{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T16:03:20Z","timestamp":1785168200548,"version":"3.55.0"},"reference-count":14,"publisher":"Oxford University Press (OUP)","issue":"15","license":[{"start":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T00:00:00Z","timestamp":1770854400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,7,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>Acute cocaine intoxication remains a common emergency department presentation, with well-described symptoms including agitation, tachycardia, hypertension, and hyperthermia. Cocaine also has sodium channel antagonist properties, resulting in QRS interval prolongation and ventricular dysrhythmias. Cocaine-induced QRS interval prolongation is typically treated with 8.4% sodium bicarbonate to increase the concentration of sodium at sodium channels and increase pH, thereby decreasing the amount of free drug binding to sodium channels. However, drug shortages, including recent shortages of sodium bicarbonate, have prompted the use of alternative therapies to treat drug toxicities typically treated with sodium bicarbonate.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Summary<\/jats:title>\n                    <jats:p>We report the case of a 44-year-old male with a history of cocaine use who presented to the emergency department in cardiac arrest with presumed cocaine toxicity. Because of QRS complex widening noted on telemetry, 3 boluses of sodium bicarbonate were administered but only reduced the duration of the QRS interval from 165 to 130 ms with laboratory evidence of acidemia. To help treat the patient\u2019s significant acidemia, 500 mL of 36 mg\/mL tromethamine (THAM) was administered over 60 minutes. While THAM is not typically used in the treatment of toxicity due to sodium channel antagonism, it has been used in the treatment of metabolic acidosis in the intensive care unit, acting as a buffer by directly accepting protons. Approximately 35 minutes after administration of THAM, the duration of the QRS complex had decreased to 111 ms and venous blood gas analysis showed an improvement in the pH to the normal range. Following THAM administration, the patient\u2019s QRS duration remained below 120 ms for the remainder of their hospitalization.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This case illustrates the successful use of THAM in conjunction with sodium bicarbonate for the treatment of severe acidemia and refractory QRS complex widening in presumed cocaine toxicity. While sodium bicarbonate remains the mainstay of therapy for sodium channel blocker toxicity, THAM offers a potentially valuable adjunctive treatment, especially in the context of drug shortages.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ajhp\/zxag027","type":"journal-article","created":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T12:48:08Z","timestamp":1770814088000},"page":"e556-e560","source":"Crossref","is-referenced-by-count":0,"title":["Use of tromethamine in combination with sodium bicarbonate in the treatment of a wide complex dysrhythmia from presumed cocaine toxicity"],"prefix":"10.1093","volume":"83","author":[{"given":"Fermin","family":"Suarez","sequence":"first","affiliation":[{"name":"University of Utah Health , Salt Lake City, UT ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaitlyn","family":"McLeod","sequence":"additional","affiliation":[{"name":"University of Michigan Health , Ann Arbor, MI 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