The use of synthetic cannabinoids has been steadily rising, with an associated increase in reported adverse events. There is limited data on managing these adverse events in adults mainly due to the diagnostic challenges of detecting synthetic cannabinoids compared to traditional marijuana. This unique case highlights not only the rare clinical presentation of seizures but also the subtle EKG changes and significantly elevated biomarkers, as would be seen in a myocardial infarction secondary to synthetic cannabinoids.
Marijuana, a readily available drug, can cause long-term adverse effects on overall health, including neurological and cardiovascular events [1]. The National Institute of Drug Abuse has declared marijuana as “the most commonly used illicit drug in the US and the third most common cause of drug-related emergency department visits between 2004-2011.” Presentations can include but are not limited to stroke, myocardial infarction, and other conditions. However there have been very few reported cases of young adults and adolescents with seizures [2], and coronary vasospasms in literature, making this case of a young adult lady who presented with altered mental status and seizures, and was found to have subtle EKG changes and elevated troponins secondary to smoking synthetic cannabinoids, particularly unique and intriguing.
A 21-year-old lady with a long-standing history of depression and polysubstance abuse presented to the emergency room after a friend witnessed a convulsive episode with altered mental status shortly after consuming synthetic marijuana. On route, she experienced convulsive episodes for which she was administered 10 mg of diazepam and 5 mg of midazolam. She was noted to be afebrile, tachycardic with a rate of 102 beats per minute, blood pressure measured at 110/76mmHg, and tachypneic with rate of 24 breaths per minute, saturating 95% on room air. Apart from agitation and altered mental status, the systemic physical exam was unrevealing. Subsequent electrocardiograms revealed nonspecific minor T wave changes in precordial leads (Figure 1). High sensitivity troponins steadily elevated before down trending at 134, 1431, 1389, 1205 ng/L with no other electrolyte abnormalities noted on the complete metabolic panel. Additional work up included leukocytosis and elevated lactic acid at 12080 uL and 10.45 mmol/L, respectively, which were deemed to be reactive as the patient was afebrile and did not have any other signs of infectious etiology. Urinalysis was significant for benzodiazepines and cannabinoids. Based on the presentation and clinical findings, the patient was admitted for acute encephalopathy likely secondary to toxins and underwent seizure and altered mental status protocol with lab work, EEG, and imaging, which revealed no abnormalities. Computed tomography and magnetic resonance imaging of the head and brain respectively revealed no acute pathology She was kept under close monitoring with adequate hydration and initiated on quetiapine nightly over four days, after which she returned to her baseline. She later revealed that she was smoking spice (a designer synthetic cannabinoid) laced with raid (insect repellant). Thus, a link between seizures secondary to the toxic effects of synthetic cannabinoids as well as coronary vasospasm causing elevated troponins was made. The patient was counseled on cessation of drug abuse and discharged home with an appointment for outpatient follow-up for monitoring and addressing her psychiatric illness.
Figure 1: Electrocardiograms.
Synthetic Cannabinoids (SCs) are chemically synthesized by adding compounds to marijuana, which can be laced with various substances and are known by different names, such as Spice, K2, and Spice X [3]. Due to their potent psychotropic effects, stemming from strong agonism of cannabinoid receptors 1 (CB1) and 2 (CB2), recreational use of SCs has become increasingly prevalent in the United States. The strong affinity of SCs to CB1 is hypothesized to cause prolonged neuropsychiatric toxicity and has a higher addictive potential than naturally sourced CB1 agonists like tetrahydrocannabinol (THC). Spice and K2, a popular alternative to marijuana, is favored due to its psychoactive properties, non-detection in routine urine drug screens, and easy availability. Reported adverse effects of SC toxicity include tachycardia, cardiac ischemia, acute kidney injury, agitation, first episodes of psychosis, seizures and death [4]. Cannabinoids decrease Glutamate and γ-Aminobutyric Acid (GABA) synaptic transmission in the brain through mechanisms that are not fully understood. Decreasing the excitatory neurotransmitter glutamate lowers seizure susceptibility while decreasing the inhibitory neurotransmitter GABA increases it. Synthetic cannabinoids, as full agonists of the CB1 receptor, inhibit glutamatergic neurotransmission. Their full agonism of the GABA CB1 receptor may lead to a more potent epileptogenic decrease in GABA synaptic transmission without the mitigating effects of Cannabidiol (CBD) and the novel cannabinoid-sensitive glutamate receptor.
The pathophysiologic effect of marijuana on myocardial ischemia involves increasing sympathetic nervous activity, leading to a higher heart rate and greater myocardial oxygen demand. Additionally, elevated carboxyhemoglobin levels reduce the capacity to supply oxygen. Differentiating vasospastic phenomena from acute myocardial infarction is nearly impossible due to their similar presentations. Synthetic cannabinoids have a higher receptor binding capacity, potentiating these side effects. The diagnosis of SC toxicity is generally made clinically based on history and physical examination, as laboratory analysis for detecting synthetic cannabinoids is complicated and limited [5]. Based on literature research and case reports, it is evident that coronary vasospasm is more likely related to synthetic marijuana use due to its higher potency, the presence of multiple chemicals, and the possible biochemical transformation of THC through interaction with other compounds in synthetic marijuana.
This case underscores the importance of obtaining a comprehensive social history regarding drug abuse and looking beyond the usual suspects like cocaine and marijuana, especially in cases with minimal to no risk factors for coronary artery disease and negative drug screens. It also highlights the need for readily available urine and blood drug detection tests to identify this potentially harmful drug abuse. More importantly, it emphasizes the need to address psychosocial determinants and a holistic approach to effectively combat the usage of recreational drugs among teens and young adults.
Citation: Kondapavuluru R, Tran V, Gonzalez E, Reckley W, Olson K, et al. (2024) Seizures and Elevated Troponins Due to Synthetic Cannabinoids. J Addict Addictv Disord 11: 179.
Copyright: © 2024 Roy Kondapavuluru, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.