Cannabinoid Hyperemesis Syndrome: The Anti-Munchies

Amy Matson, MD, PGY2
Brown University, Emergency Medicine Residency

Your next ED patient is in the department 8 times in 2 week for nausea and vomiting and abdominal pain with negative work ups.
There is a powerful skunk smell in the air.
What’s going on? And can you do something to help?

With increasing use of marijuana nationwide, there has been an increase in a marijuana-related syndrome termed cannabinoid hyperemesis syndrome (CHS) characterized by cyclic episodes of refractory nausea, vomiting, and persistent pain that is not relieved with traditional supportive care.

Although marijuana is still classified as Schedule I by DEA (Schedule I drugs, substances, or chemicals are defined as drugs with no currently accepted medical use and a high potential for abuse), the legalization for both medical use and recreational use has significantly increased over past few years. Currently, medical use is legalized in 28 states and recreational use is legalized in 8 states. In addition, numerous states have decriminalized possession of small amounts of marijuana making the consequences of marijuana use minimal.

Many people have viewed the state of Colorado as an example of how widespread marijuana use will affect the economics, policy, and health of its residents. Medical use was initially legalized in Colorado in 2000, but not frequently utilized until 2009 when federal policy changed stating they would cede jurisdiction to state governments. Recreational marijuana use approved by voters in 2012 and retail marijuana sales began in Colorado on Jan 1, 2014. Both medical and recreational marijuana use have increased over the past years and health care leaders have taken notice.

A recent study at University of Colorado reviewed ED visits pre and post recreational marijuana sales. They found an increase in burns related to manufacturing marijuana products, accidental ingestions by children, acute marijuana intoxication with psychosis, exacerbation of chronic psychiatric conditions, as well as an increase in cyclic vomiting syndrome.

A small study at 2 Denver-area hospitals revealed an increase in cyclic vomiting presentations from 41 per 113,262 ED visits to 87 per 125,095 ED visits (prevalence ratio, 1.92) after medical marijuana liberalization.

Cannabinoid hyperemesis syndrome was first described in medical literature in 2004 by Allen et al. In addition, updated proposed clinical criteria were released in 2009 based on a Mayo Clinic Case series of 98 patients. Criteria essential for diagnosis include chronic marijuana use and then major features include cyclic N/V, epigastric pain, weekly use of marijuana, resolution of symptoms with cannabis cessation. However, the diagnosis of cannabinoid hyperemesis syndrome should be a diagnosis of exclusion. It is important to remember that emergent conditions can also mimic these symptoms such as SBO, perforated ulcer, appendicitis, ischemia, renal colic, pyelonephritis.

There are multiple proposed theories regarding the development of CHS but no definitive evidence or single mechanism. Possible contributing factors include slowed gastric motility and impaired peristalsis by CB1 receptors in CNS and enteric plexus. Another proposed theory involves the chronic activation of these receptors that lead to a paradoxical emetic effect. THC in marijuana is an extremely fat soluble compound so stores for long periods of time in fat tissue. When a marijuana user inhales THC it quickly reaches the brain to give the typical euphoric “high” sensation. It then slowly absorbs into the fat tissue where is gets stored. As the THC in the blood stream from the initial use begins to decrease, there will be a slow “leech” of THC from the fat tissues back into the blood stream. With chronic marijuana use, this amount of THC that gets leeched back into the bloodstream is theorized to lead to chronic activation of CB1 receptors, potentially causing a paradoxical effect on the normal receptor activation.

A key feature of this syndrome is compulsive bathing and showering which seems to relieve symptoms. Patients have been found to shower >20 times per day or spend prolonged multiple hour periods in the shower. Again, multiple theories have been suggested for this but the most promising theory involves TRPV1 receptors that are head-gated ion channels found in the peripheral nervous system and skin. They are activated by scalding heat (>109F) and have been found to interact with the endocannabinoid system. Most patients are not forthright with the fact that they abuse marijuana, nor do they realize the link between marijuana and CHS. Asking patients who present with cyclic vomiting if they have relief with hot showers can clue you in to the diagnosis. No other cause of vomiting has shown improvement with hot showers.

Although CHS does not have a life threatening etiology, there are specific complications that can arise from the syndrome which include cutaneous burns from compulsive showering, AKI, electrolyte abnormalities, and dramatic weight loss. Supportive care for these complications should be provided as indicated.

Treatment for CHS includes traditional supportive care with IV fluid hydration and anti-emetics. Other more tailored treatment options include Haldol and capsaicin cream. Numerous case reports have been released citing significant patient improvement with Haldol. No randomized or controlled studies have been performed on this topic. Haldol acts as a D2 receptor antagonist. CB1 receptors in the nucleus accumbens and prefrontal cortex release dopamine. It is theorized that Haldol dopamine antagonism reverses some CB1 receptors that could play a role in the syndrome. Another alternative treatment option is capsaicin cream. As discussed previously, TRPV1 receptors in the peripheral nervous system (ie skin) are activated when exposed to scalding heat, potentially being the reason hot showers resolve CHS symptoms. These same receptors are activated by topical capsaicin cream. Patients should feel fairly immediate relief (at most 30 minutes from time of application) with application of capsaicin cream to skin. Some case reports have used on the abdomen, others spread across the body on the arms, legs, and torso.

Ultimately, the only treatment for CHS is marijuana use cessation. Counseling our patients on the importance of marijuana cessation should be the most important goal for their ED visit. It is the only treatment that can effectively cease the symptoms of CHS. Without marijuana cessation, the patient will continue to experience cyclic bouts of symptoms. As discussed earlier, marijuana metabolites including THC are stored in the body’s fat tissue for many days and even weeks before being excreted out of the body. Therefore, patients cannot expect to see improvement until weeks to months from the time they quit smoking. Patients should be counseled on this so they do not restart using marijuana after only a few days of abstinence.

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