Cannabis, Hallucinogens, Inhalants & Club Drugs

Cannabis and synthetic cannabinoids

Intoxication. THC activates CB1 receptors, producing euphoria, slowed time sense, impaired short-term memory and driving, conjunctival injection, dry mouth, increased appetite, and tachycardia. High-potency products can cause anxiety, paranoia, or frank psychosis, and heavy adolescent use raises the risk of later psychotic disorders. Edibles can take 1–2 hours to act, so users redose and overshoot; young children who eat them present with lethargy and ataxia. THC metabolites are fat-soluble, so urine tests stay positive for days after occasional use and for weeks in heavy users.

Cannabinoid hyperemesis syndrome. Chronic heavy users develop recurrent episodes of intense nausea, vomiting, and abdominal pain that are relieved by compulsive hot showers or baths and often resist ondansetron. Acute care is IV fluids with electrolyte correction, topical capsaicin, and haloperidol or droperidol; sustained abstinence is the only cure.

Withdrawal. After heavy use, symptoms begin within about a week (often 1–3 days): irritability, anxiety, insomnia with vivid dreams, low appetite, restlessness, and low mood. They peak in the first week and last 1–2 weeks. Treatment is supportive, and cannabis use disorder is treated with CBT, motivational enhancement, and contingency management.

Synthetic cannabinoids. Products sold as "K2" or "Spice" are full CB1 agonists far more potent than THC. They cause severe agitation, psychosis, seizures, tachycardia, and acute kidney injury, yet standard urine screens are negative. Treat with benzodiazepines and supportive care.

Dissociatives: PCP and ketamine

Phencyclidine. This NMDA antagonist produces horizontal and vertical nystagmus, hypertension, tachycardia, agitation and violence, analgesia that lets patients injure themselves, ataxia, hyperthermia, seizures, and rhabdomyolysis. Management is benzodiazepines in a quiet, low-stimulation room, cooling, and IV fluids, with CK and creatinine monitoring; prolonged struggling against physical restraints worsens hyperthermia and muscle breakdown.

Urine acidification to hasten PCP excretion is no longer used because it worsens myoglobin-induced kidney injury.

Ketamine. A shorter-acting PCP relative, ketamine causes dissociation (the "K-hole"), analgesia, amnesia, hallucinations, nystagmus, and tachycardia with relatively preserved airway reflexes, which is why it is used for anesthesia and procedural sedation; intranasal esketamine is approved for treatment-resistant depression under monitoring. Chronic recreational use causes ulcerative cystitis: dysuria, urgency, frequency, hematuria with sterile urine, and a small contracted bladder, sometimes with hydronephrosis. Stopping ketamine is essential.

Classic hallucinogens

Effects. LSD, psilocybin, and mescaline are serotonin 5-HT2A agonists. Users describe visual distortions, intensified colors, synesthesia such as "hearing colors," altered time sense, and depersonalization, usually with insight that the experience is drug-induced. Mydriasis, tachycardia, and tremor are mild. Tolerance develops within days and is shared among these agents (cross-tolerance); there is no withdrawal syndrome, fatal overdose is rare, and harm usually comes from accidents or dangerous behavior. Standard drug screens do not detect them.

Bad trips. Panic, paranoia, or terror is managed with a calm, quiet, low-light setting and reassurance that the effects will pass ("talking down"). A benzodiazepine is added for severe anxiety or agitation. Avoid restraints, and look for co-ingestants or a medical cause if vital signs are markedly abnormal.

Hallucinogen persisting perception disorder. After stopping, some users re-experience perceptual disturbances (geometric patterns, trails behind moving objects, flashes of color, halos) with intact insight, causing distress; episodes can recur for months or longer. Management is reassurance and avoidance of hallucinogens and cannabis, after excluding seizures, migraine aura, and psychosis.

Club drugs: MDMA and GHB

MDMA. "Ecstasy" or "Molly" reverses the serotonin transporter, flooding synapses with serotonin plus norepinephrine and dopamine. Users feel euphoria and empathy, with bruxism and jaw clenching, mydriasis, tachycardia, and hypertension. Hyperthermia, worsened by exertion in hot, crowded venues, can progress to rhabdomyolysis and DIC. Combined with SSRIs, MAOIs, or other serotonergic drugs it can cause serotonin syndrome, treated with cooling, benzodiazepines, and cyproheptadine.

MDMA hyponatremia. MDMA stimulates ADH release while users drink large volumes of water, causing acute hyponatremia with headache, vomiting, confusion, seizures, and cerebral edema; young women are most at risk. Seizures or coma call for a 3% hypertonic saline bolus, and free water is restricted; isotonic saline can worsen this SIADH-type picture.

GHB. This GABA-B agonist produces euphoria, then abrupt deep coma with respiratory depression, bradycardia, and hypothermia, followed by rapid spontaneous awakening within hours, sometimes with agitation. There is no antidote (naloxone and flumazenil do not work), so care is supportive airway management, and standard screens miss it. Its rapid sedation and amnesia explain its use in drug-facilitated sexual assault; prescription sodium oxybate treats narcolepsy with cataplexy.

Users who take GHB around the clock develop rapid, severe withdrawal resembling delirium tremens (tremor, hallucinations, autonomic instability, seizures) that needs high-dose benzodiazepines, with barbiturates for refractory cases.

Inhalants

Acute use. Volatile solvents such as toluene (glue, paint thinner), butane, and aerosol propellants are used mainly by adolescents. Intoxication is rapid and brief and resembles alcohol: euphoria, slurred speech, ataxia, and nystagmus. Clues include a perioral "huffer's rash," chemical odor, and paint stains on the face or hands. Sudden sniffing death occurs when halogenated hydrocarbons sensitize the myocardium to catecholamines, so a startle or exertion triggers ventricular fibrillation; asphyxia and aspiration are other causes of death.

Chronic toxicity. Toluene causes leukoencephalopathy with cognitive decline and cerebellar ataxia, plus distal renal tubular acidosis with hypokalemia; n-hexane causes peripheral neuropathy.

Nitrous oxide. Inhaled from whipped-cream chargers ("whippets"), nitrous oxide oxidizes and inactivates vitamin B12, producing subacute combined degeneration with lost vibration and position sense and a sensory ataxia. Methylmalonic acid and homocysteine are high even when serum B12 looks normal, and spinal MRI shows T2 hyperintensity of the dorsal columns (an "inverted V" on axial images). Treat by stopping nitrous oxide and replacing B12.

Nitrites. Inhaled alkyl nitrites ("poppers") cause vasodilation, headache, and hypotension, can cause methemoglobinemia (treated with methylene blue), and are dangerous with PDE-5 inhibitors.

Drug-screen blind spots

Negative is not reassuring. A typical panel detects amphetamines, cocaine, THC, morphine-type opiates, and PCP. Synthetic cathinones such as MDPV and α-PVP cause severe sympathomimetic toxicity (agitation, paranoia, hallucinations, hyperthermia, tachycardia, rhabdomyolysis, seizures) and are treated with benzodiazepines and rapid cooling. A negative screen never excludes poisoning.

False positives. Dextromethorphan, diphenhydramine, and venlafaxine can trigger the PCP assay; pseudoephedrine and bupropion can trigger the amphetamine assay; efavirenz can trigger the cannabinoid assay.