GCC Nursing Guide — Drug Overdose & Poisoning

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ABCDE Approach — Overdose / Poisoning Patient

A — Airway

Assess patency — gag reflex, secretions
GCS ≤8 or vomiting: consider airway adjunct / intubation
Position: recovery if reduced consciousness

B — Breathing

RR, SpO₂, auscultation, ABG
Opioids: RR <12 + miosis = naloxone
TCA: Kussmaul breathing (acidosis)

C — Circulation

ECG immediately — QTc, QRS width, arrhythmias
IV access ×2, bloods
TCA: wide QRS; digoxin: bradyarrhythmia

D — Disability

GCS, pupils (size, reactivity, symmetry)
BM glucose — hypoglycaemia mimics OD
Seizure activity noted and treated

E — Exposure

Full skin exam: needle tracks, rashes, burns (caustic), mottling
Temperature (hypo/hyperthermia)
Any medication packets / bottles at scene

GCC Common ODs

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Toxidrome Recognition

Anticholinergic

Causes: antihistamines, TCAs, atropine, antipsychotics, jimsonweed

Dry skin/mouth, Hot (hyperthermia), Flushed, Tachycardia, Dilated pupils, urinary retention, ileus, agitation/delirium

Mnemonic: "Dry as a bone, hot as a hare, red as a beet, blind as a bat, mad as a hatter"

Cholinergic (SLUDGE)

Causes: organophosphates, nerve agents, pilocarpine, physostigmine

Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis + miosis, bradycardia, bronchospasm, bronchorrhoea, seizures

Muscarinic (SLUDGE) + Nicotinic (muscle weakness, fasciculations)

Sympathomimetic

Causes: cocaine, amphetamines, MDMA, caffeine overdose, ephedrine

Tachycardia, Hypertension, Hyperthermia, Dilated pupils, diaphoresis, agitation, chest pain, seizures

Differentiate from anticholinergic: sympathomimetic has diaphoresis (wet skin)

Opioid

Causes: morphine, heroin, fentanyl, tramadol, codeine, methadone

Miosis (pinpoint pupils), Respiratory depression, Reduced consciousness, bradycardia, hypotension, reduced bowel sounds

GCC note: tramadol also causes seizures — naloxone may not fully reverse

Serotonin Syndrome

Causes: SSRIs + MAOIs, SSRIs + tramadol, linezolid + SSRI, triptans + SSRIs

Cognitive: agitation, restlessness, confusion

Autonomic: hyperthermia, tachycardia, diaphoresis, hypertension

Neuromuscular: clonus (pathognomonic), tremor, hyperreflexia, myoclonus

Hunter Criteria: clonus + serotonergic agent = serotonin syndrome

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History — AMPLE + OD-Specific Questions

AMPLE History

A — AllergiesDrug allergies / reactions

M — MedicationsRegular medications, recent changes

P — PMHPrevious OD, mental health, liver disease

L — Last oral intakeLast food/drink (empty stomach increases absorption)

E — EventsWhat led to this event

OD-Specific Questions

Which substance(s) taken?
How much / how many tablets?
What time was it taken?
Was it intentional or accidental?
Any alcohol or other substances co-ingested?
Prior overdose history
Access to other medications at home
Psychiatric history / current mental health

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Key Investigations

Urgent

ECG▼

QTc prolongation (>450ms men, >470ms women): TCAs, antipsychotics, methadone, antihistamines, fluoroquinolones

Wide QRS (>100ms): TCA toxicity — indicates sodium channel blockade; treat with sodium bicarbonate

Bradyarrhythmia: beta-blockers, calcium channel blockers, digoxin, organophosphates

Paracetamol Level▼

Take at 4 hours post-ingestion (earlier levels unreliable — still absorbing)

Plot on Rumack-Matthew nomogram to determine if NAC required

If timing uncertain or staggered: treat if any paracetamol taken >75mg/kg in 24h

Salicylate Level▼

Toxic >300mg/L. Severe toxicity >700mg/L

Features: tinnitus, hyperventilation (resp alkalosis early), metabolic acidosis, hypoglycaemia, confusion

Treatment: IV fluids, urinary alkalinisation (sodium bicarbonate), haemodialysis if severe

Standard Panel

ABG: acid-base status, metabolic acidosis, lactate
Blood glucose: hypoglycaemia mimics/complicates OD
U&E: electrolytes (hypokalaemia — diuretics, salbutamol), renal function
LFT: paracetamol hepatotoxicity baseline and monitoring
FBC: anaemia, infection
Coagulation / INR: raised in paracetamol-induced liver failure
Drug screen (urine): qualitative screen — note: false positives common

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Intentional OD: Mental health assessment, psychiatric liaison referral, safeguarding considerations, removal of further means. Never discharge without psychiatric review.

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Paracetamol Toxicity Mechanism

Normal paracetamol metabolism: mostly glucuronidation/sulphation. Small fraction converted to toxic metabolite NAPQI via CYP2E1.

NAPQI is normally detoxified by glutathione. In overdose, glutathione stores are depleted → NAPQI accumulates → centrilobular hepatic necrosis.

Stages of Paracetamol Toxicity

0–24hNausea, vomiting, malaise — may appear well

24–72hRUQ pain, rising LFTs, INR rising

72–96hPeak hepatotoxicity — jaundice, coagulopathy, AKI

>96hRecovery or fulminant hepatic failure

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Rumack-Matthew Nomogram

Plot paracetamol level (mg/L) at 4h post-ingestion on nomogram treatment line:

Time (h)	Standard Line (mg/L)	High-Risk Line (mg/L)
4h	100 mg/L	50 mg/L
8h	50 mg/L	25 mg/L
12h	25 mg/L	12 mg/L
15h	15 mg/L	7.5 mg/L
>15h	If >15h since ingestion — discuss with toxicology/start NAC

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High-risk features: Regular alcohol use, malnutrition/eating disorder, enzyme inducers (rifampicin, carbamazepine, phenytoin), HIV/AIDS. Treat at lower threshold (50% of standard line).

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N-Acetylcysteine (NAC) Protocol — Prescott 3-Bag Regimen

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NAC mechanism: Replenishes glutathione stores → detoxifies NAPQI. Most effective when given early (<8h). Still beneficial up to 24h+ in severe toxicity.

Bag 1 — Loading

150 mg/kg

In 200ml 5% dextrose

Over 1 hour

Most anaphylactoid reactions occur in this bag — monitor closely

Bag 2

50 mg/kg

In 500ml 5% dextrose

Over 4 hours

Bag 3 — Maintenance

100 mg/kg

In 1000ml 5% dextrose

Over 16 hours

NAC Anaphylactoid Reaction

Occurs in up to 15–20% (usually Bag 1)
Features: flushing, rash, urticaria, wheeze, nausea
Action: stop infusion, chlorphenamine IV, consider hydrocortisone
Restart at reduced rate once resolved — NAC is NOT contraindicated
True anaphylaxis rare — adrenaline only if cardiovascular compromise

Staggered / Unknown Timing Overdose

If exact time of ingestion unknown or multiple episodes
Treat if total paracetamol taken >75mg/kg equivalent in any 24h period
Check level and start NAC — do not delay for 4h level if history suggests significant dose
Liver transplant assessment: King's College Criteria if fulminant hepatic failure develops

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Paracetamol OD Risk Assessor & NAC Decision Tool

NAC Decision & Dose Calculator

Paracetamol Level

Time Since Ingestion (hours)

Body Weight (kg)

High-Risk Features (lower treatment threshold)

Regular alcohol use (hepatic enzyme induction) Malnutrition / eating disorder / low body weight Enzyme inducers (rifampicin, carbamazepine, phenytoin, St John's Wort) Staggered overdose / uncertain timing

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Key principle: Most overdose management is supportive. Antidotes exist for specific toxins — know the indication and limitations of each. Antidote use does not replace supportive care.

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Antidote Quick Reference

Toxin / Overdose	Antidote / Treatment	Key Notes
Opioids Morphine, fentanyl, heroin, tramadol	Naloxone 400mcg IV/IM/intranasal Repeat every 2–3 min PRN	Titrate to adequate respiration NOT full reversal (avoid acute withdrawal in opioid-dependent). Short duration — re-sedation risk. Tramadol OD: may not fully reverse; high seizure risk.
Benzodiazepines Diazepam, midazolam, lorazepam	Flumazenil 200mcg IV over 15s Repeat 100mcg every 60s (max 1mg)	CAUTION: may precipitate seizures in BZD-dependent patients. Short duration (1h) — re-sedation occurs. Avoid in mixed OD with TCAs (lowers seizure threshold). Rarely used routinely.
Tricyclic Antidepressants (TCAs) Amitriptyline, imipramine	Sodium Bicarbonate 1–2 mmol/kg IV bolus Infusion if refractory	Indicated if QRS >100ms, ventricular arrhythmia, or haemodynamic instability. Target blood pH 7.45–7.55. Avoid flumazenil and physostigmine. ICU level care.
Organophosphates / Nerve Agents	Atropine (titrate to dry secretions, NOT HR) + Pralidoxime (reactivates cholinesterase — give within 24–48h)	Atropine doses may be very large (100mg+ in severe poisoning). Pralidoxime less effective after 24–48h (cholinesterase "ageing"). PPE essential for staff decontamination.
Cyanide Poisoning Smoke inhalation, industrial, apricot kernels	Hydroxocobalamin 5g IV (Cyanokit) — 1st line Dicobalt edetate 300mg IV (if no doubt about diagnosis)	Dicobalt edetate: serious side effects if not cyanide — only use if diagnosis certain. Hydroxocobalamin preferred (safer). Also give 100% O₂.
Carbon Monoxide	100% O₂ via tight-fitting non-rebreather mask Consider hyperbaric O₂ (HBO)	HBO indications: CoHb >25%, LOC, neurological features, pregnancy. Pulse oximetry unreliable (CO-oximetry needed). Carboxyhaemoglobin level from ABG.
Beta-Blocker Overdose	Atropine → Glucagon 1–5mg IV (1st specific antidote) → High-Dose Insulin/Dextrose (HDIE) → Lipid emulsion	Glucagon bypasses beta receptor. HDIE: insulin 1 unit/kg/h + dextrose to maintain euglycaemia — improves myocardial carbohydrate utilisation. Consider pacing/ECMO in refractory cases.
Calcium Channel Blocker Amlodipine, diltiazem, verapamil	Calcium chloride 10ml 10% IV (or gluconate) → Glucagon → HDIE therapy → Lipid emulsion	Calcium competes with drug at receptor. Verapamil/diltiazem: significant bradycardia/heart block. Amlodipine: predominantly vasodilation. HDIE most effective evidence base. Consider ECMO.
Digoxin Toxicity	Digoxin-specific Fab antibody fragments (Digibind / DigiFab)	Indicated: life-threatening arrhythmia, K+ >5.5 mmol/L with toxicity, acute ingestion >10mg (adult). Dose based on digoxin level × body weight formula. Monitor K+ closely after administration.
Paracetamol	N-Acetylcysteine (NAC) 3-bag Prescott regimen	See Tab 2 for full protocol. Most effective <8h but beneficial up to 24h+. Replenishes glutathione stores.
Iron Overdose	Desferrioxamine 15mg/kg/h IV infusion	Indicated if serum iron >55 μmol/L or severe features (shock, coma, severe acidosis). Urine turns orange-red (vin rosé). Max 80mg/kg/24h.
Warfarin / Anticoagulant	Vitamin K (phytomenadione) IV/oral + Prothrombin complex concentrate (PCC) if bleeding	Superwarfarin (rodenticide) poisoning: prolonged treatment (weeks). DOAC reversal: idarucizumab (dabigatran), andexanet alfa (Xa inhibitors).

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Serotonin Syndrome vs NMS

Feature	Serotonin Syndrome	Neuroleptic Malignant Syndrome
Onset	Rapid (hours)	Gradual (days)
Cause	Serotonergic agents	Antipsychotics / dopamine blockade
Neuromuscular	Clonus, hyperreflexia, myoclonus	Rigidity, bradykinesia, lead-pipe
Hyperthermia	Present	Present (often more severe)
Treatment	Cyproheptadine, lorazepam, cooling, discontinue agent	Dantrolene, bromocriptine, cooling, stop antipsychotic

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Alcohol Withdrawal — CIWA-Ar Management

CIWA-Ar score guides treatment frequency (score ≥8 = pharmacotherapy)
Thiamine IV (Pabrinex) BEFORE glucose — prevents Wernicke's encephalopathy
Chlordiazepoxide or diazepam symptom-triggered protocol
Monitor: tremor, agitation, sweating, nausea, headache, anxiety, perceptual disturbances
Seizure risk: peaks 24–48h after last drink
Delirium tremens: 72–96h — medical emergency (mortality 5–15% untreated)

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NEVER give IV dextrose before thiamine in alcohol misuse — precipitates acute Wernicke's encephalopathy.

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Gastric Decontamination

Activated Charcoal

50g orally — most effective within 1 hour of ingestion

Contraindications

Reduced/unprotected airway (GCS <13)
Caustic substances (acids/alkalis)
Hydrocarbons / petroleum distillates
Intestinal obstruction

Does NOT bind: alcohols, metals (iron, lithium), cyanide

Whole Bowel Irrigation

PEG solution (GoLYTELY) via NGT — 1–2 L/h until rectal effluent clear

Indications

Body packers (drug mules)
Sustained-release / enteric-coated preparations
Iron or lithium overdose

Gastric Lavage

Rarely used in modern toxicology — evidence poor. Only consider within 1h of massive life-threatening ingestion with protected airway.

Risk: aspiration, oesophageal injury, vagal stimulation. Do NOT use routinely.

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Tramadol Overdose — GCC Context

Tramadol is widely prescribed across the GCC for pain management. Misuse and dependency are significant public health concerns in the region.

Clinical Features of Tramadol OD

Partial opioid mu-receptor agonist + SNRI activity
Miosis and respiratory depression (opioid effect)
High seizure risk — serotonergic mechanism
Serotonin syndrome possible, especially with co-ingested SSRIs
Naloxone may not fully reverse (only reverses opioid component)

Nursing Management

Airway protection, IV access, ECG, bloods
Naloxone 400mcg IV/IM — titrate; may need infusion
Seizure precautions — IV lorazepam/diazepam if seizures
Monitor for serotonin syndrome features (clonus)
Do NOT use flumazenil if BZDs co-ingested
Psychiatric review for intentional OD

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Cultural note: Tramadol misuse may be denied or minimised by patient/family in GCC context. Non-judgmental, culturally sensitive history essential.

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Supportive Care Bundle

Airway & Breathing

Recovery position if drowsy
Airway adjuncts (NPA/OPA)
Intubation if GCS ≤8 or airway not maintained
SpO₂ monitoring and titrated O₂

Temperature Management

Hyperthermia (serotonin, sympathomimetic): cooling — fans, ice packs, tepid sponging, sedation
Hypothermia (opioids, alcohol, barbs): active external re-warming
Target normothermia 36–37.5°C

Seizure Management

IV lorazepam 4mg (or diazepam 10mg IV/rectally) 1st line
Phenobarbital if BZD-refractory
Phenytoin: avoid in TCA OD (pro-arrhythmic)
Pyridoxine (vit B6): isoniazid-induced seizures

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Risk Assessment Post-Overdose

Columbia Suicide Severity Rating Scale (C-SSRS)

Validated tool for suicidal ideation and behaviour assessment
Ideation scale: 1 (passive wish to be dead) → 5 (active ideation with plan and intent)
Behaviour scale: identifies preparatory acts, interrupted or aborted attempts
Used across GCC regulatory frameworks (DHA, DOH, MOH)

Manchester Self-Harm Rule

Previous self-harm, psychiatric treatment, benzodiazepine OD, current psychiatric care — any present = high risk for repeat

High-Risk Indicators for Repeat Self-Harm

Previous suicide attempt
Mental health disorder (depression, psychosis, personality disorder)
Substance misuse
Hopelessness (stronger predictor than depression alone)
Social isolation
Male gender, older age
Planned act, precautions against discovery
Stated intent to repeat

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Capacity Assessment

Patient refusing treatment following intentional OD — assess capacity:

Can understand information about treatment?
Can retain that information long enough to decide?
Can weigh up pros/cons (use/balance information)?
Can communicate decision?

Capacity is decision-specific and time-specific. Acutely intoxicated patients typically lack capacity temporarily.

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If no capacity + life-threatening OD: Treat in patient's best interests. Document clearly. Mental Health Act provisions may apply. Always escalate to senior clinician.

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Safeguarding Considerations

Children & adolescents: OD in minors — mandatory reporting to child protection services in all GCC countries
Vulnerable adults: consider coercion, domestic violence, elder abuse
Document all disclosures verbatim, objective observations
Involve social work team early
Do not discharge a child without safeguarding assessment and senior review

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GCC Cultural Context: Suicide and self-harm carry social stigma and legal implications in some GCC jurisdictions. Patients/families may present OD as accidental. Approach with cultural sensitivity — non-judgmental questioning essential to obtain accurate history.

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Psychiatric Liaison & Discharge Planning

Psychiatric Liaison Referral

Mandatory for all intentional OD before discharge
Ideally same admission
Risk stratification and safety planning
Consider inpatient psychiatric admission if high risk

Means Restriction Counselling

Safe storage of all medications at home (lock box)
Limit supply of medications at discharge (prescribe ≤7 days)
Remove or transfer firearms/knives where applicable
Involve family/carer with consent

Safety Planning

Written safety plan — warning signs, coping strategies, support contacts
Crisis line numbers provided
Follow-up appointment arranged before discharge
Family psychoeducation with patient consent

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Toxidrome Recognition — Exam Table

Toxidrome	Pupils	HR	Temp	Skin	Bowel Sounds	Key Drug Examples
Anticholinergic	Dilated ▲	Tachycardia ▲	High ▲	Dry, flushed, hot	Absent ▼	TCAs, antihistamines, atropine, antipsychotics
Cholinergic	Miosis ▼	Bradycardia ▼	Normal/Low	Wet, diaphoretic	Hyperactive ▲	Organophosphates, carbamates
Sympathomimetic	Dilated ▲	Tachycardia ▲	High ▲	Wet, diaphoretic	Normal	Cocaine, amphetamines, MDMA, ephedrine
Opioid	Miosis (pinpoint) ▼	Bradycardia ▼	Low ▼	Dry, pale	Absent ▼	Morphine, heroin, fentanyl, tramadol, codeine
Serotonin Syndrome	Dilated ▲	Tachycardia ▲	High ▲	Wet, flushed	Hyperactive ▲	SSRIs + MAOIs, SSRIs + tramadol
Sedative / Hypnotic	Normal/small	Bradycardia ▼	Low ▼	Normal/pale	Absent ▼	Benzodiazepines, barbiturates, alcohol

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Antidote Quick Reference — Exam Format

Drug / Toxin	Antidote
Paracetamol	N-Acetylcysteine (NAC)
Opioids	Naloxone
Benzodiazepines	Flumazenil (use with caution)
TCA (arrhythmia/wide QRS)	Sodium Bicarbonate
Organophosphates	Atropine + Pralidoxime
Cyanide	Hydroxocobalamin (Cyanokit)

Drug / Toxin	Antidote
Carbon Monoxide	100% O₂ / Hyperbaric O₂
Beta-Blocker	Glucagon → HDIE → Lipid emulsion
Calcium Channel Blocker	Calcium salts → HDIE
Digoxin	Digoxin-specific Fab (Digibind)
Iron	Desferrioxamine
Warfarin	Vitamin K + PCC

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QTc-Prolonging Drugs — Common Exam Topic

QTc >500ms = high risk of Torsades de Pointes. Correct electrolytes (K+, Mg2+) — hypokalaemia and hypomagnesaemia increase risk.

Psychiatric / Neurological

Cardiac

Anti-infectives

GI / Other

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Exam tip: TCA OD causes wide QRS (sodium channel block) + QTc prolongation. Treat with sodium bicarbonate.

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DHA / DOH / SCFHS / QCHP High-Yield Toxicology Questions

Q: What is the most important investigation timing in paracetamol OD? ▼

Answer: Paracetamol level at 4 hours post-ingestion. Earlier levels are unreliable as absorption may be incomplete. Level is plotted on the Rumack-Matthew nomogram to determine NAC treatment need.

Q: What is the mechanism of NAC in paracetamol toxicity? ▼

Answer: NAC replenishes glutathione stores, which detoxify the toxic metabolite NAPQI. In overdose, hepatic glutathione is depleted → NAPQI accumulates → hepatocellular necrosis. NAC is most effective within 8 hours but still beneficial up to 24h+.

Q: Why is flumazenil relatively contraindicated in mixed BZD + TCA overdose? ▼

Answer: In TCA overdose, TCAs lower the seizure threshold. BZDs may be providing seizure prophylaxis. Reversing BZDs with flumazenil can precipitate refractory seizures. Additionally, flumazenil has a short half-life — re-sedation occurs (1–2h vs BZD duration).

Q: What ECG finding in TCA OD indicates sodium bicarbonate treatment? ▼

Answer: QRS >100ms (wide QRS complex) indicates sodium channel blockade by TCA. Sodium bicarbonate reverses this by increasing sodium gradient. Also treat if ventricular arrhythmia or haemodynamic instability. Target arterial pH 7.45–7.55.

Q: Describe the clinical triad of opioid toxidrome. ▼

Answer: Classic triad — Miosis (pinpoint pupils) + Respiratory depression (RR <12) + Reduced consciousness. Treatment: naloxone titrated to adequate spontaneous respiration. Note: tramadol OD (common in GCC) may also cause seizures — naloxone only reverses opioid component.

Q: What is the pathognomonic feature of serotonin syndrome? ▼

Answer: Clonus — particularly inducible or spontaneous clonus — is pathognomonic of serotonin syndrome. Hunter Criteria: clonus + serotonergic drug = serotonin syndrome. Differentiated from NMS (which has lead-pipe rigidity, not clonus) and anticholinergic toxidrome (no clonus, dry skin).

Q: Why must thiamine be given BEFORE glucose in alcohol misuse? ▼

Answer: Chronic alcohol misuse causes thiamine (B1) deficiency. Glucose metabolism requires thiamine as a cofactor. Administering glucose first rapidly depletes remaining thiamine stores, precipitating Wernicke's encephalopathy (confusion, ophthalmoplegia, ataxia). IV Pabrinex (thiamine) must be given FIRST.

Q: What are the King's College Criteria for liver transplant in paracetamol OD? ▼

Answer (paracetamol OD): pH <7.3 after resuscitation, OR all three of: PT >100s (INR >6.5) + Creatinine >300 μmol/L + Grade III/IV hepatic encephalopathy. These patients require urgent liver transplant assessment.

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NAC Protocol Summary — Quick Reference

Bag	Dose	Diluent	Duration	Rate per 70kg (approx)
1 (Loading)	150 mg/kg	200ml 5% dextrose	1 hour	10,500mg in 200ml over 1h
2	50 mg/kg	500ml 5% dextrose	4 hours	3,500mg in 500ml over 4h
3 (Maintenance)	100 mg/kg	1000ml 5% dextrose	16 hours	7,000mg in 1000ml over 16h
Total duration		21 hours