Hemodialysis Reversed Bradyarrhythmia and Sinus Nodal Dysfunction From Acute Lithium Toxicity American Thoracic Society Saad E, Abdulrahman A, Faris ME. Hemodialysis Reversed Bradyarrhythmia and Sinus Nodal Dysfunction From Acute Lithium Toxicity. InC44. TOXIDROMES AND ADVERSE MEDICATION REACTIONS IN THE ICU 2024 May (pp. A5666-A5666). American Thoracic Society.
Date
05/21/2024Abstract
Background: Serious multisystemic complications can occur as adverse events from
lithium therapy. The authors present a case of a 50-year-old male who developed lithium-induced
acute kidney injury and subsequent cardiac toxicity which manifested as bradyarrhythmia with
frequent sinus pauses necessitating emergent hemodialysis. The bradyarrhythmia and sinus nodal
abnormalities were promptly reversed after the normalization of lithium levels post-dialysis sparing a
need for cardiac pacing. Case Presentation: A 50-year-old Caucasian male with a past medical
history of hypertension, hypothyroidism, and bipolar disorder presented with nausea, tremors, and
generalized weakness for 3 days. Regular medications included levothyroxine, lisinopril, lithium
carbonate, and furosemide. The patient was somnolent but arousable. Vital signs revealed
bradycardia with hypotension (85/50 mmHg). The physical exam was notable for bilateral upper
extremity coarse tremors. Initial EKG showed bradycardia (32 beats/minute) with ventricular escape
rhythm. Laboratory work-up revealed a serum creatinine of 3.9 mg/dl (0.6 -1.3 mg/dl) and BUN of 45
mmol/L (5.0- 22.0 mg/dl) (baseline levels were normal before three weeks), potassium of 4.1
mmol/L (3.5- 5.2 mmol/L), and bicarbonate of 23 mmol/L (22.0- 29.0 mmol/L) with normal venous
pH. The thyroid function test was normal. The initial lithium level was supra-therapeutic at 2.5
mmol/L (upper normal limit 1.2 mmol/L). Urinalysis revealed trace proteinuria and renal ultrasound
was unremarkable. Lisinopril and furosemide were held, and blood pressure improved following
initial fluid resuscitation. Repeat lithium level after 4 hours was trending up to 3.1 mmol/L with no
significant interval worsening of renal function or serum electrolytes. At this juncture, the telemetry
monitor depicted frequent short-lasting sinus pauses suggestive of sinus nodal dysfunction. The
patient’s mental status remained unchanged with no signs of acute cardiac decompensation. A
decision was made for emergent hemodialysis for lithium-induced renal and cardiac toxicity.
Cardiology consultation recommended pacing should hemodynamic status deteriorate, or
metabolic-related sinus nodal dysfunction persist despite hemodialysis. Prompt resolution of
bradyarrhythmia with the restoration of the normal sinus rhythm was observed upon normalization of
lithium levels after hemodialysis. Renal function recovered and lithium was switched to cariprazine
per psychiatry consultation. Discussion. Lithium-induced cardiac toxicity is a rare occurrence that
should deserve serious attention. The most common manifestations include sinus nodal
abnormalities and profound bradycardia. The available literature described the reversibility of
bradyarrhythmia and restoration of nodal function with lithium levels normalization post-dialysis, as
demonstrated in our case, although temporary (and rarely permanent) cardiac pacing was
warranted in some patients
Author List
E Saad, A Abdulrahman, ME FarisAuthor
Mohammed Elamin Faris MBBS Assistant Professor in the Medicine department at Medical College of WisconsinView Online
