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Hyponatremia due to antidepressant medications
CASE REPORT antidepressants, hyponatremia; hyponatremia, antidepressants
Hyponatremia Due to Antidepressant Medications Presented is the case of an elderly woman who developed severe hyponatremia while taking tricyclic antidepressants. She met the criteria for the syndrome of inappropriate antidiuretic hormone secretion induced by drugs. Her symptoms of lethargy, weakness, and gastrointestinal disturbances developed insidiously, allowing the hyponatremia to reach severe levels before a diagnosis was made. A variety of psychoactive drugs, most prominently tricyclic antidepressants, have been reported to produce hyponatremia idiosyncratically in elderly persons. [Abbott R: Hyponatremia due to antidepressant medications. Ann Emerg Med 12:708-710, November 1983.]
INTRODUCTION A wide variety of drugs, including the tricyclic antidepressants and other psychoactive drugs, have been reported as causes of hyponatremia via the mechanism of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)J In the case of the psychoactive drugs, the mild hyponatremic syndrome of weakness, lethargy, anorexia, nausea, and vomiting may resemble the underlying psychiatric disorder for which the drugs had been prescribed. A more severe clinical picture of coma and seizures due to hyponatremia could mimic an overdose in the patient known to be taking psychoactive medications. This case is presented to remind emergency physicians to be aware of the occasional association of hyponatremia with these as well as other drugs, and to obtain appropriate studies when any patient using psychoactive drugs develops an altered level of consciousness.
Rick Abbott, MD Lewis'con, Maine From the Department of Emergency Medicine, Central Maine Medical Center, Lewiston, Maine. Received for publication October 1, 1982. Revision received May 2, 1983. Accepted for publication June 20, 1983. Address for reprints: Rick Abbott, MD, Department of Emergency Medicine, Central Maine Medical Center, Lewiston, Maine 04240.
CASE REPORT A 57-year-old woman presented with a complaint of weakness. Four days prior she had developed progressive diffuse weakness. One day prior to admission she was too weak to leave her bed. In addition, she had vomited early in her illness, and had been anorexic, although she continued to ingest liquids. Over a period of many years, she had repeatedly complained of and been hospitalized for similar complaints: weakness, lightheadedness, and anorexia. She had undergone intermittent treatment with a variety of antidepressants during that time. In addition, mild hypertension had been treated on a long-term basis with propranolol (Inderal) and hydrochlorothiazide with triamterene (Dyazide). Sixteen days prior to the visit, she had been hospitalized for complaints of weakness. Extensive medical and neurological investigations had shown no evidence of neurological or metabolic disease, and there were no electrolyte abnormalities. During that admission, she was treated with amoxapine (Asendin) 50 mg daily, and with doxepin (Sinequan, Adapin) 75 mg daily in divided doses. Following institution of antidepressant therapy, her symptomatology rapidly improved and she was discharged, remaining well until the onset of her present illness. On examination, the patient had a blood pressure of 160/100 m m Hg and a pulse of 84 with no orthostatic change. She was afebrile, and respirations 12:11 November 1983
Annals of Emergency Medicine
708/85
HYPONATREMIA Abbott
were 22/min and unlabored. She was awake, but rather subdued in affect. She attempted to answer questions but her speech was slightly slurred, her attention wandered, and she was unable to express herself except in simple phrases. She was oriented in three spheres. Motor examination showed that she could overcome gravity but fatigued rapidly and could not overcome additional resistance. Sensory examination was normal. Deep tendon reflexes were absent in the upper extremities and symmetrically decreased in the lower extremities. There were no pathological reflexes, and cerebellar function was intact. Respiratory and cardiac examinations were normal, and there was no edema. The abdomen was normal, except for a bladder distended to the umblicus that resolved with catheterization and did not recur. Initial laboratory values showed a normal CBC, glucose of 154 mg/dL, and BUN of 15 mg/dL. Sodium was 95 mEq/L; chloride, 67 mEq/L; potassium, 4 mEq/L; and carbon dioxide, 22 mEq/L. The calculated osmolality was 218 m o s m / k g , and the m e a s u r e d osmolality was 223 mosm/kg. The urinary osmolality was 492 mosm/kg, and urinary sodium was 56 mEq/L. The electrolytes were redrawn and rerun, and additional controls were run to confirm the above values. Thyroid function studies and a serum cortisol were later reported normal. The patient was initially treated with a total of 700 mL of 5% saline (600 mEq of sodium) over 12 hours. Her serum sodium rose to 102 mEq/L at 6 hours, and to 126 mEq/L after 15 hours. Water was restricted during the next 24 hours, at which time her electrolytes had returned to normal. Doxepin and amoxapine had been discontinued on admission. After the first 36 hours she was allowed free access to water, and her serum electrolytes remained normal for the remainder of her hospitalization. Return of her depressive symptoms required treatment by the fifth day of hospitalization, and she was given amitriptyline (Elavil). Repeated determinations of electrolytes were normal during the hospitalization, and remained normal as an outpatient 10 weeks later. Her depression remains under reasonable control, and her activities are normal taking amitriptyline. 86/709
DISCUSSION
Hyponatremia, as well as other electrolyte disturbances, may result in n o n s p e c i f i c and p o o r l y localized symptoms. Commonly reported clinical findings of hyponatremia include lethargy, weakness, anorexia, vomiting, coma, and seizures. The severity of these symptoms relates to the level of the serum sodium and to the rapidity of development of hyponatremia. When hyponatremia develops gradually, the symptoms likely result from diffuse cellular dysfunction. With rapid development of hyponatremia, intraceflular fluid shiftsmay cause intracellular swelling and increased intracranial pressure, clinically manifested as coma and seizures. The e v a l u a t i o n of patients w i t h such symptoms and findings requires measurement of serum electrolytes as part of the initial evaluation. 2 When hyponatremia is identified, the differential diagnosis includes gastrointestinal loss, renal loss, volume depletion, edematous states, excessive free water intake, adrenal insufficiency, osmotic changes due to mannitol or hyperglycemia, artifactual hyponatrernia due to measurement in the presence of marked hyperlipemia or hyperproteinemia, and the syndrome of inappropriate antidiuretic hormone secretion.1 The specific criteria for the diagnosis of SIADH are hyponatremia, hyposmolality, urinary sodium that is less than maximally conserved, and urinary osmolality greater than serum osmolality. 3 These changes define a situation in which the inappropriate continued secretion of ADH permits the continued renal loss of sodium in the face of serum hypotonicity. In order to confirm the diagnosis of SIADH, these findings must occur in the absence of Volume depletion, cardiac failure, renal failure, hypothyroidism, or adrenal insufficiency.3 SIADH can be caused by central nervous system or pulmonary lesions, and by drugs. 3 Central nervous system l e s i o n s - trauma, tumors, meningitis, and encephalitis- have been thought to cause SIADH via stimulation of pituitary production of ADH. 1'3 Pulmonary tumors and infections have been considered to produce a substance of p u l m o n a r y origin w i t h ADH-like activity. 1,3 A variety of drugs have been found to produce SIADH. The mechanism of action has not been clarified. The origAnnals of Emergency Medicine
inal, drugs identified as producing SIADH were the oral hypoglycemic agents, 3 with chlorpropamide being the prototype. 3 Some of the cancer chemotherapeutic agents commonly produce hyponatremia. Of these, vincristine and cyclophosphamide have been most widely recognized. 4 Because these drugs are used in relatively restricted settings, and because they are recognized as frequent causes of hyponatremia, few problems are encountered in recognizing SIADH in association with their use. The final group of drags reported to p r o d u c e S I A D H are the psychotherapeutic agents. The occurrence of hyponatremia due to this group of drugs seems to be rare and idiosyncratic. 5 When hyponatremia causes coma or seizures in a known user of tricyclics, the consideration of possible overdosage may prompt urgent t r e a t m e n t prior to availability of routinely requested electrolyte values - - a potentially dangerous situation. The most commonly reported psychoactive drugs producing SIADH have been amitriptyline (Elavil), carbamazepine (Tegretol), and haloperidol (Haldol). 6-1s Others that have been reported include desipramine (Norprarain), n o r t r i p t y l i n e (Aventyl and Pamelor).hs'16 All the reported cases, as well as ours, have occurred in patients over the age of 50. Several cases have demonstrated return of the hyponatremia upon rechallenge with the same drug. 5,9 In others, patients have been treated with another psychoactive drag, even one known to sometimes produce SIADH. without return of the hyponatremia.' In our case, after treatment with amoxapine and doxepin was discontinued, treatment with amitriptyline did not reproduce the hyponatremia. In our patient, two recently administered drugs were in use at the time of development of SIADH: doxepin and amoxapine. Neither of these drugs has previously been reported to cause SIADH, and because rechallenge was not carried out, it is impossible to be sure which drug was causative. Doxepin is a tricyclic similar in structure to the other tricyclic drugs known to cause the syndrome, such as amitriptyline and carbamazepine. 6 Amoxapine is a recently released antidepressant with a dibenzoxazepine structure more similar chemically to the antipsychotic drugs. 17 This group has also been previously reported to 12:11 November 1983
cause SIADH. Treatment of hyponatremia due to SIADH consists of three stages. First, all drugs p o t e n t i a l l y c o n t r i b u t i n g should be discontinued pending firm i d e n t i f i c a t i o n of t h e source of t h e SIADH. Second, if the level of hyponatremia or the severity of the symptomatology requires urgent treatment, therapy should be initiated w i t h 5% saline, administering several hundred milliliters intravenously over several hours while following serum sodium and the symptoms, and watching for signs of fluid overload. Finally, after the initial phase of t r e a t m e n t or in less urgent situations, t r e a t m e n t is readily a c c o m p l i s h e d by r e s t r i c t i n g water intake to 1,000 mL per day. Our patient was treated by administration of 700 mL of 5% saline over the first 12 hours, followed by water restriction. Six hours after beginning treatmen L the serum sodium had risen from 95 to 102, and at 15 hours was 126. W i t h w a t e r restriction, it continued to rise to normal within 24 hours, and r e m a i n e d w i t h i n n o r m a l limits.
SUMMARY The evaluation of any patient presenting w i t h poorly localized symptoms or w i t h altered consciousness, p a r t i c u l a r l y in t h o s e u s i n g d r u g s k n o w n to cause h y p o n a t r e m i a , requires consideration of electrolyte disturbance. SIADH can be produced by a n u m b e r of drugs, and possible drug
12:11 November 1983
etiology should be considered when this s y n d r o m e is identified. Of part i c u l a r i m p o r t a n c e for e m e r g e n c y p h y s i c i a n s is t h e p o t e n t i a l for psychoactive drugs to cause idiosyncratic, severe hyponatremia in patients over 50 years of age. Treatment of hyponatremia depends on severity of symptoms, and m a y be carried out with 5% saline administration when severe, or w i t h water restriction in m i l d cases.
REFERENCES 1. Streeten D, Moses A, Miller M: Disorders of the neurohypophysis, in Isselbacher K, et ah Harrison's Principles of Internal Medicine, ed 9. New York, McGraw-Hill, 1980, p 1691-1694. 2. Weiner M, Epstein FH: Signs and symptoms of electrolyte disorders. Yale J Biol Med 43:76, 1970. 3. Bartter FC, Schwartz WB: The syndrome of inappropriate secretion of antidiuretic hormone. A m J Med 42:790-805, 1967. 4. Miller M, Moses AM: Drug-induced states of impaired.water secretion. Kidney lnt [Suppl] 10:9G 1976. 5. Weitzel WD, Shraberg D, Work J: Inappropriate ADH secretion: The role of drug rechallenge. Psychosomatics 21:771779, 1980. 6. Beckstrom D, Reding R, Cerletty J: Syndrome of inappropriate antidiuretic hormone secretion associated with amitriptyline administration,-(letter). JAMA 241:133, 1979. 7. Garson M: Syndrome of dilutional hyponatremia secondary to tricyclic antidepressant. Practitioner 222:4tl-412, 1979.
Annals of Emergency Medicine
8. Hamburger S, Langley H, Bowers G: The syndrome of inappropriate secretion of antidiuretic hormone associated with amitriptyline or trifluoperazine administration. J Kans Med Soc 81:469-470, 1980. 9. Luzecky M, Barmon K, Schuhz ER: The syndrome of inappropriate secretion of antidiuretic hormone associated with amitriptyline administration. South Med J 67:495-497, 1974. 10. Madhusoodanan S, Osnos R: Amitriptyline induced hyponatremia: A case report. Mt Sinai J Med 48:431-433, 1981. 11. Solammadevi SV: Inappropriate antidiuresis during amitriptyline therapy, (letter). South Med J 74:775-776, 1981. 12. Husband C, Mai FM, Carruthers G: Syndrome of inappropriate secretion of antidiuretic hormone in a patient treated with haloperidol. Can J Psychiatry 26:196197, 1981. 13. Kosten TR, Camp W: Inappropriate secretion of antidiuretic hormone in a patient receiving piperazine phenothiazines. Psychosomatics 21:354-355, 1980. 14. Peck V, Shenkman L: Haloperidolinduced syndrome of inappropriate secretion of antidiuretic hormone. Clin Pharmacol Ther 26:442-444, 1979. 15. Flegel KM, Cole CH: Inappropriate antidiuresis during carbamazepine treatment. Ann Intern Med 87:722-723, 1977. 16. Dhar SK, Ramos RR: Inappropriate antidiuresis during desipramine therapy, (letter). Arch Intern Med 138:1750-1751, 1978. 17. Amoxapine ( A s e n d i n ) - A new antidepressant. Med Lett 23:39-40, 1981.
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Hyponatremia Due to Antidepressant Medications Presented is the case of an elderly woman who developed severe hyponatremia while taking tricyclic antidepressants. She met the criteria for the syndrome of inappropriate antidiuretic hormone secretion induced by drugs. Her symptoms of lethargy, weakness, and gastrointestinal disturbances developed insidiously, allowing the hyponatremia to reach severe levels before a diagnosis was made. A variety of psychoactive drugs, most prominently tricyclic antidepressants, have been reported to produce hyponatremia idiosyncratically in elderly persons. [Abbott R: Hyponatremia due to antidepressant medications. Ann Emerg Med 12:708-710, November 1983.]
INTRODUCTION A wide variety of drugs, including the tricyclic antidepressants and other psychoactive drugs, have been reported as causes of hyponatremia via the mechanism of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)J In the case of the psychoactive drugs, the mild hyponatremic syndrome of weakness, lethargy, anorexia, nausea, and vomiting may resemble the underlying psychiatric disorder for which the drugs had been prescribed. A more severe clinical picture of coma and seizures due to hyponatremia could mimic an overdose in the patient known to be taking psychoactive medications. This case is presented to remind emergency physicians to be aware of the occasional association of hyponatremia with these as well as other drugs, and to obtain appropriate studies when any patient using psychoactive drugs develops an altered level of consciousness.
Rick Abbott, MD Lewis'con, Maine From the Department of Emergency Medicine, Central Maine Medical Center, Lewiston, Maine. Received for publication October 1, 1982. Revision received May 2, 1983. Accepted for publication June 20, 1983. Address for reprints: Rick Abbott, MD, Department of Emergency Medicine, Central Maine Medical Center, Lewiston, Maine 04240.
CASE REPORT A 57-year-old woman presented with a complaint of weakness. Four days prior she had developed progressive diffuse weakness. One day prior to admission she was too weak to leave her bed. In addition, she had vomited early in her illness, and had been anorexic, although she continued to ingest liquids. Over a period of many years, she had repeatedly complained of and been hospitalized for similar complaints: weakness, lightheadedness, and anorexia. She had undergone intermittent treatment with a variety of antidepressants during that time. In addition, mild hypertension had been treated on a long-term basis with propranolol (Inderal) and hydrochlorothiazide with triamterene (Dyazide). Sixteen days prior to the visit, she had been hospitalized for complaints of weakness. Extensive medical and neurological investigations had shown no evidence of neurological or metabolic disease, and there were no electrolyte abnormalities. During that admission, she was treated with amoxapine (Asendin) 50 mg daily, and with doxepin (Sinequan, Adapin) 75 mg daily in divided doses. Following institution of antidepressant therapy, her symptomatology rapidly improved and she was discharged, remaining well until the onset of her present illness. On examination, the patient had a blood pressure of 160/100 m m Hg and a pulse of 84 with no orthostatic change. She was afebrile, and respirations 12:11 November 1983
Annals of Emergency Medicine
708/85
HYPONATREMIA Abbott
were 22/min and unlabored. She was awake, but rather subdued in affect. She attempted to answer questions but her speech was slightly slurred, her attention wandered, and she was unable to express herself except in simple phrases. She was oriented in three spheres. Motor examination showed that she could overcome gravity but fatigued rapidly and could not overcome additional resistance. Sensory examination was normal. Deep tendon reflexes were absent in the upper extremities and symmetrically decreased in the lower extremities. There were no pathological reflexes, and cerebellar function was intact. Respiratory and cardiac examinations were normal, and there was no edema. The abdomen was normal, except for a bladder distended to the umblicus that resolved with catheterization and did not recur. Initial laboratory values showed a normal CBC, glucose of 154 mg/dL, and BUN of 15 mg/dL. Sodium was 95 mEq/L; chloride, 67 mEq/L; potassium, 4 mEq/L; and carbon dioxide, 22 mEq/L. The calculated osmolality was 218 m o s m / k g , and the m e a s u r e d osmolality was 223 mosm/kg. The urinary osmolality was 492 mosm/kg, and urinary sodium was 56 mEq/L. The electrolytes were redrawn and rerun, and additional controls were run to confirm the above values. Thyroid function studies and a serum cortisol were later reported normal. The patient was initially treated with a total of 700 mL of 5% saline (600 mEq of sodium) over 12 hours. Her serum sodium rose to 102 mEq/L at 6 hours, and to 126 mEq/L after 15 hours. Water was restricted during the next 24 hours, at which time her electrolytes had returned to normal. Doxepin and amoxapine had been discontinued on admission. After the first 36 hours she was allowed free access to water, and her serum electrolytes remained normal for the remainder of her hospitalization. Return of her depressive symptoms required treatment by the fifth day of hospitalization, and she was given amitriptyline (Elavil). Repeated determinations of electrolytes were normal during the hospitalization, and remained normal as an outpatient 10 weeks later. Her depression remains under reasonable control, and her activities are normal taking amitriptyline. 86/709
DISCUSSION
Hyponatremia, as well as other electrolyte disturbances, may result in n o n s p e c i f i c and p o o r l y localized symptoms. Commonly reported clinical findings of hyponatremia include lethargy, weakness, anorexia, vomiting, coma, and seizures. The severity of these symptoms relates to the level of the serum sodium and to the rapidity of development of hyponatremia. When hyponatremia develops gradually, the symptoms likely result from diffuse cellular dysfunction. With rapid development of hyponatremia, intraceflular fluid shiftsmay cause intracellular swelling and increased intracranial pressure, clinically manifested as coma and seizures. The e v a l u a t i o n of patients w i t h such symptoms and findings requires measurement of serum electrolytes as part of the initial evaluation. 2 When hyponatremia is identified, the differential diagnosis includes gastrointestinal loss, renal loss, volume depletion, edematous states, excessive free water intake, adrenal insufficiency, osmotic changes due to mannitol or hyperglycemia, artifactual hyponatrernia due to measurement in the presence of marked hyperlipemia or hyperproteinemia, and the syndrome of inappropriate antidiuretic hormone secretion.1 The specific criteria for the diagnosis of SIADH are hyponatremia, hyposmolality, urinary sodium that is less than maximally conserved, and urinary osmolality greater than serum osmolality. 3 These changes define a situation in which the inappropriate continued secretion of ADH permits the continued renal loss of sodium in the face of serum hypotonicity. In order to confirm the diagnosis of SIADH, these findings must occur in the absence of Volume depletion, cardiac failure, renal failure, hypothyroidism, or adrenal insufficiency.3 SIADH can be caused by central nervous system or pulmonary lesions, and by drugs. 3 Central nervous system l e s i o n s - trauma, tumors, meningitis, and encephalitis- have been thought to cause SIADH via stimulation of pituitary production of ADH. 1'3 Pulmonary tumors and infections have been considered to produce a substance of p u l m o n a r y origin w i t h ADH-like activity. 1,3 A variety of drugs have been found to produce SIADH. The mechanism of action has not been clarified. The origAnnals of Emergency Medicine
inal, drugs identified as producing SIADH were the oral hypoglycemic agents, 3 with chlorpropamide being the prototype. 3 Some of the cancer chemotherapeutic agents commonly produce hyponatremia. Of these, vincristine and cyclophosphamide have been most widely recognized. 4 Because these drugs are used in relatively restricted settings, and because they are recognized as frequent causes of hyponatremia, few problems are encountered in recognizing SIADH in association with their use. The final group of drags reported to p r o d u c e S I A D H are the psychotherapeutic agents. The occurrence of hyponatremia due to this group of drugs seems to be rare and idiosyncratic. 5 When hyponatremia causes coma or seizures in a known user of tricyclics, the consideration of possible overdosage may prompt urgent t r e a t m e n t prior to availability of routinely requested electrolyte values - - a potentially dangerous situation. The most commonly reported psychoactive drugs producing SIADH have been amitriptyline (Elavil), carbamazepine (Tegretol), and haloperidol (Haldol). 6-1s Others that have been reported include desipramine (Norprarain), n o r t r i p t y l i n e (Aventyl and Pamelor).hs'16 All the reported cases, as well as ours, have occurred in patients over the age of 50. Several cases have demonstrated return of the hyponatremia upon rechallenge with the same drug. 5,9 In others, patients have been treated with another psychoactive drag, even one known to sometimes produce SIADH. without return of the hyponatremia.' In our case, after treatment with amoxapine and doxepin was discontinued, treatment with amitriptyline did not reproduce the hyponatremia. In our patient, two recently administered drugs were in use at the time of development of SIADH: doxepin and amoxapine. Neither of these drugs has previously been reported to cause SIADH, and because rechallenge was not carried out, it is impossible to be sure which drug was causative. Doxepin is a tricyclic similar in structure to the other tricyclic drugs known to cause the syndrome, such as amitriptyline and carbamazepine. 6 Amoxapine is a recently released antidepressant with a dibenzoxazepine structure more similar chemically to the antipsychotic drugs. 17 This group has also been previously reported to 12:11 November 1983
cause SIADH. Treatment of hyponatremia due to SIADH consists of three stages. First, all drugs p o t e n t i a l l y c o n t r i b u t i n g should be discontinued pending firm i d e n t i f i c a t i o n of t h e source of t h e SIADH. Second, if the level of hyponatremia or the severity of the symptomatology requires urgent treatment, therapy should be initiated w i t h 5% saline, administering several hundred milliliters intravenously over several hours while following serum sodium and the symptoms, and watching for signs of fluid overload. Finally, after the initial phase of t r e a t m e n t or in less urgent situations, t r e a t m e n t is readily a c c o m p l i s h e d by r e s t r i c t i n g water intake to 1,000 mL per day. Our patient was treated by administration of 700 mL of 5% saline over the first 12 hours, followed by water restriction. Six hours after beginning treatmen L the serum sodium had risen from 95 to 102, and at 15 hours was 126. W i t h w a t e r restriction, it continued to rise to normal within 24 hours, and r e m a i n e d w i t h i n n o r m a l limits.
SUMMARY The evaluation of any patient presenting w i t h poorly localized symptoms or w i t h altered consciousness, p a r t i c u l a r l y in t h o s e u s i n g d r u g s k n o w n to cause h y p o n a t r e m i a , requires consideration of electrolyte disturbance. SIADH can be produced by a n u m b e r of drugs, and possible drug
12:11 November 1983
etiology should be considered when this s y n d r o m e is identified. Of part i c u l a r i m p o r t a n c e for e m e r g e n c y p h y s i c i a n s is t h e p o t e n t i a l for psychoactive drugs to cause idiosyncratic, severe hyponatremia in patients over 50 years of age. Treatment of hyponatremia depends on severity of symptoms, and m a y be carried out with 5% saline administration when severe, or w i t h water restriction in m i l d cases.
REFERENCES 1. Streeten D, Moses A, Miller M: Disorders of the neurohypophysis, in Isselbacher K, et ah Harrison's Principles of Internal Medicine, ed 9. New York, McGraw-Hill, 1980, p 1691-1694. 2. Weiner M, Epstein FH: Signs and symptoms of electrolyte disorders. Yale J Biol Med 43:76, 1970. 3. Bartter FC, Schwartz WB: The syndrome of inappropriate secretion of antidiuretic hormone. A m J Med 42:790-805, 1967. 4. Miller M, Moses AM: Drug-induced states of impaired.water secretion. Kidney lnt [Suppl] 10:9G 1976. 5. Weitzel WD, Shraberg D, Work J: Inappropriate ADH secretion: The role of drug rechallenge. Psychosomatics 21:771779, 1980. 6. Beckstrom D, Reding R, Cerletty J: Syndrome of inappropriate antidiuretic hormone secretion associated with amitriptyline administration,-(letter). JAMA 241:133, 1979. 7. Garson M: Syndrome of dilutional hyponatremia secondary to tricyclic antidepressant. Practitioner 222:4tl-412, 1979.
Annals of Emergency Medicine
8. Hamburger S, Langley H, Bowers G: The syndrome of inappropriate secretion of antidiuretic hormone associated with amitriptyline or trifluoperazine administration. J Kans Med Soc 81:469-470, 1980. 9. Luzecky M, Barmon K, Schuhz ER: The syndrome of inappropriate secretion of antidiuretic hormone associated with amitriptyline administration. South Med J 67:495-497, 1974. 10. Madhusoodanan S, Osnos R: Amitriptyline induced hyponatremia: A case report. Mt Sinai J Med 48:431-433, 1981. 11. Solammadevi SV: Inappropriate antidiuresis during amitriptyline therapy, (letter). South Med J 74:775-776, 1981. 12. Husband C, Mai FM, Carruthers G: Syndrome of inappropriate secretion of antidiuretic hormone in a patient treated with haloperidol. Can J Psychiatry 26:196197, 1981. 13. Kosten TR, Camp W: Inappropriate secretion of antidiuretic hormone in a patient receiving piperazine phenothiazines. Psychosomatics 21:354-355, 1980. 14. Peck V, Shenkman L: Haloperidolinduced syndrome of inappropriate secretion of antidiuretic hormone. Clin Pharmacol Ther 26:442-444, 1979. 15. Flegel KM, Cole CH: Inappropriate antidiuresis during carbamazepine treatment. Ann Intern Med 87:722-723, 1977. 16. Dhar SK, Ramos RR: Inappropriate antidiuresis during desipramine therapy, (letter). Arch Intern Med 138:1750-1751, 1978. 17. Amoxapine ( A s e n d i n ) - A new antidepressant. Med Lett 23:39-40, 1981.
710/87