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DOI: 10.1055/s-0035-1567858
Junctional Bradycardia as Early Sign of Digoxin Toxicity in a Premature Infant with Congestive Heart Failure due to a Left to Right Shunt
Publication History
29 July 2015
06 October 2015
Publication Date:
20 November 2015 (online)
![](https://www.thieme-connect.de/media/ajpr/201601/lookinside/thumbnails/10-1055-s-0035-1567858_150058-1.jpg)
Abstract
Introduction Congestive heart failure due to left to right cardiac shunt is usually managed medically with diuretics, angiotensin converting enzyme inhibitors, and, in some cases, with the addition of digoxin.
Case We report a 31-week gestation premature male infant who did not respond to such treatment and developed hyperaldosteronism and severe hypokalemia secondary to activation of the renin angiotensin aldosterone system. The hypokalemia was not responsive to intravenous KCL supplementation and induced digoxin toxicity despite a relatively normal digoxin level. The earliest signs of digoxin toxicity in the patient were junctional rhythm and bradycardia. The discontinuation of digoxin and the administration of digoxin specific immunoglobulin fragments (Fab) reversed those changes. The addition of spironolactone (an aldosterone antagonist) had a dramatic effect, resulting in clinical improvement of the patient coupled with normalization of Q4 serum and urine electrolytes.
Conclusion Serum Digoxin level alone may fail as an independent guide in the diagnosis of digoxin toxicity when hypokalemia is present. In premature infants with congestive heart failure and hypokalemia, addition of an aldosterone antagonist should be considered.
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References
- 1 Borlaug BA, Paulus WJ. Heart failure with preserved ejection fraction: pathophysiology, diagnosis, and treatment. Eur Heart J 2011; 32 (6) 670-679
- 2 Friedman WF. The intrinsic physiologic properties of the developing heart. Prog Cardiovasc Dis 1972; 15 (1) 87-111
- 3 Tait JF, Little B, Tait SA, Flood C, Bougas J. Splanchnic extraction and clearance of aldosterone in subjects with minimal and marked cardiac dysfunction. J Clin Endocrinol Metab 1965; 25: 219-228
- 4 Lelievre LG, Lechat P. Mechanisms, manifestations and management of digoxin toxicity. Heart Metab 2007; 35: 9-11
- 5 Gheorghiade M, Adams Jr KF, Colucci WS. Digoxin in the management of cardiovascular disorders. Circulation 2004; 109 (24) 2959-2964
- 6 Wang W, Chen JS, Zucker IH. Carotid sinus baroreceptor sensitivity in experimental heart failure. Circulation 1990; 81 (6) 1959-1966
- 7 Smith TW, Antman EM, Friedman PL, Blatt CM, Marsh JD. Digitalis glycosides: mechanisms and manifestations of toxicity. Part I. Prog Cardiovasc Dis 1984; 26 (5) 413-458
- 8 Park MK. Use of digoxin in infants and children, with specific emphasis on dosage. J Pediatr 1986; 108 (6) 871-877
- 9 Bhatia SJ. Digitalis toxicity—turning over a new leaf?. West J Med 1986; 145 (1) 74-82
- 10 Sundar S, Burma DP, Vaish SK. Digoxin toxicity and electrolytes: a correlative study. Acta Cardiol 1983; 38 (2) 115-123
- 11 Ma G, Brady WJ, Pollack M, Chan TC. Electrocardiographic manifestations: digitalis toxicity. J Emerg Med 2001; 20 (2) 145-152
- 12 Felicilda-Reynaldo RF. Cardiac glycosides, digoxin toxicity, and the antidote. Medsurg Nurs 2013; 22 (4) 258-261