Digitalis Toxicity Research Articles

Atrial fibrillation with Slow Ventricular response as a sign of Digoxin toxicity Secondary to Acute Renal failure.

Digoxin is a cardiac glycoside that has been used for centuries for atrial fibrillation (AFib) and congestive heart failure (CHF). Digoxin has a narrow therapeutic index with a potential for toxicity that can be life-threatening1-5. Toxicity can result from accidental or intentional overdose, renal failure, and/or hypokalemia. Cardiac manifestations of digoxin toxicity cause dysrhythmias of different types2,6. Bidirectional ventricular tachycardia is a specific dysrhythmia in the setting of digitalis toxicity, but AFib with slow ventricular response (SVR) is another digoxin toxicity-related dysrhythmia7. Here, we report AFib with SVR as a sign of digoxin toxicity secondary to acute renal failure (ARF).

Estimating the Concentration of Heavy Metals in Oleander/Pink and white Oleander Plants

Oleander is a large ornamental evergreen shrub that may grow 20–25 ft in height. During the summer months’ large clusters of white, pink, red, or yellow (yellow oleander) flowers appear at the ends of the branches. All parts of the plant contain cardiac glycosides. Oleander is a common source of serious plant poisoning. In South Asia, particularly Sri Lanka, also present in Libya desert and some house gardens with white and pink types, oleander has become a notorious method of suicide. Toxicity is largely characterized by gastrointestinal symptoms and cardiac abnormalities. Tachy or bradydysthythmias may be present in addition to slowed conduction and heart block. Hyperkalemia is common and correlates with severity of poisoning. A specific antidote—digoxin-specific fragment antigen-binding region (Fab region)- is available. In Mediterranean climates oleanders can be expected to bloom from April through October, with the heaviest bloom usually occurring between May and June. Free-flowering varieties like 'Petite Salmon' or 'Mont Blanc' require no period of rest and can flower continuously throughout the year if the weather remains warm. The exact nature of plant poisoning varies from region to region, but certain plants are almost ubiquitous in distribution and among these, Oleander is a garden plant that features in many homes. Incidents of poisoning from these plants are therefore not uncommon and may be the result of accidental exposure or deliberate, suicidal ingestion of the toxic parts. An attempt has been made to review the management principles with regard to toxicity of these plants and survey the literature in order to highlight current concepts in the treatment of poisoning resulting from both plants. Ingestion of its seeds results in a clinical picture similar to digoxin toxicity. It contains cardiac glycosides that are toxic to cardiac myocytes and autonomic system. Cardiac glycosides of oleander cause poisoning by inhibiting plasmalemmal Na+/K+-ATPase. Results: The poisoning effects of plant or their active alkaloids induced infiltration of cells with hemorrhage and sever negative changes in the lung, induce lesions, and infiltration of inflammatory cells into the portal spaces with scattered necrosis of hepatocytes in the liver, cardiac toxicity of the plant in the heart were included, induced varying degrees of hemorrhage, myocardial degeneration, and necrosis. It also induced arrhythmia, sinus bradycardia, and prolonged P-R interval in electrocardiographic records. Conclusions: The toxic effects of N. oleander are mostly related to its inhibitory effects on the Naþ-Kþ ATPase pump in the cellular membrane. However, the exact molecular mechanism involved in the toxicity of N. oleander is not clear.

Acute ellipsoid zone thickening: A sign of probable digoxin toxicity?

A 62-year-old gentleman presented with blurred vision in both eyes associated with excessive sleepiness and headache for 5 days. Optical coherence tomography (OCT) showed thickening of ellipsoid zone (EZ) with subtle separation from retinal pigment epithelium in both eyes. Patient was on digoxin 0.25 mg once daily for the past 2 years. As OCT was suggestive of photoceptor involvement, we sought an opinion from the cardiologist to consider withholding digoxin. Patient reported visual improvement at 1 week. At 6 months, OCT showed normalization of EZ. We propose that acute EZ thickening would be a sign of digoxin toxicity.

Thirty-day risk of digoxin toxicity among older adults co-prescribed trimethoprim-sulfamethoxazole versus amoxicillin: A population-based cohort study.

Trimethoprim-sulfamethoxazole (TMP-SMX) may increase digoxin concentration, a medication with a narrow therapeutic index. Small changes in digoxin concentration could predispose individuals to the risk of toxicity. To characterize the risk of digoxin toxicity in older adults taking digoxin following co-prescription of TMP-SMX compared with co-prescription of amoxicillin. Retrospective population-based cohort study in Ontario, Canada (2002-2020) using linked health care data. Participants comprised 47,961 older adults taking digoxin (58% women; median age 80 years [interquartile range 74-86]) who were newly treated with TMP-SMX (n = 10,273) compared with those newly treated with amoxicillin (n = 37,688). Co-prescription of TMP-SMX versus amoxicillin in older adults concurrently taking digoxin. The primary outcome was a hospital encounter (i.e., hospital admission or emergency department visit) with digoxin toxicity within 30 days of the antibiotic prescription. Inverse probability of treatment weighting on the propensity score was used to balance comparison groups on indicators of baseline health. Weighted risk ratios (RR) were obtained using modified Poisson regression and weighted risk differences (RD) using binomial regression. The number needed to harm (NNH) was calculated as 1/RD. A hospital encounter with digoxin toxicity occurred in 49/10,273 (0.48%) patients treated with TMP-SMX versus 32/37,688 (0.08%) in those treated with amoxicillin (weighted RR, 5.71 [95% confidence interval (CI), 3.19 to 10.24]; weighted RD, 0.39% [95% CI, 0.25% to 0.53%]; NNH 256 [95% CI, 233 to 400]). In older adults taking digoxin, the 30-day risk of a hospital encounter with digoxin toxicity was nearly 6 times higher in those co-prescribed TMP-SMX versus amoxicillin, although the absolute risk difference was low (0.4%). Physicians should prescribe an alternative antibiotic when clinically appropriate. If TMP-SMX must be co-prescribed with digoxin (if the benefit is believed to outweigh the risk), digoxin should be dose-reduced on an individual basis.

Not only Van Gogh: a case of BRASH syndrome with concomitant digoxin toxicity

BackgroundBradycardia, renal failure, atrioventricular (AV) node blocking, shock, and hyperkalemia syndrome is a potentially life-threatening clinical condition characterized by bradycardia, renal failure, atrioventricular (AV) node blocking, shock, and hyperkalemia. It constitutes a vicious circle in which the accumulation of pharmacologically active compounds and hyperkalemia lead to hemodynamic instability and heart failure.Case presentationA 66-year-old Caucasian female patient was admitted to the emergency department presenting with fatigue and bradycardia. Upon examination, the patient was found to be anuric and hypotensive. Laboratory investigations revealed metabolic acidosis and hyperkalemia. Clinical evaluation suggested signs of digoxin toxicity, with serum digoxin concentrations persistently elevated over several days. Despite the implementation of antikalemic measures, the patient’s condition remained refractory, necessitating renal dialysis and administration of digoxin immune fab.ConclusionBradycardia, renal failure, atrioventricular (AV) node blocking, shock, and hyperkalemia syndrome is a life-threatening condition that requires prompt management. It is important to also consider potential coexisting clinical manifestations indicative of intoxication from other pharmacological agents. Specifically, symptoms associated with the accumulation of drugs eliminated via the kidneys, such as digoxin. These manifestations may warrant targeted therapeutic measures.

Characterizing Utilization and Outcomes of Digoxin Immune Fab for Digoxin Toxicity.

Digoxin is a widely prescribed drug for congestive heart failure and atrial fibrillation. Digoxin has a narrow therapeutic index and toxicity can develop quite easily. Digoxin immune fab (DIF) is an effective treatment for toxicity, however there are limited studies characterizing its impact on clinical outcomes in real-world clinical practice. The aim of this study was to identify factors and healthcare outcomes associated with digoxin immune fab (DIF) treatment in patients with confirmed/suspected digoxin toxicity. An IRB-approved retrospective chart review of digoxin toxic patients (2011-2020) presenting at an academic healthcare system was conducted. Demographic and clinical data were collected. Patients were stratified by DIF treatment versus non-DIF treatment. DIF utilization patterns (appropriate, use when not indicated, or underutilized) were determined using pre-defined criteria. Severe digoxin toxicity was defined as having one or more of the following: mental status disturbances, antiarrhythmic therapy, acute renal impairment or dehydration, serum digoxin concentration (SDC) > 4ng/mL, or serum K+ > 5mEq/mL. Logistic multivariable regression analysis evaluated factors associated with DIF use. All statistical analyses were performed in R version 4.1. Data from 96 patients (non-DIF treated group = 49; DIF treated group = 47) were analyzed. DIF was used appropriately in 70 patients (73%), underutilized in 19 (20%), and administered to 7 (7%) patients when it was not indicated. Several clinical parameters differentiated the DIF from the non-DIF group (p<0.05) including higher mean SDC (3.41±1.63 vs 2.87±1.17), higher mean potassium (5.33±1.48 vs 4.55±0.87), more toxicity severity (85% vs 49%), and more likely to require cardiac pacing (26% vs 4%). Digoxin toxicity resolved sooner in the DIF group (coefficient - 0.702, 95% CI - 1.137 to - 0.267) (p<0.01) and they had shorter intensive care unit lengths of stay (12.4±20.3 vs 24.4±28.7 days; p=0.018). The all-cause mortality rate in patients appropriately managed with DIF therapy versus those patients where DIF was underutilized was 11% and 21%, respectively. Based on our study population, DIF therapy appears to be beneficial in limiting duration of toxicity and intensive care unit lengths of stay in digoxin toxic patients. Although DIF was appropriately utilized in most cases, there was a relatively high proportion of cases in which DIF treatment was either underutilized or not indicated.

Characteristics of digoxin toxicity attended in Spanish emergency departments according to type of poisoning and administration of digoxin antibodies: the DIGITOX study

Characteristics of digoxin toxicity attended in Spanish emergency departments according to type of poisoning and administration of digoxin antibodies: the DIGITOX study

Seven- and thirty-day mortality in digoxin poisoning: Results from the DIGITOX study

BackgroundDigoxin poisonings are relatively common and potentially fatal, requiring immediate therapeutic intervention, with special attention to the patient's hemodynamic status and the presence of electrocardiographic and electrolytic disturbances. ObjectiveTo identify factors associated with seven-day and thirty-day mortality in digoxin poisoning. Design, settings and participantsA retrospective, observational, multicenter study was conducted across 15 Hospital Emergency Departments (HED) in Spain. All patients over 18 years of age who presented to participating HEDs from 2015 to 2021 were included. The inclusion criteria encompassed individuals meeting the criteria for digoxin poisoning, whether acute or chronic. Outcomes measure and analysisTo identify independent factors associated with 7-day and 30-day mortality, a multivariate analysis was conducted. This analysis included variables of clinical significance, as well as those exhibiting a trend (p < 0.1) or significance in the bivariate analysis. Main findingsA total of 658 cases of digoxin poisoning were identified. Mortality rates were 4.5% (30 patients) at seven days and 11.1% (73 patients) at thirty days. Regarding 7-day mortality, the mean age of deceased patients was comparable to survivors (84.7 (8.9) vs 83.9 (7.9) years; p = ns). The multivariate analysis revealed that factors independently associated with 7-day mortality encompassed the extent of dependence assessed by the Barthel Index (BI 60–89 OR 0.28; 95% CI 0.10–0.77; p = 0.014 and BI>90 OR 0.22; 95% CI 0.08–0.63; p = 0.005), the identification of ventricular arrhythmias (OR 1.34; 95% CI 1.34–25.21; p = 0.019), and the presence of circulatory (OR 2.84; 95% CI 1.19–6.27; p = 0.019) and neurological manifestations (OR 2.67; 95% CI 1.13–6.27; p = 0.025). Factors independently associated with 30-day mortality encompassed extent of dependence (BI 60–89 OR 0.37; 95% CI 0.20–0.71; p = 0.003 and BI>90 OR 0.18; 95% CI 0.09–0.39; p < 0.001) and the identification of circulatory (OR 2.13; 95% CI 1.10–4.15; p = 0.025) and neurological manifestations (OR 2.39; 95% CI 1.25–3.89; p = 0.006). ConclusionsThe study identifies the degree of dependency assessed by the Barthel Index and the presence of cardiovascular and neurological symptoms as independent predictors of both 7-day and 30-day mortality. Additionally, the detection of ventricular arrhythmia is also an independent factor for 7-day mortality.

A case report on digoxin toxicity

Digoxin is an inotropic drug that is commonly prescribed in patient with heart related diseases. The effective dose of digoxin is 0.8-2.0 ng/ml beyond which digoxin causes toxic effects like visual dysfunction, irregular heartbeat, and cardiovascular collapse. Digoxin toxicity is caused due to increased automaticity and inotropy due to intracellular calcium and decreased dromotropy due to poisoning of sodium potassium transporter and AV nodal blockade. Digoxin toxicity should be assessed by continuous hemodynamic and cardiac monitoring including 12-lead electrocardiogram. There should be timely and immediate evaluation of electrolyte levels like potassium, calcium, serum creatinine and digoxin levels and prompt intensive care unit admission, if necessary. In this case study we studied a 43 old female patient prescribed with digoxin 0.25 mg, who had a medical history of congestive cardiac failure presented with symptoms of digoxin toxicity. The patient was assessed with electrocardiography (ECG) and managed by keeping digoxin on hold and effective patient counselling.

Treatment with Digoxin – is it a clinical challenge? A Retrospective Analysis of Hospitalizations due to Digoxin intoxication

Introduction and purpose: Digoxin, a cardiac glycoside derived from Digitalis lanata, has stood as a cornerstone in the treatment of various cardiovascular disorders for centuries. This study aims to delve into the demographic aspects, clinical characteristics, and outcomes associated with Digoxin poisoning. By drawing upon a dataset involving 22 patients hospitalized for Digoxin intoxication at the Clinical Department of Toxicology and Cardiology in Lublin, Poland, spanning from April 2014 to December 2023, our investigation seeks to provide an understanding of this issue.Brief description of the state of knowledge: Despite the efficacy of Digoxin, the potential risk of intoxication, especially in the elderly, necessitate a comprehensive examination. Age-related changes, such as declining renal function, electrolyte imbalances, comorbidities and polypharmacy affect how drugs like Digoxin work. The symptoms of Digoxin poisoning can manifest in various organ systems such as cardiovascular, gastrointestinal, nervous system, highlighting the importance of prompt recognition to seek medical attention.Methods and results: In our study, we analyzed data from 22 patients hospitalized due to Digoxin intoxication, focusing on demographic aspects, clinical characteristics and outcomes. The cases of Digoxin poisoning were categorized according to several factors, including the quantity and nature of substances consumed, the cause of intoxication, gender, age brackets, health conditions, peak serum Digoxin levels, length and outcomes of hospitalization.Conclusions: Our study provides insights into the characteristics and outcomes of patients hospitalized due to Digoxin intoxication. The findings underscore the association of Digoxin poisoning, and emphasize the importance of monitoring serum levels to prevent adverse outcomes. As Digoxin continues to be relevant in treating cardiovascular conditions, our study calls for careful management and monitoring.

Two Cases of Digoxin Intoxication: Insights into ECG Findings and Visual Disturbances

Digoxin, a widely prescribed cardiac glycoside, is known for its therapeutic benefits in managing various cardiac conditions. However, its narrow therapeutic index poses a significant risk of toxicity. We present two cases of digoxin intoxication with pathognomic electrocardiographic (ECG) findings and visual disturbances. The detailed analysis of ECG abnormalities and visual disturbances associated with digoxin toxicity will aid in prompt diagnosis and appropriate management, ultimately improving patient outcomes

Successful management of massive digoxin overdose using DIGIFab and therapeutic plasma exchange: a case report

BackgroundDespite the efficacy and safety of DIGIFab, it is relatively expensive and has limited availability. In addition, alternative interventions, such as therapeutic plasma exchange, may need to be considered in massive digoxin overdoses. Although few case reports describe its efficacy.Case presentationWe report a case of a 17-year-old white male patient brought by family members to our emergency department in Riyadh, Saudi Arabia. After intentionally ingesting 48 mg of digoxin tablets to commit suicide, the patient’s initial digoxin serum level was 8.04 ng/mL. The patient was resuscitated in the emergency department. After admission to the intensive care unit, the patient underwent therapeutic plasma exchange, because of insufficient DIGIFab doses. Afterward, the serum digoxin levels drastically decreased, and his symptoms reverted. The patient was successfully managed and discharged 7 days after admission.ConclusionDespite insufficient evidence and a limited number of case reports describing the use of extracorporeal treatment in digoxin overdose, we noted the significant impact of therapeutic plasma exchange on our patient. However, therapeutic plasma exchange’s use in routine treatment requires stronger evidence to confirm its benefits.

Severe Digoxin Toxicity in a Child Managed with Cholestyramine. A Case Report.

ABSTRACT Digoxin toxicity is a common problem in clinical practice because its therapeutic window is relatively narrow (from 0.5 to 2 ng/ml). The toxic effects occur at concentrations &amp;gt; 2.8 ng/ml and are mainly related to disturbances of cardiac function and of circulatory system as well as GI and CNS disturbances. We report a case of digoxin toxicity in a 2.5years old male child who accidently ingested 15 tablets of digoxin x 0.25mg. During his stay in pediatric ICU, typical symptoms of toxicity were observed. Digoxin-specific antibody (Fab) fragments have become the mainstay of treatment in severe digoxin toxicity. However, due to its high cost and limited availability, alternative measures are used to manage severe intoxications in countries like Pakistan, where Fab fragments are not available. Here we successfully treated severe digoxin intoxication with Cholestyramine.

Двунаправленная желудочковая тахикардия как осложнение бесконтрольного приема дигоксина: клиническое наблюдение

Cardiac glycosides (CG) are one of the first drug groups that have been used in the treatment of cardiac diseases for more than 200 years. Despite this, their use is still a matter of dispute and constant discussion within the medical community. It is known that CG increases the myocardial contractility, slows down conduction in the atrioventricular node, which helps delaying the heart rate and improves systemic hemodynamics in atrial fibrillation (AF) during heart failure. Despite this, CG has not been a first-line drug for a long time. Among CGs, digoxin is used as the most studied drug in many clinical studies. Taking digoxin is commonly associated with the development of adverse events such as bradycardia, ventricular extrasystole, nausea, vomiting. One of the most dangerous side effects of CG is considered to be a pro-arrhythmogenic effect, in particular, their ability to provoke ventricular tachycardia. The authors present a case study of rare bidirectional ventricular tachycardia in a 78-year-old female patient with a persistent AF during long-term uncontrolled digoxin intake. Analyzing this case, the authors conclude that more careful follow-up of long-term digoxin intake is necessary to exclude the development of its side effects. KEYWORDS: case study, bidirectional ventricular tachycardia, atrial fibrillation, cardiac glycosides, digitalis toxicity. FOR CITATION: Peterburgsky D.V., Sinitsyn E.A., Smolyakova E.V., Zykov K.A. Bidirectional ventricular tachycardia as a complication of uncontrolled digoxin intake: case report. Russian Medical Inquiry. 2024;8(7):386–390 (in Russ.). DOI: 10.32364/2587-6821-2024-8-7-2.

Digoxin‐induced retinal toxicity after acute kidney injury in a patient with dilated cardiomyopathy: A case report

Aims/Purpose: We would like to report a case of digoxin‐induced retinal toxicity.Methods: Observational case report. Clinical follow‐up was performed using optical coherence tomography and electroretinography.Results: A 50‐year‐old female patient was referred to our clinic with symptoms of blurred vision and a whitening of the central visual field. She had no prior ophthalmic history but had underlying diseases including hypertension, hyperlipidaemia, dilated cardiomyopathy, systemic lupus erythematosus and chronic kidney disease. She had been admitted to the department of nephrology due to acute renal impairment, presenting with flank pain and oliguria. At the initial examination, her best‐corrected visual acuity was 0.5 in the right eye and 0.4 in the left eye. The Ishihara colour vision test revealed 3/17 and 1/17 in the right and left eye, respectively. Optical coherence tomography showed blurring and thickening of the ellipsoid zone in both eyes. Electroretinography demonstrated decreased cone cell function. She had been taking digoxin 0.125 mg for dilated cardiomyopathy for the past 2 years. Following the onset of acute renal impairment, her serum digoxin level was found to be 2.95 ng/mL, more than twice the normal range [0.6–1.2]. Suspecting digoxin intoxication, we consulted with her cardiologist and decided to discontinue digoxin. 3 weeks after discontinuing the medication, she reported improvement in the whitening of central visual field. Her best‐corrected visual acuity improved to 0.7 in the right eye and 0.6 in the left eye, and the Ishihara colour vision test showed 16/17 in both eyes. OCT demonstrated normalization of the ellipsoid zone thickness, and ERG showed ongoing recovery of cone cell function.Conclusions: Digoxin toxicity is known to result in visual disturbances—including decreased visual acuity, blurry vision and central scotoma with altered colour perception—caused by direct dysfunction of photoreceptors. Symptoms are gradually recovered within days to months after discontinuation of the medication. When facing visual problems in a patient with comorbidities, it is important to elicit a complete history, with all drug and detailed complaints, and to include a drug adverse effect. If a drug intoxication was suspected, medical consultations should be obtained.

P Glycoprotein Mediated Drug Interaction between Digoxin and Orange Juice- Exploratory Study by In-vitro Approach

P.gp is an efflux transporter that plays a vital role in drug transportation. Aim: This exploratory study is aimed to find the P-glycoprotein (P-gp) mediated drug interaction between digoxin and orange juice, conducted for a period of six months. The 3D structure of the human P-gp was predicted from the peptide by molecular threading using default settings. The structural analysis and verification server and the PDB were used to assess the stereo-chemical quality of these structures. The molecular structure of P-gp in a transport cycle has been investigated using a variety of methods. Molecular docking has been performed to predict the highest binding affinity to P gp with ligands of orange juice and ligands of ketoconazole. In 50% ethyl acetate extract of orange juice was prepared and a transcellular transport study was done using MDR1 transfectants and MRP2 transfectants LLC-PK1, LLC-GAS-COL150, LLC-pCI and LLC-MRP cells grown in M199 medium supplemented with 10% fetal calf serum at 37℃ in a humidified atmosphere of 5% CO2/95% air. The minimum inhibitory concentration is found to be 125 mcg/mL. Hence, the loading concentration along with orange juice is found to be 24.562 mcg/mL and the concentration less than that is found with poor sensitivity. Whereas the concentration above 125 mcg/mL loaded with orange juice is found to inhibit P-gp. The absorbance of orange juice and digoxin was measured at 470 nm. Since digoxin is not sensitive to orange juice beyond the concentration of 125 mcg/mL, it is considered as the MIC. Hence orange juice is a moderate p-gp Inhibitor and it escalates the serum digoxin toxicity. Orange juice is inhibiting the P-gp which increases the serum toxicity levels of digoxin.

Safety profile of intravenous digoxin in Chinese patients with acute heart failure with reduced ejection fraction: a small-scale prospective cohort study.

Background: Adverse effects of intravenous digoxin vary from patients and disease status, which should be closely monitored. Aims: To explore the safety profile of intravenous digoxin in acute heart failure with reduced ejection fraction (HFrEF) among Chinese patients. Methods: A clinical prospective, single-center, single-arm, open-label exploratory clinical trial was performed in patients with acute HFrEF at Wuhan Asia Heart Hospital. A fixed dose of 0.5mg digoxin was used intravenously once per day for 3days. The normalized dosage of digoxin (NDD), toxic serum digoxin concentration (SDC), and adverse reactions of intravenous digoxin were recorded. Results: A total of 40 patients were recruited in the study. The SDC increased from 1.03 ± 0.34ng/mL to 1.95 ± 0.52ng/mL during treatment. 50% (20/40) patients reached a toxic SDC of 2.0ng/mL, and toxic effects were seen in 30% (12/40) patients. Estimated glomerular filtration rate (eGFR) < 60mL/min [HR: 5.269; 95% CI: 1.905-14.575, p = 0.001], NDD ≥7μg/kg [HR: 3.028; 95% CI: 1.119-8.194, p = 0.029], and ischemic cardiomyopathy [HR: 2.658; 95% CI: 1.025-6.894, p = 0.044] were independent risk factors for toxic SDC. Toxic SDC was effectively identified [area under the receiver operating characteristic (ROC) curve = 0.85, p < 0.001] using this model, and patients would have a higher risk of toxicity with more risk factors. Conclusion: Intravenous digoxin of 0.5mg was safe and effective for initial dose but not suitable for maintenance treatment in Chinese patients with acute HFrEF. Patients who had lower eGFR, received higher NDD, and had ischemic cardiomyopathy should be closely monitored to avoid digoxin toxicity.

Digoxin-specific antibodies: anovel dosing strategy.

Digoxin-specific antibodies (digoxin-Fabs) are of value in the treatment of astrongly suspected or aknown, potentially life-threatening digoxin toxicity. These antibodies are not registered for use in Europe; therefore Dutch hospital pharmacies are not allowed to keep them in stock. In the Netherlands, digoxin-Fabs are stored in anational calamity stock of emergency medicines at the National Institute for Public Health and the Environment. In the case of amedical emergency, digoxin-Fabs are available after contact with the Dutch Poisons Information Centre. Recent studies have shown that the dose of digoxin-Fabs required to effectively treat digoxin toxicity is lower than previously thought. In this article, we present the adjusted digoxin-Fab dosing strategy currently recommended by the Dutch Poisons Information Centre ( www.vergiftigingen.info ). This new dose titration strategy is safe and effective and has acost-saving side-effect.

Diagnosis and practical management of digoxin toxicity: a narrative review and consensus.

There are currently no universally accepted guidelines for the management of digoxin toxicity. In the absence of clinical practice guidelines, a set of consensus recommendations for management of digoxin toxicity in the clinical setting were developed through a modified Delphi approach. The recommendations highlight the importance of early recognition of signs of potentially life-threatening toxicity that requires immediate treatment with digoxin-specific antibodies. The consensus identifies a straightforward approach to dosing immune antibody fragments according to the presence or absence of signs of life-threatening toxicity. Supportive measures and management of specific signs of toxicity are also covered.

Development and validation of a risk prediction nomogram for serious arrhythmias in acute digoxin toxicity among pediatrics: A multicenter study

Digoxin is a cardiac glycoside obtained from the leaves of the foxglove plant, Digitalis lanata. Several studies have described the safety of digoxin including various life-threatening events, notably cardiac arrhythmias. Early identification of high-risk patients and subsequent initiation of the utmost medical care are associated with a better prognosis. The assessment of serum digoxin levels, which is not always convenient, is the only tool used to evaluate the severity of digoxin exposure. However, the feasibility of this tool, particularly in resource-restricted countries, remains unclear. Therefore, the current study aimed to establish and validate a feasible alternative tool, a bedside nomogram, to identify pediatric patients diagnosed with acute digoxin intoxication who are at risk of developing serious arrhythmias. This was a two-phase, multicenter, retrospective study. The prevalence of serious arrhythmias was approximately 17%. Patients diagnosed with serious arrhythmias showed significantly higher serum digoxin, random blood glucose, and potassium levels but lower sodium, magnesium, and hemoglobin levels. Serious arrhythmias were associated with significantly lower P-R intervals, shorter QTc intervals, and more frequent digoxin effects (p < 0.05). The proposed nomogram showed that combining age and initial random blood glucose, sodium, and potassium levels could predict the future incidence of serious arrhythmia with an accuracy of 96.2% (sensitivity = 94.4%, specificity = 96.5%), an area under the curve (AUC) of 0.977, and p < 0.001. Validation of the proposed nomogram yielded an AUC for the nomogram probability of approximately 81%, and the AUC for the predicted probability using the developed model was 98.3%, indicating that both the validated model and the developed nomogram were significant predictors of serious arrhythmia. The utility of using the four-factor nomogram to determine the risk of serious arrhythmia in children exposed to an overdose of digoxin is comparable, if not superior, to the serum digoxin level.