Aetna considers electroconvulsive therapy (ECT) medically necessary for members diagnosed with any of the following conditions.
Note: More than 20 sessions of ECT in a treatment series is rarely medically necessary.
Aetna considers multiple monitored ECT experimental and investigational because its effectiveness has not been established.
Aetna considers ultrabrief bilateral ECT experimental and investigational because its effectiveness has not been established.
Aetna considers adjunctive ketamine in ECT experimental and investigational because the effectiveness of this approach has not been established.
Aetna considers ECT experimental and investigational for the treatment of the following indications because its effectiveness for these indications has not been established (not an all-inclusive list):
Electroconvulsive therapy (ECT, also known as electroshock therapy) involves the intentional induction of generalized seizures by administering electrical impulses to the anesthetized patient. Treatments are typically administered by a psychiatrist and an anesthesiologist or anesthetist.
Electroconvulsive therapy is generally administered in an inpatient setting, but can be administered on an outpatient basis in a facility with treatment and recovery rooms. It is usually administered 2 or 3 times a week, although ECT may be administered daily if tolerated.
The primary indication for ECT is major depressive disorder. Electroconvulsive therapy is usually considered when medications fail, can not be tolerated, or may be dangerous, but it is a first-line treatment for severely depressed patients who require a rapid response because of a high suicide or homicide risk, extreme agitation, life-threatening inanition, psychosis, or stupor. The average course of treatment for depression is 6 to 12 treatments, but some patients may require as many as 20 treatments.
Electroconvulsive therapy has been found to be as or more effective than lithium in the treatment of manic episodes and is also a potential treatment for patients experiencing mixed episodes. It is generally reserved for those patients with bipolar disorder who are unable to safely wait until a medication becomes effective, who are not responsive to or unable to safely tolerate one of the effective medications, is preferred by the patient in consultation with the psychiatrist, or who have had a good response to ECT in the past. The number of ECT treatments reported to be effective for mania has ranged from 8 to 20.
Electroconvulsive therapy is not effective for chronic schizophrenia. However, ECT may be effective for psychotic schizophrenic exacerbations when affective symptomatology is prominent, in catatonic schizophrenia, and when there is a history of a prior favorable response to ECT. Schizophrenia may require 17 or more ECT treatments.
A small number of ECT treatments often reverse catatonia, a nonspecific symptom that can occur in mood disorders, schizophrenia, cognitive disorders, and medical and neurological illnesses. Up to 12 treatments may be required in some patients.
There is very limited evidence that ECT is effective for delirium. In addition, there may be considerable risks with ECT in medically unstable patients. For these reasons, the American Psychiatric Association (APA) (1999) concluded that ECT “has not been shown to be an effective treatment for general cases of delirium.” The APA recommends that ECT be “considered only rarely for patients with delirium due to specific etiologies such as neuroleptic malignant syndrome and should not be considered initially as a substitute for more conservative and conventional treatments.”
A few clinicians have reported the successful use of ECT in severe obsessive-compulsive disorder (OCD), anorexia nervosa, atypical psychosis, cycloid psychosis, epilepsy with alternating psychosis, and chronic pain disorder, but those disorders are not usually considered indications for ECT. Electroconvulsive therapy is not an effective treatment for body dysmorphic disoder, dysthymic disorder, neuroses, dissociative disorders, hypochondriasis, conversion disorder, substance-related disorders, and personality disorders. Dell'Osso and colleagues (2005) noted that in addition to pharmacological, behavioral, and neurosurgical interventions, different brain stimulation methods such as transcranial magnetic stimulation, deep brain stimulation, as well as ECT have been examined in treatment-resistant patients with OCD. However, available data about the use of these techniques in OCD treatment are quite limited in terms of sample size and study design, given the difficulty in conducting standard blinded trials for these procedures. Furthermore, none of the mentioned treatments has received approval for the treatment of OCD from the Food and Drug Administration. This is in agreement with the observation of Schruers et al (2005) who stated that serotonin reuptake inhibitors augmentation strategies with a variety of drugs and ECT have demonstrated results in individual cases, but no conclusive evidence has been found in placebo-controlled trials. In addition, the National Institute for Health and Clinical Excellence (NICE, 2006) guidelines on OCD stated that there is insufficient evidence on which to base a recommendation for the use of ECT in the treatment of OCD, especially given potential associated risks with ECT. Furthermore, the NICE report stated that there is no evidence that ECT or psychosurgery is beneficial in treating patients with body dysmorphic disorder.
Clinical experience suggests that ECT be continued until the patient has shown a maximal response; there is no evidence that administering 1 or 2 additional treatments results in a better outcome. Indeed, increased confusion from additional treatments may produce clinical deterioration. Electroconvulsive therapy is discontinued in patients who have had a partial but substantial improvement but show no change after 2 more treatments and in patients who have not responded at all after 6 to 10 treatments.
Prophylactic ECT may be needed for patients who do not tolerate or respond to prophylactic medications or who respond better to ECT. After remission, prophylactic ECT treatments are initially administered at weekly intervals, and the frequency of treatments is usually decreased gradually to once a month or less. Treatment has been continued for periods of 4 or 6 months to five years or longer; some patients apparently require indefinite prophylactic ECT.
Relative contraindications to ECT include space-occupying lesions of the brain, high intracranial pressure, intracerebral bleeding, recent myocardial infarction, retinal detachment, pheochromocytoma, high anesthesia risk, adolescents and children, or a significant medical illness in which risk outweighs potential benefit.
In multiple monitored electroconvulsive therapy (MMECT), a patient undergoes ECT in the usual manner, but before regaining consciousness, undergoes another session of ECT designed to elicit a second (or additional) seizure. The effectiveness of MMECT has not been established. The National Institutes of Health 1985 Consensus Development Conference Statement on ECT states that “Multiple monitored ECT (several seizures during a single treatment session) has not been demonstrated to be sufficiently effective to be recommended…”.
In an open, prospective study, Margoob et al (2010) examined the effects of ECT in the treatment of patients with chronic, severe, antidepressant- and congitive behavioral therapy (CBT)-refractory post-traumatic stress disorder (PTSD). A total of 20 consenting adults were prospectively treated with a fixed course of 6 bilateral ECT treatments administered on an outpatient basis at a twice-weekly frequency. The primary outcome measure was improvement on the Clinician-Administered Post-traumatic Stress Disorder Scale (CAPS). Baseline refractoriness was defined as a failure to respond to an adequate course of at least 4 different antidepressant drugs along with 12 sessions of CBT. Response to ECT was defined as at least 30 % attenuation of CAPS ratings, and remission as an end point CAPS score of 20 or less. After ECT, patients were prescribed sertraline (100 to 150 mg/day) or mirtazapine (15 to 30 mg/day). All but 3 patients completed the ECT course. An intent-to-treat analysis (n = 20) showed statistically and clinically significant improvement in the sample as a whole: CAPS scores decreased by a mean of 34.4 %, and depression scores by a mean of 51.1 %. Most of the improvement in CAPS and depression ratings developed by the third ECT; that is, by day 10 of treatment, itself. The improvement in CAPS ratings was independent of the improvement in depression ratings; and improvement in CAPS did not differ significantly between patients with less severe versus more severe baseline depression. The response rate was 70 %; no patient remitted. In the completer analysis (n = 17), mean improvements were 40 % and 57 % for CAPS and depression ratings, respectively, and the response rate was 82 %. Treatment gains were maintained at a 4 to 6 month follow-up. The authors concluded that ECT may improve the core symptoms of PTSD independently of improvement in depression, and may therefore be a useful treatment option for patients with severe, chronic, medication- and CBT-refractory PTSD. The findings of this small study need to be validated by well-designed studies.
Ujkaj et al (2012) examined the safety and effectiveness of ECT for agitation and aggression in dementia patients. A total of 16 patients with a diagnosis of dementia treated with ECT for agitation/aggression during 2004 to 2007 were included in this analysis. Clinical charts were rated on the Pittsburgh Agitation Scale as the primary outcome; the Clinical Global Impression scale and the Global Assessment of Functioning pre- and post-ECT were also used. Patients of mean age 66.6 +/- 8.3 years were studied. Their average overall and pre-ECT lengths of stay were 59.7 +/- 39.7 days and 23 +/- 15.7 days, respectively. Patients received a mean of 9 ECT treatments, mostly bilateral. Patients showed significant reductions in their total Pittsburgh Agitation Scale scores from baseline after ECT (from 11.0 +/- 5.0 to 3.9 +/- 4.3 [F = 30.33, df = 1, 15, p < 0.001]). Clinical Global Impression scale decreased significantly (from 6.0 +/- 0.6 pre-ECT to 2.1 +/- 1.6 post-ECT [F = 112.97, df = 1, 15, p < 0.001]). Global Assessment of Functioning change was not significant (from 23.0 +/- 4.9 to 26.9 +/- 6.9 [F = 5.73, df = 1, 13, p = 0.32]). Only 1 patient, in whom ECT was discontinued following 11 bilateral treatments, showed no improvement; 8 patients showed transient postictal confusion, which typically resolved within 48 hours. Two patients showed more severe postictal confusion that required modification of treatment. The authors concluded that these results suggested that ECT is an effective and safe treatment for agitation and aggression in dementia. Moreover, they stated that further prospective studies are warranted.
Oudman (2012) noted that depression is one of the most frequently diagnosed psychiatric disorders in patients with dementia with a prevalence of up to 50 %. The detrimental effects of depression in dementia include disability in daily living, worse quality of life, and faster cognitive decline. Although ECT is a well-established and effective treatment for depression in the elderly, it is currently an over-looked treatment option in the elderly with dementia and depression. The aim of this review was to provide a critical analysis of the safety and effectiveness of ECT in depression super-imposed on dementia by reviewing the current literature on this topic. Current evidence suggests that ECT is an effective treatment for depression in dementia, although the relatively small number of controlled studies hampers the comparison of effectiveness between healthy non-geriatric patients and those with dementia. Moreover, the systematic reports on cognitive side effects are very limited in number and currently only apply to moderately mild or mild dementia of non-vascular origin. Some studies do suggest that cognitive side effects are likely in later stages of dementia and in patients with vascular dementia. The author concluded that it is therefore of crucial relevance to prospectively study effects of ECT in different types and phases of dementia in controlled trials.
Loo and colleagues (2012) noted that the effect of shortening the pulse width of the electrical stimulus when administering ECT has recently been systematically studied with promising results. These investigators examined outcomes from 3 randomized controlled trials that compared ultrabrief (less than or equal to 0.3 ms) with brief (0.5 to 1.5 ms) pulse width ECT, and other recent clinical trials of ultrabrief pulse width ECT. The emerging evidence for ultrabrief pulse right unilateral (RUL) ECT suggested clinically meaningful efficacy and substantially reduced neuropsychological side effects compared with standard (brief) pulse ECT; this may represent a generational advance in the ECT technique. However, it is unclear if patients receiving ultrabrief pulse RUL ECT may have a slower speed of response and require additional treatments compared with brief pulse ECT. Therefore, until further data are available, clinicians may be well advised to use brief pulse ECT in situations requiring an urgent clinical response. The authors concluded that the evidence base for ultrabrief bilateral ECT is limited, with findings that efficacy may be reduced compared with brief pulse width ECT. They stated that ultrabrief bilateral ECT should not be used outside the research setting.
Lima et al (2013) reviewed the recent and classical aspects regarding ECT use in adolescents. These researchers performed a systematic review that conformed to the PRISMA statement. From the 212 retrieved articles, only 39 were included in the final sample. The reviewed studies brought indications of ECT use in adolescents, evaluated the efficiency of this therapy regarding remission, and explored the potential risks and complications of the procedure. The authors concluded that the use of ECT in adolescents is considered a highly efficient option for treating several psychiatric disorders, achieving high remission rates, and presenting few and relatively benign adverse effects. Risks can be mitigated by the correct use of the technique and are considered minimal when compared to the efficiency of ECT in treating psychopathologies.
Leiknes et al (2015) explored practice, use, and risk of ECT in pregnancy. These investigators performed a systematic search using the databases Medline, Embase, PsycINFO, SveMed and CINAHL (EBSCO). Only primary data-based studies reporting ECT undertaken during pregnancy were included. Two reviewers independently checked study titles and abstracts according to inclusion criteria and extracted detailed use, practice, and adverse effects data from full text retrieved articles. Studies and extracted data were sorted according to before and after year 1970, due to changes in ECT administration over time. A total of 67 case reports were included and studies from all continents represented. Altogether, 169 pregnant women were identified, treated during pregnancy with a mean number of 9.4 ECTs, at mean age of 29 years. Most women received ECT during the 2nd trimester and many were Para I. Main diagnostic indication in years 1970 to 2013 was depression/bipolar disorder (including psychotic depression). Missing data on fetus/child was 12 %. Electroconvulsive therapy parameter report was often sparse. Both bilateral and unilateral electrode placement was used and thiopental was the main anesthetic agent. Adverse events such as fetal heart rate reduction, uterine contractions, and premature labor (born between 29 and 37 gestation weeks) were reported for nearly 1/3 (29 %) of the cases. The overall child mortality rate was 7.1 %. Lethal outcomes for the fetus and/or baby had diverse associations. The authors concluded that ECT during pregnancy is advised only as last resort treatment under very stringent diagnostic and clinical indications.
The American Academy of Neurology’s evidence-based guideline on “Treatment of tardive syndromes” (Bhidayasiri et al, 2013) stated that “Data are insufficient to determine the efficacy of electroconvulsive therapy for TDD [tardive dyskinesias] treatment”.
The National Collaborating Centre for Mental Health’s clinical guideline on “Bipolar disorder: The assessment and management of bipolar disorder in adults, children and young people in primary and secondary care” (NICE, 2014) recommended ECT for the treatment of severe mania that has not responded to other interventions (e.g., anti-convulsants, anti-psychotics, and lithium).
Termine et al (2013) stated that Tourette syndrome (TS) is a neurodevelopmental disorder characterized by multiple motor/phonic tics and a wide spectrum of behavioral problems (e.g., complex tic-like symptoms, attention deficit hyperactivity disorder, and obsessive-compulsive disorder). Tourette syndrome can be a challenging condition even for the specialists, because of the complexity of the clinical picture and the potential adverse effects of the most commonly prescribed medications. Expert opinions and consensus guidelines on the assessment and treatment of tic disorders have recently been published in Europe and Canada. All pharmacological treatment options are mere symptomatic treatments that alleviate, but do not cure, the tics. There is still a lack evidence of their effects on the natural long-term course and on the prognosis of TS and how these treatments may influence the natural course of brain development. The most commonly prescribed drugs are dopamine antagonists, such as typical (e.g., haloperidol, pimozide) and atypical neuroleptics (e.g., aripiprazole, risperidone), and alpha-2-adrenoreceptor agonists (e.g., clonidine). However, several studies have investigated the efficacy and tolerability of alternative pharmacological agents that may be effective, including the newest atypical antipsychotic agents (e.g., paliperidone, sertindole), tetrabenazine, drugs that modulate acetylcholine (e.g., nicotine) and GABA (e.g., baclofen, levetiracetam), tetrahydrocannabinol, botulinum toxin injections, anti-convulsant drugs (e.g., carbamazepine, topiramate), naloxone, lithium, norepinephrine, steroid 5-alpha reductase, and other neuroactive agents (buspirone, metoclopramide, phytostigmine, and spiradoline mesylate). As regards non-pharmacological interventions, some of the more recent treatments that have been studied included ECT and repetitive transcranial magnetic stimulation. The authors noted that their review focused primarily on the safety and effectiveness of these emerging treatment strategies in TS.
Furthermore, an UpToDate review on “Tourette syndrome” (Jankovic, 2015) does not mention EXT as a therapeutic option.
Roshanaei-Moghaddam and Pauly (2014) reviewed the literature to explore whether the use of ECT for the treatment of methamphetamine dependence can be justified by scientific rationale and/or evidence. These investigators reviewed the literature on the use of ECT in addictive disorders. They described a patient with methamphetamine dependence treated with ECT; and then offered a historical review of the moral and ethical difficulties encountered in the treatment of addictive disorders. These researchers proposed a dynamic understanding as to why clinicians might deploy such brutal actions in the face of hopeless and emotionally intense encounters. They found no scientific evidence or justification for ECT as a treatment of methamphetamine dependence or as the first-line treatment for methamphetamine-induced psychiatric co-morbidities. The authors concluded that the current available evidence does not support using ECT for the treatment of addictive disorders, and hence is unethical, unacceptable and inhumane and warrants immediate social and political attention.
Okazaki et al (2015) stated that autism spectrum disorders (ASD) are heterogeneous neurodevelopmental disorders that are reportedly characterized by aberrant neural networks. Recently developed multi-scale entropy (MSE) analysis can characterize the complexity inherent in electroencephalography (EEG) dynamics over multiple temporal scales in the dynamics of neural networks. These researchers encountered an 18-year old man with ASD whose refractory catatonic obsessive-compulsive symptoms were improved dramatically after ECT. In this clinical case study, these investigators attempted to clarify the neurophysiological mechanism of ECT in ASD by assessing EEG complexity using MSE analysis. Along with ECT, the fronto-central region showed decreased EEG complexity at higher temporal scales, whereas the occipital region expressed an increase at lower temporal scales. Furthermore, these changes were associated with clinical improvement associated with the elevation of brain-derived neurotrophic factor, which is a molecular hypothesis of ECT, playing key roles in ASD pathogenesis. Changes in EEG complexity in a region-specific and temporal scale-specific manner that were found might reflect atypical EEG dynamics in ASD. The authors concluded that although MSE analysis is not a direct approach to measuring neural connectivity and the results were from only a single case, they might reflect specific aberrant neural network activity and the therapeutic neurophysiological mechanism of ECT in ASD. Well-designed studies are needed to ascertain the clinical value of ECT, if any, for the treatment of ASD.
Adjunctive Ketamine in Electroconvulsive Therapy:
Fond et al (2014) stated that ketamine's effectiveness in depressive disorders has been established in several controlled trials. These researchers determined whether or not ketamine administration significantly improves depressive symptomatology in depression and more specifically in major depressive disorder (MDD), bipolar depression, resistant depression (non-ECT studies), and as an anesthetic agent in ECT for resistant depression (ECT studies). Secondary outcomes were the duration of ketamine's effect, the efficacy on suicidal ideations, the existence of a dose effect, and the safety/tolerance of the treatment. Studies were included if they met the following criteria (without any language or date restriction): design: randomized controlled trials (RCTs), intervention: ketamine administration, participants: diagnosis of depression, and evaluation of severity based on a validated scale. These investigators calculated standardized mean differences (SMDs) with 95 % confidence intervals (CIs) for each study. They used fixed and random effects models. Heterogeneity was assessed using the I2 statistic. The authors included 9 non-ECT studies in their quantitative analysis (192 patients with MDD and 34 patients with bipolar depression). Overall, depression scores were significantly decreased in the ketamine groups compared to those in the control groups (SMD = -0.99; 95 % CI: -1.23 to -0.75; p < 0.01). Ketamine's efficacy was confirmed in MDD (resistant to previous pharmacological treatments or not) (SMD = -0.91; 95 % CI -1.19,-0.64; p < 0.01), in bipolar depression (SMD = -1.34; 95 % CI -1.94 to -0.75), and in drug-free patients as well as patients under medication. Four ECT trials (118 patients) were included in the quantitative analysis. A total of 103 patients were diagnosed with MDD and 15 with bipolar depression. Overall, depression scores were significantly improved in the 58 patients receiving ketamine in ECT anesthesia induction compared to the 60 patients (SMD = -0.56; 95 % CI: -1.10 to -0.02; p = 0.04; I2 = 52.4 %). The duration of ketamine's effects was assessed in only 2 non-ECT studies and seemed to persist for 2 to 3 days; this result needs to be confirmed; 3 of 4 studies found significant decrease of suicidal thoughts and 1 found no difference between groups, but suicidal ideations were only studied by the suicide item of the depressive scales. It was not possible to determine a dose effect; 0.5 mg/kg was used in the majority of the studies. Some cardiovascular events were described (mostly transient blood pressure elevation that may require treatment), and ketamine's use should remain cautious in patients with a cardiovascular history. The authors concluded that the present meta-analysis confirmed ketamine's efficacy in depressive disorders in non-ECT studies, as well as in ECT studies. They stated that the results of this first meta-analysis were encouraging, and further studies are needed to detail efficacy in bipolar disorders and other specific depressed populations; middle- and long-term safety and effectiveness have yet to be explored. They also noted that extrapolation should be cautious since patients included had no history of psychotic episodes and no history of alcohol or substance use disorders, which is not representative of all the depressed patients that may benefit from this therapy.
Naughton et al (2014) (i) reviewed the clinical literature on low-dose ketamine as a rapid-acting anti-depressant in affective disorders, (ii) provided a critical overview of the limitations of ketamine and research attempts to overcome these, (iii) discussed the proposed mechanisms of action of ketamine, and (iv) pointed towards future research directions. The electronic database PubMed, Web of Science and sciencedirect were searched using the keywords: ketamine, N-methyl-d-aspartate receptor antagonist, rapid-acting antidepressant, depression, treatment-resistant depression, bipolar depression, suicidal ideation, electroconvulsive therapy, mechanism of action. The literature demonstrated evidence supporting a rapid-acting antidepressant effect of low-dose intravenous ketamine in MDD, in bipolar depression and in depression with suicidal ideation. There were mixed results as to whether ketamine leads to a reduction in time to remission in patients undergoing ECT. Ketamine's limiting factors are the transient nature of its anti-depressant effect and concerns regarding abuse, and research efforts to overcome these were reviewed. The authors concluded that current and future research studies are using ketamine as a promising tool to evaluate the glutamatergic neurotransmitter system to learn more about the pathophysiology of depression and develop more specific rapid-acting anti-depressant treatments.
McGirr et al (2015) noted that ECT remains one of the most effective tools in the psychiatric treatment armamentarium, particularly for refractory depression. Yet, there remains a subset of patients who do not respond to ECT or for whom clinically adequate seizures cannot be elicited, for whom ketamine has emerged as a putative augmentation agent. These investigators searched EMBASE, PsycINFO, CENTRAL, and MEDLINE from 1962 to April 2014 to identify RCTs evaluating ketamine in ECT. Clinical remission, response, and change in depressive symptom scores were extracted by 2 independent raters. Adverse events were recorded. Drop-outs were assessed as a proxy for acceptability. Meta-analyses employed a random effects model. Data were synthesized from 5 RCTs, representing a total of 182 patients with major depressive episodes (n = 165 MDD, n = 17 bipolar disorder). Electroconvulsive therapy with ketamine augmentation was not associated with higher rates of clinical remission (Risk Difference (RD) = 0.00; 95 % CI: -0.08 to 0.10), response (RD = -0.01; 95 % CI: -0.11 to 0.08), or improvements in depressive symptoms (SMD = 0.38; 95 % CI: -0.41 to 1.17). Ketamine augmentation was associated with higher rates of confusion/disorientation/prolonged delirium (odds ratio [OR] = 6.59, 95 % CI: 1.28 to 33.82, number needed to harm [NNH] = 3), but not agitation, hypertension or affective switches. The authors concluded that the findings of this meta-analysis of RCTs of ketamine augmentation in the ECT setting suggested a lack of clinical effectiveness, and an increased likelihood of confusion. Individuals for whom adequate seizures or therapeutic response cannot be obtained have not been studied using randomized controlled designs. They stated that additional research needed to address the role of ketamine in this population.
Erdil et al (2015) evaluated the effects of a sub-anesthetic dose of ketamine, which was administered as an adjunct to sevoflurane, on duration of seizure activity, hemodynamic profile, and recovery times during ECT in patients with major depression. Patients were randomly allocated to a group receiving either sevoflurane-ketamine (group SK) or sevoflurane-saline (group SS). Sevoflurane was initiated in both groups at 8 % for anesthesia induction until loss of consciousness was achieved, at which point it was discontinued. After loss of consciousness, ketamine was administered to the group SK in the form of a 0.5 mg/kg intravenous bolus; patients in the group SS received saline in the same manner. Mean arterial pressure (MAP) and heart rate were recorded before anesthetic induction (T1); after anesthetic induction (T2); as well as 0, 1, 3, and 10 minutes after the seizure had ended (T3, T4, T5, and T6, respectively). Motor and EEG seizure durations were recorded. Motor and EEG seizure durations in the group SS were similar to those observed for the group SK. The heart rate increased significantly during T2 to T6 in both group SS and group SK compared with the baseline. The MAP increased in the group SS during the period between T3 and T6 as well as in the group SK during the same period compared with the baseline. The MAP increased more in the group SK, in comparison with the group SS, during T2 (p < 0.05). The authors concluded that the addition of ketamine at sub-anesthetic doses, for the purposes of anesthetic induction with sevoflurane, yielded results similar to those in the control group in terms of both seizure duration and hemodynamic stability.
Furthermore, an UpToDate review on “Overview of electroconvulsive therapy (ECT) for adults” (Kellner, 2015) does not mention ketamine as an adjunctive therapy.
Selection Criteria for ECT:
|CPT Codes / HCPCS Codes / ICD-9 Codes|
|CPT codes covered if selection criteria are met:|
|00104||Anesthesia for electroconvulsive therapy|
|90870||Electroconvulsive therapy (includes necessary monitoring) [not covered for ultrabrief bilateral electroconvulsive therapy]|
|ICD-9 codes covered if selection criteria are met:|
|291.0 - 294.9||Organic psychotic conditions|
|295.00 - 298.96||Other psychoses|
|311||Depressive disorder, not elsewhere classified|
|ICD-9 codes not covered for indications listed in the CPB (not all-inclusive):|
|290.0 - 290.9||Dementias|
|299.00 - 299.91||Autistic disorder|
|300.00 - 300.9||Anxiety, dissociative and somatoform disorders|
|301.0 - 301.9||Personality disorders|
|303.00 - 305.93||Alcohol dependence syndrome, drug dependence, and nondependent abuse of drugs|
|309.81||Post-traumatic stress disorder|
|333.85||Subacute dyskinesia due to drugs|
|337.20 - 337.29||Reflex sympathetic dystrophy|
|781.0||Abnormal involuntary movements|
|CPT Codes / HCPCS Codes / ICD-10 Codes|
|Information in the [brackets] below has been added for clarification purposes.  Codes requiring a 7th character are represented by "+":|
|ICD-10 codes will become effective as of October 1, 2015:|
|CPT codes covered if selection criteria are met:|
|00104||Anesthesia for electroconvulsive therapy|
|90870||Electroconvulsive therapy (includes necessary monitoring) [not covered for ultrabrief bilateral electroconvulsive therapy]|
|ICD-10 codes covered if selection criteria are met:|
|F06.1||Catatonic disrder due to known physiological condition|
|F10.10 - F19.99||Alcohol and drug induced mental disorders [Codes not listed due to expanded specificity]|
|F20.0 - F20.89||Schizophrenia|
|F30.10 - F30.9||Manic episode|
|F31.0 - F31.9||Bipolar disorder|
|F32.0 - F33.9||Major depressive disorder|
|ICD-10 codes not covered for indications listed in the CPB (not all-inclusive):|
|F01.50 - F03.91||Dementia|
|F40.00 - F48.9||Anxiety, dissociative, stress-related, somatoform and other non-psychotic disorders|
|F60.0 - F60.9||Specific personality disorders|
|F84.0 - F84.9||Pervasive developmental disorders|
|G24.01||Drug induced subacute dyskinesia|
|G24.4||Idiopathic orofacial dystonia|
|G90.50 - G90.59||Complex regional pain syndrome I (CRPS I)|
|Numerous options||Alcohol and drug, abuse, dependence and use [Codes not listed due to expanded specificity]|
|R25.0 - R25.9||Abnormal involuntary movements|
Adjunctive Ketamine in ElectroconvulsiveTherapy: