Labetalol-induced hyperkalemia in acute aortic dissection: A rare but clinically relevant adverse effect

Clicks: 3
ID: 332138
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #221 of 228 articles by views in American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 228 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
BACKGROUND: Hyperkalemia is a potentially life-threatening electrolyte abnormality often associated with renin-angiotensin-aldosterone system (RAAS) inhibitors, renal dysfunction, or potassium-sparing agents. Non-selective beta-blockers, including labetalol, may also precipitate hyperkalemia through beta-2 (β-2)-adrenergic blockade, although this adverse effect is underrecognized, particularly in patients without underlying renal disease. CASE PRESENTATION: A 59-year-old man with hypertension, diabetes, asthma, and polysubstance use disorder presented with severe chest pain and hypertensive emergency (243/132 mmHg). Imaging revealed aortic dilatation and confirmed acute type B aortic dissection. After initial medical management with intravenous (IV) esmolol and nicardipine, oral labetalol was initiated and escalated to 600 mg for anti-impulse therapy. The patient developed persistent, non-hemolyzed hyperkalemia (5.2 to 5.8 mmol/L) temporally correlating with labetalol dose escalation, despite preserved renal function (serum creatinine 1.4 to 1.8 mg/dL) and absence of RAAS inhibitors or heparin exposure. Conservative management failed, and the patient underwent thoracic endovascular aortic repair (TEVAR) with thoracic branch endoprosthesis (TBE). Post-operatively, labetalol was discontinued and replaced with carvedilol. Serum potassium (K+) normalized within 48 hours and remained without further K+ lowering agents. Naranjo Adverse Drug Reaction Probability Scale assessment yielded a score of 7, indicating a probable adverse drug reaction. CONCLUSIONS: Labetalol may induce clinically significant hyperkalemia independent of renal impairment or typical precipitating medications. This case highlights the importance of monitoring K+ in patients receiving labetalol for acute aortic syndromes and supports carvedilol as a potentially safer non-selective beta-blocker alternative with respect to K+ homeostasis.
Reference Key
openalex_W7221506819 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Faizan Butt, Zoha Khan, Paul Matthew Madua
Journal American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
Year 2026
DOI
10.1093/ajhp/zxag297
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.