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Moderate hyponatremia and death in a polydipsic schizophrenic on lithium
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Moderate Hyponatremia and Death in a Polydipsic Schizophrenic on Lithium Morris B. Goldman i
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Hill
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K e y W o r d s : Hyponalremia, schizophrenia, lithium, bradycardia, polydipsia, fatal
Introduction Acute dilutional hyponatremia in psychotic patients causes morbidity and mortality as a function of the brain's response to cellular edema and to the rapid rise or fall in solute concentration (Vieweg et al 1985; Goldman 1991). Symptomatic hyponatremia in inputients can usually be eliminated by a target weight procedure in which the patient is isolated from water duriug periods when plasma sodium is falling (Goldman 1991). The patient reported here died, however, despite maintaining sodium concentration above levels previously associated with symptomatic hyponatremia. Lithium and moderate hyponatremia may have contributed to her demise.
Case Report The patient was a 38-year-old female with schizoaffecfive disorder. She was in good physical health with normal plasma cholesterol levels and routine electrocardiograms. Her maternal uncle died of a heart attack at the age of 41; other close family members had coronary insufficiency, but not prior to their 60th birthdays. The patient had a 10-year history of polydipsia. Her first episode of water intoxication occurred in July i 990 when she was found to be seizing. Sodium level at that time was i 16 mEq/l, with a urine osmolality of 236 mOsm/kg, and urine sodium of 86 mEq/l. She had two subsequent seizures in May 1991 and ! 992 (sodium levels of !!3 and 116 ~ , respectively). Basal sodium levels were between 130 and 140 mEq/l, and no known factors could account for defective urinary dilution. From Elgin Mental Health Center, Elgin, IL: Illinois State Psychiatric Institute, Chicago. IL: and University of Chicago Pritzker School of Medicine. Chicago. It.. Addressreprint requests to Morris B. Goldman, MD, University of Chicago Pritzker School of Medicine. Depanmem of Psychiatry. 5841 South Maryland Ave. MC3077. Chicago, EL.60637; FAX: 312-702-6454. Received January 10,1994: revised April I !, 1994. © 1994 Societyof BieloglcalPsychiatry
The patieat was taken to the emergeocy room on two occasions following vasovagal episodes while receiving lithium, In Augu~ 1990she was lightheaded lint alert, with a heart rate of 40bpm. Her scram sodium was 120 mEq/i, serum potassium was 3.6 mEq/l, and lithium was 0.6 ~ . In a ~ episode in May 1992, she vomited and her heart rate dropped to 32 bpm with first-degree atrioventricular (AV) block (sodium = 120 mF~q, potassium = 3.5 mEqB, lithium =0.8 mEq/i). The patient was alert. She was given atropine and admitted to a coronary care unit for observation. Lithium was stopped, and fluid restriction was imposed. No evidence of primary heart disease was uncovered, and follow-up cardiograms were normal. Following another exacerbation of her psychiatric illness, she was wausferred to Elgin Mental Health Center. Because of her history of water intoxication and mild hypona~remiaon admission (125 mEq/l), a target weight procedure was instituted. She was begun on lithium because of her good response to this medication in the past. Other medications included mesoridazine 250 mg/day and lorazepum ! m g bid. Her psychiatric symptoms improved, and she maintained her weight within the prescribed guidelines (Goldman 1991). Three months after admission, the patient was found in a toilet stall leaning upright against the wail. Her pupils were fixed and dilated. Blood chemistries obtained at that time revealed a sodium level of 119 trdEq/!and lithium of 0.6 mEq/l. Two routine sodium levels obtained in the month prior to this incident were 134 and ! 36 rnEq/I. She was transferred to the intensive care unit of a nearby hospital and treated with isotonic saline and inotropic agents. No evidence of myocardial infarction was obtained. The patient died the next day. Autopsy of the brain revealed diffuse anoxia and mild edema.
Discussion While the cause of death remains unclear, the data do not implicate either coronary artery disease or classic water intoxication. Thus 0006-3223/94/'Y}7.00
tttcx t~YCtltATI~Y Itg,t;36:4$5-4116
prior evaluation in a coronary care unit. and laboratory tests performed after she succumbed, did not disclose cardiac ischemia or damage. The absence of severe cerebral edema and her prior history of being mentally alert at a similar level of hyponatremia argue against water intoxication as the only cause of her death. Instead. the patient's previous history of bradycardia, and the conditions under which she was found (i.e., leaning uptight against a toilet stall) suggest that a vasovagal episode induced a fatal arrhythmia. While such an arrhythmia could be solely a function of underly-
Case Reports
ing cardiac disease, the resolution of her previously identified conduction defect with water restriction and discontinuation of lithium suggest that these two factors may have contributed. Volume expansion may inhibit the sympathetic nervous system response to ~ (Agius and C'utajor 1991). and lithium may suppress sinus and AV nodal function (Brady and Morgan 1988). Thus it may be appropriate in hyponatremic patients with a histot3, of bradyc~ia to impose more stringent target weight limits, and to avoid lithium therapy.
References Agius AM, Cutajar CL (1991): Hyponatremia after transurethral resection of the prostate. J Royal Coil Surg Edin 36:109- I ! 2. Brady MB, Morgan JH 0988): Lithium and the heart. Chest 93:166-169. Goldman MB 0991): A rational approach to disorders of water
balance in psychiatric patients. Hosp Community Psychiatry 42:488--494. Vieweg WVR, David JJ, Rowe WT (1985): Death from selfinduced water intoxication among patients with schizophrenic disurders. J Nerv MentDis 173:161-165.
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Moderate Hyponatremia and Death in a Polydipsic Schizophrenic on Lithium Morris B. Goldman i
lliH
Hill
ImlIH
Hlllll
I
K e y W o r d s : Hyponalremia, schizophrenia, lithium, bradycardia, polydipsia, fatal
Introduction Acute dilutional hyponatremia in psychotic patients causes morbidity and mortality as a function of the brain's response to cellular edema and to the rapid rise or fall in solute concentration (Vieweg et al 1985; Goldman 1991). Symptomatic hyponatremia in inputients can usually be eliminated by a target weight procedure in which the patient is isolated from water duriug periods when plasma sodium is falling (Goldman 1991). The patient reported here died, however, despite maintaining sodium concentration above levels previously associated with symptomatic hyponatremia. Lithium and moderate hyponatremia may have contributed to her demise.
Case Report The patient was a 38-year-old female with schizoaffecfive disorder. She was in good physical health with normal plasma cholesterol levels and routine electrocardiograms. Her maternal uncle died of a heart attack at the age of 41; other close family members had coronary insufficiency, but not prior to their 60th birthdays. The patient had a 10-year history of polydipsia. Her first episode of water intoxication occurred in July i 990 when she was found to be seizing. Sodium level at that time was i 16 mEq/l, with a urine osmolality of 236 mOsm/kg, and urine sodium of 86 mEq/l. She had two subsequent seizures in May 1991 and ! 992 (sodium levels of !!3 and 116 ~ , respectively). Basal sodium levels were between 130 and 140 mEq/l, and no known factors could account for defective urinary dilution. From Elgin Mental Health Center, Elgin, IL: Illinois State Psychiatric Institute, Chicago. IL: and University of Chicago Pritzker School of Medicine. Chicago. It.. Addressreprint requests to Morris B. Goldman, MD, University of Chicago Pritzker School of Medicine. Depanmem of Psychiatry. 5841 South Maryland Ave. MC3077. Chicago, EL.60637; FAX: 312-702-6454. Received January 10,1994: revised April I !, 1994. © 1994 Societyof BieloglcalPsychiatry
The patieat was taken to the emergeocy room on two occasions following vasovagal episodes while receiving lithium, In Augu~ 1990she was lightheaded lint alert, with a heart rate of 40bpm. Her scram sodium was 120 mEq/i, serum potassium was 3.6 mEq/l, and lithium was 0.6 ~ . In a ~ episode in May 1992, she vomited and her heart rate dropped to 32 bpm with first-degree atrioventricular (AV) block (sodium = 120 mF~q, potassium = 3.5 mEqB, lithium =0.8 mEq/i). The patient was alert. She was given atropine and admitted to a coronary care unit for observation. Lithium was stopped, and fluid restriction was imposed. No evidence of primary heart disease was uncovered, and follow-up cardiograms were normal. Following another exacerbation of her psychiatric illness, she was wausferred to Elgin Mental Health Center. Because of her history of water intoxication and mild hypona~remiaon admission (125 mEq/l), a target weight procedure was instituted. She was begun on lithium because of her good response to this medication in the past. Other medications included mesoridazine 250 mg/day and lorazepum ! m g bid. Her psychiatric symptoms improved, and she maintained her weight within the prescribed guidelines (Goldman 1991). Three months after admission, the patient was found in a toilet stall leaning upright against the wail. Her pupils were fixed and dilated. Blood chemistries obtained at that time revealed a sodium level of 119 trdEq/!and lithium of 0.6 mEq/l. Two routine sodium levels obtained in the month prior to this incident were 134 and ! 36 rnEq/I. She was transferred to the intensive care unit of a nearby hospital and treated with isotonic saline and inotropic agents. No evidence of myocardial infarction was obtained. The patient died the next day. Autopsy of the brain revealed diffuse anoxia and mild edema.
Discussion While the cause of death remains unclear, the data do not implicate either coronary artery disease or classic water intoxication. Thus 0006-3223/94/'Y}7.00
tttcx t~YCtltATI~Y Itg,t;36:4$5-4116
prior evaluation in a coronary care unit. and laboratory tests performed after she succumbed, did not disclose cardiac ischemia or damage. The absence of severe cerebral edema and her prior history of being mentally alert at a similar level of hyponatremia argue against water intoxication as the only cause of her death. Instead. the patient's previous history of bradycardia, and the conditions under which she was found (i.e., leaning uptight against a toilet stall) suggest that a vasovagal episode induced a fatal arrhythmia. While such an arrhythmia could be solely a function of underly-
Case Reports
ing cardiac disease, the resolution of her previously identified conduction defect with water restriction and discontinuation of lithium suggest that these two factors may have contributed. Volume expansion may inhibit the sympathetic nervous system response to ~ (Agius and C'utajor 1991). and lithium may suppress sinus and AV nodal function (Brady and Morgan 1988). Thus it may be appropriate in hyponatremic patients with a histot3, of bradyc~ia to impose more stringent target weight limits, and to avoid lithium therapy.
References Agius AM, Cutajar CL (1991): Hyponatremia after transurethral resection of the prostate. J Royal Coil Surg Edin 36:109- I ! 2. Brady MB, Morgan JH 0988): Lithium and the heart. Chest 93:166-169. Goldman MB 0991): A rational approach to disorders of water
balance in psychiatric patients. Hosp Community Psychiatry 42:488--494. Vieweg WVR, David JJ, Rowe WT (1985): Death from selfinduced water intoxication among patients with schizophrenic disurders. J Nerv MentDis 173:161-165.