A 15-year-old boy with acute onset abdominal pain and hypertension

A 15-year-old boy with a current history of depression and attention deficit hyperactivity disorder presented to a paediatric emergency department with sudden onset of nausea and severe diffuse abdominal pain. At the time of presentation, he had been prescribed dextroamphetamine/amphetamine salts, methylphenidate osmotic-controlled release oral delivery system, clonidine and sertraline, but acknowledged he had been inconsistently taking these medications. Four days prior to presentation, he had been assessed for intentional acetaminophen overdose following peer and family conflict. At that time, he was evaluated to have nontoxic serum level of acetaminophen (<20 µmol/L) 5 hours following reported ingestion, with normal blood pressure of 119/74. He was subsequently discharged home to his family following psychiatric evaluation with community supports in place. On subsequent presentation, history revealed marijuana use (4 g smoked with two friends to relieve stress) 2 days prior with denied use of alcohol, over the counter or prescribed psychoactive medications. Physical examination revealed stage 1 hypertension (blood pressure 140/93), with remainder of vitals within normal limits. There was tenderness to deep palpation on abdominal examination with absence of peritonitic signs. The remainder of his examination was unremarkable with symmetric normal pupillary examination, and normal temperature of 37.0°C measured axillary. Investigations showed a creatinine level of 182 µmol/L (previously normal 73 µmol/L 4 days prior) with normal blood urea nitrogen and electrolytes. Repeated serum acetaminophen level was noted to be <20 µmol/L. Urinalysis showed 3+ blood and 3+ protein with normal urine electrolytes and fractional excretion of sodium was calculated to be 13%. A urine drug screen was negative for drugs of abuse, including cannabis and amphetamines. Complete blood count, creatinine kinase, Venous gas, LDH, C3 and C4 were all within normal limits. Renal ultrasound showed mildly echogenic kidneys and no other abnormalities. Home medications were held during his inpatient admission. The patient was admitted to the general paediatric service with nephrology and adolescent medicine consultations. Consent from the patient was obtained for toxicological analysis of a sample of the marijuana he had smoked and ‘bong’ (water pipe) he used, which confirmed suspicion of the diagnosis. The patient was diagnosed with acute kidney injury (AKI) believed to be secondary to nephrotoxicity associated with synthetic cannibinoid use. Our patient’s report of recent marijuana use with negative cannabis screen prompted consideration of this diagnosis. Toxicology studies revealed that JWH-018, JWH-073 and JWH-122, known synthetic cannabinoid (SC) receptor agonists, were detected in residue within patient’s supplied sample (1). Serum creatinine levels for our patient increased with peak measurement of 282 µmol/L on the second day of admission. His hypertension persisted and treatment was initiated with amlodipine. He maintained adequate urine output and was managed with aggressive fluid restriction. On his fourth day of admission, he began to demonstrate improving renal function, with no subsequent need for hemodialysis or renal biopsy. The patient expressed a desire to reduce his marijuana use and was referred to a community problematic substance use program for youth. On follow-up, he was found to have normal renal function, with resolution of hypertension and normal urinalysis. SCs are a diverse group of chemical compounds available in Canada in numerous forms (2). Little is known about their specific pharmacological profile and toxicology (3). SCs are proposed to function similarly to THC (Δ9-tetrahydrocannabinol), the main psychoactive ingredient in cannabis. The desired effect, or ‘high’ associated with smoking SCs or marijuana occurs when THC or SCs bind to the CB1 receptor in the brain. While THC is a partial agonist at this receptor, many SCs function as full agonists and are said to bind to the receptor with a much greater affinity than THC (4,5). It has been demonstrated that metabolism of SCs can differ based on the drug and the individual user (6). These formulations, originally created in laboratories dedicated to drug development research, are now produced and advertised as recreational drugs with more intense cannabis-like effects. They are also marketed with the added benefit that many are not detectable on standard drug test screening (7). Typically, SCs are comprised of mixtures of unknown plant products (not marijuana) that have been sprayed with liquid forms of SC material (8). As of 2014, there were over 84 different forms of SCs identified (2). They currently exist under various names such as ‘legal high’, ‘Spice’ and ‘K2’ (9). Despite including a label that states ‘not for human consumption’ (some believe an attempt to divert drug laws in regions where they are sold), they are typically smoked in a pipe or bong. A new concerning development includes SCs prepared in liquid cartridges used in electronic cigarettes, which may reflect a targeted approach by drug manufacturers to market directly to young people, a population where the practice of ‘vaping’ has become more popular (7,10). The use of SCs is growing in North America (7). While some are illegal in Canada under the CDSA (Controlled Drugs and Substances Act), SCs are available in convenience stores and ‘head shops’ ranging from $10 to $20 per 1.25 g (2,11,12). The number of calls Poison Control Centres in the USA received related to SCs grew from zero in 2010, to approximately 41,000 SC-related calls in 2012 (13). In Canada, the 2014 Youth Smoking Survey revealed 1% of students in grades 7 to 12 reported using ‘synthetic marijuana’ in the past year, representing 30,000 youth nationwide (2). There is a growing body of literature on the nature and extent of harm associated with SC product use. There have been deaths attributed to SC use in the USA (both from direct effects as well as indirect such as suicide related to psychosis). Long-term effects of SCs remain unknown (3). The most commonly recognized clinical manifestations include delusions, hallucinations, anxiety, agitation, nausea, vomiting, palpitations, tachycardia, hypertension and conjunctival injection. More serious complications include seizures, psychosis, myocardial infarction and AKI (5,7). AKI associated with SC use was first reported in the USA in 2012 (14). To date, published case series represent 21 cases (all but one male, median age 20 years). Presenting symptoms included nausea, abdominal and back pain. Urinalysis was abnormal in most cases with renal ultrasound findings showing increased echogenicity. Renal biopsies were performed in 13 cases, showing acute tubular necrosis in most and findings consistent with acute interstitial nephritis in three cases. Five patients required hemodialysis, with the rest recovering following supportive management similar to what happened with our patient (15). To our knowledge, this is the first reported Canadian paediatric case within the literature. The current case emphasizes the need for paediatricians and adolescent care providers to become familiar with these drugs and their typical presentations as they continue to be perceived as low risk by inexperienced users and have the tremendous potential to lead to severe health consequences. The pathogenesis of AKI in SC use is unknown. One theory proposes that SC products contain an as yet unidentified nephrotoxic contaminant and that SCs are inherently nephrotoxic. An additional proposed theory relates to a common presenting feature of vomiting (which was not present in our case) and proposes that acute tubular necrosis arises from hypovolaemia. Whatever the identified cause of nephrotoxicity, the association between SC exposure and AKI in adolescents reinforces the need for awareness of emerging drugs of abuse, which are easily accessible and potentially dangerous (15). Synthetic cannabinoids continue to be readily available to adolescents in Canada, with new variations developing, each with the potential for adverse effects. Adolescent health care providers should advocate for policy makers to address synthetic cannabinoids as a drug control issue. Paediatricians and adolescent health care providers should ask about newer drugs such as synthetic cannabinoids during adolescent history taking. Collaboration and engagement with adolescents remains key to diagnostic clarity when addressing important medical issues.

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