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Toxicology & Poisoning Nursing Guide

Gulf Cooperation Council (GCC) Clinical Reference — Emergency & Critical Care

GCC Edition 2025

H History Taking: AMPLE + Substance Profile

AMPLE Framework

  • A — Allergies (drug allergies, cross-reactivity)
  • M — Medications (prescribed, OTC, herbal, supplements)
  • P — Past medical/psychiatric history
  • L — Last meal / last known well time
  • E — Events leading to presentation & environment (scene info)

Substance Profile (6 questions)

  • Name — exact drug/substance (brand + generic)
  • Formulation — IR vs. modified-release, concentration
  • Amount — number of tablets/capsules or volume; calculate mg/kg
  • Time — time of ingestion / duration of exposure
  • Route — oral, IV, inhalation, dermal, rectal
  • Intention — accidental, deliberate self-harm, recreational, occupational

Always gather collateral history from family, ambulance crew, pharmacy records. In intentional OD, patients may minimise amounts taken.

T Toxidromes — Recognisable Clinical Syndromes

SLUDGE / Cholinergic (Organophosphates, Carbamates)

  • Salivation
  • Lacrimation
  • Urination
  • Defecation
  • GI cramping / emesis
  • Emesis
  • + Bronchospasm, bradycardia, miosis, muscle fasciculations

Sympathomimetic (Cocaine, Amphetamines, Cathinones)

  • Tachycardia / hypertension
  • Hyperthermia
  • Mydriasis (dilated pupils)
  • Agitation, tremor, diaphoresis
  • Seizures (high dose)
  • Chest pain / MI risk

Opioid (Morphine, Heroin, Tramadol, Fentanyl)

  • Miosis (pinpoint pupils)
  • Bradypnoea / respiratory depression
  • Altered / depressed consciousness
  • Hypotension, bradycardia
  • Decreased bowel sounds
  • Classic triad: miosis + bradypnoea + coma

Anticholinergic (TCAs, Antihistamines, Atropine)

  • Mad as a hatter — agitation, delirium
  • Dry as a bone — dry skin & mucosa, urinary retention
  • Blind as a bat — mydriasis, blurred vision
  • Red as a beet — flushed skin
  • Hot as a hare — hyperthermia
  • Tachycardia, decreased bowel sounds

Sedative-Hypnotic (Benzodiazepines, Barbiturates, GHB)

  • CNS depression (drowsiness → coma)
  • Respiratory depression
  • Slurred speech, ataxia
  • Nystagmus (barbiturates)
  • Normal or small pupils
  • Hypothermia

V Vital Signs Interpretation in Poisoning

ParameterElevatedDecreased
Heart RateSympathomimetic, anticholinergic, TCA, hyperthermia, salicylatesOpioid, beta-blocker, CCB, digoxin, organophosphate
Blood PressureSympathomimetic, MAOIsBeta-blocker, CCB, TCA, opioid, iron (late)
TemperatureSympathomimetic, anticholinergic, serotonin syndrome, salicylatesOpioid, sedative, beta-blocker, ethanol
Respiratory RateSalicylates (early), CO (compensatory), metabolic acidosisOpioid, sedative-hypnotic, botulism
SpO2—Opioid, CO (falsely normal with standard pulse ox), methaemoglobinaemia
Pupil SizeMydriasis: sympathomimetic, anticholinergicMiosis: opioid, organophosphate, clonidine

CO poisoning: SpO2 reads falsely normal. Use co-oximetry or blood gas carboxyhaemoglobin level when CO suspected.

G GCS Trajectory Monitoring

Serial GCS in Poisoning

  • Document baseline GCS on arrival with time stamp
  • Repeat every 15-30 min in acute phase
  • Trend is more important than single value
  • Declining GCS: anticipate need for airway protection
  • GCS ≤8: consider early intubation (cannot protect airway)

Alert anaesthetics/ICU early when GCS declining or ≤10. Do not wait for GCS 8 to call for help.

Neurological Assessment Points

  • Pupil size and reactivity (bilateral)
  • Gag reflex assessment
  • Muscle tone and reflexes
  • Clonus (serotonin syndrome screening)
  • Tremor, fasciculations (organophosphate)
  • Seizure activity — timing, type, duration
  • Posturing (decerebrate/decorticate)

E ECG in Poisoning

QRS Widening (>100 ms)

  • Sodium channel blockade
  • Tricyclic antidepressants (TCAs)
  • Type Ia antiarrhythmics (quinidine, procainamide)
  • Cocaine (sodium channel effect)
  • Diphenhydramine (high dose)
  • Treatment: Sodium bicarbonate 1-2 mmol/kg IV bolus

QTc Prolongation (>500 ms high risk)

  • Methadone, tramadol
  • Antipsychotics (haloperidol, quetiapine)
  • Antifungals (fluconazole)
  • Fluoroquinolones
  • Tricyclic antidepressants
  • Risk: Torsades de pointes → VF
  • Treatment: Magnesium sulfate 2g IV over 10 min; correct K+, Mg2+

12-lead ECG mandatory in ALL intentional poisoning. Repeat at 2-4h. Continuous monitoring in TCA/cardiac drug OD.

C Activated Charcoal (AC)

Dosing & Administration

  • Dose: 1 g/kg, maximum 50 g
  • Given orally or via NG tube
  • Mix as slurry in water
  • Optimal within 1 hour of ingestion
  • Consider up to 2h for modified-release preparations
  • Multi-dose AC: dapsone, carbamazepine, phenobarbital, quinine, theophylline

AC adsorbs most drugs. Call poisons centre if unsure whether it is indicated for a specific substance.

Contraindications

Corrosives (acids/alkalis) Hydrocarbons Comatose without airway protection Bowel obstruction/perforation Unprotected airway (GCS ≤8)

Does NOT Adsorb (AILM)

Iron Lithium Alcohols (ethanol, methanol, ethylene glycol) Metals (lead, mercury) Potassium Cyanide

If GCS declining: secure airway BEFORE administering AC. Aspiration of AC causes severe chemical pneumonitis. Never give AC to a patient who is drowsy or vomiting uncontrollably.

L Gastric Lavage

Indications (Rarely Used)

  • Life-threatening ingestion within 1 hour
  • Substance not adsorbed by charcoal
  • Patient must be intubated (if airway at risk) OR fully cooperative and alert
  • Use largest possible orogastric tube (36-40 Fr adult)
  • Warm normal saline 200-300 mL aliquots, repeat until clear
  • Left lateral, Trendelenburg position

Contraindications

Corrosive ingestion Hydrocarbon ingestion Impaired airway reflexes without intubation Oesophageal varices/recent GI surgery

Risks

  • Aspiration pneumonia
  • Oesophageal/gastric perforation
  • Laryngospasm
  • Hypoxia, fluid/electrolyte shifts

POSITION CHECK before lavage: confirm OGT placement. Never perform gastric lavage in an unprotected, obtunded patient — intubate first.

W Whole Bowel Irrigation (WBI)

Indications

  • Modified/sustained-release preparations (calcium channel blockers, metformin-XL)
  • Iron tablets
  • Lithium
  • Body packers (cocaine, heroin packets)
  • Substances not adsorbed by AC

Regimen

Polyethylene glycol (PEG-ELS) solution:
Adults: 1.5-2 L/h via NG tube
Children 6-12 years: 1 L/h
Continue until rectal effluent is clear

Contraindications

Bowel obstruction Perforation Ileus Haemodynamic instability Unprotected airway

Antiemetics (ondansetron/metoclopramide) may be needed to prevent vomiting during WBI. Sit patient upright at 45°.

X Obsolete & Contraindicated Methods

Ipecac Syrup — OBSOLETE. DO NOT USE.
Withdrawn globally. Causes prolonged vomiting, delays AC administration, no outcome benefit demonstrated. Removed from toxicology guidelines worldwide.

Induced Emesis — CONTRAINDICATED.
Risk of aspiration especially with CNS depressants. Absolutely contraindicated with corrosives, hydrocarbons, and any patient with impaired airway reflexes.

A N-Acetylcysteine (NAC) for Paracetamol

Standard IV 21-Hour Regimen

Bag 1 (Loading dose)

150 mg/kg in 200 mL 5% dextrose over 1 hour

Bag 2

50 mg/kg in 500 mL 5% dextrose over 4 hours

Bag 3 (Maintenance)

100 mg/kg in 1000 mL 5% dextrose over 16 hours

Total NAC dose = 300 mg/kg over 21 hours. Use 5% dextrose (NOT normal saline for bags 2 & 3 in children <20kg — hyponatraemia risk).

Key Nursing Points

  • Rumack-Matthew nomogram: plot paracetamol level against time since ingestion
  • Treat if level above treatment line (100 mg/L at 4h, 15 mg/L at 15h)
  • If time of ingestion unknown: treat empirically
  • Late presentation (>24h): discuss with poisons centre; continue NAC if any hepatotoxicity
  • Monitor: LFTs, INR, creatinine, paracetamol level, blood glucose

Anaphylactoid reactions to NAC occur in ~15% (urticaria, bronchospasm). Slow infusion rate, give chlorphenamine. Rarely need to stop treatment.

N Naloxone for Opioids

Dosing

  • IV/IM: 0.4 mg – 2 mg
  • Intranasal: 2-4 mg (atomiser device)
  • Repeat every 2-3 min as needed
  • Goal: adequate ventilation, NOT full reversal (avoids acute withdrawal)
  • Children: 0.01 mg/kg IV (min 0.1 mg)

Critical Nursing Consideration

Re-sedation risk: Naloxone half-life is 60-90 min. Most opioids last much longer. Patient MUST be monitored for 4-6 hours after last naloxone dose. Consider naloxone infusion at 2/3 of effective bolus dose per hour for long-acting opioids (methadone, modified-release morphine).

Tramadol: naloxone only partially reverses CNS depression. Also manage seizures with benzodiazepines.

F Flumazenil for Benzodiazepines

Dosing

  • 0.2 mg IV over 30 sec, repeat 0.1 mg every 60 sec
  • Maximum dose: 1 mg (3 mg in ICU setting)
  • Half-life 1 hour — shorter than most benzodiazepines

RARELY Used — Key Dangers

Precipitates seizures in:
• Mixed overdose (co-ingested TCAs/stimulants)
• Benzodiazepine-dependent patients
• Epileptics controlled with BZ
Avoid in chronic BZ users. Seek toxicology advice before use.

O Atropine & Pralidoxime for Organophosphates

Atropine (Muscarinic Blocker)

  • Initial dose: 2-4 mg IV
  • Double dose every 5-10 min until secretions dry
  • Endpoint: dry secretions (NOT tachycardia or mydriasis)
  • Severe cases may require 20-100+ mg total

Titrate to SECRETIONS not heart rate. Giving insufficient atropine is the most common error in organophosphate management.

Pralidoxime (Acetylcholinesterase Reactivator)

  • 30 mg/kg IV loading dose over 30 min
  • Then 8-10 mg/kg/h infusion
  • Reactivates acetylcholinesterase if given early (within 24-48h; “ageing” occurs after)
  • Reverses nicotinic effects (muscle weakness/fasciculations) better than atropine
  • Use alongside atropine, not instead of

D Specific Antidotes Reference Table

Poison / DrugAntidoteKey Notes
ParacetamolN-Acetylcysteine (IV)150 mg/kg load → 21h regimen; use nomogram
OpioidsNaloxone0.4-2 mg IV/IM/IN; re-sedation risk; infusion for long-acting
BenzodiazepinesFlumazenilRarely indicated; seizure risk in mixed OD or BZ dependence
OrganophosphatesAtropine + PralidoximeAtropine: dry secretions endpoint; pralidoxime: early use only
DigoxinDigoxin-specific Fab fragments (Digibind/DigiFab)Dose based on serum level or amount ingested; rebound toxicity possible
Beta-blockersGlucagon + High-dose insulinGlucagon 5-10 mg IV; insulin 1 U/kg/h + dextrose; IV calcium
Calcium channel blockersHigh-dose insulin + IV calciumInsulin 1 U/kg/h; lipid emulsion for refractory cases
IronDeferoxamine15 mg/kg/h IV; chelation; serum iron >500 mcg/dL or symptomatic
Methanol / Ethylene glycolFomepizole (preferred) or EthanolFomepizole: 15 mg/kg IV load; inhibits alcohol dehydrogenase
CyanideHydroxocobalamin (Cyanokit)5 g IV over 15 min; also sodium thiosulfate; turn urine red-pink
HeparinProtamine sulphate1 mg per 100 units heparin; max 50 mg
Warfarin / superwarfarinsVitamin K + Prothrombin Complex ConcentrateIV vitamin K + PCC for active bleeding; superwarfarins need weeks of oral K
TCA / sodium channel blockersSodium bicarbonate1-2 mmol/kg bolus for QRS >100ms or arrhythmia; target pH 7.45-7.55
Carbon monoxide100% Oxygen (HBO in selected cases)High-flow O2 via non-rebreather mask; HBO for severe/pregnant/cardiac
MethaemoglobinaemiaMethylene blue1-2 mg/kg IV; avoid in G6PD deficiency

P Paracetamol Overdose

Clinical Phases

  • Phase 1 (0-24h): N/V, malaise, pallor — can be asymptomatic
  • Phase 2 (24-72h): RUQ pain, elevated ALT/AST, INR rising
  • Phase 3 (72-96h): Hepatic necrosis peak; jaundice, coagulopathy, encephalopathy
  • Phase 4: Recovery or fulminant hepatic failure

Hepatotoxicity is DELAYED 48-72h. Normal initial LFTs do NOT mean safe. Treat based on nomogram, not symptoms.

Monitoring & Management

  • 4-hour paracetamol level (earliest meaningful level)
  • LFTs, INR, creatinine, pH at baseline then every 12-24h
  • Blood glucose (hypoglycaemia in hepatic failure)
  • NAC 21-hour IV regimen if above treatment line

King's College Criteria (Transplant)

  • pH <7.30 after resuscitation, OR
  • All 3: INR >6.5 + Creatinine >300 mcmol/L + Grade III-IV encephalopathy

S Salicylate (Aspirin) Overdose

Clinical Features

  • Tinnitus, hearing loss (early sign)
  • Tachypnoea, hyperpnoea
  • Early: Respiratory alkalosis (direct respiratory centre stimulation)
  • Late: High anion-gap metabolic acidosis
  • Hyperthermia, diaphoresis
  • Pulmonary oedema (non-cardiogenic)

Management

  • Serial salicylate levels (rising level = continued absorption)
  • Urinary alkalinisation: sodium bicarbonate IV; target urine pH 7.5-8.5 (traps salicylate in urine as ionised form)
  • IV fluids to maintain urine output
  • Haemodialysis (HD) indications: severe acidosis, CNS effects, level >700 mg/L, renal failure, pulmonary oedema
  • DO NOT intubate unless absolutely necessary (hypoventilation accelerates acidosis)

T Tricyclic Antidepressant (TCA) Overdose

Clinical Features

  • Anticholinergic syndrome (tachycardia, dry, agitated, flushed)
  • QRS widening >100 ms → ventricular arrhythmias, VT
  • QTc prolongation
  • Hypotension (alpha blockade)
  • Seizures (lowers seizure threshold)
  • Rapid deterioration possible

TCA OD can deteriorate rapidly from alert to cardiac arrest in minutes. All TCA patients need continuous cardiac monitoring.

Management

  • QRS >100 ms or arrhythmia: NaHCO3 1-2 mmol/kg IV bolus (target pH 7.45-7.55)
  • Repeat NaHCO3 boluses as needed, max until pH 7.55
  • Treat seizures: benzodiazepines (avoid phenytoin — worsens cardiac toxicity)
  • Hypotension: IV fluids, then noradrenaline
  • Avoid physostigmine (risk of cardiac arrest)
  • Lipid emulsion if refractory

C Calcium Channel Blocker (CCB) Overdose

Features

  • Bradycardia (often profound), heart blocks
  • Hypotension
  • Hyperglycaemia (inhibits insulin release)
  • Modified-release CCBs: delayed/prolonged toxicity up to 18-24h

High-Dose Insulin Therapy (HDIT)

  • Regular insulin 1 unit/kg/h IV infusion
  • 50% dextrose co-infusion — monitor glucose every 30 min
  • Target blood glucose: 8-14 mmol/L
  • IV calcium: 10% calcium gluconate 30 mL IV over 5 min (may repeat)
  • Lipid emulsion (Intralipid 20%): 1.5 mL/kg bolus for refractory cardiac toxicity
  • Atropine, cardiac pacing, vasopressors as needed

B Beta-Blocker Overdose

Features

  • Bradycardia, hypotension, heart blocks
  • Bronchospasm (especially non-selective)
  • Hypoglycaemia (especially paediatric)
  • Seizures (propranolol: membrane stabilising effect)
  • Modified-release preparations: prolonged toxicity

Management

  • Glucagon 5-10 mg IV bolus; then 2-5 mg/h infusion
  • High-dose insulin (1 U/kg/h) + dextrose (similar to CCB)
  • IV calcium chloride / gluconate
  • Atropine (often ineffective but first-line)
  • Cardiac pacing (transcutaneous)
  • Lipid emulsion for lipid-soluble beta-blockers (propranolol)

I Iron Poisoning

Clinical Phases

  • Phase 1 (0-6h): GI toxicity — N/V/D, haematemesis, abdo pain
  • Phase 2 (6-24h): Apparent recovery (false reassurance)
  • Phase 3 (12-48h): Metabolic acidosis, cardiovascular collapse
  • Phase 4 (2-6 weeks): GI obstruction from scarring

Management

  • AXR to quantify tablet burden
  • Serum iron level at 4h (toxic >500 mcg/dL)
  • Whole bowel irrigation for significant ingestion
  • Deferoxamine: 15 mg/kg/h IV continuous infusion
  • Indications for deferoxamine: serum Fe >500 mcg/dL, symptoms of systemic toxicity, metabolic acidosis
  • Urine colour: orange-pink ("vin rosé") indicates deferoxamine working

Phase 2 "lucid interval" can lull clinicians into false security. Monitor any symptomatic iron poisoning for ≥24 hours.

OP Organophosphate Pesticide Poisoning

Context in GCC

Agricultural workers, particularly South Asian (Indian, Pakistani, Bangladeshi, Sri Lankan) farmhands in date palm farms and crop agriculture. Accidental occupational exposure most common; intentional self-poisoning also seen in migrant workers under psychosocial stress.

  • Common agents: chlorpyrifos, dimethoate, malathion, diazinon
  • Routes: dermal, inhalational, ingestion

Management Priorities

  • Decontaminate: remove clothing, wash skin with soap & water
  • Staff PPE during decontamination (nitrile gloves, gown)
  • SLUDGE toxidrome → identify severity
  • Atropine: 2-4 mg IV bolus, double every 5-10 min until secretions dry
  • Pralidoxime: 30 mg/kg IV over 30 min, then infusion (early only)
  • Diazepam 5-10 mg IV for seizures
  • Intermediate syndrome: may develop 24-96h post-exposure (proximal weakness, respiratory failure)

Intermediate syndrome (24-96h later): proximal limb weakness + respiratory failure. Monitor respiratory function for at least 4 days post-exposure.

TR Tramadol Misuse — GCC Concern

Epidemiology

Tramadol is widely misused across the GCC and Middle East, particularly in Egypt, Saudi Arabia, UAE, and Qatar. Available illegally; used recreationally for stimulant/euphoric effect at low doses, and as a labour endurance drug.

Pharmacology

  • Weak mu-opioid agonist
  • SNRI (serotonin-noradrenaline reuptake inhibitor) properties
  • Mixed opioid + serotonin syndrome risk in overdose

Clinical Features in OD

  • Seizures — most distinctive feature (lowers seizure threshold)
  • QTc prolongation → Torsades risk
  • CNS depression (opioid effect)
  • Serotonin syndrome features (clonus, hyperthermia, rigidity)
  • Respiratory depression (less severe than classic opioids)

Management

  • Naloxone for opioid effects (partially effective)
  • Benzodiazepines for seizures (NOT phenytoin)
  • ECG monitoring for QTc
  • Cooling measures if hyperthermic
  • Cyproheptadine for serotonin syndrome features

K Khat (Qat) Toxicity

Background

Khat (Catha edulis) is a plant chewed for stimulant effects, predominantly by Yemeni and Somali expat communities in GCC countries. Active compounds: cathinone (more potent, fresh leaves) and cathine (norpseudoephedrine).

  • Legal status varies by GCC country (banned in Saudi Arabia, UAE, Qatar; regulated elsewhere)
  • Social chewing sessions common; heavy daily use in communities

Toxicity Features

Tachycardia Hypertension Insomnia Agitation Anorexia Constipation (chronic) Psychiatric: paranoia/psychosis (chronic)

Management

  • Largely supportive; benzodiazepines for severe agitation
  • Beta-blockers for symptomatic tachycardia/hypertension
  • Psychiatric follow-up for chronic psychosis

H2 Hydrogen Sulphide (H2S) — Petrochemical Hazard

Occupational Context

H2S is a significant occupational hazard in GCC petrochemical, oil & gas industry (Saudi Aramco, ADNOC, Qatar Energy facilities). Nurses may see workers from these sectors.

  • "Rotten egg" smell at low concentrations
  • Olfactory paralysis at high concentrations — smell disappears; creates false sense of safety
  • "Knockdown" effect: sudden collapse at high concentrations (>700 ppm) — one breath can cause death
  • 100 ppm: immediate life-threatening; impairs sense of smell

Clinical Features & Management

  • Eye and airway irritation at low levels
  • Pulmonary oedema
  • CNS depression, seizures, coma
  • Inhibits cytochrome c oxidase (similar to cyanide)

Treatment

  • Remove from environment (trained rescuers only — SCBA)
  • High-flow 100% oxygen
  • Sodium nitrite 300 mg IV (forms methaemoglobin which binds sulphide)
  • Supportive care; HBO in severe cases

Rescuers MUST use SCBA. Multiple rescuer casualties documented from entering H2S-contaminated spaces without PPE.

SC Scorpion Envenomation — UAE/GCC

Species of Concern

  • Androctonus crassicauda (fat-tailed scorpion) — most lethal in Middle East
  • Leiurus quinquestriatus (deathstalker) — UAE/Saudi border regions
  • Paediatric patients at highest risk of severe envenomation
  • Season: warmer months; nocturnally active

Clinical Features & Management

  • Local pain, paraesthesia
  • Severe: autonomic storm — hypertension/hypotension, tachycardia, diaphoresis
  • Pulmonary oedema (catecholamine surge)
  • Myocarditis (direct venom effect)

Treatment

  • Local wound care; IV access
  • Antivenom (where available & species confirmed)
  • Prazosin for hypertensive crisis
  • Supportive: oxygen, IV fluids, analgesics
  • Paediatric ICU admission for grade III-IV

TR Traditional Remedies & Date-Related Toxicity

Traditional/Herbal Toxicity

  • Senna (overuse): electrolyte disturbance, hypokalemia
  • Zamzam water (counterfeit products): heavy metal contamination reported
  • Frankincense (Boswellia) misuse: GI effects, rare hepatotoxicity
  • Black seed (Nigella sativa) oil in high doses: hepatotoxicity
  • Camel milk (raw): MERS-CoV risk, bacterial infections
  • Habbatus sawda (combination products): variable herb toxicity

Key Nursing Approach

  • Always ask about traditional remedy use in history (culturally common)
  • Do not dismiss — many cause real herb-drug interactions
  • Herbal-warfarin interactions particularly important
  • Document herbal/traditional substance in medication list
  • Contact poisons centre if unsure about specific substance

Many patients will not volunteer traditional remedy use unless specifically asked. Include in your medication history for all GCC patients.

PC GCC Poison Control Centres

Saudi Arabia

Saudi Poison Control Centre

0800-2464-672

24/7 Free hotline

UAE — Abu Dhabi

Abu Dhabi Poison Control Centre

+971-2-581-3333

SEHA network

Qatar

HMC Poison Control Centre

16000

Hamad Medical Corporation

Kuwait

Kuwait Poison Control

+965-2224-5307

Ministry of Health

Bahrain

National Toxicology Centre

+973-1744-4444

Salmaniya Medical Complex

International Reference

UK NPIS (Toxbase)

+44-344-892-0111

Available to registered HCPs

Call the regional poison control centre EARLY for all significant poisoning cases — before the patient deteriorates. They provide real-time management guidance 24/7.

MH Documentation — Self-Harm Poisoning

Mandatory Documentation

  • Time of ingestion vs. time of presentation
  • Exact substance(s) and amount(s)
  • Stated intention (must be documented clearly)
  • Mental health history, previous attempts
  • Social circumstances (living alone, recent stressors)
  • Safeguarding concerns (minors, domestic violence)
  • Psychiatric team referral documented with time

Mandatory Referrals

DO NOT DISCHARGE without:
1. Medical clearance by physician
2. Psychiatric risk assessment completed
3. Social work involvement if safeguarding concern
4. Discharge plan documented
5. Follow-up arranged (psychiatric outpatient or inpatient)

In many GCC countries, intentional self-harm requires notification to specific government agencies. Know your facility's local policy.

DS Drug Screening — Urine Immunoassay

Common False Positives

Screen TargetFalse-Positive Cause
OpiatesQuinolone antibiotics, rifampicin, dextromethorphan, quinine
PCP (phencyclidine)Ibuprofen, tramadol, dextromethorphan, venlafaxine
AmphetaminesPseudoephedrine, MDMA, labetalol, promethazine, bupropion
BenzodiazepinesSertraline, oxaprozin, efavirenz
THC (cannabis)NSAIDs, proton pump inhibitors (rare)
CocaineTopical benzocaine/lidocaine metabolites

Key Principles

  • Immunoassay is a screening test — not confirmatory
  • Confirmatory test: GC-MS (Gas Chromatography-Mass Spectrometry)
  • False negatives also occur (especially for novel psychoactive substances, synthetic opioids)
  • Fentanyl is NOT detected on standard opiate screen
  • Synthetic cannabinoids (Spice) NOT detected on standard THC screen
  • Always correlate with clinical picture, not screen alone

A positive urine drug screen does NOT mean the patient is intoxicated NOW — many drugs are detected for days to weeks after last use.

D Disposition Criteria

Medical Clearance for Discharge

  • GCS 15, protecting airway, haemodynamically stable
  • Appropriate observation period completed (varies by drug)
  • Serial ECG normal (if relevant)
  • LFTs/INR stable (paracetamol)
  • Pain controlled
  • Tolerating oral fluids/food

Minimum Observation Periods

SubstanceMin. Obs.
Modified-release drugs24h (may extend)
ParacetamolUntil LFTs stable post-NAC
TCA6h from ingestion if asymptomatic
Beta-blocker/CCB12-24h (MR: 24-48h)
Organophosphates4 days (intermediate syndrome risk)
SalicylatesUntil falling serum level confirmed

Intentional self-harm poisoning: PSYCHIATRIC ASSESSMENT mandatory before discharge in all cases. Never discharge on night shift without day-team psychiatric review documented.

BP Body Packers ("Drug Mules")

Clinical Scenario

Individuals swallowing wrapped packets of cocaine or heroin ("body packing") to smuggle drugs across borders. Relevant in GCC airports (Dubai, Doha, Riyadh). Packets may rupture causing massive overdose.

Investigations

  • Abdominal X-ray (AXR): radiopaque packets visible
  • CT abdomen (more sensitive, shows packet number/location)
  • Urine drug screen

Management

  • Asymptomatic: Whole bowel irrigation with PEG-ELS
  • DO NOT use activated charcoal (may degrade packet integrity)
  • Symptomatic / suspected rupture: Emergency surgery
  • Naloxone infusion if opioid toxicity while awaiting surgery
  • Cocaine rupture: benzodiazepines for agitation/seizures; no specific antidote
  • NEVER perform endoscopic retrieval (risk of packet rupture)

Packet rupture = toxicological emergency. Cocaine packet rupture can cause near-immediate massive toxicity. Alert surgical team early for all body packers.

Paracetamol OD Risk Tool — Rumack-Matthew Nomogram

Enter time since ingestion and paracetamol level OR amount ingested to assess treatment need. For single acute ingestions only.

NAC Infusion Rate Calculator (21-Hour IV Regimen)

Enter patient weight to generate NAC dose and infusion rates for all three bags.

Q Practice MCQs — Toxicology & Poisoning

Test your knowledge. Click an answer to see instant feedback.