A Life-threatening Bradyarrhythmia in the ICU: Beware of Phenytoin AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICIN Faris ME, Saad E, Abdulrahman A, Albanna M, Friedman H. A Life-threatening Bradyarrhythmia in the ICU: Beware of Phenytoin Loading!. InB44. MITIGATING HARM: MANAGING EXPECTED AND UNEXPECTED COMPLICATIONS IN THE ICU 2024 May (pp. A3646-A3646). American Thoracic Society.
Date
05/01/2024Abstract
Background: Phenytoin is an anticonvulsant medication that has Class 1B antiarrhythmic
characteristics and has been used to treat tachyarrhythmias. The most common adverse drug reactions
(ADRs) include skin and soft tissue manifestations followed by gastrointestinal problems. Cardiac
ARDs are a rare phenomenon that should, however, deserve serious attention as they may manifest as
life-threatening bradyarrhythmias. The authors presented a case of bradycardia and hypotension in a
critically ill patient following an infusion of a phenytoin loading dose which necessitated cardiac pacing.
Case Presentation: A 75-year-old female with a medical history of hypertension, epilepsy (on
phenytoin), type II diabetes mellitus, and hypothyroidism was brought with poor oral intake and lethargy
for 4 days. On arrival at the emergency room (ER), she was hypotensive (60/40 mmHg) and tachycardic
(132 beats/minute). Initial fluids resuscitation was administered, and vasopressors were started
(norepinephrine initially at 30 mcg/minute). CXR was unremarkable, urinalysis revealed bacteria and
leukocytes, and blood cultures grew gram-negative rods. The patient became hemodynamically stable,
and she was weaned off vasopressors on day 2, but she experienced two generalized tonic seizures
with a subtherapeutic phenytoin level and an unremarkable metabolic profile. Neurology consultation
recommended parenteral phenytoin loading. Following the infusion of a phenytoin loading (20 mg/kg
dose, infusion rate of 60 mg/minute) the patient suddenly became bradycardic (30 beats/minutes) and
hypotensive at 70/44 mmHg. EKG demonstrated bradycardia without ischemic changes (Figure 1)
which was unresponsive to transcutaneous pacing. Inotropes were commenced (epinephrine at 5
mcg/minute/kg and dopamine at 15 mcg/kg/minute) and a transvenous pacer was placed per
cardiology consultation. The thyroid function test was normal, and there were no significant metabolic
derangements to cause bradycardia. The intrinsic sinus rhythm was restored, and inotropes were
discontinued on day 3. A permanent pacemaker was placed on day 4 per electrophysiology
consultation for life-threatening bradycardia in a high-risk patient. Phenytoin was switched to an
alternative antiepileptic after the occurrence of this cardiac ADR which was probably attributed to
phenytoin infusion. Discussion: Phenytoin-induced bradycardia and hypotension represent a rare but
serious ADR, with a reported incidence of 0.05% that was mostly observed following an intravenous
loading. Phenytoin inhibits sodium channels in atrial tissues and the AV node resulting in various
bradyarrhythmias and conduction block syndromes. Prompt identification of these bradyarrhythmias
with immediate phenytoin discontinuation is needed. Hemodynamic support with atropine, fluids
resuscitation, inotropes, and often temporary cardiac pacing may be warranted as demonstrated in our
case.
Author List
M Faris, E Saad, A Abdulrahman, M Albanna, H FriedmanAuthor
Mohammed Elamin Faris MBBS Assistant Professor in the Medicine department at Medical College of WisconsinView Online
