Synthetic marijuana is a street drug sold under various names at various convenient stores, tobacco stores and through the internet. SCB are mostly smoked or inhaled while some use it as an additive to herbal teas or food [6]. The major engineered compound in SCB mimics the active constituent, delta-9-tetrahydrocanabinol (THC), of marijuana that binds to the G protein-coupled cannabinoid receptors (CB), cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2) [2,7,8]. SCB can contain multiple active ingredients and little is known about the metabolism of those compounds [8,9]. Nonetheless, multiple studies have revealed more toxicity associated with SCB compared to marijuana due to the higher potency of the synthetic ingredients [2,8,10,11]. This increased toxicity is mostly explained by the full agonism of synthetic compounds towards CB compared to the partial agonism of THC to CB [10].

The Food and Drug Administration (FDA) has thus far approved three different cannabis-related drug products including dronabinol (oral and liquid formulations), and nabilone [12]. Similarly, there is only one cannabis-derived drug product approved by the FDA, known as cannabidiol [12]. All of the four aforementioned cannabis-like substances are available only by prescription from a licensed health-care provider. Any other form of SCB, such as the one consumed by our patient named K2 (unknown active ingredient), is not approved by FDA for consumption. The unregulated SCB are sold with a disclaimer on the package, ‘not for human consumption.’ [10,13] The packages of SCB available in the market have various quality and quantity of ingredients. Type and concentration of SCB present between batches of SCB as well as packets of same brand-named SCB can also be variable [6,14].

Although CBs are found predominantly in central nervous system (CB1 receptors) and peripherally in the immune cells (CB2 receptors), both these receptors have also been reported in various other tissues including peripheral nervous system, cardiovascular system, gastrointestinal tract, liver, adipose tissue, bone, and reproductive system [15–17]. Many of the serious adverse effects of SCB toxicity can, therefore, be explained by the presence of CB receptors throughout the body. Table 1 shows various adverse effects of SCB toxicity affecting multiple organs.

SCB intoxication can present as a clinical conundrum. The constellation of clinical effects can range from behavioral abnormalities to more serious consequences including various organ system dysfunction as described in Table 1. There is no known antidote for SCB intoxication, making supportive care the primary treatment. Standard urine toxicology does not detect SCB, therefore obtaining a detailed history about the recreational use of these substances becomes a paramount to solving the diagnostic dilemma of SCB intoxication. In this case, we believe that the chemicals present in the new packets of K2 caused him to become hypertensive, and rapidly progressed to PRES manifesting as altered mental status and seizures. To our knowledge, this is the first case reporting SCB induced posterior reversible encephalopathy syndrome (PRES). In our patient’s case, although common viral etiology as a cause of his clinical manifestations was eliminated, the presence of uncommon viruses was not tested and remains a limitation of our study. Further, patient’s urine toxicology upon admission revealed benzodiazepine, yet he refused the use of any other substance except cannabis and SCB. In this setting, the use of any other substance, undisclosed by the patient, cannot be totally excluded. Further, since SCB consumption is a growing public health issue with little understanding of dose-related toxicity future studies on dose-related severity of adverse effects of SCBs are warranted to understand the SCB toxicity better.