Psychosomatics 41:442-445, October 2000
© 2000 The Academy of Psychosomatic Medicine
Breast Cancer, Bipolar Disorder, Catatonia, and Life-Preserving Electroconvulsive Therapy
Kathy Waller, M.D.,
Alla Borik, M.D., and
Connie Choi, M.D.
Received September 1, 1999; revised December 29, 1999; accepted March 16, 2000. From the Department of Psychiatry and Langley Porter Psychiatric Institute, University of California, San Francisco, 401 Parnassus Avenue, San Francisco, California. Address reprint requests to Dr. Waller, Department of Psychiatry and Langley Porter Psychiatric Institute, University of California, San Francisco, 401 Parnassus Avenue, San Francisco, CA 94143.
Key Words: Cancer • Depression • ECT
The following is a case report of a woman with a history of metastatic breast cancer and bipolar disorder who developed a long and complicated course of catatonia that was successfully treated with electroconvulsive therapy (ECT). This case illustrates catatonia as a potentially lethal neuropsychiatric syndrome with multiple etiologies, complications, and a promising cure rate when treated adequately with medications, ECT, or both. It also illustrates relative medical contraindications to ECT and the medicolegal obstacles in California that can prevent the timely delivery of life-preserving ECT.
Case Report
Mrs. M. was a 42-year-old White woman with a 15-year history of bipolar affective disorder that had been stable for the past 8 years on lithium (600 mg) and fluoxetine (30 mg/day). She also had a history of breast cancer, with cerebral, pulmonary, and bone metastases. Her cancer was thought to be in remission after having received whole brain and gamma knife radiotherapy and chemotherapy over the year before admission. Small cerebral lesions located in the left parietal and right frontal lobes were no longer evident on brain imaging. Three months before admission, Mrs. M. had a brief episode of word finding difficulty and restlessness that responded to an increase in her lithium dose. After this episode, Mrs. M. had returned to her baseline state of health, active and feeling well until 1 week before admission. At that time she had a sudden onset of word-finding difficulty and lapses in concentration during conversations. Over the next several days her ability to communicate deteriorated while she became progressively more restless and unable to sleep. Mrs. M. tried taking repeated doses of lorazepam (1 mg for a total of 5 mg) and flurazepam (30 mg for a total of 150 mg) over the 2 days before admission, but her symptoms did not respond. Mrs. M. was brought into the neurology clinic by her husband and admitted to the hospital with confusion, psychomotor agitation, frequent screaming, and decreased speech production with occasional incomprehensive speech.
Mrs. M.'s condition progressively worsened after admission to the hospital. She had altered consciousness, became almost mute, and was unresponsive to questions and commands, with frequent echolalia, staring, and grimacing. Her level of activity alternated from stupor to agitation and combativeness. She exhibited waxy flexibility, cogwheel rigidity, tremor, shuffling gate, and stereotypy. Her vital signs were initially stable, and her physical exam was normal except for a chronic lower extremity deep venous thrombosis (DVT). Enoxaparin was started for treatment and pulmonary embolus prophylaxis. Admission laboratory studies showed a therapeutic lithium level of 0.8, and normal complete blood count, electrolytes, liver function tests, and thyroid function tests. Cerebrospinal fluid (CSF) cell count and differential were normal from a lumbar puncture; cytology on this CSF was benign. Additional tests included a chest x-ray and electrocardiogram, which were normal; an electroencephalogram, which showed bilateral generalized slowing; and brain computer topography, which showed diffuse degrees of brain atrophy but no evidence of hemorrhage or recurrent metastases.
Mrs. M was diagnosed with catatonia, but the etiology was unclear. The initial management was the addition of 1 dose of lorazepam (2 mg) while continuing lithium (600 mg), fluoxetine (30 mg), and flurazepam (30 mg). With Mrs. M.'s condition worsening on Day 2, the following changes were made: lorazepam (1 mg) was given intravenously and (0.5 mg) was given 5 times throughout the day, lithium was increased (600 mg to 750 mg), and haloperidol (1 mg) doses were used to target agitation and delirium. However, after receiving only 2 doses of haloperidol, severe muscular rigidity ensued, in the absence of fever or autonomic instability. In addition, her lithium level increased from 0.8 to a toxic level of 1.5. Because of these adverse effects and a known association with catatonia, haloperidol, lithium, and fluoxetine were discontinued. Mrs. M.'s other medications before admission had been filgrastin, epoetin alfa, and ondansetron, none of which were a concern for an association with catatonia. Management was changed to lorazepam, used in increasing doses of 1–4 mg, with up to 23 mg a day by Day 9. Because she was not responding to lorazepam, a second benzodiazepine, clonazepam, was tried up to 14 mg per day, but Mrs. M. still did not respond and ultimately clonazepam was discontinued and lorazepam was restarted. Divalproex sodium was added as an alternative mood stabilizer to target her bipolar disorder as the possible underlying etiology of her catatonia. However, at a therapeutic valproic acid level of 53, Mrs. M. had only minimal improvement in her condition: increased sleep, mildly increased speech volume, and decreased thrashing. As pharmacotherapy proved to be failing, ECT became the recommendation despite relative medical contraindications.
However, medicolegal procedures for the practice of ECT in California became a serious obstacle over the next few weeks. California law dictates that when a patient does not have capacity to give informed consent for ECT, as Mrs. M. did not because of her condition, the case must be treated as an "Involuntary" ECT, requiring consent from the Superior Court. Procedures include evaluations and recommendations for ECT from three psychiatrists in the form of petitions to the court, a court hearing to declare the patient incompetent, and a second hearing to obtain consent for the specific procedure of ECT. During these legal procedures Mrs. M.'s catatonic syndrome continued and complications arose. As mentioned, she had a DVT. While hospitalized, she had two brief episodes of tachypnea, labored breathing, hypoxia, and obtundation. The first resolved with supplemental oxygen, but the second required short-term intubation. These events fortunately did not prove to be because of pulmonary embolism as expected; they appeared to have been because of a mucus plug and resolved with supportive measures. On Day 12, brain magnetic resonance imaging showed very small but new subdural hematomas over the convexities from the vertex to the temporal regions bilaterally, which had not been present on brain computer topography between Mrs. M.'s admission and Day 11. The bleeding was likely because of minor head trauma from her physical agitation in the context of vulnerability from brain radiation and anticoagulation started when the DVT was discovered. Enoxaparin was discontinued and an inferior vena cava filter was eventually placed. However, the subdural hematomas continued to expand requiring neurosurgical evacuation on Day 30. Remarkably Mrs. M.'s catatonic symptoms remained unchanged before and after surgery. Cytology done on CSF obtained during surgery was positive for adenocarcinoma malignant cells, although no masses were seen on imaging studies. Medicolegal procedures were ongoing during the course, and one the Superior Court authorized ECT, Mrs. M. underwent a series of three bilateral ECT treatments within a 3- day period beginning on Day 45. Following the third treatment, Mrs. M. was awake, alert, verbal, and like her old self, according to her family. She was unable to recall any events before or during her hospitalization. Her condition remained stable, and she did not require further ECT or psychiatric medications during the remainder of her hospitalization. Discharge medications included only albuterol and tylenol. In the weeks following discharge, lithium and fluoxetine were restarted.
Three months after discharge, follow-up was obtained via telephone. Mrs. M. reported having a stable mood and overall feeling well. Her cancer was thought to be in remission. However, shortly after the follow-up, the cancer was found to have recurred and again metastasized extensively to her brain in the right frontoparietal region, bone, lungs, and liver. Some agitation returned and she opted to try ECT again. However, it was not helpful for this limited symptom and at that time she was treated with comfort care only. Mrs. M. died shortly thereafter from metastatic breast cancer.
Discussion
Mrs. M. had a prolonged catatonic syndrome successfully treated with ECT despite an unusually complicated course. The underlying etiology of her catatonia was a diagnostic dilemma because of her history of bipolar disorder and metastatic cancer. Subdural hematomas and neurosurgical evacuation during the course of her catatonia contributed to relative contraindications for ECT. In addition, medicolegal procedures delayed prompt treatment. Remarkably, despite the complexity of her case and failure of standard pharmacotherapy for catatonia, ECT resulted in a complete resolution of her symptoms.
The diagnosis of catatonia was made based on Mrs. M.'s following symptoms: motoric immobility, excessive motor activity, mutism, bizarre movements, and echolalia.1 Although her syndrome was severe and complicated, it was still "simple" catatonia because she did not have hyperthermia or autonomic instability, which would have categorized it as "malignant." Although "malignant" catatonia is more immanently lethal, complications arising from "simple" catatonia may also be lethal. The presence of a DVT put Mrs. M. at high risk for a pulmonary embolism. According to McCall et al.'s2 report on cases of fatal pulmonary embolism during catatonia, anticoagulation can be a particularly delicate balance in catatonia because of alternating states of mobility. Although prophylaxis for pulmonary embolism may be lifesaving, the increased risk for bleeding, manifested by Mrs. M. as expanding subdural hematomas, also has the potential of being life threatening.
The general approach to catatonia is to treat the underlying condition if identifiable. Catatonia can be caused by either medical or psychiatric conditions. Mrs. M. had both. Because some medications have been shown to be associated with catatonia,3 stopping all possible medications is reasonable. Mrs. M. had been on lithium and fluoxetine, which are both associated with catatonia, so these were discontinued. However, her condition did not change. The most concerning possible etiology was a recurrence of cerebral metastases from primary breast carcinoma. Brain computer topography showed no anatomic evidence for cancer recurrence compared with previous imaging studies, and it ruled out a cerebrovascular event. Initial cytology done on CSF was benign although later cytology was positive for malignant cells. The presence of cells postradiation was difficult to interpret because malignant cells could have represented new metastases or remnant cells from previously irradiated tumors. Subdural hematomas did not appear to be related to the severity of Mrs. M.'s syndrome because they developed after the problem was evident, and there was no improvement after surgery. Recent cancer treatments were considered also. However, postradiation encephalopathy is not known to manifest as catatonia, and although the patient had recently finished a cycle of chemotherapy, there were no metabolic abnormalities on laboratory studies. There was also no evidence of infection. Highly suspect was her long history of bipolar affective disorder because a strong relationship exists between affective disorders and catatonia.4 As the evaluation evolved, the suspected possible etiologies narrowed to an idiopathic syndrome related to her history of cerebral metastases versus bipolar affective disorder or a combination of both.
While evaluating potential causes of catatonia, treatment was initiated with benzodiazepines, a safe and effective first-line treatment regardless of etiology. Lorazepam has been the one most studied. In Hawkins' 1995 review of the literature of catatonia treatment, response rates ranged from 70% to 79% with a mean daily dose of lorazepam (3.0 mg).5 Bush et al.6 reported a 76% complete response with lorazepam (4–8 mg/day for up to 5 days), with 69% responding in the first day of treatment. Over 1 to 5 days the response rate decreased and at the end of 5 days nonresponders were referred to ECT. In Mrs. M.'s case, high doses over weeks of treatment with lorazepam and clonazepam failed, leading to serious considerations of ECT.
Everyone involved in Mrs. M.'s care exercised extreme caution regarding ECT because of the patient's history of neurologic involvement of the cancer and more recent subdural hematomas. Historically, evidence of cerebral lesions or malignant tumors in any location have been absolute contraindications to ECT.7 This clinical judgment was based on cases reported before the existence of brain imaging. Current imaging techniques allow for evaluation of cerebral lesions, most importantly with respect to increased intracranial pressure. Recent expert opinion holds that ECT is safe if lesions are not obstructing CSF or causing increased intracranial pressure.7 Mrs. M. had no current masses; however, she did have recent subdural hematomas. Craniotomy itself was a concern as there is no evidence defining a safe interval between neurosurgery and ECT.7 However, with no sign of improvement and known efficacy of ECT, the family was willing to accept the risks of ECT 2 weeks after her surgery. In Hawkins' review, ECT administered to catatonic patients had an 85% complete response rate when used alone and high efficacy when used in combination with other treatments. Many authors agree that patients should be promptly referred for ECT if not responding to benzodiazepines within a few days.6,7 ECT is considered by some to be another first-line treatment, especially in cases of malignant catatonia when rapid resolution of the syndrome is lifesaving. Although the literature endorses timely administration of ECT as a safe and successful procedure, even in the context of relative medical contraindications, the medicolegal obstacles to administering ECT in California did not allow it.
Although the patient's husband had Durable Power of Attorney for medical decisions, California legislation prohibits it from being used to authorize ECT. Therefore, the court approached the case as "Involuntary" ECT despite her family's desire for her to receive it. The following procedures were required to obtain legal consent: an initial Superior Court hearing to establish conservatorship, letters petitioning the Superior Court from the treating psychiatrists and two consulting psychiatrists with evaluations and recommendations for ECT, and a second Superior Court hearing to declare the patient incompetent to specifically refuse ECT. The time required for these procedures far exceeded the recommendation to refer patients for ECT if there is no response to benzodiazepines in 3 to 5 days.
Conclusion
The search for this patient's underlying cause of catatonia did not result in a definitive etiology. It appears in retrospect to have been a combination of her cancer recurrence and bipolar disorder. However, despite the unclear etiology, ECT proved to be a safe and effective treatment when benzodiazepines failed. Many of the complications of Mrs. M.'s hospital course might have been avoided with earlier administration of ECT. Medicolegal procedures required in the state of California prevented timely administration of ECT and placed the patient at increased risk for morbidity and mortality. Although government regulations are well- intentioned to protect the public, excessive regulations interfere with quality of care and ultimately do society a costly disservice. There was a 30-day delay for Mrs. M. from the time ECT was recommended until it was authorized and delivered. The cost to Mrs. M. was a delay in treatment for a life-threatening condition. In addition to medical expenses, her family also paid legal fees of approximately $2,000 for the ECT legal procedures. The cost to the system for additional hospital days, procedures, and tests exceeded $75,000. In order to provide the best possible treatment for patients with catatonic syndromes in the future, the current understanding of catatonia and available treatments must be accepted, practiced, and used to reform ECT legislation.
REFERENCES
-
Bush G, Fink M, Petrides G, et al: Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand 1996; 93:129–136[Medline]
-
McCall WV, Mann SC, Shlep FE, et al: Fatal pulmonary embolism in the catatonic syndrome: two case reports and a literature review. J Clin Psychiatry 1995; 56:21–25[Medline]
-
Philbrick KL, Rummans TA: Malignant catatonia. J Neuropsychiatry Clin Neurosci 1994; 6:1–13[Abstract/Free Full Text]
-
Friccione G, Bush G, Manish F, et al: Recognition and treatment of the catatonic syndrome. J Intensive Care Med 1997; 12:135–147
-
Hawkins JM, Archer KJ, Strakowski SM, et al: Somatic treatment of catatonia. Int J Psychiatry Med 1995; 25:345–369[Medline]
-
Bush G, Fink M, Petrides G, et al: Catatonia. II. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand 1996; 93:137–143[Medline]
-
Zwil AS, Pelchat RJ: ECT in the treatment of patients with neurological and somatic disease. Int J Psychiatry in Med 1994; 24:1–29[Medline]
Get information about faster international access.
Privacy Policy
Copyright © 2000
Academy of Psychosomatic Medicine.
All rights reserved.
Home
| Search
| Current Issue
| Past Issues
| Subscribe
| All APPI Journals
| Help
| Contact Us
|
