BRIEF REPORTS
Brief reports of new clinical or laboratory observations, cases of unusual importance, and new developments in medical care will be considered for publication in this section. Manuscripts must be typed double-spaced. Text length must not exceed 750 words; no more than 10 references and one figure or table can be used. See "Information for Authors" on page 1-6 for form of references. Manuscripts should include an abstract of not over 100 words. Reports will be reviewed by consultants when, in the opinion of the editors, such review is needed. The Editor reserves the right to shorten reports and to make changes in style.
Formed Visual Hallucinations as Digitalis Toxicity BRUCE T. VOLPE, M.D.; and ROSEMARY SOAVE, M.D. Cornell University Medical Center; New York, New York
W H I L E the cardiac symptoms of digitalis excess are well known and their recognition is facilitated by data on the serum digitalis level, the noncardiac neurologic symptoms of digitalis toxicity may precede the arrhythmia and obscure the diagnosis (1, 2). We report the cases of three patients who had digitalis intoxication and an unusual central nervous system toxic manifestation, formed visual hallucinations. The lack of electrocardiographic clues and the failure to recognize that hallucinations may be associated with digitalis toxicity resulted in delayed diagnosis. The apparitions experienced by our patients were more complex than the scotomas, flashing geometric patterns, zigzags, or whorls of color previously described as visual manifestations of digitalis toxicity (3). Further, our patients did not have concurrent metabolic or neurologic disorders known to exacerbate or precipitate visual hallucinations (4, 5). A 68-year-old man was admitted for evaluation of repetitive formed visual hallucinations. For several days before admission he reported the intermittent and sudden appearance of butterflies, bird houses, and Confederate soldiers, all in appropriate size and color and without visual field preference. He also reported that some brown objects had an unusual yellow hue. He was an oriented, calmly conversant man without hemodynamic compromise who had been taking digoxin, quinidine, furosemide, and a potassium supplement. He had no focal neurologic or ophthalmologic abnormalities. His electrocardiogram revealed sinus bradycardia, rate 45/min, with a second-degree variable atrioventricular block unchanged over the past 2 years. His digoxin level at admission was 5.0 ng/mL (intoxication range, 2.3 + 1.6 ng/mL). Hallucinations persisted during the first few hospital days but resolved completely when digoxin was withheld, and the serum level fell to 1.7 ng/mL. He has had no recurrence of the hallucinations during the subsequent 12-month period, and his serum digoxin level has remained in the therapeutic range. A 66-year-old man was brought to the hospital because of confusion and disorientation. Two days before admission he experienced, without visual field preference, the appearance of friends who wore unusually bright colored clothes. A month before, his digoxin dose had been increased to 0.375 mg twice
daily to control congestive heart failure secondary to rheumatic heart disease. He also took furosemide and potassium supplement. Although he was actively hallucinating and, at times, disoriented, he was easily calmed and had no other focal neurologic or ophthalmologic deficit. His electrocardiogram, unchanged from previous tracings, revealed atrial fibrillation with a rate of 70/min and an old anteroseptal myocardial infarction. Admission serum digoxin level was 6.5 ng/mL. The drug was withdrawn, and his hallucinations ceased when his serum digoxin level fell to 2.0 ng/mL. An 82-year-old chronically demented woman was admitted to the hospital with a right olecranon fracture. She was actively hallucinating, noting that former friends as well as familiar household objects intermittently appeared at the foot of her bed. She took digoxin, furosemide, and a potassium supplement. She had no focal neurologic or ophthalmologic deficits. Electrocardiogram revealed atrial fibrillation at a rate of 80/ min and an old left bundle branch block. Her serum digoxin level was 2.7 ng/mL, and the drug was withdrawn. Although the hallucinations ceased when the digoxin level fell to 1.0 ng/ mL, she remained demented. In all three patients, thyroid, renal, and liver function, acid-base balance, arterial oxygen saturation, serum calcium, magnesium, and potassium were normal. There was no sepsis and no alcohol abuse. Computerized tomographic brain scans, electroencephalography, and cerebrospinal fluid analysis in each case did not contribute to the diagnosis. The wide spectrum of digitalis effects on the central nervous system ranges from fatigue and somnolence to coma, and from agitated delirium to psychosis (4-6). Perhaps the most frequent side effect is disordered vision, which usually includes scotomas and changes in color perception or acuity (7). True formed visual hallucinations have not been reported as an isolated symptom of digitalis intoxication. Formed visual hallucinations are uncommon phenomena usually associated with focal epileptic discharge, hallucinogenic drugs, infection, alcohol withdrawal, sensory deprivation, and psychosis (8). They contain elements that appear real, so that the patient may consider the hallucination as one of the possible perceptual choices among real stimuli. Our patients had neither signs to indicate focal brain disease nor symptoms of an associated dreamy or fearful state suggesting uncinate fits. Further, they did not suffer an exacerbation of an underlying illness, as reported in other patients who were hallucinating while digitalis toxic (4, 5). When serum digoxin levels decreased to therapeutic levels in all our patients, the formed visual hallucinations subsided and never recurred. Although there is evidence to suggest that the presence of digitalis in the central nervous system correlates with the cardiac (9) or gastrointestinal (10) toxic effects, the mechanism for the primary neurologic symptoms is unknown. Digitalis toxicity should be considered in the differential diagnosis of patients with formed visual hallucinations, even in the absence of well-recognized cardiac and gastrointestinal side effects. Brief Reports
Downloaded from https://annals.org by Karolinska Institute user on 01/18/2019
865
REFERENCES 1. S M I T H TW, H A B E R E. Digitalis: I. N Engl J Med.
1973;289:945-52.
2. D O E R I N G W, K O N I G E. Digitalis intoxication: specificity of clinical and electrocardiographic signs. In: B O D E M G, B E N G L O R HJ, eds. Cardiac
Glycosides. New York: Springer-Verlag; 1978:358-66. 3. CARROLL F D . Visual symptoms caused by digitalis. Am J Ophthalmol. 1945;28:373-6. 4. C H U R C H G, M A R R I O T T HJL. Digitalis delirium: a report on three cases. Circulation. 1959;20:549-53. 5. SHEAR M K , SACKS M. Digitalis delirium: psychiatric manifestations. Int J Psychiatry Med. 1977-1978;8:371-81. 6. LELY AH, VAN E N T E R CHJ. Non-cardiac symptoms of digitalis intoxication. Am Heart J. 1972;83:149-52. 7. R O B E R T S O N D M , H O L L E N H O R S T RW, C A L L A H A N JA. Ocular manifes-
tations of digitalis toxicity. Arch Ophthalmol. 1966;76:640-5. 8. L A N C E JW. Simple formed hallucinations confined to the area of specific visual field defect. Brain. 1976;99:719-34. 9. SOMBERG JC, S M I T H TW. Localization of the neurally mediated ar-
rhythmogenic properties of digitalis. Science. 1979;204:321-3. 10. BORISON HL, W A N G SC. Physiology and pharmacology of vomiting. Pharmacol
Rev.
1953;5:193-230.
© 1 9 7 9 American College of Physicians
8 6 6
December
1979 • Annals of Internal Medicine • Volume 91 • Number
Downloaded from https://annals.org by Karolinska Institute user on 01/18/2019
6
Brief reports of new clinical or laboratory observations, cases of unusual importance, and new developments in medical care will be considered for publication in this section. Manuscripts must be typed double-spaced. Text length must not exceed 750 words; no more than 10 references and one figure or table can be used. See "Information for Authors" on page 1-6 for form of references. Manuscripts should include an abstract of not over 100 words. Reports will be reviewed by consultants when, in the opinion of the editors, such review is needed. The Editor reserves the right to shorten reports and to make changes in style.
Formed Visual Hallucinations as Digitalis Toxicity BRUCE T. VOLPE, M.D.; and ROSEMARY SOAVE, M.D. Cornell University Medical Center; New York, New York
W H I L E the cardiac symptoms of digitalis excess are well known and their recognition is facilitated by data on the serum digitalis level, the noncardiac neurologic symptoms of digitalis toxicity may precede the arrhythmia and obscure the diagnosis (1, 2). We report the cases of three patients who had digitalis intoxication and an unusual central nervous system toxic manifestation, formed visual hallucinations. The lack of electrocardiographic clues and the failure to recognize that hallucinations may be associated with digitalis toxicity resulted in delayed diagnosis. The apparitions experienced by our patients were more complex than the scotomas, flashing geometric patterns, zigzags, or whorls of color previously described as visual manifestations of digitalis toxicity (3). Further, our patients did not have concurrent metabolic or neurologic disorders known to exacerbate or precipitate visual hallucinations (4, 5). A 68-year-old man was admitted for evaluation of repetitive formed visual hallucinations. For several days before admission he reported the intermittent and sudden appearance of butterflies, bird houses, and Confederate soldiers, all in appropriate size and color and without visual field preference. He also reported that some brown objects had an unusual yellow hue. He was an oriented, calmly conversant man without hemodynamic compromise who had been taking digoxin, quinidine, furosemide, and a potassium supplement. He had no focal neurologic or ophthalmologic abnormalities. His electrocardiogram revealed sinus bradycardia, rate 45/min, with a second-degree variable atrioventricular block unchanged over the past 2 years. His digoxin level at admission was 5.0 ng/mL (intoxication range, 2.3 + 1.6 ng/mL). Hallucinations persisted during the first few hospital days but resolved completely when digoxin was withheld, and the serum level fell to 1.7 ng/mL. He has had no recurrence of the hallucinations during the subsequent 12-month period, and his serum digoxin level has remained in the therapeutic range. A 66-year-old man was brought to the hospital because of confusion and disorientation. Two days before admission he experienced, without visual field preference, the appearance of friends who wore unusually bright colored clothes. A month before, his digoxin dose had been increased to 0.375 mg twice
daily to control congestive heart failure secondary to rheumatic heart disease. He also took furosemide and potassium supplement. Although he was actively hallucinating and, at times, disoriented, he was easily calmed and had no other focal neurologic or ophthalmologic deficit. His electrocardiogram, unchanged from previous tracings, revealed atrial fibrillation with a rate of 70/min and an old anteroseptal myocardial infarction. Admission serum digoxin level was 6.5 ng/mL. The drug was withdrawn, and his hallucinations ceased when his serum digoxin level fell to 2.0 ng/mL. An 82-year-old chronically demented woman was admitted to the hospital with a right olecranon fracture. She was actively hallucinating, noting that former friends as well as familiar household objects intermittently appeared at the foot of her bed. She took digoxin, furosemide, and a potassium supplement. She had no focal neurologic or ophthalmologic deficits. Electrocardiogram revealed atrial fibrillation at a rate of 80/ min and an old left bundle branch block. Her serum digoxin level was 2.7 ng/mL, and the drug was withdrawn. Although the hallucinations ceased when the digoxin level fell to 1.0 ng/ mL, she remained demented. In all three patients, thyroid, renal, and liver function, acid-base balance, arterial oxygen saturation, serum calcium, magnesium, and potassium were normal. There was no sepsis and no alcohol abuse. Computerized tomographic brain scans, electroencephalography, and cerebrospinal fluid analysis in each case did not contribute to the diagnosis. The wide spectrum of digitalis effects on the central nervous system ranges from fatigue and somnolence to coma, and from agitated delirium to psychosis (4-6). Perhaps the most frequent side effect is disordered vision, which usually includes scotomas and changes in color perception or acuity (7). True formed visual hallucinations have not been reported as an isolated symptom of digitalis intoxication. Formed visual hallucinations are uncommon phenomena usually associated with focal epileptic discharge, hallucinogenic drugs, infection, alcohol withdrawal, sensory deprivation, and psychosis (8). They contain elements that appear real, so that the patient may consider the hallucination as one of the possible perceptual choices among real stimuli. Our patients had neither signs to indicate focal brain disease nor symptoms of an associated dreamy or fearful state suggesting uncinate fits. Further, they did not suffer an exacerbation of an underlying illness, as reported in other patients who were hallucinating while digitalis toxic (4, 5). When serum digoxin levels decreased to therapeutic levels in all our patients, the formed visual hallucinations subsided and never recurred. Although there is evidence to suggest that the presence of digitalis in the central nervous system correlates with the cardiac (9) or gastrointestinal (10) toxic effects, the mechanism for the primary neurologic symptoms is unknown. Digitalis toxicity should be considered in the differential diagnosis of patients with formed visual hallucinations, even in the absence of well-recognized cardiac and gastrointestinal side effects. Brief Reports
Downloaded from https://annals.org by Karolinska Institute user on 01/18/2019
865
REFERENCES 1. S M I T H TW, H A B E R E. Digitalis: I. N Engl J Med.
1973;289:945-52.
2. D O E R I N G W, K O N I G E. Digitalis intoxication: specificity of clinical and electrocardiographic signs. In: B O D E M G, B E N G L O R HJ, eds. Cardiac
Glycosides. New York: Springer-Verlag; 1978:358-66. 3. CARROLL F D . Visual symptoms caused by digitalis. Am J Ophthalmol. 1945;28:373-6. 4. C H U R C H G, M A R R I O T T HJL. Digitalis delirium: a report on three cases. Circulation. 1959;20:549-53. 5. SHEAR M K , SACKS M. Digitalis delirium: psychiatric manifestations. Int J Psychiatry Med. 1977-1978;8:371-81. 6. LELY AH, VAN E N T E R CHJ. Non-cardiac symptoms of digitalis intoxication. Am Heart J. 1972;83:149-52. 7. R O B E R T S O N D M , H O L L E N H O R S T RW, C A L L A H A N JA. Ocular manifes-
tations of digitalis toxicity. Arch Ophthalmol. 1966;76:640-5. 8. L A N C E JW. Simple formed hallucinations confined to the area of specific visual field defect. Brain. 1976;99:719-34. 9. SOMBERG JC, S M I T H TW. Localization of the neurally mediated ar-
rhythmogenic properties of digitalis. Science. 1979;204:321-3. 10. BORISON HL, W A N G SC. Physiology and pharmacology of vomiting. Pharmacol
Rev.
1953;5:193-230.
© 1 9 7 9 American College of Physicians
8 6 6
December
1979 • Annals of Internal Medicine • Volume 91 • Number
Downloaded from https://annals.org by Karolinska Institute user on 01/18/2019
6
