first trimester. An obstetrical exam should occur prior to the initiation of ECT with documentation of fetal heart rate. Adequate preoxygenation is essential as the pregnant woman will desaturate faster than her non-pregnant peers as her functional residual capacity (FRC) starts to decrease secondary to the upward displacement of the gravid uterus. The pregnant woman is always regarded as having a full stomach and at increased risk of aspiration as early as the 12th week. Therefore the administration of a non-particulate antacid (Bicitra/sodium citrate 30 ml) and/or histamine-2 receptor blockers (ranitidine 50 mg IV 30–60 min prior to the procedure) should be considered. After 20 weeks gestation a wedge should be placed under the right hip for left uterine displacement of the uterus from the aorta and inferior vena cava (IVC). After 24 weeks gestational age, the patient should be intubated for airway protection with a rapid-sequence induction with cricoid pressure and maintenance via sevoflurane which can reduce the risk of uterine contractions. Non-invasive fetal heart monitoring is advised after ECT performed in the second and third trimester. Complications include premature labor due to increased levels of oxytocin produced after ECT and spontaneous abortion, and thus prophylactic tocolytic therapy may be useful in women with a history of premature labor who need ECT. Other complications include uterine contractions, vaginal bleeding, fetal arrhythmias specifically fetal bradycardia, and abruption of the placenta. The most prudent way to optimize the chance of a safe anesthetic in obstetric patients is vigilance and close monitoring of both the mother and fetus before, during, and after ECT. Finally, it would be wise (depending on gestational age) to perform ECT on the pregnant patient in sites with immediate access to obstetrical care in the event that an emergency caesarian section is required. Certainly ECT is not without risk, and should be reserved for those with grave disability and psychiatric disorders recalcitrant to pharmacotherapy.