Cannabinoid Hyperemesis Syndrome

Public Health Implications and a Novel Model Treatment Guideline

Jeff Lapoint, DO; Seth Meyer, MD; Charles K. Yu, MD; Kristi L. Koenig, MD; Roneet Lev, MD; Sayone Thihalolipavan, MD, MPH; Katherine Staats, MD; Christopher A. Kahn, MD, MPH

Disclosures

Western J Emerg Med. 2018;19(2):380-386. 

In This Article

Pathophysiology of CHS

The pathophysiology of CHS is unclear.[7] Paradoxically, there are long-recognized antiemetic effects of cannabis, thus leading to its approved use for treatment of nausea and vomiting associated with chemotherapy and appetite stimulation in HIV/AIDS patients. The factors leading to the development of CHS among only a portion of chronic marijuana users are not well understood. Basic science research has identified two main cannabinoid receptors: CB1 and CB2, with CB1 receptors primarily in the central nervous system, and CB2 receptors primarily in peripheral tissues. This categorization has recently been challenged and researchers have identified CB1 receptors in the gastrointestinal tract.[7,9] Activity at the CB1 receptor is believed to be responsible for many of the clinical effects of cannabis use, including those related to cognition, memory, and nausea/vomiting.[13] Scientists hypothesize that CHS may be secondary to dysregulation of the endogenous cannabinoid system by desensitization or downregulation of cannabinoid receptors.[14,15] Some investigators have postulated that disruption of peripheral cannabinoid receptors in the enteric nerves may slow gastric motility, precipitating hyperemesis.[16,17]

Relief of CHS symptoms with very hot water (greater than 41°C) has highlighted a peripheral tissue receptor called TRPV,[1] a G-protein coupled receptor that has been shown to interact with the endocannabinoid system, but is also the only known capsaicin receptor.[13,18] This has led some to advocate for the use of topical capsaicin cream in the management of acute CHS.[18–21]

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