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Spironolactone-Associated Hyponatremic Coma
Author(s) -
Michael M. Hirschl,
Dan Seidler,
Anton N. Laggner
Publication year - 1994
Publication title -
˜the œnephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000188036
Subject(s) - icon , spironolactone , citation , medicine , vetting , library science , computer science , heart failure , computer security , programming language
Dr. Michael M. Hirschl, Department of Emergency Medicine, New General Hospital, Währinger Gürtel 18-20, A-1090 Vienna (Austria) Admission Dear Sir, Hyponatremia is the most common electrolyte abnormality observed in a general hospitalized population, seen in about 2% of patients [1]. Common causes of hyponatremia are the syndrome of inappropriate secretion of antidiuretic hormone, water intoxication, advanced renal failure, nephrotic syndrome, congestive heart failure, liver cirrhosis, diarrhea, excessive vomiting and therapy with thiazide diuretica [2]. We present an unusual causes of a hyponatremic coma associated with the use of spironolactone. Case report: A 93-year-old woman presented to the emergency department with coma of unknown origin. Prior to admission the patient had had severe diarrhea for the last 48 h with 10-15 watery stools. At 11:00 h the patient was found by a nurse lying on the floor and did not respond to painful stimuli. Her last medication included spironolactone (200 mg/Aldactone; Boehringer) and oxaze-pam (10 mg/Adumbron; Bender). On presentation the patient was comatose, spontaneously breathing and hemodynamically stable (RR 150/45 mm Hg). Physical status established no cardiac murmur, normal vesicular breathing and no peripheral edema. Neurological examination revealed a compromised alertness and a severe reduced response to painful stimuli. Pupillary reaction was delayed but without differences between both sides as well as after painful stimuli all four extremities were moved without differences. According to the neurological status a focal cerebral lesion seemed rather unlikely. Chest X-ray showed no signs of edema. Laboratory data demonstrated a severe hyponatremia with a serum sodium of 104 mmol/l. Urinalysis revealed a sodium of 150 mmol/l, potassium of 22 mmol/l and an osmolarity of 360 mosm/1. The urine volume was 1,600 ml/ 24 h. On admission, blood samples were taken to determine thyroid and adrenal hormones. According to the high urine sodium level combined with a severe hyponatremia, a

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