Toxicology and Emergency Pharmacy

Toxicology is the study of poisons — their identification, mechanisms of action, and the management of poisoning. Emergency pharmacy encompasses the preparation, dispensing, and management of medicines used in acute medical emergencies. In South Africa, where poisoning from traditional medicines (muti), household chemicals, pesticides, and bites/stings is a significant presenting problem to emergency departments, and where the pharmacist may be the first healthcare professional consulted for advice in an acute poisoning, the pharmacist must have a solid foundation in toxicology. The SAPC examination tests candidates on the general principles of toxicology, specific antidotes and their indications, and the management of common poisonings and envenomations in the South African context.

This topic builds on pharmacodynamics (pharma-006), pharmacokinetics (pharma-003 through pharma-007), drug interactions (pharma-008), adverse drug reactions (pharma-009), and central nervous system drugs (pharma-013 for drugs of abuse).

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General Principles of Toxicology

Definitions

Toxicology: The science of poisons — their sources, chemical properties, mechanisms of action, detection, and treatment.

Poison: Any substance that, when introduced into or applied to the body, produces a deleterious effect on health.

Toxicity: The degree to which a substance can cause a harmful effect.

Dose-response relationship: The fundamental principle of toxicology — the effects of a poison are directly related to the dose received.

LD50: The dose that causes death in 50% of a population of test animals. Used to compare toxicity of substances.

Therapeutic index (TI): TD50/ED50 — the ratio of toxic to therapeutic dose. A narrow TI indicates a more dangerous drug.

Routes of Toxic Exposure

Route	Characteristics
Ingestion	Most common; delay before systemic absorption; some poisons not absorbed (caustic agents); activated charcoal ineffective for caustics, metals, hydrocarbons
Inhalation	Rapid absorption via pulmonary capillary bed; occupational exposure; chemical pneumonitis from some gases
Dermal/Transcutaneous	Corrosives, pesticides; absorption enhanced by skin breaks or occlusion
Ocular	Corrosive splash; immediate irrigation essential
Injection	IV (immediate effect); IM/SC (slower); IV drug users at risk of infections, overdose
Rectal/ Vaginal	Some poisons absorbed; used for drug smuggling (bodypacking)

Toxicokinetics

Toxicokinetics describes the absorption, distribution, metabolism, and elimination of toxic substances. These processes determine:

• Onset of toxic effects
• Duration of toxicity
• Whether there is an antidote or intervention that can alter the toxicokinetic profile

Key concepts:

• First-pass metabolism — ingested poisons may be extensively metabolised by the liver before reaching systemic circulation (reducing toxicity) or may be activated by liver metabolism (increasing toxicity — e.g., methanol, paracetamol)
• Volume of distribution (Vd) — poisons with large Vd (extensive tissue binding) are not effectively removed by haemodialysis
• Half-life — determines duration of effect and whether repeated dosing of antidote is needed
• Enterohepatic recirculation — some poisons (e.g., digoxin) recirculate through liver and gut, prolonging toxicity
• Active metabolites — some poisons are metabolised to more toxic products (paracetamol → NAPQI; methanol → formaldehyde/formic acid; ethylene glycol → oxalic acid)

General Management of Poisoning

Primary Survey (ABCDE approach)

A — Airway: Ensure airway is patent; protect from aspiration (positioning, suction); consider airway protection if reduced consciousness

B — Breathing: Ensure adequate ventilation; supplemental oxygen if needed; monitor SpO2; identify pneumonitis or pulmonary oedema

C — Circulation: Establish IV access; fluid resuscitation for hypotension; continuous cardiac monitoring; identify arrhythmias

D — Disability: Assess level of consciousness (AVPU or GCS); pupillary size and reaction; identify seizures

E — Exposure: Fully undress patient; examine entire body for signs of poisoning (injection sites, odours, skin findings); take rectal temperature (hypo/hyperthermia)

Decontamination

Gastrointestinal decontamination:

Method	Indication	Contraindication	Efficacy
Activated charcoal (AC)	Ingested poisons within 1–2 hours (if still in stomach); useful for many drugs and chemicals; multiple-dose AC for enterohepatic recirculating poisons	Caustic ingestion, hydrocarbons, metals (not adsorbed), compromised airway, ingested poisons with no adsorption to AC	Reduces absorption if given early; efficacy decreases with time
Gastric lavage	Rarely indicated; potentially within 1 hour of life-threatening ingestion; used in centres with appropriate equipment and trained staff	Caustics, hydrocarbons, risk of aspiration, ingestions where AC is effective	Removes variable amounts; not recommended as routine
Cathartics (sorbitol, magnesium citrate)	Promote elimination; used with AC	Not used alone; contraindicated in children <1 year; avoid in diarrhoea, abdominal pain, renal impairment	Limited evidence
Whole bowel irrigation (PEG solution)	Bodypackers (drug smugglers), sustained-release preparations, metals (iron, lithium)	Bowel obstruction, ileus, GI perforation	Reasonable evidence for bodypackers
Induced emesis (ipecac)	NOT recommended	Never — ipecac no longer recommended for any poisoning	Not recommended

Activated charcoal is the preferred GI decontamination method when indicated. Dose: 1 g/kg (or 50 g in adults) as a suspension in water. Can be repeated every 4 hours for drugs with enterohepatic recirculation.

Skin decontamination: Remove clothing; wash skin with water and soap (or appropriate solvent for specific chemicals); irrigate eyes with normal saline or water for at least 15–20 minutes.

Inhalation exposure: Remove from source; 100% oxygen; adequate ventilation; bronchodilators for bronchospasm.

Enhanced Elimination

Method	Indication	Mechanism
Urinary alkalinisation	Salicylate (aspirin) poisoning, phenobarbital poisoning	Ion trapping — weak acids are ionised in alkaline urine, reducing tubular reabsorption
Urinary acidification	Amphetamine, PCP (limited use)	Ion trapping — weak bases ionised in acidic urine
Haemodialysis	Lithium, ethylene glycol, methanol, salicylate (severe), metformin, phenobarbital (severe), theophylline (severe)	Direct removal from blood; bypasses organ of elimination
Haemoperfusion	Severe poisoning with poisons that bind to charcoal or resin	Blood passed through cartridge; toxin adsorbed
Exchange transfusion	Rare; severe poisoning in neonates	Replaces patient’s blood with donor blood

Supportive Care

This is the cornerstone of poisoning management — specific antidotes are the exception rather than the rule.

Parameter	Monitoring	Intervention
Airway	GCS, oxygen saturation	Intubation if GCS <8; positioning; suction
Breathing	RR, SpO2, blood gases	Oxygen; ventilate if respiratory depression
Circulation	HR, BP, ECG, urine output	IV fluids; vasopressors for hypotension; treat arrhythmias
Disability	GCS, pupils, glucose	Treat seizures (benzodiazepines); correct glucose
Temperature	Rectal temperature	Active cooling for hyperthermia; warming for hypothermia
Metabolic	Blood gases, electrolytes, glucose	Correct acid-base disturbances; correct electrolytes

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Specific Poisonings and Antidotes

Paracetamol (Acetaminophen) Poisoning

Mechanism: Paracetamol is metabolised primarily by glucuronidation (~50%) and sulfation (~30%) to non-toxic metabolites. A small fraction (~5%) is oxidised by CYP2E1 to the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI). At therapeutic doses, NAPQI is detoxified by glutathione. In overdose, glutathione is depleted, NAPQI accumulates, and binds covalently to hepatocyte proteins → centrilobular necrosis.

Toxic dose: >150 mg/kg (>10 g total in a typical adult) is potentially hepatotoxic; >250 mg/kg is frequently associated with severe hepatotoxicity; >500 mg/kg is potentially fatal.

Stages of paracetamol poisoning:

Time	Features
0–24 hours	Often asymptomatic; nausea, vomiting, pallor, sweating; may have normal LFTs
24–48 hours	Right upper quadrant pain, nausea, elevated transaminases (AST/ALT >1000 common)
48–72 hours	Peak hepatotoxicity; jaundice, coagulopathy, hepatic encephalopathy, renal failure; may be fatal
4–14 days	Recovery (if survive) or progressive liver failure; possible deaths from multi-organ failure

Treatment — N-acetylcysteine (NAC): NAC replenishes glutathione and directly scavenges NAPQI. Most effective when given within 8 hours of ingestion. Administer regardless of ingestion time if presentation >8 hours (late presentation still benefits).

SA protocol for NAC administration:

IV regimen (preferred in SA for severe cases):

• Loading dose: 150 mg/kg NAC IV over 60 minutes
• Maintenance dose 1: 50 mg/kg NAC IV over 4 hours
• Maintenance dose 2: 100 mg/kg NAC IV over 16 hours

Oral regimen:

• 140 mg/kg loading dose PO; then 70 mg/kg every 4 hours for 72 hours (or 18 doses)
• Less commonly used in SA due to GI side effects and requirement for prolonged administration

Who requires NAC treatment?

• Paracetamol level on nomogram above the treatment line (use Rumack-Matthew nomogram)
• Ingestion >150 mg/kg (or >10 g in adults) within 24 hours
• Unknown time of ingestion with potentially toxic dose
• Clinical evidence of hepatotoxicity (elevated AST/ALT, coagulopathy)

Prophylactic NAC: All patients with significant ingestion should receive NAC regardless of level if presentation is >8 hours.

Additional management: Supportive care; monitor INR, glucose, electrolytes, renal function; no specific role for activated charcoal (late presentation most common reason to consider).

Opioid Poisoning

Presentation: Triad of CNS depression, respiratory depression, and miosis (pinpoint pupils). May also have hypotension, bradycardia, hypothermia.

Specific antidote: Naloxone

Mechanism: Competitive μ-opioid receptor antagonist; displaces opioids from receptors; rapid onset IV (1–2 minutes).

Dosing:

• Adults: 0.4–2 mg IV initially; repeat every 2–3 minutes to total of 10 mg
• If no response with 10 mg, consider alternative diagnosis (not opioid poisoning)
• May need infusion (naloxone short half-life ~30–60 min; opioids longer) or repeat IM injections
• Paediatric: 0.1 mg/kg IV; repeat as needed

Naloxone formulations:

• IV, IM, SC: standard formulations
• Intranasal: 2 mg in one nostril (for community use; available in some settings)
• Auto-injector: for community responders

Higher potency opioids (fentanyl analogues, carfentanil): May require higher naloxone doses; carfentanil (used as a chemical weapon or in veterinary practice) may require massive naloxone dosing.

Important consideration: Naloxone precipitates withdrawal in opioid-dependent patients (agitation, sweating, nausea, vomiting, diarrhoea). In chronic pain patients on opioids, reverse carefully to avoid precipitating pain crisis.

Benzodiazepine Poisoning

Presentation: CNS depression, respiratory depression, hypotension, hypothermia, ataxia, nystagmus, normal pupils.

Specific antidote: Flumazenil

Mechanism: Competitive antagonist at the benzodiazepine binding site on GABA-A receptors.

Dosing: 0.2 mg IV initially; repeat 0.2 mg every minute to total of 1 mg; or 0.3 mg initially, repeat up to 2 mg total if no response.

Important cautions:

• Do not use in patients with benzodiazepine dependence (precipitates withdrawal seizures)
• Do not use in mixed overdose with tricyclic antidepressants (can cause seizures)
• Short half-life (~1 hour); may need infusion
• Use in young children only if life-threatening and ingested benzodiazepine only

Supportive care (preferred approach): With airway protection, oxygen, IV fluids, observation — flumazenil rarely needed.

Methanol and Ethylene Glycol Poisoning

Methanol (wood alcohol): Found in solvents, antifreeze, fuel; metabolised by alcohol dehydrogenase to formaldehyde → formic acid → metabolic acidosis, optic nerve damage (blindness), CNS damage.

Ethylene glycol: Found in antifreeze, coolants; metabolised by alcohol dehydrogenase to glycoaldehyde → glycolic acid → oxalic acid → calcium oxalate crystal deposition in kidneys (acute renal failure), CNS damage, cardiopulmonary complications.

Treatment — Fomepizole (4-methylpyrazole, 4-MP):

• Inhibits alcohol dehydrogenase → prevents metabolism of methanol/ethylene glycol to toxic metabolites
• Loading dose: 15 mg/kg IV; then 10 mg/kg every 12 hours for 4 doses, then 15 mg/kg every 12 hours
• Preferred over ethanol because it does not cause CNS depression, has predictable kinetics, and does not require blood level monitoring

Ethanol as alternative antidote:

• Competes with methanol/ethylene glycol for alcohol dehydrogenase (higher affinity)
• Loading dose: 0.8 g/kg (1 mL/kg of 95% ethanol) orally; then maintenance dose (0.15 g/kg/hour; double if on dialysis)
• Requires blood ethanol level monitoring (target 1–1.5 g/L)
• Causes intoxication, CNS depression; not preferred where fomepizole is available

Haemodialysis: Indicated for severe methanol or ethylene glycol poisoning (metabolic acidosis, visual impairment for methanol, renal failure for ethylene glycol, or levels >20 mmol/L).

Additional management: Urinary alkalinisation to enhance excretion of formic acid (methanol); correct metabolic acidosis; supportive care.

Organophosphate and Carbamate Poisoning

Mechanism: Organophosphates irreversibly inhibit acetylcholinesterase → accumulation of acetylcholine at muscarinic and nicotinic receptors → cholinergic crisis.

SLUDGE/BBMUSH effects (muscarinic):

• Salivation
• Lacrimation
• Urination
• Defecation/Diarrhoea
• GI distress
• Emesis
• Bronchorrhoea/Bronchospasm/Bradycardia

Nicotinic effects: Muscle weakness, fasciculations, paralysis (including respiratory muscles).

Management — Atropine:

• 2–4 mg IV initially; repeat every 5–10 minutes until atropinisation (drying of secretions, mydriasis, HR >80 bpm)
• Often massive doses required (hundreds of mg over days)
• Atropine does not reverse nicotinic effects (muscle weakness)
• Atropine infusion may be required

Management — Pralidoxime (2-PAM):

• Reactivates acetylcholinesterase if given before “ageing” (irreversible phosphorylation); most effective within 24 hours
• Dose: 1–2 g IV over 30 minutes; then 1 g/hour infusion
• More effective for organophosphates than carbamates
• Does not replace need for atropine

Additional management: Decontamination (remove clothing; wash skin); ventilate for respiratory muscle paralysis; treat bradycardia; control seizures (benzodiazepines); supportive care.

In South Africa: Organophosphate poisoning occurs through agricultural use, ingestion of pesticide-contaminated food/water, and intentional poisoning. Emergency departments in rural areas and agricultural regions should have atropine and pralidoxime available.

Carbon Monoxide Poisoning

Mechanism: CO binds to haemoglobin with ~240× greater affinity than oxygen → functional anaemia, left shift of oxyhaemoglobin dissociation curve → tissue hypoxia.

Presentation: Headache, dizziness, nausea, confusion, syncope, cherry-red skin (not always present), chest pain, arrhythmias, coma.

Treatment — Oxygen:

• 100% oxygen via non-rebreather mask → reduces half-life of carboxyhaemoglobin from ~5 hours (room air) to ~60–90 minutes
• Hyperbaric oxygen (HBO): reduces half-life to ~20–30 minutes; indicated for severe poisoning (LOC, neurological signs, cardiac ischaemia, pregnancy)
• SA context: HBO chambers limited to major centres; availability a challenge

Additional management: Maintain airway; continuous cardiac monitoring; check carboxyhaemoglobin (CO-oximetry — standard pulse oximetry unreliable); identify source of CO; treat complications.

Digoxin Poisoning

Mechanism: Digoxin inhibits Na⁺/K⁺-ATPase → intracellular K⁺ depletion, increased automaticity, AV block, hyperkalaemia.

Presentation: Nausea, vomiting, diarrhoea, abdominal pain; bradyarrhythmias (sinus bradycardia, AV block), tachyarrhythmias (ectopic ventricular beats, bidirectional ventricular tachycardia); visual disturbances (yellow-green halos); confusion.

Specific antidote — Digoxin-specific antibodies (Fab fragments):

• Indications: life-threatening arrhythmias, hyperkalaemia (>6 mmol/L), ingestion >10 mg in adults, ingestion >4 mg in children, level >12 ng/mL
• Dose: 10 vials IV for acute ingestion of 10 mg digoxin; adjust for chronic toxicity based on serum digoxin level and body weight
• Reverses digoxin effects within 20–30 minutes
• Very expensive; use in life-threatening cases

Additional management: Correct hyperkalaemia (avoid calcium — can worsen arrhythmias); bradycardia (atropine, temporary pacing); control arrhythmias (phenytoin, lignocaine, magnesium); supportive care.

Sodium Cyanide Poisoning

Mechanism: Cyanide inhibits cytochrome c oxidase (Complex IV in mitochondrial electron transport chain) → blocks cellular respiration → tissue hypoxia despite adequate oxygen → rapid cellular death.

Sources: Smoke inhalation (synthetic materials burning), industrial exposure, ingestion of cyanide salts (pesticides, rodenticides), cassava (if poorly processed).

Presentation: Rapid onset — headache, confusion, dyspnoea, seizures, loss of consciousness, cardiovascular collapse. The classic finding is bright venous blood (oxygen extracted but not used).

Antidote — Hydroxocobalamin (Cyanokit):

• Binds cyanide to form cyanocobalamin (vitamin B12), which is renally excreted
• Dose: 5 g IV over 15 minutes; repeat 1 g if needed
• Preferred antidote; can be given empirically in smoke inhalation
• SA: registered and available in some centres

Alternative — Sodium nitrite + sodium thiosulfate:

• Sodium nitrite: induces methaemoglobinaemia → binds cyanide (but reduces oxygen-carrying capacity — problematic in smoke inhalation with concurrent CO poisoning)
• Sodium thiosulfate: provides sulfur donor for rhodanese → converts cyanide to thiocyanate (renally excreted)
• Less preferred than hydroxocobalamin; combination in SA may be used if hydroxocobalamin unavailable

Snake Envenomation in South Africa

South Africa has several venomous snakes: puff adder, Mozambique spitting cobra, rinkhals, Cape cobra, black mamba, green mamba, boomslang.

Venom types:

Venom Type	Snakes	Effects	Treatment
Cytotoxic (tissue necrosis)	Puff adder, spitting cobras, rinkhals	Local swelling, pain, tissue necrosis; delayed effects	Polyvalent antivenom (SAIMR) for systemic spread
Neurotoxic (paralysis)	Cape cobra, black mamba, green mamba	Descending paralysis → respiratory paralysis	Polyvalent antivenom
Haemotoxic (coagulopathy)	Boomslang, vine snake	Haemorrhagic manifestations; delayed onset	Monovalent antivenom for boomslang

SAIMR polyvalent antivenom (polyvalent snake antivenom):

• Effective against: puff adder, Mozambique spitting cobra, rinkhals, Cape cobra, black mamba, green mamba
• NOT effective against: boomslang (requires monovalent), puff adder cytotoxic effects alone
• Dose: 10–20 mL (1–2 vials) IV after test dose (to detect hypersensitivity); diluted in 200 mL saline, infused over 30–60 minutes
• Adverse reactions: acute anaphylaxis (urticaria, bronchospasm, hypotension) — treat with adrenaline IM; serum sickness (delayed, 5–14 days later)

General management of snakebite:

1. Immobilise limb (movement spreads venom via lymphatics)
2. Remove rings, watches, tight clothing
3. Pressure immobilisation bandage (for neurotoxic snakes — mambas, cobras): bandage firmly from digits to above site, immobilise with splint
4. DO NOT: Cut wound, suck venom, apply tourniquet, give alcohol, apply ice
5. Transport to hospital — do not attempt to catch or kill snake (photograph if safely possible for identification)
6. Monitor: Vital signs, wound site, coagulation (for boomslang)
7. Antivenom as indicated; treat reactions

SA context: Snakebite is common in rural areas; district hospitals in endemic areas should have antivenom. SAIMR (South African Institute for Medical Research) polyvalent antivenom is available through the South African Vaccine Producers (SAVP) and through provincial health departments.

Scorpion Stings

Most dangerous scorpion in SA: Parabuthus transvaalicus (Transvaal thick-tailed scorpion) — found in semi-arid regions; neurotoxic venom.

Venom effects: Pain, local swelling, hyper-salivation, lacrimation, sweating, tachycardia, hypertension, muscle twitching, hyperreflexia; severe cases: pulmonary oedema, cardiovascular collapse.

Management:

• Analgesia: NSAIDs, opioids for severe pain; local anaesthetic infiltration (without adrenaline) for severe local pain
• Benzodiazepines for muscle spasm
• Atropine for cholinergic symptoms (bradycardia, bronchorrhoea)
• Vasopressors for hypotension unresponsive to fluids
• Scorpion antivenom (limited availability in SA); reserved for severe cases
• Monitor cardiac and respiratory function

Spider Bites

Black widow (button spider — Latrodectus species):

• Venom: α-latrotoxin → massive neurotransmitter release → severe muscle pain, rigidity, hypertension, sweating
• Systemic effects: chest and abdominal muscle pain (mimics acute abdomen or MI)
• Treatment: analgesics (opioids), benzodiazepines for muscle spasm; calcium gluconate IV (controversial); antivenom rarely needed
• SA: found in dry, sheltered areas; not aggressive unless threatened

Brown violin spider (Loxosceles species):

• Venom: sphingomyelinase D → dermonecrotic effects
• Local necrosis (loxoscelism): slow-developing necrotic ulcer; may take weeks to heal
• Rarely systemic (loxoscelism): fever, rash, haemolysis, DIC
• Treatment: supportive; wound care; debridement only after demarcation; antibiotics for secondary infection; antivenom not available in SA

Other Important Poisonings in South Africa

Petrol (benzine/gasoline) ingestion:

• Pulmonary aspiration → chemical pneumonitis
• CNS depression, arrhythmias
• Management: supportive; do NOT induce vomiting (aspiration risk); activated charcoal not effective

Muti (traditional medicine) poisoning:

• Traditional medicines may contain toxic substances; heavy metal contamination (lead, mercury, arsenic) documented
• Presentation highly variable; suspect in unexplained lead poisoning, abdominal pain, neurological symptoms
• Treatment: supportive; specific heavy metal chelation therapy if indicated (see below)

Lead poisoning:

• Sources: old paint, contaminated soil, traditional medicines, occupational exposure
• Presentation: abdominal pain, encephalopathy, peripheral neuropathy, anaemia, gingival lead lines, wrist drop
• Diagnosis: blood lead level
• Treatment: chelation therapy (British anti-Lewisite/BAL, EDTA, DMSA) for levels >70 mcg/dL or symptomatic patients

Paraquat poisoning:

• Highly toxic herbicide; ingested accidentally or intentionally
• Mechanism: generation of reactive oxygen species → multi-organ failure (lung fibrosis, renal failure, hepatic necrosis)
• No specific antidote; treatment: supportive; haemodialysis early (before multi-organ failure)
• Prognosis poor if ingested >40 mL; often fatal

Heavy Metal Chelation Therapy

Metal	Chelator	Notes
Lead (and other heavy metals)	EDTA (ethylenediaminetetraacetic acid)	IV; causes renal damage if prolonged; careful monitoring
Lead, arsenic, mercury	BAL (British anti-Lewisite/dimercaprol)	IM; painful; side effects
Lead, mercury, arsenic	DMSA (dimercaptosuccinic acid/succimer)	Oral; better tolerated; used especially in children
Mercury, arsenic	DMSA or DMPS (dimercaptopropane sulfonate)	DMPS more effective for mercury
Iron	Deferoxamine	IV for acute iron poisoning; oral deferasirox for chronic overload

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Emergency Pharmacy

Cardiopulmonary Resuscitation (CPR) Drugs

Drug	Indication	Dose (adult)	Notes
Adrenaline (epinephrine)	VF/pVT (refractory), asystole, PEA	1 mg IV every 3–5 min	Standard CPR dose
Amiodarone	VF/pVT refractory to 3 shocks	300 mg IV (first dose); 150 mg (second dose)	Preferred over lignocaine
Lignocaine (lidocaine)	VF/pVT (if amiodarone unavailable)	1–1.5 mg/kg IV	Second line to amiodarone
Atropine	Symptomatic bradycardia, asystole	0.5 mg IV every 3–5 min; max 3 mg	May not be needed for asystole
Adenosine	SVT (AVNRT, AVRT)	6 mg rapid IV push; then 12 mg if needed	Requires IV access and cardiac monitoring
Sodium bicarbonate	Severe metabolic acidosis (pH <7.1), hyperkalaemia, tricyclic overdose (QRS widening)	1 mEq/kg IV	Not routine — use specific indications
Calcium chloride	Hyperkalaemia with cardiac effects, calcium channel blocker toxicity, magnesium overdose	10 mL of 10% CaCl2 IV	Central line preferred

Anaphylaxis Management

Presentation: Urticaria, angioedema (especially laryngeal), bronchospasm, hypotension, tachycardia.

Treatment:

• Adrenaline IM: 0.3–0.5 mg (0.3 mL of 1:1000) IM into lateral thigh; repeat every 5–15 minutes as needed
• Oxygen: 100% via mask
• IV fluids: 0.9% NaCl for hypotension
• Nebulised salbutamol: for bronchospasm
• Antihistamines (diphenhydramine): for histamine-mediated symptoms (secondary)
• Corticosteroids (hydrocortisone IV): for delayed/rebound reactions (secondary)
• Observe: at least 4–6 hours; rebound can occur

Status Epilepticus Management

Stage	Time	Treatment
Early	0–5 min	Position patient safely; do not force anything in mouth; monitor
Established	5–20 min	IV benzodiazepine: lorazepam 0.1 mg/kg (max 4 mg) OR diazepam 0.15–0.2 mg/kg (max 10 mg) OR midazolam IM/intranasal 0.2 mg/kg
Refractory	>20 min	IV anaesthetics: phenytoin/fosphenytoin OR levetiracetam OR valproic acid OR phenobarbital
Super-refractory	>60 min	Continuous midazolam infusion OR propofol infusion OR thiopentone coma

Acute Asthma Exacerbation

Severity assessment: Tachypnoea, accessory muscle use, inability to speak full sentences, silent chest (ominous sign), SpO2 <92%, PEF <50% personal best.

Treatment:

• Oxygen: 2–4 L/min via mask to maintain SpO2 ≥92%
• Salbutamol: 2–5 puffs via spacer; repeat every 20 min × 3 if severe; or nebulise 2.5–5 mg if severe
• Ipratropium: 0.5 mg nebulised with salbutamol (for moderate-severe exacerbation)
• Prednisone/prednisolone: 40–50 mg PO (or IV methylprednisolone if unable to take orally)
• Magnesium sulfate: 2 g IV over 20 minutes for severe exacerbation (if poor response to bronchodilators)
• If poor response: IV aminophylline (load 5 mg/kg over 20 min; maintenance infusion); ICU referral; intubation if needed

Acute Coronary Syndrome (ACS)

STEMI management:

• Aspirin: 150–300 mg chewed immediately (unless contraindicated)
• Clopidogrel: 300–600 mg loading dose (or ticagrelor 180 mg)
• Anticoagulation: Heparin (UFH or enoxaparin) or bivalirudin
• Reperfusion: Primary PCI (if available within 90 min) or fibrinbolysis (if PCI not within 120 min)
• Morphine: 1–3 mg IV for chest pain (if not relieved by nitrates)
• Supplemental oxygen: if SpO2 <94%
• Nitrates: for chest pain unrelieved by aspirin and clopidogrel; avoid if hypotensive or inferior STEMI (right ventricular involvement)

NSTEMI/UA:

• Anticoagulation (enoxaparin SC or UFH IV)
• Antiplatelet (aspirin + clopidogrel or ticagrelor)
• Anticoagulant
• Risk stratify (TIMI, GRACE scores)
• Early invasive strategy vs conservative management

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SAPC Examination Focus Areas

High-yield topics for the SAPC exam:

1. Paracetamol poisoning — NAPQI mechanism, NAC antidote (dose and regimen), 8-hour window, Rumack-Matthew nomogram
2. Opioid poisoning — naloxone (dose, short half-life, infusion), CNS/respiratory/miosis triad
3. Benzodiazepine poisoning — flumazenil (caution in dependence, mixed overdose), supportive care preferred
4. Methanol/ethylene glycol poisoning — fomepizole vs ethanol, alcohol dehydrogenase inhibition, haemodialysis indications
5. Organophosphate poisoning — cholinergic crisis (SLUDGE), atropine (massive doses), pralidoxime
6. Carbon monoxide poisoning — 100% oxygen, hyperbaric indications, CO-oximetry
7. Snake envenomation — pressure immobilisation, SAIMR antivenom indications and dosing, local vs systemic effects
8. Digoxin poisoning — arrhythmias, hyperkalaemia, digoxin-specific Fab fragments indications and dosing
9. Cyanide poisoning — hydroxocobalamin (Cyanokit), mechanism (cytochrome c oxidase inhibition), bright venous blood
10. Anaphylaxis — adrenaline IM (0.3–0.5 mg of 1:1000), positioning, oxygen, fluids, observation
11. Status epilepticus — benzodiazepines first line (lorazepam/diazepam/midazolam), second-line (phenytoin/levetiracetam/valproate)
12. Acute asthma — salbutamol nebulisation, ipratropium, steroids, magnesium sulfate, oxygen
13. Activated charcoal — indications (within 1–2 hours), contraindications (caustics, hydrocarbons), dosing
14. Lead poisoning — chelation therapy (BAL, EDTA, DMSA)
15. Urinary alkalinisation — salicylate poisoning, phenobarbital; ion trapping mechanism

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Summary of Key Concepts

• Toxicology management follows ABCDE approach; decontamination methods (activated charcoal preferred) and enhanced elimination (haemodialysis for specific poisons) are adjunctive
• Supportive care is the cornerstone of poisoning management — antidotes are the exception
• Paracetamol poisoning: NAPQI mechanism; NAC antidote within 8 hours; monitor transaminases and INR
• Opioid poisoning: naloxone reversal; CNS/respiratory/miosis triad; consider longer-acting opioids
• Methanol and ethylene glycol: fomepizole inhibits alcohol dehydrogenase; haemodialysis for severe cases
• Organophosphate poisoning: atropine (massive doses until secretions dry) and pralidoxime
• Snake envenomation: pressure immobilisation for neurotoxic snakes; SAIMR polyvalent antivenom for systemic effects; do not cut, suck, or tourniquet
• Scorpion stings: analgesia, benzodiazepines for spasm, atropine for cholinergic symptoms
• Scorpion and spider envenomation: differs by species; supportive care primary
• Emergency pharmacy: adrenaline for anaphylaxis, standard CPR drug doses, status epilepticus and acute asthma management
• South African context: traditional medicine (muti) poisoning, organophosphate pesticide exposure, snakebite in rural areas — all require knowledge of local context and availability of SA-specific antivenoms
• Pharmacists can play a critical role in poison information (advice lines), antidote stocking, and emergency preparedness in both hospital and community settings