Inhalant-related disorders — chroming, sudden sniffing death, and N2O myeloneuropathy (MEQ)

(i) Immediate medical priorities and sudden sniffing death. Treat as medical emergency: ABC, remove residual bags/paint exposure, oxygen as needed, glucose, ECG and cardiac monitoring after collapse with recent hydrocarbon/chroming use, observe for arrhythmia, aspiration and trauma. Avoid framing as trivial "behavioural only." Sudden sniffing death (hydrocarbon-associated sudden collapse) is classically a fatal ventricular arrhythmia on a sensitised myocardium, often precipitated by exertion, fright or catecholamine surge during or immediately after use — this case's running after police is a classic trigger context. Witnessed collapse needs ACLS-ready care.[2][3]

(ii) Adolescent assessment and comorbidity. Structured history of products, methods (bagging/chroming), frequency, solitary vs group use, access, last use; MSE; suicide and accidental-death risk; capacity; collateral from family/school. Screen trauma, mood, psychosis, ADHD/conduct, other SUD. Clinical samples with inhalant use disorders show high psychiatric and behavioural comorbidity — not isolated curiosity when disorder-level use is present.[1][7][8]

(iii) Ongoing management and pharmacotherapy position. Backbone is psychosocial: engagement, motivational work, family/school involvement, youth AOD case management, counselling and structured programmes (recreation/engagement/residential in selected cases). State explicitly: Cochrane review found no eligible RCTs establishing a licensed anti-craving or substitution pharmacotherapy for inhalant dependence — do not invent methadone-equivalent. Treat comorbid conditions on their merits.[5][6][8]

(iv) Cousin — N2O myeloneuropathy. Subacute sensory ataxia after heavy recreational nitrous oxide with borderline B12 suggests functional B12 deficiency myeloneuropathy. Stop N2O immediately; check MMA and homocysteine (may be elevated even if B12 not frankly low); start parenteral B12 early (teaching example: hydroxocobalamin 1 mg IM daily for several days per local neurology protocol, then spaced dosing), folate support, MRI cord/neurophysiology as indicated, rehab. Dual-formulate other myelopathy differentials.[4]

(v) Harm reduction and disposition. Product access control at home, education about first-use sudden death risk, avoid solitary bagging, fire/burns awareness; for N2O address peer supply and local retail laws. Disposition: medical clearance and observation after collapse; youth MH + AOD follow-up; neurology for myelopathy; culturally safe community responses if petrol sniffing cluster context; written safety plan for suicide and when to return (chest pain, syncope, progressive numbness).[3][8]