Monitoring Digoxin TherapyTHE USE OF PLASMA DIGOXIN CONCENTRATION MEASUREMENTS IN THE DIAGNOSIS OF DIGOXIN TOXICITY

QJM ◽  
1978 ◽  
1997 ◽  
Vol 16 (12) ◽  
pp. 733-735 ◽  
Author(s):  
Julian AJH Critchley ◽  
Lester AH Critchley

1 Digoxin toxicity can result from overdose or iatrogenic causes, especially if renal function is impaired. 2 We present a case of digoxin toxicity presenting with severe bradycardia and hypotension in a 66 year old man with chronic renal failure. Regular haemodia lysis had, as predicted, failed to reduce his plasma digoxin concentration. Digoxin specific antibody fragments (Fab) were not readily available and their use was probably inappropriate as they are normally renally eliminated. 3 The patient was successfully treated by two prolonged courses of intestinal dialysis with repeated doses of activated charcoal over 48 and 72 h and totaling 400 g and 600 g, respectively. However, the patient found the activated charcoal extremely unpalatable. 4 Multiple dose activated charcoal intestinal dialysis (MDACID) has been recently advocated for use in a wide range of poisonings. The technique takes advantage of the large surface area of the small intestine to eliminate drugs and metabolites, over several days if necessary. The pharmacokinetics of digoxin toxicity in chronic renal failure make intest inal dialysis an appropriate method of treatment but the realisation of the true potential of this technique awaits a more palatable absorbent or formulation.


1972 ◽  
Vol 10 (1) ◽  
pp. 1.2-3

Digoxin toxicity is a relatively common problem.1 It occurs often in the elderly, in patients with renal failure and in those with hypokalaemia; in all these the diagnosis is particularly difficult as many of the indications of toxicity, such as anorexia, nausea, vomiting and most of the arrhythmias are apt to be caused by the underlying disease. The problem can be resolved in normokalaemic patients by knowing the plasma digoxin concentration, for in these patients there is a good correlation between the concentration of digoxin in the plasma and the development of therapeutic or toxic effects.


Author(s):  
B. F. Johnson ◽  
D. J. Chapple ◽  
R. Hughes ◽  
J. LaBrooy ◽  
I. Smith

1997 ◽  
Vol 31 (7-8) ◽  
pp. 864-866 ◽  
Author(s):  
James J. Nawarskas ◽  
David M. McCarthy ◽  
Sarah A. Spinier

OBJECTIVE: To report a case of digoxin toxicity thought to be secondary to clarithromycin therapy. CASE SUMMARY: A 78-year-old white woman with congestive heart failure taking digoxin 0.25 mg po qd presented to our hospital with nausea, vomiting, and diarrhea. She had taken clarithromycin 500 mg po bid for 3 days, and a serum digoxin concentration obtained the day of admission was 4.4 μg/L. An electrocardiogram (ECG) done on admission revealed ST segment changes consistent with digoxin effect and later asymptomatic, nonsustained ventricular tachycardia (NSVT). Clarithromycin was discontinued and digoxin was withheld at admission, resulting in the resolution of symptoms, ECG abnormalities, and NSVT on day 3 of hospitalization. On day 5 her serum digoxin concentration was 1.5 μg/L and digoxin therapy was reinstituted at a dose of 0.125 mg/d po. DISCUSSION: This is the fourth published case implicating clarithromycin as the cause of digoxin toxicity. This interaction is most likely due to clarithromycin eradication of digoxinmetabolizing gut flora, thereby increasing digoxin bioavailability. CONCLUSIONS: Approximately 10% of patients are thought to be extensive presystemic metabolizers of digoxin and may therefore be most susceptible to a drug interaction with clarithromycin. Serum digoxin concentrations in such patients should be monitored closely during clarithromycin therapy.


2021 ◽  
pp. 033-037
Author(s):  
Eslami Vahid ◽  
Mortezapour Fatemeh ◽  
Samavat Shiva ◽  
Ziae Shadi ◽  
Gheymati Azin

2009 ◽  
Vol 218 (2) ◽  
pp. 229-232 ◽  
Author(s):  
KNUD ERIK PEDERSEN ◽  
JAN LYSGAARD MADSEN ◽  
NIELS ANDERS KLITGAARD ◽  
KAREN KJAER ◽  
STEFFEN HVIDT

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