CHS is a constellation of symptoms including severe cyclical nausea and vomiting and epigastric or periumbilical abdominal pain as a result of long-term cannabis use. In this study, we compared costs incurred by patients in various settings to determine if there is a difference between patients with and without CHS. The pathophysiologic processes underlying CHS are unclear at this time. Many hypotheses exist, yet there is very limited evidence to support any one unifying mechanism. The best evidence suggests a dynamic interplay between cannabinoid metabolism and complex pharmacodynamics at the CB-1 receptor.
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The best characterized endocannabinoids are anandamide and 2-arachidonylglycerol (2-AG) [9]. The endocannabinoids are present in both the central nervous system [8] and enteric nervous system [15]. Anandamide and 2-AG are released locally on demand by neurons, are present in small quantities, and undergo rapid inactivation [8]. Endocannabinoids are thought to act as either neuromodulators or neurotransmitters [11]. Anandamide and 2-AG possess similar biochemical structures, but each has a distinct pathway for biosynthesis and degradation. Anandamide is synthesized from the precursor N-arachidonoyl phosphatidylethanolamine, while 2-AG is produced from an inositol-1,2-diacylglycerol precursor [8,16,17].
Diagnosis of CHS
- CHS has been reported numerous times in [9–11] large case series, small case series, and more than 80 individual case reports [6, 8, 11–82].
- A case series from Spain from 2012 to 2016 involved 6 patients (5 men) with an average age of 28.3 years who, on average, began to use marijuana at age 16.
- Haloperidol should also be used with caution in patients with dementia and Parkinson’s disease, as dopamine blockade can dramatically worsen symptoms causing extrapyramidal side effects and incapacitation [46].
For example, THC has two main metabolites (11-hydroxy-delta9-tetrahydrocannabinol or 11-OH- THC and 11-nor-9-carboxy-THC-delta9-tetrahydrocannabinol or THC-COOH) but it also has over 100 minor metabolites [40]. The 11-OH-THC metabolite is psychoactive and is equipotent to THC in terms of psychoactive effects; THC-COOH is not psychotropic and has anti-inflammatory and analgesic properties [41, 42]. CBD is not psychotropic, has little affinity for the CB1/CB2 receptors, and appears to be a partial agnostic at the serotonin receptors [43]. CBD enhances the expression of the CB1 receptors in the hypothalamus, plus it amplifies the hypothermic effects of THC [44]. In preclinical studies, toxin-induced vomiting treated with CBD showed a biphasic response, that is, low doses of CBD had an antiemetic effect while higher doses had a proemetic effect [37, 45]. CBG is not psychotropic and acts as an antagonist at both CB1 and serotonin receptors [46].
How is cannabis hyperemesis syndrome treated?
Exposure characteristics are generally related to excessive use in adults and inadvertent ingestions in small children. This has been well documented throughout the recent legalization of recreational marijuana in Colorado, and now other states. Synthetic cannabinoids are the most abused synthetic drug and second most abused drug among adolescents. [7]Reports of abuse and toxicity are steadily growing, as the number of synthetic cannabinoids produced increases. Increasing varieties of synthetic cannabinoids have been synthesized over the last ten years to avoid classification as illegal agents by making chemical modifications to compounds.
Lang said of the 800 to 1,000 patients seen in Calgary emergency departments per day, it wouldn’t surprise him if they were treating upwards of five to 10 cases of CHS. Experts also aren’t clear on what causes CHS, or why some people develop it while others don’t. Since it was first identified in 2004 in Australia, researchers have looked at the effects of cannabis on the vomiting centers of the brain.
- The exact mechanism, however, remains unknown, and it is out of scope for this review to explore it further.
- CBD enhances the expression of CB1 receptors in the hypothalamus and amplifies the hypothermic effects caused by THC [29].
- One theory behind CHS is that chronic overstimulation of the body’s endocannabinoid receptors leads to your body not being able to control nausea and vomiting.
- This immoderate stimulation of the endocannabinoid system leads to the aforementioned erratic neurotransmitter modulation that can lead to toxicity.
Differentiating Cyclic Vomiting, PV, and CHS
With more states liberalizing the use of cannabis, many cases of toxicity are now being reported, esp in children and teenagers. These patients typicallly present to the emergency department with varying mental status changes. The cannabinoid hyperemesis syndrome toxicity is best managed by the emergency department physician, posion control, an internist, nurses, neurologist and or psychiatrist. Most cases of cannabis toxxicity are managed with supportive care with close monitoring.
