A 12-year-old boy presented to the emergency room with acute onset altered sensorium. His parents gave history of multiple episodes of non-bilious and non-projectile vomiting two hours after returning from school and having lunch. Following which he became drowsy, spoke in appropriately, had history sugges-tive of visual and auditory hallucinations, and bladder incontinence. There was no history of fever, seizures, weakness in any limb or cranial nerve palsies. There was no past history of altered sensorium or seizures and the child was not on any medications.

The child had a heart rate of 120 per minute, respiratory rate of 32 per minute, blood pressure of 100/60 mm Hg (50th to 90th centile), was febrile with a temperature of 1010F and was in a minimally conscious state (Glasgow coma scale 8). Both pupils were mid-dilated and were sluggishly reacting to light. The child had an involuntary pill rolling movement of his fingers which disappeared on sleeping. Rest of the motor examination was normal. There were no cerebellar signs, signs of meningeal irritation or signs of raised intracranial tension.

A provisional diagnosis of acute onset encephalopathy with mydriasis was kept with differential diagnosis of viral encephalitis, metabolic encephalopathies (including uremic and hepatic), intoxication, post-ictal state and snake envenomation. The child was managed empirically with intravenous fluids, injection ceftriaxone (1 g/kg/d) and acyclovir. On investigation, dextrose was 107 mg/dL, hemoglobin 10.5 g/dL, leukocyte count 6.7×109/L, platelet count 260×109/L, sodium 142 mEq/L, pota-ssium 4.2 mEq/L and ionized calcium 4.5 mEq/L. Serum creati-nine, bilirubin and alanine transaminase were within normal limits. Blood gas revealed a pH of 7.43, bicarbonate 23 mmol/L and lactate 1.3 mmol/L.

The child’s vitals remained stable and with continued supportive care his sensorium improved to normal in the next 36 hours. Urine toxicology screen by qualitative radio immune assay (threshold for detection >50 ng/mL) showed presence of tetrahydrocannabinol (THC), thus supporting toxin ingestion (marijuana) as the cause of encephalopathy. After regaining his sensorium, the child revealed that he had consumed a chocolate- like sweet that had been given to him by a friend on the day of symptom onset.

Cannabis is consumed in different forms such as dried leaves (marijuana), resin (hashish), and concentrated resin extract (hashish oil). Hashish may be easily mistaken for a chocolate by a child, and this may be the reason why hashish is the most common (38%) documented oral ingestion [1]. THC is the main psychoactive ingredient that binds to brain canna-binoid receptors, producing dose- and time-dependent stimulant, hallucinogenic or sedative effects. Effects of cannabis starts from 30 minutes to 3 hours of ingestion and lasts up to 12 hours. With the increased bioavailability of cannabis concentrates and the smaller body mass in children, childhood cannabis ingestion results in high serum THC levels, even if small amounts are consumed [2].

Paediatric cannabis intoxication has a variable presen-tation, most commonly neurological (confusion, lethargy, coma or agitation) followed by ophthalmological (bilateral reactive mydriasis), cardiovascular (tachycardia, hyper-or hypotension) and respiratory depression needing mechanical ventilation [3]. These symptoms are nonspecific and mimic postictal state, encephalitis, metabolic causes and sympathomimetic agent poisonings which may lead to a delayed diagnosis and unnecessary diagnostic evaluation, particularly in a drowsy child. High index of clinical suspicion and early urine screening can prevent invasive and costly investigations like lumbar puncture and neuroimaging respectively, and may reduce the need for prolonged empirical treatment with intravenous antibiotics and antivirals. Its rare availability in most settings, lack of expertise in testing and high cost limits its widespread use. Initial urine screening is typically performed with enzyme multiplied immunoassay technique, which is then confirmed by gas chromatography-mass spectrometry [4,5]. Results of screening test are available in a few hours (reduced to minutes with point of care testing) whereas the confirmatory test requires a few days.

Examination of the pupils provides a valuable clue to the underlying disease, especially in cases of suspected toxin. Mydriatic pupils are seen in anticholinergic (atropine, anti-histaminic, antipsychotic), sympathomimetic (cocaine, amphe-tamine, lysergic acid diethylamide, etc) toxidromes and cannabis ingestion, whereas miotic pupils are seen in cholinergic (organophosphate, carbamate) and opioid (morphine, heroin, codeine) toxidromes [6]. In this case of unexplained encephalopathy with reactive mydriatic pupils, we narrowed our differentials to the former category of intoxicants.

Clinical recognition of altered mental status by marijuana exposure can be challenging in children. However, increased awareness regarding childhood drug abuse, its clinical effects especially on pupils, as well as utilization of toxicology screen in those with high suspicion facilitates early diagnosis, limits extensive investigations and facilitates implementation of preventative measures, especially in a resource-constrained setting like ours.

1. Richards JR, Smith NE, Moulin AK.Unintentional cannabis ingestion in children: A systematic review. J Pediatr. 2017; 190:142-52.

2. Levene RJ, Pollak-Christian E, Wolfram S.A 21st century problem: Cannabis toxicity in a 13-month-old child. J Emerg Med. 2019;56:94-6.

3. Claudet I, Mouvier S, Labadie M, et al. Unintentional cannabis intoxication in toddlers. Pediatrics. 2017;140: e20170017.

4. Thomas AA,Mazor S. Unintentional marijuana exposure presenting as altered mental status in the paediatric emergency department: A case series. J Emerg Med. 2017; 53:e119-e123.

5. Moeller KE, Lee KC, Kissack JC. Urine drug screening: Practical guide for clinicians. Mayo Clin Proc. 2008;83:66-76.

6. Davies E, Connolly DJ, Mordekar SR. Encephalopathy in children: An approach to assessment and management. Arch Dis Child. 2012;97:452-8.