Cannabinoid hyperemesis syndrome (CHS) is a condition in which patients experience abdominal pain, nausea, and persistent vomiting following prolonged and heavy cannabis use. With the recent legalization of medical and recreational marijuana in many regions, CHS has become increasingly recognized worldwide, and its diagnosis has increased. In a study conducted in Colorado, researchers found that emergency department (ED) visits related to vomiting increased following the legalization of recreational marijuana.1 This increase was amplified in counties with additional dispensaries. While CHS is not exclusive to legalized areas, health systems in legalized regions throughout the world have reported more frequent encounters with persistent vomiting that ultimately are diagnosed as CHS. These findings have been reflected in many regions of the world where recreational marijuana is legalized. The question remains, however, as to how hospitalists should anticipate, monitor, and respond to this uptick in CHS. This article examines the demographic and clinical patterns of CHS, discusses potential pathophysiological mechanisms, and explores how hospitalists can more effectively identify and treat CHS.
Clinical Features of CHS
CHS affects those with chronic, high-dose cannabis use. Earlier studies reported a higher incidence in male patients; however, studies have shown that visits by female patients have increased significantly following cannabis legalization.2 Additionally, the age-profile of these patients tends to be their late teens and twenties, with a history of approximately 1.5 grams of cannabis a day for approximately 10 years.3 Often these are individuals who have developed a tolerance and dependency on cannabis, sometimes using extremely potent forms or concentrates.
Notably, comorbid psychiatric conditions and substance use disorders are common in CHS patients. In a study conducted by Myran et al., approximately 24% to 25% had a documented ED visit or hospitalization for a mental health condition or other substance use in the two years before their CHS episode.2 The presence of psychiatric comorbidities can complicate management, as these patients may be using cannabis both recreationally and as an attempt to alleviate anxiety or nausea, creating a vicious cycle in CHS.
CHS often follows a stereotypical clinical course with three phases: a prodromal phase, a hyperemetic phase, and a recovery phase. During the prodromal phase, patients develop mild nausea, especially in the mornings, and may increase their cannabis use in attempts to settle their stomach.4 This phase may last for weeks or months and is insidious. Once CHS progresses to the hyperemetic phase, patients experience the hallmark symptoms of CHS. These symptoms include profuse, repetitive vomiting, often up to five times an hour, severe retching, and diffuse abdominal pain. Patients in this phase often report compulsive hot bathing or showering to relieve symptoms, a learned behavior. Taking frequent hot showers for symptom relief is considered pathognomonic for CHS, and almost two-thirds of patients find that the remedy significantly eases their nausea and abdominal pain.5 The duration of the vomiting episodes can range from about 24 to 48 hours, and five to seven days in more severe cases. Initially, CHS episodes might remit within a day or two with supportive care, especially if cannabis use is halted. If cannabis use continues between episodes, however, the intervals often shorten, and the hyperemetic episodes can intensify over time, further dysregulating the physiology of the gut-brain axis.
Patients experiencing CHS often initially use cannabis to self-treat their nausea. At low doses, THC can be antiemetic, but at high chronic doses, it becomes proemetic.6 Many CHS sufferers describe that when the nausea first starts, they smoke marijuana or use edibles to try to suppress it. While this attempt might give brief relief due to THC’s short-term anti-nausea effect, the vomiting worsens as the CHS pathophysiology progresses. This self-medicating behavior delays recognition of CHS and often brings patients into the hospital only after they reach a point where no amount of cannabis stops the vomiting.
Clinically, CHS can be distinguished from other vomiting syndromes by a combination of history and exam findings, including a history of heavy cannabis use, normal GI investigations, relief with hot showers, and failure to improve with standard antiemetics. Patients are often tachycardic and volume-depleted from fluid losses. They may have epigastric or periumbilical abdominal tenderness from forceful retching. There are typically no peritoneal signs and no clear triggers like food poisoning. CHS closely resembles cyclic vomiting syndrome (CVS), but CVS occurs in non-cannabis-users and often has migraine-like or stress triggers.7 Importantly, CVS patients respond to conventional anti-nausea medications, whereas CHS patients do not.
Pathophysiology of CHS
The exact pathophysiological mechanism of CHS is not fully elucidated, but several interrelated hypotheses exist. The leading theory is that chronic overstimulation of the endocannabinoid system, particularly CB1 receptors, disrupts the body’s normal emetic/antiemetic balance.8 THC, the primary psychoactive cannabinoid, acts on CB1 receptors, which are abundant in the central nervous system and the enteric nervous system of the gut. Acute cannabis exposure usually activates pathways that suppress nausea. With heavy, prolonged exposure, however, it is thought that CB1 receptor signaling becomes dysregulated or desensitized. Essentially, the threshold for nausea and vomiting becomes reset due to chronic THC saturation.
Another contributing factor to the pathophysiology is the transient receptor potential vanilloid 1 (TRPV1) receptor system. TRPV1 receptors are involved in pain and thermoregulation and can influence nausea pathways. They are activated by heat and capsaicin. Although it’s not clear how exactly TRPV1 is implicated in CHS, one hypothesis is that chronic cannabis use leads to desensitization or alteration of TRPV1 function, and the act of applying heat restores some balance by releasing substance P.8 Substance P is a key mediator of emesis in the brainstem, and overstimulating TRPV1 may deplete substance P, thereby reducing vomiting. In summary, there are several hypotheses explaining how CHS arises, including a combination of chronic cannabinoid receptor overstimulation and derangement of TRPV1.
Management and Treatment Strategies
CHS requires a multifaceted treatment approach that addresses both the physical causes of vomiting and any underlying anxiety or stress responses that may exacerbate symptoms. In addition to relief from hot showers, many patients benefit from anti-anxiety medications, suggesting an anxiety-related component to the syndrome. Key acute treatments for CHS include haloperidol, benzodiazepines, hot showers, and topical capsaicin.
Haloperidol is a dopamine D2-receptor antagonist and can be an effective acute treatment for CHS, outperforming standard antiemetics like ondansetron in clinical trials. One study found that IV haloperidol was shown to provide greater relief of nausea, vomiting, and abdominal pain at two hours than ondansetron 8 mg, with patients on haloperidol requiring fewer rescue antiemetics and leaving the emergency department sooner on average.3 These findings align with multiple case reports and clinical experiences in which haloperidol aborted CHS symptoms even when ondansetron failed. Other antipsychotics with dopamine-blocking activity, such as droperidol or olanzapine, have also been reported to alleviate CHS, presumably via similar blockade of the brain’s chemoreceptor trigger zone.
From an anxiety perspective, while haloperidol’s primary benefit in CHS comes from blocking dopamine, thereby suppressing the emetic pathway, it also has sedative and tranquilizing properties. CHS patients in a hyperemesis episode are typically distressed or agitated and exhibit a surge in sympathetic activity, including tachycardia, hypertension, and sweating.6 EDs now use IV haloperidol as a first-line agent in CHS protocols, reflecting its efficacy.
Benzodiazepines such as lorazepam are also frequently cited as useful in CHS, especially in cases where anxiety is amplifying the emetic reflex. Benzodiazepines are among the most consistently effective acute therapies. Lorazepam or similar benzodiazepines can break the cycle of anxiety and vomiting by relaxing the patient and dampening the hyperemetic response by exerting antiemetic effects through the central GABA system.6
In addition to hot baths, some clinicians have used a topical capsaicin cream applied to the abdomen. A pilot study demonstrated that capsaicin cream notably reduces nausea within 60 minutes and shortens hospital stays for CHS patients.9 While large multi-center trials are lacking, the existing evidence and low risk profile of capsaicin make it a recommended adjunct in many CHS protocols.5
While antiemetics and anti-anxiety measures are pursued, clinicians must pay close attention to electrolyte abnormalities, fluid status, and cardiac rhythm, including QT intervals, and treat appropriately.
Pediatric Perspective
While most evidence for cannabinoid hyperemesis syndrome comes from adult data, CHS is an increasingly recognized disease entity in pediatric populations. Multiple studies have demonstrated an increasing incidence among adolescents, especially with recreational cannabis legalization and commercialization.10,11 Clinical presentation in adolescents and teens seems to closely parallel adult presentations, with nausea followed by recurrent vomiting, abdominal pain, and relief with hot showers.12,13 In addition, standard antiemetic therapies (ondansetron and metoclopramide) likewise have been largely ineffective. While robust pediatric data are lacking, some case series have demonstrated promising results with dopamine antagonists, benzodiazepines, and topical capsaicin. Sustained cessation of cannabinoid products remains the only intervention that has demonstrated longitudinal efficacy.14 These findings reinforce the applicability of adult CHS principles but concurrently demonstrate the need for pediatric-specific research into CHS in this population.
Conclusion
CHS has emerged as an important and increasingly common diagnosis in the era of cannabis legalization. The pathophysiology involves a paradoxical effect of long-term cannabinoid use on the emesis pathways, possibly mediated by CB1 receptor desensitization and TRPV1 receptor activation. Hospitalists should be aware that CHS patients often have coexisting psychiatric needs and may initially deny cannabis as a cause, given their prior reliance on it for symptom relief.
While conventional antiemetics alone are usually insufficient for CHS, growing clinical experience has identified more effective treatments for acute episodes, including dopamine antagonists, benzodiazepines, and topical capsaicin. Adopting protocols that include these agents can significantly improve patient comfort and shorten hospital stays. However, the ultimate treatment is patient education and cessation of cannabis use, which may require compassionate counseling and addiction support.
Ongoing research and surveillance are needed to fully understand this syndrome’s mechanisms and to develop more targeted treatments. In the meantime, heightened awareness and recognition of CHS by hospitalists can lead to appropriate therapy, reduced healthcare utilization, and better outcomes for these patients.
Ms. Chamoun
Dr. Kovaleski
Dr. Eckerle
Dr. Poonacha
Ms. Chamoun is a first-year medical student at the University of Minnesota Medical School in Minneapolis. Dr. Eckerle is a professor of pediatrics at the University of Minnesota Medical School in Minneapolis and sees patients in outpatient clinics and pediatric emergency settings. Dr. Kovaleski is an assistant professor in the division of pediatric emergency medicine at the University of Minnesota Medical School in Minneapolis. Dr. Poonacha is a hospitalist and medical director for care management and clinical documentation improvement at Emory Johns Creek Hospital and assistant professor of medicine at Emory University Medical School, both in Atlanta. He is also on The Hospitalist’s editorial board.
References
1. Wang GS, et al. Changes in emergency department encounters for vomiting after cannabis legalization in Colorado. JAMA Network Open. 2021;4(9):e2125063. doi:10.1001/ jamanetworkopen.2021.25063.
2. Myran DT, et al. Changes in emergency department visits for cannabis hyperemesis syndrome following recreational cannabis legalization and subsequent commercialization in Ontario, Canada. JAMA Netw Open. 2022;5(9):e2231937. doi: 10.1001/jamanetworkopen.2022.31937.
3. Ruberto AJ, et al. Intravenous haloperidol versus ondansetron for cannabis hyperemesis syndrome (HaVOC): a randomized, controlled trial. Ann Emerg Med. 2021;77(6):613- 619. doi: 10.1016/j.annemergmed.2020.08.021.
4. Fleming JE, Lockwood S. Cannabinoid hyperemesis syndrome. Fed Pract. 2017;34(10):33-36. PMID:30766236.
5. Richards JR, et al. Pharmacologic treatment of cannabinoid hyperemesis syndrome: a systematic review. Pharmacotherapy. 2017;37(6):725-734. doi: 10.1002/phar.1931.
6. Loganathan P, et al. A comprehensive review and update on cannabis hyperemesis syndrome. Pharmaceuticals (Basel). 2024;17(11):1549. doi: 10.3390/ph17111549.
7. Blumentrath CG, et al. Cannabinoid hyperemesis and the cyclic vomiting syndrome in adults: recognition, diagnosis, acute and long-term treatment. Ger Med Sci. 2017;15:Doc06. doi: 10.3205/000247.
8. Cue L, et al. Cannabinoid hyperemesis syndrome. 2023. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan. PMID: 31751105.
9. Dean DJ, et al. A pilot trial of topical capsaicin cream for treatment of cannabinoid hyperemesis syndrome. Acad Emerg Med. 2020;27(11):1166-1172. doi: 10.1111/ acem.14062.
10. Toce MS, et al. Emergency department visits for cannabis hyperemesis syndrome among adolescents. JAMA Netw Open. 2025;8(7):e2520492. doi: 10.1001/jamanetworkopen.2025.20492.
11. Dosani K, et al. Cannabinoid hyperemesis syndrome in pediatrics: an emerging problem. Pediatr Rev. 2021;42(9):500-506. doi: 10.1542/pir.2019-0097.
12. Zhu JW, et al. Diagnosis and acute management of adolescent cannabinoid hyperemesis syndrome: a systematic review. J Adolesc Health. 2021;68(2):246-254. doi: 10.1016/j. jadohealth.2020.07.035.
13. Geraci E, et al. Comparison of antiemetics in the management of pediatric cannabinoid hyperemesis syndrome. J Pediatr Pharmacol Ther. 2023;28(3):222-227. doi: 10.5863/1551-6776-28.3.222.
14. Reinert JP, et al. Management of pediatric cannabinoid hyperemesis syndrome: a review. J Pediatr Pharmacol Ther. 2021;26(4):339-345. doi: 10.5863/1551-6776-26.4.339.
