With the large prevalence of marijuana use in the world, why does it appear that so few patients develop CHS? Certain individuals may have a genetic polymorphisms in the cytochrome P450 enzymes responsible for the metabolism of the cannabinoids [62,72]. This could result in excessive levels of pro-emetic cannabinoids or emetogenic metabolites. Such genetic variations have yet to be studied in patients diagnosed with CHS and represent an area for future research. Cannabinoid hyperemesis syndrome (CHS) can affect people who use cannabis (marijuana) long-term. The syndrome happens when you have cycles of nausea, vomiting, and abdominal pain after using cannabis (marijuana) for a long time.

Clinical Features, Diagnosis and Treatment

• Since there are so many active chemicals in cannabis, the exact cause of cannabinoid hyperemesis syndrome is unknown.
• One possible treatment option involves the use of benzodiazepines, such as lorazepam, to control nausea and vomiting.
• In the first phase of CHS (the prodromal phase), you don’t vomit.
• Researchers are currently studying several treatment options to manage the hyperemetic phase of CHS.
• Hot showers for symptomatic relief were reported by 17/19 patients [128].

During his last hospitalization he was given conventional antiemetic therapy but his symptoms persisted for 2 more days. He consented to IV haloperidol 1 mg which relieved his symptoms and produced no adverse effects; he subsequently received two more IV doses of 2 mg before he was discharged [114]. An 18-year-old patient diagnosed with CHS refused to stop using marijuana and was treated in-clinic with haloperidol followed by outpatient 5 mg haloperidol which relieved her symptoms of nausea and vomiting.

Excessive vomiting (hyperemesis) phase

• The full text of all relevant articles were obtained and reviewed.
• However, after abstaining from alcohol for long periods, the patient had continued recurrence of the symptoms and increased frequency of presentations to the ED.
• The metabolism of anandamide is principally carried out via fatty acid amide hydrolase (FAAH), whereas the major enzyme metabolizing 2-AG is monoacylglycerol lipase (MAGL) [18].
• THC accumulates largely within body fat which serves as a long-term storage site for the drug [20,22].
• If administering antiemetics, the nursing staff should be familiar with the adverse event profile so they can report any concerns that may arise.

Similarly, Allen et al., Simonetto et al., Patterson et al., and Soriano-Co et al. reported symptom resolution in seven out of seven [6], six out of six [9], four out of four [11], and four out of five [12] patients, respectively. The cumulative synthesis (see Table ​Table1)1) demonstrated that among 64 patients with documented cannabis cessation, 62 (96.8%) had complete resolution of symptoms. The two patients who reported no resolution of symptoms did not have urine testing performed to confirm abstinence [8, 56].

• In a study in Spain, a questionnaire was sent out to all patients over 18 years of age who attended a single outpatient marijuana rehabilitation center in 2014; of the 22 respondents, 18.2% reported symptoms suggestive of CHS [71].
• Sometimes called “weed sickness,” CHS can cause excessive vomiting, abdominal pain, and dehydration.
• For one participating ED with seven patients enrolled in the study, the median charge for ED visits and hospital admissions over the course of a patient’s illness was $95,023 (range $62,420 to 268,110).
• It’s important to be honest about your marijuana use if you have symptoms of CHS.
• It is not clear if there is a comorbid association between CHS and anxiety or whether the symptoms of CHS are so distressing that patients become anxious.
• If symptoms persist and you continue to use cannabis, you may experience more severe problems that require hospitalization for treatment.

Medical Marijuana: How Does It Affect Your Health?

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. In addition, our study identified three unique cases of CHS caused by synthetic cannabinoids [23, 41, 182]. These agents are potent agonists of the cannabinoid CB1 receptors, similar to THC, suggesting that agonism at the CB1 receptor may be responsible for CHS. Supportive care with IV fluids and anti-emetics is the mainstay of treatment in the acute phase of illness.

Low-quality outcomes are those for which further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate. https://ecosoberhouse.com/ Very low-quality outcomes are those for which any estimate of effect is very uncertain. Probably, a crucial factor in the genesis of CHS is the composition of cannabis.

Cyclic Vomiting Syndrome (CVS)

Cannabidiol, in contrast to THC, is non-psychotropic, has a low affinity for CB1 and CB2 receptors [27], and acts as a partial agonist at the 5-HT1A receptor [28]. CBD enhances the expression of CB1 receptors in the hypothalamus and amplifies the hypothermic effects caused by THC [29]. In animals the effect of CBD on toxin-induced vomiting cannabinoid hyperemesis syndrome displays a biphasic response with low doses producing an anti-emetic effect whereas higher doses enhance vomiting [30,31]. Two distinct cannabinoid receptors, CB1 and CB2, have been identified in human and animal models. The CB1 and CB2 receptors function as G-protein coupled receptors that act by inhibiting adenylate cyclase [7].

• There are many suggested pathophysiologic mechanisms of CHS, though evidence for each is minimal (see Table ​Table3).3).
• These two conditions are hard to distinguish between and the main difference is CHS happens with using a lot of marijuana.
• Nearly 100 different metabolites have been identified for THC [24].
• Marijuana has a lot of active chemical compounds called cannabinoids.
• For patients on psychiatric pharmacological regimens, CHS can have a destabilizing effect on the patient [126].

While any amount of long-term cannabis use can lead to CHS, daily cannabis use seems to be more likely to cause CHS than using it less often. Clinical guidelines for the diagnosis of CHS do not currently exist. Some researchers have published their findings from their personal experience with the condition in clinical journals. Researchers have identified two receptors called CB1 and CB2 to which marijuana molecules attach.

Marijuana Cessation