Cannabis dominates the global recreational drug market with regards to consumer numbers. Its use has dramatically increased over recent years, with production doubling from 1992 to 2006.1
The United Nations Office on Drugs and Crime estimates that approximately 166 million people used cannabis in 2006, which is equivalent to 3.9% of the global population from age 15–64 years. Additionally, cannabis has become more potent with higher levels of the active ingredient THC being detected.1
With the increase in availability and potency and consumers being exposed to higher doses of THC, it is perhaps for this reason that a new syndrome titled cannabinoid hyperemesis emerged in the literature in 2004. Allen et al2
described a series of 19 cases. de Moore et al
described an earlier case of psychogenic vomiting complicated by cannabis use and pneumomediastinum.12
Since then several other authors have described similar symptoms in their patients.3–8
Patients present with a clinical syndrome of episodic vomiting often relieved by hot water bathing or showering. These symptoms arise after heavy chronic cannabis use and abstinence leads to symptom resolution.
Cannabinoids have been found to have an antiemetic effect, mediated by CB1 receptors in the CNS9 13
via a process known as depolarisation-induced suppression of inhibition where stimulation of the CB1 receptor activates a G-protein leading to a reduction in neurotransmitter release.13
CB1 receptors are found in high concentrations throughout the CNS, including the specific areas involved in nausea and vomiting—for example, the nucleus tractus solitaries, which has multiple communications, including inputs from vagal afferents and the area postrema (the chemoreceptor trigger zone), and outputs to the brainstem emetic centre.13
CB1 receptors are also found in the higher cortical and limbic regions where the senses of taste, smell, sight and memory are modulated. These areas have been found to be involved in anticipatory nausea and vomiting—for example, secondary to chemotherapy. Nabilone is a synthetic cannabinoid which has been used for treatment of chemotherapy induced nausea and vomiting.13
Paradoxically, chronic cannabis use results in hyperemesis. It has been proposed that in chronic use, the long half-life of cannabinoids leads to accumulation. Cannabis causes delayed gastric emptying10 11
and at toxic levels this could result in gastric stasis; hence, counteracting the centrally mediated antiemetic effect at the CB1 receptors.2
Vaziri et al
noted an emetic response to an intravenous injection of crude marijuana extract.14
The ‘hot water’ seeking behaviour of patients is thought to be due to possible deregulation of the thermoregulatory systems of the hypothalamus.10
- With the ongoing increase in cannabis use and its increasing potency, it is likely that cannabinoid hyperemesis will become more prevalent.
- It is probable that the condition is under-reported in the literature and under-diagnosed in the clinic and emergency setting.
- History taking should include a detailed account of recreational drug use and a diagnosis of cannabinoid hyperemesis should be considered in patients who have a history of heavy cannabis use.