While marijuana use in pregnancy is expected to rise due to increase in its liberalization and popularity, there has been lack of studies on its pharmacokinetic effect on pregnant women and their fetuses. The current preliminary data suggest that delta-9-tetrahydrocannabinol (THC), a main active ingredient in marijuana, crosses the placenta, and the prenatal exposure to THC may negatively impact the child's future higher cognitive functions as well as psychological development [10–14]. Therefore, it is recommended that pregnant women refrain from marijuana use until further information is available and proven otherwise.

Although cannabis is usually known for reducing nausea and vomiting, various theories have been proposed to explain the pathophysiology of CHS. While THC produces an antiemetic effect by activating the G-protein coupled cannabinoid 1 (CB1) receptors in the dorsal vagal complex, some suggest its greater effect on the CB1 receptors in the enteric nervous system, which decreases peristalsis and gastric emptying, inducing emesis [15]. There is also an evidence that synthetic marijuana may cause CHS by overactivating the CB1 receptors [5]. In addition, THC's tendency to sequester in fat tissue may explain why chronic, heavy users of marijuana are more prone to CHS [16]. On the other hand, other nonpsychoactive components of marijuana, such as cannabidiol and cannabigerol, may also have a similar correlation with vomiting. In their study, Parker et al. showed that cannabidiol acts as an antiemetic in low levels and proemetic in higher levels in shrews [17].

As seen with our patient, frequent hot bathing has been reported to relieve symptoms of nausea and vomiting in CHS. Among several theories to explain this interesting response, one proposes that increased body temperature may turn off chronic hypothalamic activation by cannabinoids. Another theory posits that dilation of cutaneous vessels may decrease blood flow to the cannabinoid-vasodilated splanchnic vessels, which may reduce nausea and vomiting [4]. Regardless of the mechanism, frequent hot bathing may exacerbate dehydration, leading to hypotension and increased risk of falls. Increased dehydration with heat exposure diverts blood flow to the skin, away from the maternal organs and fetus, and increases antidiuretic hormone and oxytocin release, inducing preterm labor [8]. Moreover, consequent maternal weight loss further increases the risk of preterm labor and small gestation for age [18]. Maternal use of hot tubs for over 30 minutes during the first trimester—which many patients with CHS greatly exceed—has also been associated with neural tube defects, esophageal atresia, omphalocele, and gastroschisis [6].

Dehydration is a common consequence of repetitive nausea and vomiting, and therefore, fluid resuscitation is usually required in the CHS patients [3, 4]. In alleviating symptoms of CHS, traditional antiemetic medications such as ondansetron, promethazine, and metoclopramide have been reported to be fairly ineffective. Alternatively, benzodiazepines, haloperidol, and capsaicin have been shown to be effective in the management of acute and tricyclic antidepressants in that of chronic CHS [19]. Although traditionally used in treatment of psychosis, haloperidol has an effect on dopamine D2 receptors in the chemoreceptor zone and potentially on cannabinoid 1 (CB1) receptors in the central nervous system. In a report by Hickey et al., IV haloperidol (5 mg) was administered in a patient with CHS, and he reported relief of symptoms within one hour with no vomiting for the subsequent eight hours [20]. Topical capsaicin had been explained to produce an antiemetic effect by binding to the transient receptor potential vanilloid 1 receptor, located near CB1 receptors throughout the body, and inhibiting the release of substance P, involved in nausea and vomiting [21, 22]. While our patient was managed with traditional antiemetics, earlier diagnosis of CHS and treatment with benzodiazepines or haloperidol could have led to faster resolution of symptoms. Future prospective trials are needed to evaluate and define optimal pharmacologic treatment of CHS.

The best treatment is, nevertheless, cessation of marijuana use, which could take up to a week for noticeable improvement [2]. Patients often attempt to treat their symptoms with more marijuana consumption, which can worsen or prolong their episodes of emesis [4]. Therefore, education, counseling, and cognitive behavioral therapy can be crucial components in successful treatment and prevention of these episodes.