Cannabinoid Hyperemesis Syndrome: A Rising Complication

cannabinoid hyperemesis syndrome

In serious cases, doctors might Oxford House insert a nasogastric tube, which goes through your nose into your stomach. Liquid nutrition can be delivered this way, letting your system rest while still getting the calories you need. You’ll stay in the hospital until you can hold down regular meals and your vomiting subsides. Dr. Joshua Yager is an Atlanta native, board-certified family practice physician who is dedicated to the health and wellbeing of his community. As the laws regarding the possession and use of marijuana change, CHS may become more prevalent because more people will have legal access to the drug. Doctors have a lack of knowledge of CHS, and this makes it hard to identify people with the condition.

cannabinoid hyperemesis syndrome

What is Cannabinoid Hyperemesis Syndrome?

Others are exploring the use of probiotics or specific dietary interventions. It’s a bit like throwing spaghetti at the wall to see what sticks, but in a scientific, controlled manner. While our understanding of CHS has come a long way since it was first described in 2004, there’s still much to learn. Researchers are exploring new potential treatments and working to better understand the underlying mechanisms of the condition.

Clinical Features, Diagnosis and Treatment

Until more studies are done on cannabis in all its new forms, putting cannabis “under the umbrella of a safe, legal drug is wrong,” she said. The combination of severe vomiting, dehydration, and potential organ stress means CHS can be life-threatening if not treated. People have landed in the hospital with acute kidney failure or needed intensive care after extended vomiting spells. If you’re seeing signs of severe dehydration—like dizziness, confusion, https://ecosoberhouse.com/ or fainting—seek emergency medical help immediately. But science hasn’t pinned down an exact formula that says, “X amount of cannabis over Y years always leads to CHS.” Instead, it’s more like a storm of factors that eventually converge.

Cannabis hyperemesis syndrome: an update on the pathophysiology and management

cannabinoid hyperemesis syndrome

This variability in recovery time is partly attributable to its accumulation in adipose tissue and due to the extended half-life of THC. Historically, cannabis has been used to stimulate appetite and as an anti-emetic. The FDA approves its use for chemotherapy-induced nausea and vomiting when other anti-emetic treatments fail. Cannabis broadly affects the gastrointestinal system, affecting its secretions, appetite, inflammation, and motility 13,14,15. Cannabis has over 100 cannabinoids in it and has varied effects and toxicity dependent on the THC-to-other-cannabinoids ratio 16.

  • Researchers have only recently discovered CHS, so some doctors or healthcare professionals may not recognize the condition.
  • It’s a bit like throwing spaghetti at the wall to see what sticks, but in a scientific, controlled manner.
  • Darmani has suggested that cannabis increases the core body temperature while concomitantly decreasing skin temperature thus increasing blood flow to the skin and dissipating excess core body heat 72.

Unraveling the CHS Mystery: Symptoms, Phases, and Puzzles

  • Other researchers theorize that the effects of marijuana can change with chronic use.
  • Despite this trend, a strict criterion for the diagnosis of CHS is lacking.
  • Treatment during the hyperemetic phase includes rehydration with bolus intravenous (IV) crystalloid fluids, IV dextrose-containing fluids (to arrest ketosis), correction of electrolyte abnormalities, and treatment of nausea (Table 2).

This suggests that this once “rare” condition is going to emerge as an increasingly common presentation in emergency departments (ED) and clinics. CHS is not trivial; there are fatal cases of CHS (as cause of death or contributing to death) reported in the literature. Cannabinoid hyperemesis syndrome is an uncommon reaction to cannabis use.

  • This systematic review is the first and most comprehensive characterization of the CHS literature.
  • With the continued use of cannabis and a lack of treatment, symptoms become more intense.
  • CHS is also underdiagnosed because people sometimes use marijuana to suppress nausea and vomiting.
  • His vital signs were within normal limits and he was found to have mild epigastric tenderness with no peritonism.
  • Immersing oneself in very hot water relieves vomiting symptoms in CHS patients but has no antiemetic effect on patients with other types of CVS or PV.

Clinical Considerations

Low-quality studies are defined as double-downgraded randomized trials or observational studies. Very low-quality studies are defined as triple-downgraded randomized trials or downgraded observational studies or case series/case reports. For each treatment modality, reviewers explored the evidence and the study design. For each mechanism proposed, chs syndrome reviewers explored the supportive evidence and the study design.

In patients treated at home, recommendations are emphasized to consume fluids containing glucose and electrolytes between vomiting episodes to ensure adequate hydration. CHS patients generally do not experience significant weight loss, as periods of regular oral intake often compensate for the days of vomiting. The primary modes of psychosocial intervention in cannabis use disorder are CBT and motivational approaches, which include the importance of the individual or the social environment. More specifically, CBT and relapse prevention approaches primarily focus on the identification and management of thoughts, as well as external triggers, that lead to its use. These approaches teach coping and problem-solving skills and promote the substitution of cannabis-related behaviors with healthier alternative behaviors 93. In contrast, motivational interviewing attempts to build motivation in an empathic and non-judgemental environment and emphasize the importance of self-efficacy and positive change.

How Common Is CHS?

For CHS patients, these tests typically offer normal-range results, but they are expensive, time-consuming, and place a hardship on the patient as well as the healthcare system. Thus, prompt diagnosis of CHS can save valuable clinical time and resources. CHS tends to affect younger people; the patients reported in Table 2 ranged in age from 15 to 47 years. It has been suggested that this is due to the fact that cannabinoid use is about double in younger people compared to older individuals 135. The authors found no cases of geriatric CHS (≥65 years), but there is no reason evident why geriatric individuals who used marijuana long term would be immune from CHS. It is not known why the syndrome develops in some, but not all, long-term marijuana users and why symptoms take longer to manifest in some patients than others.

cannabinoid hyperemesis syndrome

3. Recovery Phase

cannabinoid hyperemesis syndrome

These symptoms can reoccur in a cyclical pattern for as long as cannabis use continues. This cycle can send patients on repeated visits to the ER, and in rare cases, can even lead to death from kidney failure. Use of topical capsaicin for treatment of CHS seems promising as previously reported in several case reports and studies. However, further studies are warranted to support this finding to be used as a first-line treatment option for CHS management.

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. 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. Understanding the ECS and its effects on the vomiting center of the brain are fundamental to explain the effect of cannabis for this biphasic response 21. The ECS is composed of ligands, receptors, signaling, and enzymes (its regulators and inhibitors) 22.