Serum digoxin concentrations and clinical signs and symptoms of digoxin toxicity in the paediatric population

2015 ◽  
Vol 26 (3) ◽  
pp. 493-498 ◽  
Author(s):  
Brady S. Moffett ◽  
April Garner ◽  
Troy Zapata ◽  
Jeffrey Orcutt ◽  
Mary Niu ◽  
...  

AbstractBackgroundSerum digoxin levels have limited utility for determining digoxin toxicity in adults. Paediatric data assessing the utility of monitoring serum digoxin concentration are scarce. We sought to determine whether serum digoxin concentrations are associated with signs and symptoms of digoxin toxicity in children.MethodsWe carried out a retrospective review of patients <19 years of age who received digoxin and had serum digoxin concentrations assessed between January, 2007 and June, 2013. Data collection included patient demographics, digoxin indication, serum digoxin concentrations, signs and symptoms of digoxin toxicity, electrocardiograms, and co-morbidities. Reviewers performing chart review and electrocardiogram analysis were blinded to digoxin levels. Descriptive statistical methods were used and comparisons were made between patients with and without toxic serum digoxin concentrations (>2 ng/ml).ResultsThere were 87 patients who met study criteria (male 46%, mean age 8.4 years). CHD was present in 67.8% and electrocardiograms were performed in 72.4% of the patients. The most common indication for digoxin toxicity was heart failure symptoms (61.5%). Toxic serum digoxin concentrations were present in 6.9% of patients (mean 2.6 ng/ml). Symptoms associated with digoxin toxicity occurred in 48.4%, with nausea/vomiting as the most common symptom (36.4%), followed by tachycardia (29.5%). Compared with those without toxic serum digoxin concentrations, significantly more patients with toxic serum digoxin concentrations were female (p=0.02). The presence of electrocardiogram abnormalities and/or signs and symptoms of digoxin toxicity was not significantly different between patients with and without serum digoxin concentrations (p>0.05).ConclusionSerum digoxin concentrations in children are not strongly associated with signs and symptoms of digoxin toxicity.

1994 ◽  
Vol 10 (6) ◽  
pp. 246-249
Author(s):  
Augustine S. Aruna ◽  
Sandra G. Jue

Objective: To report a case of digoxin immune Fab (DIF) administration following an unexplained increase in serum digoxin concentration in an asymptomatic patient with chronic renal failure. Case Summary: A 70-year-old man presented to the hospital with congestive heart failure, atrial fibrillation, chronic renal failure, and suspected digoxin toxicity. By day 3, he developed a more stable cardiac rhythm with nodal beats. His last known digoxin dose was 12 hours prior to admission. No explanation for an elevated serum digoxin concentration 48 hours after admission could be found. Despite absence of other signs of digoxin toxicity, DIF 80 mg iv was administered, and was immediately followed by 40 mg. Discussion: This case illustrates that elevated digoxin concentrations may be observed in patients with renal failure. These may not be true high concentrations because of the following potential factors: (1) the presence of digoxin-like factors, (2) increased biotransformation of digoxin, and (3) accumulation of metabolites that interfere with the assay. Digoxin metabolites are known to cross-react with the antibodies in commonly used digoxin immunoassays, and may be inappropriately interpreted to signal digoxin toxicity. Both the accuracy and reliability of digoxin immunoassay techniques have been questioned or challenged over the years. It is difficult to determine whether a reported toxic serum digoxin concentration represents the true concentration or cross-reactivity between digoxin metabolites and antibodies used in most digoxin immunoassays. Data Sources: Data collection sources included retrospective review of patient medical records, personal contact with one of the physicians involved in rendering patient care for interpretation of the electrocardiogram changes, clinical symptoms and rationale for DIF administration, and contact with the immunoassay technologist, who indicated that the fluorescence polarization immunoassay technique was used for analysis of digoxin concentrations. The medical literature then was reviewed. Conclusions: DIF should be reserved for use in symptomatic patients. Elevated digoxin concentrations must be evaluated for various factors that can cause falsely elevated values. Clinical signs and symptoms are critical in making the decision to use Fab. Antidotal measures should be based on correlation of patient symptoms with serum digoxin concentrations.


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.


2015 ◽  
Vol 10 (4) ◽  
pp. 342-347
Author(s):  
Adriana Sarah NICA ◽  
◽  
Gilda MOLOGHIANU ◽  
Roxana NARTEA ◽  
Mariana-Isabela CONSTANTINOVICI ◽  
...  

Painful hand of aged people is a very common symptom but is often disregarded in comparaison with other clinical signs and symptoms analyzed in these patients. When is reported, are rarely taken into account the multiple pathophysiological and clinical aspects of aging that characterize also the hand. Pain and all these other signs induce unexpected aspects of dysfunctions, from functional impairment to disability. Our aim was to present a review of the most common situations related to painful hand in elderly patients, especially in rheumatological and posttraumatic context. This paper is an update of the most common situations in older patients, that often neglect their distal upper limb in a context of polipathology or in a problematically family and social environment. Also are presented the associated functional consequences and the main therapeutic objectives related to pathophysiological, clinical and functional outcomes.


2019 ◽  
Vol 61 (2) ◽  
pp. 244 ◽  
Author(s):  
Mehmet Mutlu ◽  
Yakup Aslan ◽  
Şebnem Kader ◽  
Filiz Aktürk-Acar ◽  
Embiya Dilber

CHD remains one of the largest causes of premature death in the UK. Angina is the most common symptom of CHD. It is usually described as a central, retrosternal pain or ache that is crushing or choking in nature. Pain may radiate down the left arm and/or up into the neck and is often accompanied by shortness of breath and sweating. Some patients may describe it as chest discomfort. The presentation of CHD, however, covers a broad spectrum of clinical signs and symptoms that vary in severity. An individual may be asymptomatic despite disease within the coronary arteries; may present with gradually worsening symptoms of angina; or the first presentation may be death following an acute MI. The progress of the disease is variable, depending on the individual’s risk factors and the coronary arteries affected. Terminology varies but, generally speaking, CHD is divided into two subtypes: stable angina—with reversible ischaemia, and acute coronary syndromes—which is an umbrella term that includes unstable angina and MI. This chapter outlines the pathophysiology and clinical management of stable angina.


Although rates of premature death from coronary heart disease (CHD) have fallen 80% over the past 40 years, it is still a significant cause of premature death in the UK. Angina is the most common symptom of CHD. It is usually described as a central, retrosternal pain or ache that is crushing or choking in nature. Pain may radiate down the left arm and/or up into the neck and is often accompanied by shortness of breath (SOB) and sweating. Some patients may describe it as chest discomfort. The presentation of CHD, however, covers a broad spectrum of clinical signs and symptoms that vary in severity. An individual may be asymptomatic despite disease within the coronary arteries; may present with gradually worsening symptoms of angina; or the first presentation may be death following an acute myocardial infarction (MI). This chapter outlines the pathophysiology and clinical management of stable angina.


Geriatrics ◽  
2021 ◽  
Vol 6 (1) ◽  
pp. 5
Author(s):  
Donatella Rita Petretto ◽  
Gian Pietro Carrogu ◽  
Luca Gaviano ◽  
Lorenzo Pili ◽  
Roberto Pili

Over 100 years ago, Alois Alzheimer presented the clinical signs and symptoms of what has been later called “Alzheimer Dementia” in a young woman whose name was Augustine Deter [...]


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