Transient bilateral chorea secondary to digoxin toxicity in a female with acute kidney injury: a case report

Background Chorea secondary to digoxin toxicity is rare, with only three published cases describing the phenomenon. We report the case of a 78-year-old female presenting with intermittent vomiting and diarrhoea for 4 weeks. She had a history of chronic kidney disease and digoxin use for atrial fibrillation. Case summary A 78-year-old lady presented to the emergency department with a 4-week history of intermittent vomiting and diarrhoea. These symptoms commenced after a course of antibiotics prescribed by her general practitioner for a urinary tract infection. Her admission electrocardiogram demonstrated atrial fibrillation at a rate of 32, with evidence of digitalis toxicity. Her creatinine was 396 µmol/L (44–80 µmol/L) with digoxin level 8.1 nmol/L (0.77–1.5 nmol/L). Initially, treatment was with digoxin-specific antibody (FAB) and fluid resuscitation. Within 24 h, she developed transient head, neck, and bilateral upper limb chorea. Review of medications revealed no other likely causative agent. Neuroimaging showed no new ischaemia, but stable established bilateral infarcts of the basal ganglia. Haloperidol 0.5 mg twice daily was commenced. Three days later as digoxin levels normalized, the chorea resolved entirely without recurrence. Discussion We have identified three reported cases of digoxin-induced chorea. Our case resembles two of the published cases where a transient bilateral chorea, associated with digitalis toxicity and resolving within a few days of normalization of digoxin levels was demonstrated. There were no other focal neurological signs or symptoms. It has been postulated that an alteration to dopaminergic neuronal activity is a potential mechanism, as digoxin also demonstrates neuropsychiatric side effects such as psychosis and depression.

SAT-507 Myxedema Coma: A Fatal Diagnosis in a Patient with No Known History of Hypothyroidism

Myxedema coma is a rare yet commonly missed diagnosis. Early detection is key to management as this diagnosis carries a high mortality rate. We report a case of a 108-year-old female with a past medical history of CKD stage 3, hypertension, CHF, and atrial fibrillation who was brought to the emergency department (ED) by her grandson for seizures. The patient has no history of seizures, hypothyroidism (previous TSH 6 years back was 2.29 micro IU/mL), diabetes, or previous radiation exposure. The family noticed the first seizure 8 hours prior to admission with eyes rolling backward, shaking for 1 minute and slurred speech upon awakening. She had 2 other seizure episodes prior to arrival to the ED. Vitals in the ED showed a temperature of 31.7°C, BP of 85/50, HR of 35, RR of 8, and SpO2 was 83% on room air. Given the patient’s age, code status was changed to DNR/DNI. Blood work in the ED revealed a sodium of 146 mMol/L (136-145), anion gap of 25, Creatinine of 2.67 mg/dL (last creatinine prior to this admission was 1.65 mg/dL), and a troponin of 0.04 ng/mL (<0.04). Thyroid function testing was not done in the ED. Home medications included Lasix, digoxin, isosorbide mononitrate, and atenolol. The patient was admitted to the medical floor for workup of bradycardia and was being worked up for beta-blocker/digoxin toxicity but continued to be bradycardic despite atropine. She became hypoglycemic to 37 mg/dL. The patient was admitted to the CCU at night on day 1 of admission and was started on dopamine and glucagon drips. Sulfonylurea screen was negative, and the patient did not have further hypoglycemic episodes. While in the CCU, blood work showed a lactic acid of 10 mMol/L (0.4-2.0), TSH of 21.03 micro IU/mL (0.45-5.33), free T4 of 0.61 ng/dL (0.70-1.70), and total T3 71 ng/dL (87-178). Myxedema score was >130. Digoxin level came back elevated at 4.5 ng/ml (0.9-2.0). Cosyntropin stimulation testing was negative for adrenal insufficiency and thus the patient was not started on steroids. Urinalysis revealed pyuria with blood, but no urine cultures were done. Blood cultures were negative. The patient was given levothyroxine 200 mcg IV in the AM on Day 2 of admission and was started on antibiotics with azithromycin, cefepime, vancomycin, and metronidazole given concern for sepsis. Hypoglycemia resolved and glucagon was discontinued. In the evening of Day 2 of admission, despite being on a dopamine drip, the patient became increasingly bradycardic, hypotensive, and short of breath. She was initially stabilized after a dose of bicarb, atropine, and epinephrine. However, her BP and respiratory status continued to decline, and the patient passed away. In conclusion, myxedema coma should be suspected in patients presenting with typical symptoms and should be tested for on presentation even when no prior history of hypothyroidism exists.

Plasma digoxin levels and ejection fraction in pediatric heart failure

Background Digoxin has long been prescribed in children with heartfailure, but its efficacy has not been evaluated. A previous study atthe Department of Child Health, Dr. Cipto Mangunkusumo Hospitalrevealed that plasma digoxin levels, following a maintenance doseof 15 μg/kg/d, were sub-therapeutic. Regarding its narrow margin ofsafety, the trend is to use digoxin in even lower dose. Thus, the drug’simpact on cardiac performance need to be evaluated.Objective To evaluate whether a lower maintenance dose of digoxin(10 μg/kg/d) is sufficient to achieve a therapeutic level and to assess forpossible correlations between plasma digoxin level and left ventricularejection fraction (LVEF) as well as fractional shortening (LVFS).Methods A cross-sectional study was conducted on 20 pediatricheart failure patients at the Department of Child Health, Dr. CiptoMangunkusumo Hospital, Jakarta, from January to May 2012. Plasmadigoxin levels were measured by ELISA method after one month ormore of treatment; LVEF and LVFS were measured by echocardiography.Correlations between plasma digoxin level and LVEF or LVFSwere analyzed by Spearman’s correlation test. The LVEF before andafter digoxin treatment were compared by paired T-test.Results Thirteen out of 20 patients had plasma digoxinlevels within therapeutic range (0.5-1.5 ng/mL; 95%CI0.599 to 0.898) and 7 had sub-therapeutic levels (<0.5 ng/mL; 95%CI 0.252 to 0.417). No significant correlationswere observed between plasma digoxin level and LVEF(r=-0.085; P=0.722) or LVFS (r=-0.105; P=0.659). There was asignificant increase in LVEF before [42.18 (SD 14.15)%] and afterdigoxin treatment [57.52 (SD 11.09)%], (P < 0.0001).Conclusion Most patients in this study have plasma digoxin levelswithin therapeutic range. There are no significant correlationsbetween plasma digoxin level at the time point of measurementand LVEF or LVFS. However, an increase of LVEF is observed inevery individual patients following digoxin treatment.