Intussusception is an uncommon process outside of the pediatric population and AI accounts for 5% of all small bowel obstructions. It occurs when one segment of bowel ‘telescopes’ into an adjacent segment, usually due to a lead point (secondary intussusception), resulting in potential obstruction and vascular compromise. The cause is usually benign in children and is managed by pneumatic or hydrostatic reduction with high success rates. In contrast, AI raises concern for tumors (≥65%) or other harboring pathology, whether intra-luminal or extra-luminal (e.g. diverticula, adhesions, polyps, celiac disease, Crohn’s disease) [4, 5]. An unknown cause (primary or idiopathic) in adults has been reported up to 20% of the time. CT is the best modality for diagnosis, showing sausage-shaped mass, target sign, vascular compromise and sometimes a lead point. Intussusception in adults has traditionally been highly associated with a malignant lead point and, thus, required surgical exploration. Due to such high tumor rates, the traditional approach to AI has been surgery; however, consideration to a more conservative management has been warranted more recently in the absence of warning signs [6, 7].

There are proposed mechanisms that explain the role of cannabis on intestinal function. These mechanisms attempt to describe the symptoms associated with CHS. CHS occurs in chronic marijuana smokers and is characterized by abdominal pain associated with intractable nausea and vomiting, often relieved by hot showers or smoking cessation [3]. Proposed mechanisms on a cellular level include G-coupled CB (CB₁ and CB₂) receptors located throughout the body producing various effects, i.e. the exogenous CB Δ9-tetrahydrocannabinol (THC) binds to CB₁ receptors in the central nervous system leading to alterations in psychomotor behavior, appetite stimulation, as well as anti-emetic effects.

CB₁ receptors located within the enteric nervous system, when stimulated by CBs, produce effects that include alterations in gastric and intestinal motility, decreased gastric emptying and LES relaxation [8, 9]. Exogenously applied CB receptor agonists inhibit enteric neuronal activity. In a publication by Boesmans et al. shows that CB1 receptor activation on myenteric neurons maintained in primary culture can suppress neuronal activity, presynaptic release of acetylcholine and mitochondrial transport along axons. They also provide initial evidence that myenteric neurons release endocannabinoids and which activate CB1 receptors constitutively [10]. As we develop a deeper understanding of these mechanisms and interactions, it seems reasonable to believe that both exogenous and endogenous CBs interacting with CB receptors may cause alterations in gut motility significant enough to cause an intussusception.