CASE REPORT
Electroconvulsive Therapy Malpractice Verdict for the Defense
Theodore Goodman, MD* and W. Vaughn McCall, MD, MS† Objectives: Malpractice cases involving electroconvulsive therapy (ECT) are rare. Even rarer are those malpractice cases alleging ECT-related brain damage. The few cases of ECT malpractice lawsuits are not described in the medical literature in detail. Methods: We provide a detailed account of a case of a patient and subsequent alleged ECT-related malpractice. The details of the case were collated using the handwritten notes of one of the authors who was present at the trial and the pretrial documents of discovery that were entered into evidence. Results: The plaintiff alleged complete autobiographical amnesia after ECT, supposedly as a result of ECT-related brain damage. The defense was aided by the presence of extensive neurological examination and brain imaging both before and after ECT. The defense team also offered to the jury the concept of “dissociative amnesia” as an alternative explanation for the plaintiff's memory complaints. The case went to trial and was successfully defended. Discussion: Electroconvulsive therapy malpractice cases alleging brain damage can be successfully defended, and the successful defense is aided by adequate documentation before, during, and after ECT. Conclusions: Malpractice cases, especially if they are baseless, can occur unpredictably, but they can be defended if the medical documentation is thorough. Key Words: electroconvulsive therapy, malpractice, amnesia (J ECT 2015;31: 155–158)
R
ates of malpractice litigation against psychiatrists are low. Decades ago, claims against a psychiatrist represented only 0.3% of all malpractice claims against physicians.1 Although electroconvulsive therapy (ECT) produces dramatic effects on the electroencephalogram (EEG) and on the cardiovascular system, ECT is remarkably safe and rates of malpractice claims are not disproportionately high among psychiatrists who provide ECT. As a result, some medical liability companies, including the American Psychiatric Association's medical liability product, dropped the premium surcharges for ECT years ago.2 In those rare instances when ECT does become the focus of a malpractice case, the plaintiff's complaint most often is related to failure to diagnose a concurrent medical condition, or dental injury, or a post-ECT fall, and the like.2–4 Electroconvulsive therapy malpractice cases related to a complaint of brain damage are very uncommon, and the medical
From the *Sutter Center for Psychiatry, Sacramento, CA; and †Department of Psychiatry and Health Behavior, the Medical College of Georgia, Augusta, GA. Received for publication September 3, 2014; accepted September 23, 2014. Reprints: W. Vaughn McCall, MD, MS, Department of Psychiatry and Health Behavior, the Medical College of Georgia, Georgia Regents University, 997 St Sebastian Way, Augusta, GA 30912 (e‐mail: [email protected]). Dr Goodman was a defendant in the described case, and Dr McCall is the editor of The Journal of ECT and he was an expert witness for the defense in this trial; otherwise they have no conflicts of interest in this report. Supplemental digital contents are available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.ectjournal.com). Copyright © 2014 by Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/YCT.0000000000000196
literature contains only outline sketches of particular cases.5 Herein, we provide a detailed description of an ECT malpractice case alleging brain damage.
CASE At the time of initial ECT in 2010, the patient presented as a man in his sixth decade, who was hospitalized for initiation of ECT upon referral by his outpatient psychiatrist. He had a long history of treatment-resistant depression. He first became depressed 12 years before admission, after a right knee surgery. He was prescribed fluoxetine by his primary care physician, responded rapidly, and returned to work. Despite returning to work, he struggled for the next 9 years with chronic knee and back pain, had 4 knee surgeries over a period of 7 years, and began treatment with hydrocodone/acetaminophen 7.5/750 twice per day and tramadol 100 mg up to 4 times per day, which were taken continuously until the time of admission for ECT. Over the years, he filed a series of workers compensation claims, first in 1995 for the right knee injury, then in 2003 for a low back injury, claimed to be secondary to his knee injuries, then finally for his depression, which was claimed as a “work-related psychological injury” in 2008. He was first seen by a psychologist 3 years before the ECT because of a family conflict between the patient and his children and was noted by the clinician to be high functioning, well connected emotionally to family members, socially engaged, well groomed, and demonstrative of a good sense of humor. Eight months later, now 2 years before the admission, he was seen again by the same psychologist, who noted that he was now clearly depressed. The psychologist was particularly concerned about his complaints of significant problems with memory and concentration. The cognitive impairment was felt to be clinically significant, but no neuropsychological testing was performed at that time. He was treated with citalopram 20 mg daily and, later, 40 mg daily as prescribed by his primary care physician. He continued in weekly psychotherapy but remained depressed. He struggled at work and, 1½ years before the admission, got a negative work review in his job. One month later, he took a disability leave from work on the basis of chronic pain and depression. He was referred to a psychiatrist who augmented his citalopram with aripiprazole, but this caused agitation and was discontinued. He then was treated in a partial hospital program for 2 months; after discharge, he became suicidal and was hospitalized for approximately 1 week. His medication regimen during this time was changed ultimately to bupropion 300 mg daily, mirtazapine 30 mg nightly, and clonazepam 1 mg twice per day. After discharge, he resumed the partial hospital program for another 2 months, and a new outpatient psychiatrist added back citalopram 40 mg daily to his medication regimen. During this time, his psychologist, whom he continued to see, became increasingly more concerned about his cognition and asked his outpatient psychiatrist to refer him to a neurologist. He then had a thorough neurological assessment approximately 4 months before the initiation of his ECT. The evaluation included magnetic resonance imaging (MRI), EEG, and brain positron
Journal of ECT • Volume 31, Number 3, September 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.ectjournal.com
155
Journal of ECT • Volume 31, Number 3, September 2015
Goodman and McCall
emission tomography (PET), along with neurological clinical evaluation and laboratory studies, and the evaluation results showed no abnormalities. The diagnosis of the neurologist was pseudodementia of depression. At that time, he remained severely depressed, with social and emotional withdrawal from his family, persistent suicidal ideation, and, now, paranoid ideation about his wife; as a result, he had become increasingly angry toward her. He became aggressive to the point that he assaulted her when she spurned him sexually. Later in his psychotherapy, he claimed he could not remember this assault, a fact whose relevance became more apparent as the legal case unfolded.
Course of ECT After the hospital admission for initiation of ECT, tramadol was tapered to discontinuation and hydrocodone was discontinued, replaced by a brief methadone taper because it was felt that the narcotics might be contributing to his cognitive clouding. Gabapentin and bupropion were also discontinued, and mirtazapine and clonazepam were tapered to discontinuation. After obtaining written, informed consent from the patient, ultra-brief-pulse ECT commenced with right unilateral (RUL) lead placement. The patient had 3 inpatient RUL sessions, followed by a fourth RUL session after discharge to outpatient. He did not respond to the 4 RUL ECT, and so bitemporal (BT) ECT was begun. After his first BT ECT, he expressed suicidal ideation, was briefly rehospitalized, and then continued thrice-weekly BT ECT as an outpatient for a total of 13 thrice-weekly sessions (including 9 BT sessions). He was begun on lamotrigine in low dose and olanzapine, 10 mg daily, and then twice daily to control his paranoia, anger, and irritability. Unfortunately, he developed a rash, so his lamotrigine had to be discontinued. After the completion of his acute course of ECT, he was started on lithium carbonate with instructions to hold the lithium the entire day before each ECT. Trough lithium level was 0.6 at a dose of 900 mg daily, and olanzapine was tapered to discontinuation as he improved. At the time of his last acute treatment, the patient stated that he was approximately “60%” better but that “if the treatments weren't affecting my memory, I'd be 80% to 90% better.” Selfreported Patient Health Questionnaire-9 scores showed no consistent improvement during the ECT course, but these scores were not considered valid because he was clinically judged moderately improved; hence, weekly continuation of ECT was begun. The clinical assessment of improvement was based on the observation that his suicidality had resolved, that he had become more verbal and better able to address and discuss psychological problems, that affect was much improved, and that the patient had become more interactive in interview and with his family. At his second weekly treatment, he continued to complain about memory dysfunction. Hence, his treatment interval was extended to 2 weeks to allow time for his memory to recover, and lithium was increased to 1125 mg daily. Within the 2-week treatment interval, the patient did well only for 1 week, and in the second week, he was much more depressed and withdrawn. After a lengthy discussion with the patient and his wife regarding treatment frequency and potential effects on memory, weekly ECTwas resumed (due to the fact that another brief acute series of treatments was not an option because of the patient's memory complaints). With the resumption of weekly ECT and with the addition of aripiprazole of 5 mg daily, he began to progress again after 2 treatments, but mood still worsened approximately 5 days after each treatment. This deterioration in mood seemed to be at least in part triggered by conflict with his children and wife, and they were referred to couples counseling, but they did not follow through with this recommendation.
156
www.ectjournal.com
In the third weekly visit, there was no progression, so aripiprazole was discontinued, and the patient was begun on tranylcypromine at 30 mg daily while continuing lithium carbonate. By the next week, the patient had again begun to improve but expressed more concern about his memory, stating “I fear it won't get better and I won't be able to return to work” (he had not worked for the past 1½ years since March 2008). The patient and his wife were offered the option to extend his treatment interval once again to 2 weeks, but given his residual symptoms and the duration of observed improvement after each treatment, the couple agreed to the continuation of weekly treatments. He ultimately had 6 once-per-week treatments and the interval was again extended to 2 weeks, but with resumption of the 2-week interval, his mood again slowly deteriorated. At this point, after a total of 23 ECT treatments (13 acute and 10 continuation treatments for a period of 9 weeks), ECT was discontinued because sustained improvement was not achieved and because the patient continued to complain of memory difficulties, precluding the option of further acute treatments, although he had clearly shown response to his acute series of treatments. Across all sessions, the mean (SD) dynamic energy of the ECT stimulus was 46.2 (18.0) J (range, 17.7–67.6 J). The mean (SD) motor seizure duration was 38.3 (12.4) seconds (range, 17–60 seconds), and the mean (SD) EEG seizure duration was 56.2 (20.2) seconds (range, 21–98 seconds). The patient experienced no complications during any of the treatment sessions. From this point forward, the patient was treated with medication and his ongoing individual psychotherapy. Tranylcypromine was discontinued, and he was begun on nortriptyline at 75 mg while continuing lithium (trough level of 0.9) and triiodothyronine at 25 μg daily. Approximately 3 months after the completion of ECT, the patient's wife now stated that the patient was amnestic for “all memories” preceding the onset of his ECT treatments. She had also begun to explore antipsychiatry as well as anti-ECT Web sites and contacted Peter Breggin, MD. At this point, the wife cut off contact with the ECT treatment team until such time as the lawsuit was filed approximately a year later.
The Lawsuit A malpractice lawsuit was filed in Sacramento, California, alleging that the standard of care had not been met in the care of the patient, resulting in harm (Sacramento County Superior Court Case No. 34-2011-00099829). The details of the case were collated using the handwritten notes of one of the authors who was present at the trial and the pretrial documents of discovery that were entered into evidence. Defendants in the case included the 2 physicians who provided ECT, the physicians who made the referral for ECT, and several other earlier treating physicians, including the consulting neurologist. The plaintiff alleged that the standard of care had not been met in the handling of the psychotropic medications, especially around the time of initiation of ECT, and that a treatment plan that included ECT ipso facto did not meet the standard of care and produced damages. Regarding the alleged damage produced by ECT, the plaintiff claimed brain damage from ECT, resulting in global, complete retrograde autobiographical memory loss that resulted in disability. The trial began approximately 4 years after the patient's treatment ended. The plaintiff's only expert was Peter Breggin, MD. Dr Breggin has a well-established reputation of opposition toward ECTand has testified for the plaintiff in numerous ECT malpractice trials.6 His bona fides were provided to the jury as follows: that he had testified numerous times in the US Congress, that he had appeared numerous times in front of Food and Drug Administration © 2014 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Journal of ECT • Volume 31, Number 3, September 2015
panels, and that he was the author of numerous books in the field of psychiatry as well as the editor of numerous journals. After his introduction, he testified for 1½ days (see Appendix 1, Supplemental Digital Content 1, http://links.lww.com/JECT/A39). At trial, Dr Breggin testified that he had been an expert witness in approximately 80 malpractice lawsuits over the years. He stated that he thought he had been a witness for the defense in “maybe 1 or 2 cases. I can't really remember.” After the testimony of Dr Breggin, the post-ECT testing of the patient was presented. The initial post-ECT testing was done by Dr Breggin. He testified that, after he was contacted by the patient's wife, he asked for a copy of the patient's records. After a review of the records, he told her that the patient “definitely had ECT-induced brain damage” (we realized at trial that this was the point in time that the patient's wife cut off all contact with the ECT treatment team and, in fact, with any psychiatrist and discontinued her husband's medications). He arranged for the patient and his wife to travel to Ithaca, New York. Once there, he testified that he did a several-hour clinical interview and administered a Mini-Mental State Examination, confirming his tentative diagnosis based on his medical record review. He then referred the patient for follow-up neurological evaluation that was done at a university medical center and included repeat MRI, EEG, brain PET, as well as neuropsychological evaluation. The findings of laboratory studies were all negative in the opinion of the neuroimaging experts for the defense. The neuropsychological testing showed extremely poor performance across multiple domains and tests, with results beyond what is seen in significant dementia. The result of the Test of Memory Malingering (TOMM) was positive for malingering. The TOMM is a 50-question visual memory recognition test that discriminates between true memory impairment and malingering, with 2 learning trials and an optional retention trial after a delay. It was first published in 1996 and is intended for testing individuals ages 16 years and older.7 The TOMM has been shown to have high levels of sensitivity as well as specificity and is largely insensitive to depression and anxiety.7 The post-ECT diagnosis of the neurologist, based on his examination and the testing, was pseudodementia of depression with exaggeration of symptoms as demonstrated in part by an elevation of the “Fake-Bad” scale on the Minnesota Multiphasic Personality Inventory as well as the results of the TOMM. After completion of the testing, Dr Breggin then referred the patient's wife to 2 attorneys to pursue a lawsuit. The first attorney is the one he had employed on multiple prior occasions for other lawsuits; the other was a California licensed attorney because the lawsuit was in California. At trial, the progress notes of the patient's treating psychologist were entered into evidence, and she noted that, during the period before the referral for ECT and after she had requested the neurological evaluation, the patient had become almost giddy when he thought that he might have Alzheimer's disease as an explanation for his memory impairment. The theory of the defense was that, in fact, he was pleased about the prospect for such a diagnosis because it provided an explanation for his inability to function as a provider for his family, as an equal partner to his wife within this family structure, as an equal sexual partner to his wife, and as an equal parent to his children. In fact, when the patient was told that there were no neurologic abnormalities identified, he became suicidal (this only became clear during the trial), and this was a precipitating event for the patient's referral for inpatient treatment and ECT. As the discovery process unfolded, the defense attorneys thought that it became increasingly clear that the patient was exaggerating his deficits. This was thought, on the basis of the MMPI, the TOMM, and the nature of the litigation process, to be conscious.
Electroconvulsive Therapy Malpractice
During the course of the trial, the patient's wife and 2 children described many instances of their father's memory impairment. The patient himself was not in the trial and was only seen on a videotape of his deposition. On this video, he appeared disheveled, much older than his chronological age, and profoundly depressed. He was described as being a “prisoner in his own home; he rarely leaves his bedroom and never cuts his hair or beard.” Despite a claim of devastating brain damage and total autobiographical memory loss, the children testified that their father continued to drive them to school, to after-school events, and, even on 1 occasion, to San Francisco, which is a 130-mile 1-way trip. However, they described strange behaviors, such as crossing over a double yellow line to pass a car and then turning to his daughter and asking, “What's that line for?” The plaintiffs used this example, and others similar to this, to show that his memory was grossly impaired. During the trial, the defense felt that examples such as these were consistent with dissociative amnesia, a diagnosis suggested to the defense attorneys by the defendants (or psychogenic amnesia as described in the medical literature8). Thus, the theory of the defense was no longer that the patient was malingering but that his reported loss of memory was symptomatic of an unconscious process. In fact, the symptoms displayed by the patient as he was described at trial were consistent with dissociative amnesia. He claimed that he was amnestic (as stated earlier) for “all” events, people, and places before the onset of ECT. He claimed that he could not recall his siblings, that he could not recall growing up in Mexico, that he could not recall his wife before the present moment, and that he could not recall his children except for the immediate time of his engagement with them. His son testified that they lived in a rural area and had a pond near their house. Every spring, they would hear loud croaking at mating time. The croaking was so loud that they would have trouble sleeping, and this had been going on for many years. After ECT, when the croaking began, the patient exclaimed “What's that noise?” The diagnosis of dissociative amnesia was not presented to the jury directly, although one of the defenses' experts did speak that the patient need to “look away” from his problems and that ECT-associated memory loss gave him a method to do this. This diagnosis is supported when the reported loss of memory after the initiating event fails to show the expected temporal gradient of amnesia, which is worse closer to the event and better for those memories more distant form the event. The plaintiff's complaint of amnesia did fail to show a temporal gradient. Furthermore, a complaint of total autobiographical amnesia would be expected to be associated with structural or functional brain abnormalities, yet no such abnormalities were demonstrated by the extensive posttreatment evaluations. Finally, psychogenic amnesia often occurs in the setting of interpersonal difficulties such as marital discord.8 The trial continued for a total of 15 days. Subsequently, the jury deliberated for 3 hours. According to the defense attorneys, this was an extremely short deliberation for such a long and complex trial and it spoke of the weakness of the plaintiff's case. The jurors returned with an 11-1 verdict for the defense. The jury foreperson stated that the plaintiffs were unable to demonstrate that the standard of care was not met. They were unable to determine whether the ECT treatments were responsible for any harm to the patient, and they were not even sure whether any harm had, in fact, occurred.
DISCUSSION This summary of a malpractice case is among the most detailed found in the medical literature. Provision of the detail is possible because the case was tried to the point of reaching a verdict,
© 2014 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.ectjournal.com
157
Journal of ECT • Volume 31, Number 3, September 2015
Goodman and McCall
resulting in the facts of the case entering the public domain. Such transparency is not possible when cases settle before trial. In the absence of being in the jury's chambers, it is impossible to know the particulars of how the jury weighed the many pieces of evidence and testimony. However, it is possible that the plaintiff's sole reliance on the testimony of Dr Breggin did not help their case because he has been reported to be “not credible” as an expert in other ECT malpractice cases.6 The availability of brain MRI, brain PET, and EEG examination results both before and after the course of ECT was fortuitous for the defense, especially because these laboratory examinations were interpreted as normal by the defense experts. The remarkable discrepancies in the patient's cognitive functioning, such as complaints of total autobiographical amnesia, with no temporal gradient, in the face of preservation of ability to navigate long automobile trips, raised questions about the “organic” nature of the memory complaint. The patient's prior repeated history of worker's compensation litigation is consistent with the pursuit of litigation in this case as well. The litigation and the concerns about “brain damage” not only could have been a source of additional compensation but are also a distraction from focusing on real and ongoing psychosocial problems, resulting in a potential failure of the patient to access needed care. The lessons learned from this case include a need for continued vigilance on the part of ECT physicians to document all necessary aspects of ECT care, as was done in this case, to defend against unpredictable lawsuits. Some of the necessary aspects include the following: (1) documentation behind the thought processes that demonstrate the need for ECT, (2) assessment of the patient's capacity to participate in the decision making for ECT, (3) a signed consent form, (4) documentation of the technical aspects of the conduct of each treatment session, (5) documentation of the patient's progress during ECT, including both therapeutic and adverse effects, and (6) documentation of the thought processes behind extending the ECT course, moving from acute to continuation ECT, or terminating ECT, and the involvement of
158
www.ectjournal.com
the patient and/or family in the decision making. Although the presence of EEG, brain MRI, and brain PET findings before ECT were helpful in the defense of this case, we do not recommend their routine use before ECT. Finally, this case demonstrates that treating ECT physicians need to be aware of the rare emergence of psychogenic amnesia precipitated by ECT treatment and the need to deal with this complication of treatment aggressively to prevent an adverse outcome of treatment. In particular, in patients with psychological problems that could predispose a patient to the emergence of psychogenic amnesia, extra caution needs to be taken with respect to the psychological aspects of the patient's treatment, concurrently with his ECT treatment, to help insure a positive outcome of treatment.
REFERENCES 1. Slawson P, Giggenheim F. Psychiatric malpractice: a review of the national loss experience. Am J Psychiatry. 1984;141:979–981. 2. Slawson P. Psychiatric malpractice: the electroconvulsive therapy experience. Convuls Ther. 1985;1:195–203. 3. Slawson P. Psychiatric malpractice and ECT: a review of national loss experience. Convuls Ther. 1989;5:126–130. 4. Slawson P. Psychiatric malpractice and ECT: a review of 1,700 claims. Convuls Ther. 1991;7:255–261. 5. Abrams R. Malpractice litigation and ECT. Convuls Ther. 1989;5:365–367. 6. Abrams R. ECT malpractice issues. Convuls Ther. 1995;11:286–287. 7. Teichner G, Wagner M. The Test of Memory Malingering (TOMM): normative data from cognitively intact, cognitively impaired, and elderly patients with dementia. Arch Clin Neuropsychol. 2004;19:455–464. 8. Serra L, Fadda L, Bucciione I, et al. Psychogenic and organic amnesia. A multidimensional assessment of clinical, neuroradiological, neuropsychological and psychopathological features. Behav Neurol. 2007; 18:53–64.
© 2014 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Electroconvulsive Therapy Malpractice Verdict for the Defense
Theodore Goodman, MD* and W. Vaughn McCall, MD, MS† Objectives: Malpractice cases involving electroconvulsive therapy (ECT) are rare. Even rarer are those malpractice cases alleging ECT-related brain damage. The few cases of ECT malpractice lawsuits are not described in the medical literature in detail. Methods: We provide a detailed account of a case of a patient and subsequent alleged ECT-related malpractice. The details of the case were collated using the handwritten notes of one of the authors who was present at the trial and the pretrial documents of discovery that were entered into evidence. Results: The plaintiff alleged complete autobiographical amnesia after ECT, supposedly as a result of ECT-related brain damage. The defense was aided by the presence of extensive neurological examination and brain imaging both before and after ECT. The defense team also offered to the jury the concept of “dissociative amnesia” as an alternative explanation for the plaintiff's memory complaints. The case went to trial and was successfully defended. Discussion: Electroconvulsive therapy malpractice cases alleging brain damage can be successfully defended, and the successful defense is aided by adequate documentation before, during, and after ECT. Conclusions: Malpractice cases, especially if they are baseless, can occur unpredictably, but they can be defended if the medical documentation is thorough. Key Words: electroconvulsive therapy, malpractice, amnesia (J ECT 2015;31: 155–158)
R
ates of malpractice litigation against psychiatrists are low. Decades ago, claims against a psychiatrist represented only 0.3% of all malpractice claims against physicians.1 Although electroconvulsive therapy (ECT) produces dramatic effects on the electroencephalogram (EEG) and on the cardiovascular system, ECT is remarkably safe and rates of malpractice claims are not disproportionately high among psychiatrists who provide ECT. As a result, some medical liability companies, including the American Psychiatric Association's medical liability product, dropped the premium surcharges for ECT years ago.2 In those rare instances when ECT does become the focus of a malpractice case, the plaintiff's complaint most often is related to failure to diagnose a concurrent medical condition, or dental injury, or a post-ECT fall, and the like.2–4 Electroconvulsive therapy malpractice cases related to a complaint of brain damage are very uncommon, and the medical
From the *Sutter Center for Psychiatry, Sacramento, CA; and †Department of Psychiatry and Health Behavior, the Medical College of Georgia, Augusta, GA. Received for publication September 3, 2014; accepted September 23, 2014. Reprints: W. Vaughn McCall, MD, MS, Department of Psychiatry and Health Behavior, the Medical College of Georgia, Georgia Regents University, 997 St Sebastian Way, Augusta, GA 30912 (e‐mail: [email protected]). Dr Goodman was a defendant in the described case, and Dr McCall is the editor of The Journal of ECT and he was an expert witness for the defense in this trial; otherwise they have no conflicts of interest in this report. Supplemental digital contents are available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.ectjournal.com). Copyright © 2014 by Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/YCT.0000000000000196
literature contains only outline sketches of particular cases.5 Herein, we provide a detailed description of an ECT malpractice case alleging brain damage.
CASE At the time of initial ECT in 2010, the patient presented as a man in his sixth decade, who was hospitalized for initiation of ECT upon referral by his outpatient psychiatrist. He had a long history of treatment-resistant depression. He first became depressed 12 years before admission, after a right knee surgery. He was prescribed fluoxetine by his primary care physician, responded rapidly, and returned to work. Despite returning to work, he struggled for the next 9 years with chronic knee and back pain, had 4 knee surgeries over a period of 7 years, and began treatment with hydrocodone/acetaminophen 7.5/750 twice per day and tramadol 100 mg up to 4 times per day, which were taken continuously until the time of admission for ECT. Over the years, he filed a series of workers compensation claims, first in 1995 for the right knee injury, then in 2003 for a low back injury, claimed to be secondary to his knee injuries, then finally for his depression, which was claimed as a “work-related psychological injury” in 2008. He was first seen by a psychologist 3 years before the ECT because of a family conflict between the patient and his children and was noted by the clinician to be high functioning, well connected emotionally to family members, socially engaged, well groomed, and demonstrative of a good sense of humor. Eight months later, now 2 years before the admission, he was seen again by the same psychologist, who noted that he was now clearly depressed. The psychologist was particularly concerned about his complaints of significant problems with memory and concentration. The cognitive impairment was felt to be clinically significant, but no neuropsychological testing was performed at that time. He was treated with citalopram 20 mg daily and, later, 40 mg daily as prescribed by his primary care physician. He continued in weekly psychotherapy but remained depressed. He struggled at work and, 1½ years before the admission, got a negative work review in his job. One month later, he took a disability leave from work on the basis of chronic pain and depression. He was referred to a psychiatrist who augmented his citalopram with aripiprazole, but this caused agitation and was discontinued. He then was treated in a partial hospital program for 2 months; after discharge, he became suicidal and was hospitalized for approximately 1 week. His medication regimen during this time was changed ultimately to bupropion 300 mg daily, mirtazapine 30 mg nightly, and clonazepam 1 mg twice per day. After discharge, he resumed the partial hospital program for another 2 months, and a new outpatient psychiatrist added back citalopram 40 mg daily to his medication regimen. During this time, his psychologist, whom he continued to see, became increasingly more concerned about his cognition and asked his outpatient psychiatrist to refer him to a neurologist. He then had a thorough neurological assessment approximately 4 months before the initiation of his ECT. The evaluation included magnetic resonance imaging (MRI), EEG, and brain positron
Journal of ECT • Volume 31, Number 3, September 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.ectjournal.com
155
Journal of ECT • Volume 31, Number 3, September 2015
Goodman and McCall
emission tomography (PET), along with neurological clinical evaluation and laboratory studies, and the evaluation results showed no abnormalities. The diagnosis of the neurologist was pseudodementia of depression. At that time, he remained severely depressed, with social and emotional withdrawal from his family, persistent suicidal ideation, and, now, paranoid ideation about his wife; as a result, he had become increasingly angry toward her. He became aggressive to the point that he assaulted her when she spurned him sexually. Later in his psychotherapy, he claimed he could not remember this assault, a fact whose relevance became more apparent as the legal case unfolded.
Course of ECT After the hospital admission for initiation of ECT, tramadol was tapered to discontinuation and hydrocodone was discontinued, replaced by a brief methadone taper because it was felt that the narcotics might be contributing to his cognitive clouding. Gabapentin and bupropion were also discontinued, and mirtazapine and clonazepam were tapered to discontinuation. After obtaining written, informed consent from the patient, ultra-brief-pulse ECT commenced with right unilateral (RUL) lead placement. The patient had 3 inpatient RUL sessions, followed by a fourth RUL session after discharge to outpatient. He did not respond to the 4 RUL ECT, and so bitemporal (BT) ECT was begun. After his first BT ECT, he expressed suicidal ideation, was briefly rehospitalized, and then continued thrice-weekly BT ECT as an outpatient for a total of 13 thrice-weekly sessions (including 9 BT sessions). He was begun on lamotrigine in low dose and olanzapine, 10 mg daily, and then twice daily to control his paranoia, anger, and irritability. Unfortunately, he developed a rash, so his lamotrigine had to be discontinued. After the completion of his acute course of ECT, he was started on lithium carbonate with instructions to hold the lithium the entire day before each ECT. Trough lithium level was 0.6 at a dose of 900 mg daily, and olanzapine was tapered to discontinuation as he improved. At the time of his last acute treatment, the patient stated that he was approximately “60%” better but that “if the treatments weren't affecting my memory, I'd be 80% to 90% better.” Selfreported Patient Health Questionnaire-9 scores showed no consistent improvement during the ECT course, but these scores were not considered valid because he was clinically judged moderately improved; hence, weekly continuation of ECT was begun. The clinical assessment of improvement was based on the observation that his suicidality had resolved, that he had become more verbal and better able to address and discuss psychological problems, that affect was much improved, and that the patient had become more interactive in interview and with his family. At his second weekly treatment, he continued to complain about memory dysfunction. Hence, his treatment interval was extended to 2 weeks to allow time for his memory to recover, and lithium was increased to 1125 mg daily. Within the 2-week treatment interval, the patient did well only for 1 week, and in the second week, he was much more depressed and withdrawn. After a lengthy discussion with the patient and his wife regarding treatment frequency and potential effects on memory, weekly ECTwas resumed (due to the fact that another brief acute series of treatments was not an option because of the patient's memory complaints). With the resumption of weekly ECT and with the addition of aripiprazole of 5 mg daily, he began to progress again after 2 treatments, but mood still worsened approximately 5 days after each treatment. This deterioration in mood seemed to be at least in part triggered by conflict with his children and wife, and they were referred to couples counseling, but they did not follow through with this recommendation.
156
www.ectjournal.com
In the third weekly visit, there was no progression, so aripiprazole was discontinued, and the patient was begun on tranylcypromine at 30 mg daily while continuing lithium carbonate. By the next week, the patient had again begun to improve but expressed more concern about his memory, stating “I fear it won't get better and I won't be able to return to work” (he had not worked for the past 1½ years since March 2008). The patient and his wife were offered the option to extend his treatment interval once again to 2 weeks, but given his residual symptoms and the duration of observed improvement after each treatment, the couple agreed to the continuation of weekly treatments. He ultimately had 6 once-per-week treatments and the interval was again extended to 2 weeks, but with resumption of the 2-week interval, his mood again slowly deteriorated. At this point, after a total of 23 ECT treatments (13 acute and 10 continuation treatments for a period of 9 weeks), ECT was discontinued because sustained improvement was not achieved and because the patient continued to complain of memory difficulties, precluding the option of further acute treatments, although he had clearly shown response to his acute series of treatments. Across all sessions, the mean (SD) dynamic energy of the ECT stimulus was 46.2 (18.0) J (range, 17.7–67.6 J). The mean (SD) motor seizure duration was 38.3 (12.4) seconds (range, 17–60 seconds), and the mean (SD) EEG seizure duration was 56.2 (20.2) seconds (range, 21–98 seconds). The patient experienced no complications during any of the treatment sessions. From this point forward, the patient was treated with medication and his ongoing individual psychotherapy. Tranylcypromine was discontinued, and he was begun on nortriptyline at 75 mg while continuing lithium (trough level of 0.9) and triiodothyronine at 25 μg daily. Approximately 3 months after the completion of ECT, the patient's wife now stated that the patient was amnestic for “all memories” preceding the onset of his ECT treatments. She had also begun to explore antipsychiatry as well as anti-ECT Web sites and contacted Peter Breggin, MD. At this point, the wife cut off contact with the ECT treatment team until such time as the lawsuit was filed approximately a year later.
The Lawsuit A malpractice lawsuit was filed in Sacramento, California, alleging that the standard of care had not been met in the care of the patient, resulting in harm (Sacramento County Superior Court Case No. 34-2011-00099829). The details of the case were collated using the handwritten notes of one of the authors who was present at the trial and the pretrial documents of discovery that were entered into evidence. Defendants in the case included the 2 physicians who provided ECT, the physicians who made the referral for ECT, and several other earlier treating physicians, including the consulting neurologist. The plaintiff alleged that the standard of care had not been met in the handling of the psychotropic medications, especially around the time of initiation of ECT, and that a treatment plan that included ECT ipso facto did not meet the standard of care and produced damages. Regarding the alleged damage produced by ECT, the plaintiff claimed brain damage from ECT, resulting in global, complete retrograde autobiographical memory loss that resulted in disability. The trial began approximately 4 years after the patient's treatment ended. The plaintiff's only expert was Peter Breggin, MD. Dr Breggin has a well-established reputation of opposition toward ECTand has testified for the plaintiff in numerous ECT malpractice trials.6 His bona fides were provided to the jury as follows: that he had testified numerous times in the US Congress, that he had appeared numerous times in front of Food and Drug Administration © 2014 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Journal of ECT • Volume 31, Number 3, September 2015
panels, and that he was the author of numerous books in the field of psychiatry as well as the editor of numerous journals. After his introduction, he testified for 1½ days (see Appendix 1, Supplemental Digital Content 1, http://links.lww.com/JECT/A39). At trial, Dr Breggin testified that he had been an expert witness in approximately 80 malpractice lawsuits over the years. He stated that he thought he had been a witness for the defense in “maybe 1 or 2 cases. I can't really remember.” After the testimony of Dr Breggin, the post-ECT testing of the patient was presented. The initial post-ECT testing was done by Dr Breggin. He testified that, after he was contacted by the patient's wife, he asked for a copy of the patient's records. After a review of the records, he told her that the patient “definitely had ECT-induced brain damage” (we realized at trial that this was the point in time that the patient's wife cut off all contact with the ECT treatment team and, in fact, with any psychiatrist and discontinued her husband's medications). He arranged for the patient and his wife to travel to Ithaca, New York. Once there, he testified that he did a several-hour clinical interview and administered a Mini-Mental State Examination, confirming his tentative diagnosis based on his medical record review. He then referred the patient for follow-up neurological evaluation that was done at a university medical center and included repeat MRI, EEG, brain PET, as well as neuropsychological evaluation. The findings of laboratory studies were all negative in the opinion of the neuroimaging experts for the defense. The neuropsychological testing showed extremely poor performance across multiple domains and tests, with results beyond what is seen in significant dementia. The result of the Test of Memory Malingering (TOMM) was positive for malingering. The TOMM is a 50-question visual memory recognition test that discriminates between true memory impairment and malingering, with 2 learning trials and an optional retention trial after a delay. It was first published in 1996 and is intended for testing individuals ages 16 years and older.7 The TOMM has been shown to have high levels of sensitivity as well as specificity and is largely insensitive to depression and anxiety.7 The post-ECT diagnosis of the neurologist, based on his examination and the testing, was pseudodementia of depression with exaggeration of symptoms as demonstrated in part by an elevation of the “Fake-Bad” scale on the Minnesota Multiphasic Personality Inventory as well as the results of the TOMM. After completion of the testing, Dr Breggin then referred the patient's wife to 2 attorneys to pursue a lawsuit. The first attorney is the one he had employed on multiple prior occasions for other lawsuits; the other was a California licensed attorney because the lawsuit was in California. At trial, the progress notes of the patient's treating psychologist were entered into evidence, and she noted that, during the period before the referral for ECT and after she had requested the neurological evaluation, the patient had become almost giddy when he thought that he might have Alzheimer's disease as an explanation for his memory impairment. The theory of the defense was that, in fact, he was pleased about the prospect for such a diagnosis because it provided an explanation for his inability to function as a provider for his family, as an equal partner to his wife within this family structure, as an equal sexual partner to his wife, and as an equal parent to his children. In fact, when the patient was told that there were no neurologic abnormalities identified, he became suicidal (this only became clear during the trial), and this was a precipitating event for the patient's referral for inpatient treatment and ECT. As the discovery process unfolded, the defense attorneys thought that it became increasingly clear that the patient was exaggerating his deficits. This was thought, on the basis of the MMPI, the TOMM, and the nature of the litigation process, to be conscious.
Electroconvulsive Therapy Malpractice
During the course of the trial, the patient's wife and 2 children described many instances of their father's memory impairment. The patient himself was not in the trial and was only seen on a videotape of his deposition. On this video, he appeared disheveled, much older than his chronological age, and profoundly depressed. He was described as being a “prisoner in his own home; he rarely leaves his bedroom and never cuts his hair or beard.” Despite a claim of devastating brain damage and total autobiographical memory loss, the children testified that their father continued to drive them to school, to after-school events, and, even on 1 occasion, to San Francisco, which is a 130-mile 1-way trip. However, they described strange behaviors, such as crossing over a double yellow line to pass a car and then turning to his daughter and asking, “What's that line for?” The plaintiffs used this example, and others similar to this, to show that his memory was grossly impaired. During the trial, the defense felt that examples such as these were consistent with dissociative amnesia, a diagnosis suggested to the defense attorneys by the defendants (or psychogenic amnesia as described in the medical literature8). Thus, the theory of the defense was no longer that the patient was malingering but that his reported loss of memory was symptomatic of an unconscious process. In fact, the symptoms displayed by the patient as he was described at trial were consistent with dissociative amnesia. He claimed that he was amnestic (as stated earlier) for “all” events, people, and places before the onset of ECT. He claimed that he could not recall his siblings, that he could not recall growing up in Mexico, that he could not recall his wife before the present moment, and that he could not recall his children except for the immediate time of his engagement with them. His son testified that they lived in a rural area and had a pond near their house. Every spring, they would hear loud croaking at mating time. The croaking was so loud that they would have trouble sleeping, and this had been going on for many years. After ECT, when the croaking began, the patient exclaimed “What's that noise?” The diagnosis of dissociative amnesia was not presented to the jury directly, although one of the defenses' experts did speak that the patient need to “look away” from his problems and that ECT-associated memory loss gave him a method to do this. This diagnosis is supported when the reported loss of memory after the initiating event fails to show the expected temporal gradient of amnesia, which is worse closer to the event and better for those memories more distant form the event. The plaintiff's complaint of amnesia did fail to show a temporal gradient. Furthermore, a complaint of total autobiographical amnesia would be expected to be associated with structural or functional brain abnormalities, yet no such abnormalities were demonstrated by the extensive posttreatment evaluations. Finally, psychogenic amnesia often occurs in the setting of interpersonal difficulties such as marital discord.8 The trial continued for a total of 15 days. Subsequently, the jury deliberated for 3 hours. According to the defense attorneys, this was an extremely short deliberation for such a long and complex trial and it spoke of the weakness of the plaintiff's case. The jurors returned with an 11-1 verdict for the defense. The jury foreperson stated that the plaintiffs were unable to demonstrate that the standard of care was not met. They were unable to determine whether the ECT treatments were responsible for any harm to the patient, and they were not even sure whether any harm had, in fact, occurred.
DISCUSSION This summary of a malpractice case is among the most detailed found in the medical literature. Provision of the detail is possible because the case was tried to the point of reaching a verdict,
© 2014 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.ectjournal.com
157
Journal of ECT • Volume 31, Number 3, September 2015
Goodman and McCall
resulting in the facts of the case entering the public domain. Such transparency is not possible when cases settle before trial. In the absence of being in the jury's chambers, it is impossible to know the particulars of how the jury weighed the many pieces of evidence and testimony. However, it is possible that the plaintiff's sole reliance on the testimony of Dr Breggin did not help their case because he has been reported to be “not credible” as an expert in other ECT malpractice cases.6 The availability of brain MRI, brain PET, and EEG examination results both before and after the course of ECT was fortuitous for the defense, especially because these laboratory examinations were interpreted as normal by the defense experts. The remarkable discrepancies in the patient's cognitive functioning, such as complaints of total autobiographical amnesia, with no temporal gradient, in the face of preservation of ability to navigate long automobile trips, raised questions about the “organic” nature of the memory complaint. The patient's prior repeated history of worker's compensation litigation is consistent with the pursuit of litigation in this case as well. The litigation and the concerns about “brain damage” not only could have been a source of additional compensation but are also a distraction from focusing on real and ongoing psychosocial problems, resulting in a potential failure of the patient to access needed care. The lessons learned from this case include a need for continued vigilance on the part of ECT physicians to document all necessary aspects of ECT care, as was done in this case, to defend against unpredictable lawsuits. Some of the necessary aspects include the following: (1) documentation behind the thought processes that demonstrate the need for ECT, (2) assessment of the patient's capacity to participate in the decision making for ECT, (3) a signed consent form, (4) documentation of the technical aspects of the conduct of each treatment session, (5) documentation of the patient's progress during ECT, including both therapeutic and adverse effects, and (6) documentation of the thought processes behind extending the ECT course, moving from acute to continuation ECT, or terminating ECT, and the involvement of
158
www.ectjournal.com
the patient and/or family in the decision making. Although the presence of EEG, brain MRI, and brain PET findings before ECT were helpful in the defense of this case, we do not recommend their routine use before ECT. Finally, this case demonstrates that treating ECT physicians need to be aware of the rare emergence of psychogenic amnesia precipitated by ECT treatment and the need to deal with this complication of treatment aggressively to prevent an adverse outcome of treatment. In particular, in patients with psychological problems that could predispose a patient to the emergence of psychogenic amnesia, extra caution needs to be taken with respect to the psychological aspects of the patient's treatment, concurrently with his ECT treatment, to help insure a positive outcome of treatment.
REFERENCES 1. Slawson P, Giggenheim F. Psychiatric malpractice: a review of the national loss experience. Am J Psychiatry. 1984;141:979–981. 2. Slawson P. Psychiatric malpractice: the electroconvulsive therapy experience. Convuls Ther. 1985;1:195–203. 3. Slawson P. Psychiatric malpractice and ECT: a review of national loss experience. Convuls Ther. 1989;5:126–130. 4. Slawson P. Psychiatric malpractice and ECT: a review of 1,700 claims. Convuls Ther. 1991;7:255–261. 5. Abrams R. Malpractice litigation and ECT. Convuls Ther. 1989;5:365–367. 6. Abrams R. ECT malpractice issues. Convuls Ther. 1995;11:286–287. 7. Teichner G, Wagner M. The Test of Memory Malingering (TOMM): normative data from cognitively intact, cognitively impaired, and elderly patients with dementia. Arch Clin Neuropsychol. 2004;19:455–464. 8. Serra L, Fadda L, Bucciione I, et al. Psychogenic and organic amnesia. A multidimensional assessment of clinical, neuroradiological, neuropsychological and psychopathological features. Behav Neurol. 2007; 18:53–64.
© 2014 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
