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Drug management
Published in Gregory YH Lip, Atrial Fibrillation in Practice, 2020
Extracardiac manifestations of digoxin toxicity can include nausea, vomiting, visual disturbances such as yellow vision (xanthopsia), visual hallucinations and general confusion. Digitoxicity could induce any kind of cardiac arrhythmias, ranging from varying degrees of atrioventricular block, inhibition of the sino-atrial node, ventricular extrasystoles to ventricular tachycardia or fibrillation. Of the different arrhythmias seen in digitoxicity, paroxysmal atrial tachycardia with block is a characteristic feature.
Toxicology
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Chronic digoxin toxicity occurs particularly in the elderly and may be precipitated by renal impairment, hypokalaemia, hypercalcaemia and drugs such as amiodarone and quinidine. Clinical manifestations include: Nausea, vomiting, diarrhoea.Sedation, confusion, delirium.Visual disturbances, such as yellow haloes (xanthopsia).Cardiac automaticity and a wide range of ventricular and supraventricular arrhythmias.
Cardiology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Digoxin toxicity – features:1 Arrhythmias (especially AV block).2 Nausea, vomiting, diarrhoea.3 Headache; dizziness.4 Seizures.5 Xanthopsia (yellow vision).6 Skin reactions.7 Impotence.
Erythropsia and Chromatopsia: Case Study and Brief Review
Published in Neuro-Ophthalmology, 2021
Michael S. Vaphiades, Brendan D. Grondines, Christine A. Curcio
Chromatopsia is defined as the perceived increase in environmental hue, much the opposite of dyschromatopsia or achromatopsia.3 It may result from changes to normal photoreceptor cell distribution, their ability to communicate with post-synaptic neurons, or changes to the post-synaptic neurons themselves. The most common causes of acquired chromatopsia are drug effects. There are hundreds of drugs that may induce chromatopsia.8,9 The more familiar ones to clinicians include xanthopsia or yellow hue, commonly caused by digoxin, in therapeutic levels, which may also cause disturbance of colour discrimination more specifically tritanopia (blue-yellow colour blindness) and non-specific loss of colour discrimination.10 Cyanopsia, or a bluish tinge is commonly due to the inhibition of cone phosphodiesterase (PDE), a group of enzymes whose prominent function is regulating cyclic guanosine monophosphate levels and therefore rod and cone light response properties.11 Because of the presence of PDE5 in choroidal and retinal vessels, these medications increase choroidal blood flow and cause vasodilation of the retinal vasculature.12 Other than drug effects, chromatopsia also occurs after cataract extraction, retinal diseases, and medical illnesses like jaundice.13
Bibliometric profile of global scientific research on digoxin toxicity (1849–2015)
Published in Drug and Chemical Toxicology, 2020
Sa'ed H. Zyoud, William S. Waring, Samah W. Al-Jabi, Waleed M. Sweileh
Digoxin has a narrow therapeutic range, typically 1–2 micrograms per liter, and therapeutic drug monitoring may be helpful. Adverse effects include bradycardia, severe nausea and vomiting, diarrhea, headache, anorexia, and malaise. Central nervous system toxicity gives rise to distorted color perception, and a yellow visual halo (xanthopsia) has been described as manifestations. Cardiovascular adverse effects include bradycardia and hypotension. Acute toxic features include hyperkalaemia, severe bradycardia, prolongation of the PR and QRS intervals on an electrocardiograph, and atrio-ventricular block. In severe poisoning, there may be ventricular tachycardia or ventricular fibrillation, particularly in patients with electrolyte disturbances or existing heart disease (Thanacoody and Waring 2008, Palatnick and Jelic 2014). Digoxin toxicity should be considered in patients that present to the Emergency Department with unexplained severe nausea or electrocardiographic abnormalities (Limon et al. 2016).
Novel methods of self-poisoning: repeated cardenolide poisoning after accessing Cerbera odollam seeds via the internet
Published in Clinical Toxicology, 2018
Henry Fok, Punitha Victor, Sally Bradberry, Michael Eddleston
Two hours after ingestion of the seeds, she developed nausea, marked retching and recurrent vomiting. She also reported central chest and upper abdominal pain. There was no xanthopsia. On admission, she had a heart rate of 66 beats per minute and a blood pressure of 155/91 mmHg. Cardiac monitoring recorded a heart rate varying between 63 and 93 beats per minute with frequent missed beats, second degree heart block and sinus pauses, confirmed on a 12-lead electrocardiogram. Despite this, there was no evidence of haemodynamic instability. Her initial serum potassium was 5.4 mmol/L, peaking at 7.1 mmol/L within the first 24 hours of seed ingestion, which correlated with increased frequency and duration of sinus pauses and heart block; no repolarisation abnormalities were observed. She was given a 200 mg (five vials) dose of digoxin specific Fab fragments (DigiFab) six hours following seed ingestion, repeated two hours after the initial dose due to persistent hyperkalaemia. A further dose of Digifab 120 mg (three vials) was given at 19 hours after seed ingestion because the potassium rebounded to >6.5 mmol/L. This smaller dose of Digifab was due to limited local drug availability. Over the course of her admission, she also received insulin/dextrose infusions to control her hyperkalaemia. Despite the above measures, the serum potassium continued to be elevated above 6 mmol/L for 48 hours post seed ingestion. Multiple dose activated charcoal was initiated briefly but abandoned due to severe retching and vomiting. Remnants of the seeds were noted in her faeces 72 hours after seeds ingestion, but nausea and vomiting was protracted and resistant to antiemetics, lasting well over 80 hours after seed ingestion. Potassium normalised as symptoms began to settle five days after seed ingestions (Figure 1). Her renal function remained normal throughout the course of the admission. She was transferred back to the psychiatric hospital on day 6 for ongoing treatment.