Cannabis hyperemesis syndrome is increasingly encountered in emergency and inpatient settings as community cannabis potency and use rise. It is conceptualized as a disorder of gut-brain interaction with a characteristic triphasic course (prodromal, hyperemetic, and recovery) and stereotyped hot‑water bathing behavior [1,2]. Contemporary guidance from the American Gastroenterological Association (AGA) emphasizes a positive clinical diagnosis using Rome IV-aligned criteria, recurrent stereotyped emesis in the context of chronic cannabis exposure with improvement on abstinence, after the reasonable exclusion of alternative etiologies [1,3]. Our patient's long-term history of heavy daily use, cyclical hospital presentations, hot showering, and resolution with supportive care and cessation counseling are concordant with these criteria.

Prolonged retching in CHS can precipitate profound dehydration, electrolyte derangements (notably hypokalemia), acute kidney injury, and barotrauma [4]. Spontaneous pneumomediastinum and pneumothorax may occur via the Macklin effect, and, more rarely, transmural esophageal rupture (Boerhaave syndrome) may complicate severe episodes, mandating urgent cross-sectional imaging and multidisciplinary input [4-6]. Our patient's CT‑confirmed esophageal perforation with concomitant pneumomediastinum and pneumothorax underscores the need for early recognition, high‑flow oxygen, broad-spectrum antimicrobials, nil per os with parenteral nutrition, and close cardiopulmonary monitoring, consistent with established management principles for Boerhaave syndrome [7].

Haloperidol, benzodiazepines, and topical capsaicin are commonly used when first-line 5-hydroxytryptamine type 3 (5-HT3) antagonists fail. A randomized trial demonstrated haloperidol's superiority over ondansetron for acute CHS symptom relief in the ED, although dosing must be balanced against adverse effects [8]. Topical capsaicin targeting transient receptor potential vanilloid 1 (TRPV1) has supportive pilot and observational data and may shorten ED length of stay, but higher-quality trials remain limited [9]. Importantly, commonly used antiemetics can prolong the QT interval, and the risk is accentuated by hypokalemia, hypomagnesemia, and acidosis typical of refractory vomiting [10]. Meta-analytic and ED cohort data confirm clinically relevant, dose-related corrected QT (QTc) effects with ondansetron; intravenous haloperidol also carries the risk of QT prolongation and torsades de pointes, particularly at higher doses, prompting ECG and electrolyte surveillance in susceptible patients [11]. In our patient, ECG changes were consistent with hypokalemia (U waves and ST depression) without QT prolongation, highlighting the importance of aggressive electrolyte correction and judicious antiemetic selection.

Aromatherapy with isopropyl alcohol (IPA) has emerged as a rapid, inexpensive, non-pharmacological option for acute nausea. Multiple randomized trials in ED triage and treatment areas show faster short-term relief with IPA swab inhalation versus saline/placebo, and a pragmatic ED trial suggests reduced rescue antiemetic use [12]. Systematic reviews conclude a modest but clinically meaningful early effect with an excellent safety profile; benefits appear greatest within the first 10-30 minutes and may be leveraged while IV access is obtained or when QT‑prolonging agents are undesirable [13]. Although published reports specifically in CHS are sparse, our patient's prompt improvement after IPA inhalation, despite the failure of ondansetron, cyclizine, haloperidol, proton‑pump inhibition, and topical capsaicin, supports the early consideration of IPA as an adjunct in refractory CHS, particularly when accompanying electrolyte and acid-base abnormalities or suspected perforation make pharmacological escalation less appealing.

Sustained cannabis cessation remains the only disease-modifying therapy and is associated with the complete remission of CHS symptoms in observational cohorts and expert guidance [14]. Structured cessation counseling, linkage to substance‑use services, and clear discharge instructions about relapse risk are essential components of care [14].

For ED and inpatient teams, a practical strategy is to promptly recognize the CHS phenotype and assess for the presence of complications using chest radiography or computed tomography in cases where chest pain or subcutaneous emphysema is present. Management should prioritize fluid resuscitation and electrolyte replacement when clinical or laboratory findings indicate dehydration or electrolyte disturbances. The use of antiemetic regimens should be judicious and carefully monitored, particularly concerning the risk of QT interval prolongation. Adjunctive therapies such as topical capsaicin and early IPA inhalation should be considered for rapid and low-risk symptom relief. In addition, clinicians should initiate cessation counseling and ensure follow-up in accordance with AGA recommendations. Future prospective studies in CHS are warranted to determine optimal IPA dosing and frequency, evaluate comparative effectiveness against haloperidol or capsaicin, and examine patient-centered outcomes such as time to oral tolerance and ED length of stay.