This case presents a previously unreported phenomenon, the occurrence of WE in a pediatric patient with cannabinoid hyperemesis syndrome.

WE results from thiamine deficiency. Thiamine is an essential cofactor for many metabolic processes and deficiency has the potential to affect all organ systems, especially the nervous system. Thiamine is water soluble and is stored in limited quantities (on average 30−50 mg) primarily in the liver. This vitamin is not produced endogenously and must therefore be ingested in sufficient quantities to meet individual metabolic demands which varies by age and activity level. Most individuals require 0.5−1.5 mg per day. ³ Therefore, on a thiamine restricted diet, stores are typically depleted in 4−6 weeks. The adolescent male described previously developed symptoms of WE within 2 months of the onset of daily emesis. We believe that his chronic emesis contributed to decreased absorption and possibly intake of thiamine as the patient had begun to engage in restrictive eating practices to decrease likelihood of emesis. It also bears noting that emesis itself may have been a symptom of WE.

There are several unique features of this case which bear noting. Firstly, the patient described experienced significant neurologic deterioration after the administration of dextrose containing IV fluids. Thiamine acts as a cofactor for pyruvate dehydrogenase and α‐ketoglutarate dehydrogenase, two enzymes involved in the metabolism of glucose and production of adenosine triphosphate. In thiamine deficiency, administration of glucose can result in ineffective adenosine triphosphate (ATP) production and accumulation of toxic intermediates which may exacerbate neurologic symptoms. This supports the conventional advice to administer glucose concurrently with thiamine when thiamine deficiency is suspected.

This patient's young age, obesity and absence of chronic alcoholism deviates significantly from the classic patient demographics associated with WE. Atypical presentations and lack of alcohol use disorders have been found to be linked to delayed diagnosis and increased risk of incomplete recovery. ⁴ It is critical for clinicians to be aware of diverse etiologies beyond alcohol abuse for WE. ⁵ , ⁶   This case serves as a reminder to clinicians to maintain a high index of suspicion for WE in patients with persistent vomiting of any etiology. ⁷ , ⁸

Cannabinoid hyperemesis has become more prevalent in the adolescent population with increasing cannabinoid use. This is exemplified by doubled emergency room visits for cannabinoid hyperemesis in several states postcannabis legalization, signaling a pressing public health concern. ⁹

Furthermore, the case described highlights the fact that individuals with elevated body mass index may also have nutrient deficiencies. Contrary to the common perception that obesity precludes vitamin deficiencies, several reports have suggested that diets high in simple sugars and low in thiamine‐rich, whole foods may increase the risk for thiamine depletion. ¹⁰ This is especially relevant given thiamine's critical role in glucose metabolism.

Finally, the significant clinical improvement observed following thiamine supplementation in our patient reinforces the efficacy of this intervention. Given thiamine's safety profile, characterized by its water‐solubility and renal excretion, we advocate for the preemptive administration of thiamine in cases where WE is suspected, even before definitive laboratory confirmation.

The association between cannabinoid hyperemesis and WE in this adolescent patient adds a new dimension to our understanding of WE, emphasizing the diversity of its etiologies beyond chronic alcoholism. It is strongly recommended that clinicians supplement with thiamine immediately when WE is suspected to minimize adverse effects. It is also recommended clinicians consider the shifting trends of substance abuse and diet among the pediatric population and be vigilant for micronutrient deficiencies that may ensue.