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OHC Medical Officer Interview Preparation - CMO Round

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Part 1: Core OHC Knowledge Questions

• Pre-employment and periodic medical examinations
• Health surveillance for workers exposed to hazards (noise, dust, chemicals, radiation)
• Emergency and first aid management
• Statutory compliance (Factories Act, Factories Rules - Form 7, Form 32)
• Maintaining health records (EHR)
• Coordination with external hospitals and specialists
• Supervising OHC staff (nurses, paramedics, pharmacists)
• Health education and vaccination drives (tetanus, hepatitis B)

• Factories Act 1948 - Sections on health, cleanliness, first aid
• State Factories Rules - periodic medical examinations for hazardous processes
• Form 7 (accident register), Form 15 (health register)
• OSHA-equivalent guidelines for India

• Defibrillator (AED), oxygen cylinder, ambu bag, suction apparatus
• IV cannulas, fluids (NS, RL, DNS)
• Emergency drugs kit (adrenaline, atropine, hydrocortisone, diazepam, GTN, aspirin, morphine)
• Stretcher, splints, cervical collar
• Eye wash station, burn dressing tray
• Spirometer/PFT for dust-exposure workers, audiometer for noise workers

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Part 2: Emergency Case Scenarios (Most Likely to Be Asked)

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CASE 1: Worker Collapses on Shop Floor - Cardiac Arrest

1. Call for help - activate emergency response (shout, press emergency button)
2. Assess - check responsiveness (tap shoulder, shout), no breathing/no pulse
3. Call ambulance / trigger emergency code
4. Start CPR immediately - 30 chest compressions : 2 breaths (100-120/min, depth 5-6 cm)
5. Attach AED as soon as available - follow voice prompts, shock if advised
6. IV access - prepare adrenaline (1 mg IV every 3-5 min in VF/pulseless VT)
7. After ROSC (Return of Spontaneous Circulation): 100% O2, monitor ECG, prepare for transfer to cardiac centre
8. Key point to mention: Post-ROSC - avoid hypoxia, hypotension, hyperthermia (target temp 32-36°C if comatose)

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CASE 2: Chest Pain at Workplace - Acute MI

1. Sit/rest the patient, oxygen if SpO2 <94%
2. Aspirin 300 mg - chew immediately (antiplatelet)
3. Sublingual GTN (if SBP >90 mmHg) - 0.5 mg, repeat every 5 min x3
4. Morphine 2-4 mg IV for pain (controversial now but standard in STEMI)
5. Clopidogrel 300 mg loading (dual antiplatelet)
6. 12-lead ECG, IV access, send troponin, CBC, BMP
7. Immediate transfer to cath lab / hospital with PCI facility - "Time is muscle" (target door-to-balloon <90 min)
8. Thrombolysis (streptokinase/tenecteplase) if PCI not available within 120 min
9. Continuous monitoring en route (ECG, vitals, SpO2)

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CASE 3: Chemical Splash / Toxic Exposure

1. Immediately irrigate with large volumes of water/saline for at least 15-20 min (eye wash station)
2. Remove contact lenses if any
3. Check pH of eye - target neutral (7.0)
4. Refer to ophthalmologist urgently
5. Identify the chemical - acid or alkali? (Alkali burns penetrate deeper - more dangerous)

1. Remove patient from exposure area, fresh air immediately
2. Assess ABCDE - airway, breathing, consciousness
3. 100% oxygen via non-rebreather mask
4. Bronchodilators (salbutamol nebulization) if wheeze
5. Steroids (hydrocortisone 100 mg IV) if severe bronchospasm
6. Monitor for delayed pulmonary oedema (can occur 4-24 hours later - especially with chlorine, ammonia, NOx)
7. Hospitalize and observe for minimum 24 hours even if initially well
8. MSDS (Material Safety Data Sheet) of the chemical is critical - check it immediately

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CASE 4: Heat Stroke

1. Core temp >40°C + CNS dysfunction (confusion/coma) = heat stroke (not just heat exhaustion)
2. Remove from hot environment immediately
3. Rapid cooling is the priority - evaporative cooling (wet cloth + fan), ice packs to axilla/groin/neck, cold IV fluids
4. Target temp: <39°C within 30 minutes
5. IV access - NS/RL bolus for hemodynamic support
6. Avoid antipyretics (they don't work in heat stroke - different mechanism from fever)
7. Monitor for complications: rhabdomyolysis (dark urine), DIC, acute kidney injury, liver failure
8. Urine output monitoring - aim >1 ml/kg/hr
9. Transfer to ICU

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CASE 5: Electrocution / Electric Shock Injury

1. DO NOT touch the patient until power is switched off (rescuer safety first)
2. Switch off the power source, use non-conductive rod to separate if needed
3. Assess - ABCDE, check for cardiac arrest (VF is common)
4. CPR if no pulse
5. Surface burns may be minor - deep tissue damage can be extensive ("iceberg" injury)
6. IV fluids - aggressive hydration (Parkland formula for burns component)
7. Monitor ECG - arrhythmias can be delayed (admit and monitor for 24 hours)
8. Watch for rhabdomyolysis, renal failure, compartment syndrome
9. Tetanus prophylaxis, wound care

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CASE 6: Organophosphate Poisoning (Common in industrial/agricultural settings)

• Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis
• Bradycardia, Bronchospasm, Bronchorrhea

1. Remove contaminated clothing, wash skin with soap and water (decontamination - protect staff with gloves)
2. O2 and airway support
3. Atropine - first line, 2-4 mg IV bolus, repeat every 5-10 min until secretions dry (no fixed dose - titrate to endpoint: dry secretions, HR >80)
4. Pralidoxime (PAM) - 1-2 g IV over 15-30 min if within 24-48 hours of exposure (reactivates AChE)
5. Benzodiazepines for seizures
6. ICU admission, monitor cholinesterase levels

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CASE 7: Fracture / Trauma at Workplace

1. Scene safety - ensure no further hazard
2. Primary survey - ABCDE (airway, C-spine control, breathing, circulation, disability, exposure)
3. Immobilize C-spine (if fall from height)
4. Hemorrhage control - direct pressure, tourniquet if limb bleed
5. Splint fracture in position found (don't attempt to reduce at OHC)
6. IV access x2, analgesia (morphine 0.1 mg/kg IV titrated)
7. IV fluids if hemodynamically unstable
8. Tetanus prophylaxis
9. Transfer to surgical center with ambulance

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CASE 8: Anaphylaxis

1. Adrenaline (epinephrine) 0.5 mg IM (1:1000) in outer mid-thigh - FIRST and MOST IMPORTANT step
2. Lay flat, raise legs (unless dyspnoeic)
3. 100% oxygen
4. IV access - rapid fluid bolus (500 ml-1L NS)
5. Repeat adrenaline every 5-15 min if no improvement
6. Chlorpheniramine 10 mg IV (antihistamine)
7. Hydrocortisone 200 mg IV (delayed action, prevents biphasic reaction)
8. Bronchodilators (salbutamol nebulization) for bronchospasm
9. Observe for minimum 4-6 hours after recovery (biphasic anaphylaxis risk)

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Part 3: OHC-Specific Management Questions

• Comprehensive history (past illness, family history, allergies)
• Clinical examination (vision, hearing, musculoskeletal fitness)
• Investigations: CBC, blood sugar, renal/liver function, CXR, ECG, PFT/audiometry based on job profile
• Fitness certificate - "Fit," "Fit with restrictions," or "Unfit" with clear reasoning

• After illness/injury, assess if worker can safely return to their specific job
• May involve graded return, modified duties, workplace adjustments

1. Wash wound immediately with soap and water for 5 min
2. Do NOT suck the wound
3. Report to OHC/supervisor immediately
4. Assess source patient - HIV, HBV, HCV status
5. Post-exposure prophylaxis (PEP): HIV-PEP within 72 hours (ideally <2 hours) - TDF+3TC+DTG for 28 days
6. HBV PEP: HBIG + vaccine if unimmunized
7. Baseline and follow-up serology (HIV, HBsAg, anti-HCV at 6 weeks, 3 months, 6 months)
8. Counseling and documentation

• Silicosis (miners, sandblasters) - CXR, PFT
• Coal workers' pneumoconiosis
• Asbestosis (construction) - CXR, HRCT
• Byssinosis (textile) - PFT with before/after-shift testing
• Occupational asthma - serial PFT, peak flow monitoring

• Audiometry (baseline + annual)
• Engineering controls, hearing protection (ear muffs >85 dB areas)
• Permissible noise level: 90 dB for 8 hours (OSHA)
• NIHL is irreversible - prevention is the only treatment

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Part 4: Management & Leadership Questions (CMO Perspective)

• Activate on-site emergency plan (ERP)
• Triage using START system: Red (immediate), Yellow (delayed), Green (minor), Black (expectant)
• Coordinate with Works Incident Controller
• Dispatch ambulances, call nearest hospital to prepare
• Communicate with police, fire brigade
• Post-incident documentation and debrief

• Maintain records as per Factories Act (Form 7, 8, 15)
• Submit periodic health reports to the factory inspector
• Ensure all required equipment is calibrated and available
• Conduct mock drills (fire, chemical spill, mass casualty) at regular intervals

• Employee Assistance Program (EAP)
• Screening tools: PHQ-9 (depression), GAD-7 (anxiety)
• Confidentiality of mental health records
• Referral to psychiatrist when needed

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Part 5: Quick Clinical Scenarios Summary Table

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Key Points to Impress the CMO

1. Always start case scenarios with ABCDE - it shows systematic thinking
2. Mention "time is muscle" for STEMI and "time is brain" for stroke - CMOs love this
3. Rescuer safety first in electrocution, chemical exposure - shows situational awareness
4. Pralidoxime must be given within 24-48 hours in OP poisoning - a common catch question
5. Atropine dose in OP poisoning is titrated to dryness of secretions, not a fixed amount
6. Biphasic anaphylaxis - mention observation for 4-6 hours after recovery
7. For burns, mention the Parkland formula: 4 ml × kg × % BSA burned (half in first 8 hours)
8. MSDS (Material Safety Data Sheet) - always refer to it in chemical exposure

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Hepatitis B Vaccine - Dosage & Schedule

Available Vaccines

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Standard Dosage by Age Group

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Vaccination Schedules

1. Standard 3-Dose Schedule (Most common)

• Dose 1: Day 0
• Dose 2: At least 4 weeks after Dose 1
• Dose 3: At least 8 weeks after Dose 2 AND at least 16 weeks after Dose 1
• Applies to: Engerix-B, Recombivax HB
• Used for: All age groups (infants, children, adolescents, adults)

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2. 2-Dose Schedule (Adults only ≥18 years)

• Vaccine: Heplisav-B only
• Advantage: Faster completion, higher seroprotection rates (~95%)
• Not for dialysis patients

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3. Accelerated 4-Dose Schedule (Rapid protection - Travel/High risk)

• Vaccine: Twinrix (HepA + HepB combined) - for ≥18 years
• Used when travel is imminent
• Standard Twinrix schedule: 0, 1, 6 months (3 doses)

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4. Alternative 4-Dose Schedule (Children/Adolescents)

• Vaccine: Engerix-B
• Licensed for all age groups when rapid protection is needed

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Newborn / Infant Schedule (India NIS + Global)

• In India's National Immunization Schedule (NIS): HepB is given with 1st, 2nd, and 3rd doses of DPT (at 6, 10, 14 weeks) + birth dose
• The Pentavalent vaccine (DPT + HiB + HepB) at 6, 10, 14 weeks replaces separate DPT and HepB doses, but the birth dose of HepB continues separately
• Birth dose must be given within 24 hours - it is the only way to prevent vertical (perinatal) transmission effectively

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Post-Exposure Prophylaxis (PEP) - Needlestick / High-Risk Exposure

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Serological Testing After Vaccination

• Test for anti-HBs 1-2 months after completing the series
• Protective level: anti-HBs ≥10 mIU/mL
• Non-responders (<10 mIU/mL): Repeat full 3-dose series, then retest
• If still no response after 6 doses: likely a genetic non-responder (~5-10% of immunocompetent adults)
• Dialysis patients, immunocompromised, healthcare workers - mandatory post-vaccination serology

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Special Populations

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2025 Update (CDC/ACIP)

• The birth dose is now subject to shared clinical decision-making for babies born to HBsAg-negative mothers (can delay to 2 months)
• This does NOT affect adult vaccination schedules
• Adult workplace and healthcare worker requirements remain unchanged
• PreHevbrio (VBI Vaccines, 3-dose series for adults) was withdrawn from US market in late 2024

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• Red Book 2021 - Report of the Committee on Infectious Diseases, Table 3.20 (p. 388/633)
• Park's Textbook of Preventive and Social Medicine - Hepatitis B vaccine section
• CDC Hepatitis B Vaccine Administration (updated Sept 2025)

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Acute Myocardial Infarction (MI) - Emergency Management

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Step 0: Immediate on Arrival (First 10 Minutes)

1. Triage RED - highest priority
2. Assess ABCDE - be ready to defibrillate (VF is the most common early cause of death)
3. 12-lead ECG within 10 minutes of arrival - this single test defines your entire treatment pathway
4. Continuous ECG monitoring, pulse oximetry, IV access x2, vitals

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Classification Based on ECG

Chest Pain Patient
      |
   12-lead ECG
      |
 _____|______________________________
|                                   |
ST Elevation (STEMI)         No ST Elevation
or New LBBB                        |
      |                    ___________________
   URGENT              Troponin elevated?   Normal troponin
   REPERFUSION             (NSTEMI)         (Unstable Angina)

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Investigations

Mandatory (Do Simultaneously with Treatment)

ECG Territory Localisation

Key point: In inferior STEMI, always do right-sided leads (V4R) to detect RV infarction - management differs! (Avoid nitrates, aggressive fluids instead)

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Immediate Treatment (MONA + Dual Antiplatelet + Anticoagulation)

Step 1: General Measures

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Step 2: Antiplatelet Therapy (DUAL - Start Immediately)

2025 guideline: Ticagrelor or Prasugrel preferred over Clopidogrel for STEMI going to PCI. Continue DAPT for 12 months post-PCI.

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Step 3: Pain Relief

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Step 4: Anticoagulation

Start anticoagulation after 3 hours of completing thrombolysis if PCI is not immediately available.

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Step 5: Other Drugs

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Reperfusion Strategy - The Most Critical Decision

For STEMI:

STEMI Diagnosed
        |
        |---- PCI-capable centre available? ----YES----> Primary PCI
        |          within 120 min?                       Target door-to-balloon < 90 min
        |
       NO
        |
Thrombolysis (Fibrinolysis)
Target: Door-to-needle < 30 min
        |
        |--- Check ECG at 60-90 min after lysis
        |
        |--- ST resolution >50%? --> SUCCESS --> Facilitated PCI in 2-24 hours
        |
        |--- ST resolution <50%? --> FAILURE --> RESCUE PCI immediately
             (Do NOT repeat thrombolysis)

Thrombolytic Agents

• Prior intracranial haemorrhage (absolute)
• Recent (<3 months) ischaemic stroke
• Active internal bleeding
• Suspected aortic dissection
• Significant head trauma <3 months
• Uncontrolled hypertension (SBP >180 or DBP >110) - relative

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For NSTEMI / High-Risk NSTE-ACS:

• No immediate thrombolysis (not indicated)
• Risk stratify using TIMI score or GRACE score
• High-risk (TIMI ≥3): Early invasive angiography within 24 hours
• Very high-risk (ongoing ischaemia, haemodynamic instability, cardiogenic shock): Immediate angiography
• Low-risk: Medical management, elective angiography

1. Age ≥65 years
2. ≥3 CAD risk factors
3. Known CAD (stenosis >50%)
4. ASA use in last 7 days
5. Severe anginal events (≥2 in 24h)
6. ST deviation ≥0.5 mm
7. Elevated serum cardiac markers

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Post-Reperfusion / In-Hospital Monitoring

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Killip Classification (Severity of HF in MI)

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Secondary Prevention (Discharge Medications - "ABCDES")

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Key Time Targets to Memorise

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One-Liner Summary for Interview

"In STEMI - rapid diagnosis by ECG, dual antiplatelet (Aspirin + Ticagrelor), anticoagulation (UFH), O2 only if SpO2 <94%, GTN if BP allows, morphine for pain, high-dose statin, then primary PCI within 90 minutes or thrombolysis within 30 minutes if PCI unavailable. For NSTEMI - same medical management but no thrombolysis; urgency of angiography based on TIMI/GRACE risk score."

• Goldman-Cecil Medicine, Chapter 58 - ST-Elevation Myocardial Infarction
• 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for ACS Management
• National ACS Treatment Guideline 2025

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Organophosphate (OP) Poisoning

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What is it?

• Pesticides/insecticides: Parathion, Malathion, Chlorpyrifos, Dichlorvos (DDVP), Dimethoate
• Nerve agents (chemical warfare): Sarin, Soman, Tabun, VX
• Occupational exposure: Agricultural workers, pest control workers, factory workers handling pesticides

Per WHO: 1-3% of agricultural workers worldwide suffer acute pesticide poisoning annually. OP poisoning accounts for one-third of all global suicide attempts - making it a major emergency in developing countries including India.

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Pathophysiology

Normal:
Nerve impulse → ACh released into synapse → Binds receptor → Signal
                                                    ↓
                                          AChE breaks down ACh → Signal stops

In OP Poisoning:
OP compound → IRREVERSIBLY inhibits AChE
                        ↓
              ACh ACCUMULATES in synapses
                        ↓
        Overstimulation of ALL cholinergic receptors:
        - Muscarinic (M) receptors → Parasympathetic overactivity
        - Nicotinic (N) receptors → NMJ + Autonomic ganglia overactivity
        - CNS receptors → Seizures, coma

The "Aging" Process (Key Pharmacology Point)

• OP binds AChE → forms a phosphorylated enzyme complex
• This bond undergoes "aging" - one oxygen-phosphorus bond breaks, permanently strengthening the bond
• After aging, pralidoxime cannot work
• Aging with Soman: within 10 minutes
• Aging with other OPs: hours to days (so pralidoxime window is 24-48 hours)

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Routes of Absorption

• Skin (most common occupational route)
• Inhalation (spray, fumes)
• Ingestion (suicidal - most common in India)
• Conjunctiva (eye splash)

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Clinical Features

Muscarinic Features (M receptor overactivity - Parasympathetic)

The killer triad: Bronchospasm + Bronchorrhoea + Bradycardia = Death by respiratory failure

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Nicotinic Features (N receptor - NMJ + Ganglia)

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CNS Features

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Severity Grading (Peradeniya OP Poisoning Scale - POP Scale)

Higher POP score = more atropine needed, longer ICU stay, higher mortality

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Diagnosis

Clinical Diagnosis First

• OP poisoning is a CLINICAL diagnosis - do NOT wait for lab results before treating
• Classic history + SLUDGE/DUMBELS features + miosis + garlic/petroleum odour = start treatment immediately

Investigations

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Management - 4 Primary Objectives

1. DECONTAMINATE
2. STABILISE (ABCDE)
3. COUNTERACT acetylcholine (Atropine)
4. REGENERATE cholinesterase (Pralidoxime)

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Step 1: Decontamination (PROTECT YOURSELF FIRST)

• Wear PPE: Nitrile or neoprene gloves (NOT latex - latex doesn't protect against insecticides), gown, face shield
• Remove all contaminated clothing from the patient
• Skin decontamination: Wash skin thoroughly with soap and water for 15-20 min
• Eye exposure: Irrigate with water/saline for 15-20 min
• Ingestion: Gastric lavage within 1-2 hours (if airway protected) + activated charcoal 50-100 g
• Do NOT induce vomiting (aspiration risk)

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Step 2: Stabilisation - ABCDE

Intubation note: Use suxamethonium with EXTREME CAUTION - OP inhibits plasma cholinesterase which metabolises suxamethonium, causing prolonged paralysis. Prefer rocuronium or vecuronium.

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Step 3: Antidote 1 - ATROPINE (Muscarinic antagonist)

Endpoint of Atropinisation (Target - not overdose):

✅ Dry secretions (most important - secretions should dry up) ✅ Heart rate > 80 bpm ✅ SBP > 80 mmHg ✅ Clear chest on auscultation

• Muscle weakness/paralysis (nicotinic effect)
• CNS features (poor CNS penetration at standard doses)

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Step 4: Antidote 2 - PRALIDOXIME (PAM - Cholinesterase Regenerator)

• Loading: 1-2 g IV over 15-30 minutes
• Maintenance: 0.5-1 g/hour infusion or 1-2 g every 4-6 hours

• Must be given within 24-48 hours of exposure
• Ineffective after aging occurs
• After carbamate poisoning: pralidoxime is generally NOT used (carbamates spontaneously reactivate AChE; PAM may worsen toxicity)

• Muscle weakness/fasciculations (nicotinic effects) - treats what atropine cannot
• Reduces total atropine requirement

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Step 5: Benzodiazepines for Seizures

• Diazepam 5-10 mg IV (or lorazepam 2-4 mg IV)
• Repeat every 5-10 min as needed
• Do NOT use phenytoin (not effective for OP-induced seizures)

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Step 6: Supportive Care

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Intermediate Syndrome

• Occurs 24-96 hours after apparent recovery from acute toxicity
• Due to sustained NMJ dysfunction
• Features: Proximal limb weakness, neck flexor weakness, respiratory muscle paralysis
• Not prevented by pralidoxime
• Treatment: Mechanical ventilation - patient recovers over days to weeks

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Complications

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OP Poisoning vs Carbamate Poisoning - Key Differences

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Summary Flow Chart

Worker/patient with SLUDGE + miosis + garlic odour
             ↓
PROTECT YOURSELF (PPE) → Decontaminate patient
             ↓
         ABCDE
         ↓
Airway - suction, O2, intubate early if needed
(Use rocuronium, NOT suxamethonium)
         ↓
Atropine IV bolus (2-5 mg) → repeat every 5-10 min
→ titrate to DRY SECRETIONS (not fixed dose)
→ Maintenance infusion 10-20% of loading dose/hr
         ↓
Pralidoxime 1-2 g IV over 15-30 min (within 48h)
→ Maintenance infusion
         ↓
Benzodiazepines for seizures
         ↓
ICU monitoring for Intermediate Syndrome
Cholinesterase levels to monitor recovery

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Key Points for Interview

1. Most common cause of death = respiratory failure (bronchospasm + bronchorrhoea + respiratory muscle paralysis)
2. Atropine endpoint = DRY SECRETIONS, not a fixed dose - can give 100+ mg if needed
3. Pralidoxime window = within 24-48 hours - after aging, it is useless
4. Do NOT use suxamethonium for intubation (prolonged paralysis)
5. Tachycardia is NOT a contraindication to atropine
6. Carbamates = do NOT give pralidoxime (spontaneous AChE recovery, PAM may worsen)
7. Intermediate syndrome = day 1-4, respiratory paralysis, needs ventilation
8. PPE for staff = nitrile/neoprene gloves (not latex)

• Ganong's Review of Medical Physiology (26th ed.) - Clinical Box 13-2: Organophosphates
• IEM Emergency Medicine: OP & Carbamate Poisoning 2024

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Anaphylaxis - Definition, Pathophysiology & Management

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Definition (GA²LEN Consensus 2024)

"Anaphylaxis is a serious allergic (hypersensitivity) reaction that can progress rapidly and may cause death."

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Pathophysiology

IgE-Mediated (Classic / Immunologic) - Most Common

SENSITIZATION (First Exposure):
Allergen → Processed by APCs → IgE antibodies produced
→ IgE binds to Fc receptors on MAST CELLS and BASOPHILS
(patient is now sensitized - no symptoms yet)

RE-EXPOSURE (Second+ Exposure):
Same allergen → cross-links IgE on mast cells/basophils
→ DEGRANULATION
→ Release of:
   • Histamine
   • Tryptase
   • Prostaglandins
   • Leukotrienes
   • Platelet activating factor (PAF)
   • Cytokines (IL-4, IL-13)
        ↓
SYSTEMIC EFFECTS:
• Vasodilation → Hypotension → Shock
• Increased vascular permeability → Angioedema, urticaria
• Bronchospasm → Respiratory failure
• Mucus secretion → Airway obstruction

Non-IgE-Mediated (Anaphylactoid) - Clinically IDENTICAL

• Direct mast cell activation (e.g., opioids, vancomycin, radiocontrast media, NMBDs via MRGPRX2 receptor)
• Complement activation (e.g., paclitaxel/Cremophor, heparin contamination)
• Exogenous histamine ingestion (scombroid fish poisoning)

Key point: IgE and non-IgE anaphylaxis are clinically indistinguishable and treated the same way.

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Common Triggers

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Clinical Features - By Organ System

Skin (most common, ~90%)

• Pruritus, flushing
• Urticaria (hives) - raised, itchy wheals
• Angioedema - deeper swelling (lips, tongue, face, larynx)
• Erythema, morbilliform rash

Respiratory (most common cause of death)

• Stridor - laryngeal oedema / angioedema (upper airway)
• Wheeze, dyspnoea - bronchospasm (lower airway)
• Hoarse voice, change in cry (infants)
• Difficulty talking, persistent cough
• Respiratory arrest

Cardiovascular

• Tachycardia (usually), bradycardia (rare, vagal)
• Hypotension - distributive shock (vasodilation + fluid extravasation)
• Pallor, dizziness, collapse
• Cardiac arrest (from hypoxia or direct cardiac effect)

GI

• Nausea, vomiting
• Abdominal cramps, diarrhoea

CNS

• Anxiety, sense of impending doom
• Confusion, altered consciousness
• Seizures (from hypoxia/hypotension)

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Diagnostic Criteria (NIAID/FAAN - Widely Used)

Criterion 1: Acute skin/mucosal symptoms + EITHER respiratory OR cardiovascular symptoms

• Urticaria/angioedema/pruritus/flushing + (dyspnoea/wheeze/stridor/hypoxia) or (hypotension/syncope/collapse)

Criterion 2: Two or more of the following within minutes to hours after LIKELY ALLERGEN exposure:

• Skin/mucosal symptoms (urticaria, pruritus, flushing, angioedema)
• Respiratory symptoms
• Hypotension or end-organ dysfunction
• Persistent GI symptoms (abdominal pain, vomiting)

Criterion 3: Hypotension alone after exposure to a KNOWN allergen for that patient

• SBP <90 mmHg or >30% drop from baseline

Remember: Anaphylaxis is a clinical diagnosis - do NOT wait for investigations before treating.

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Biphasic Anaphylaxis (Critical Concept)

• Recurrence of symptoms after initial resolution - typically 1-8 hours later (range 1-72 hours)
• Occurs in ~5-20% of cases
• Can be equal to or worse than the initial reaction
• Mechanism: second wave of mediator release
• This is why observation for minimum 4-6 hours is mandatory after any anaphylaxis

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Investigations

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Management - Step by Step

REMOVE THE TRIGGER

• Stop the offending drug/infusion
• Remove insect stinger

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STEP 1: ADRENALINE (EPINEPHRINE) - FIRST AND MOST IMPORTANT

Nothing comes before adrenaline. Antihistamines and steroids are NOT first-line.

Paediatric Dosing Chart (IM Adrenaline 1:1000):

• Fastest absorption (high muscle perfusion even in shock)
• Can be given through clothing in emergency
• Preferred over deltoid in anaphylaxis

• Only for refractory anaphylaxis (failed 3+ IM doses) or in cardiac arrest
• IV dose: 0.1 mg (1 mL of 1:10,000) slow IV bolus with cardiac monitoring
• Continuous infusion: 1-20 mcg/min, titrated

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STEP 2: POSITION

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STEP 3: CALL FOR HELP + OXYGEN + IV ACCESS

• 100% oxygen via non-rebreather mask
• IV access x2 (large bore)
• Continuous monitoring: SpO2, ECG, BP

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STEP 4: IV FLUIDS

• NS 500 mL - 1 L rapid bolus (crystalloid) for hypotension/shock
• Repeat as needed - anaphylactic shock can require several litres
• Distributive shock = massive fluid shift into tissues

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STEP 5: ADJUNCT THERAPIES (after adrenaline and stabilisation)

Antihistamines and steroids are ADJUNCTS - they cannot treat airway compromise or cardiovascular collapse. Adrenaline does.

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STEP 6: AIRWAY MANAGEMENT

• Hoarse voice, stridor, tongue swelling = early intubation (rapidly worsening angioedema can make intubation impossible in minutes)
• Surgical airway (cricothyrotomy) if intubation fails
• Bag-mask ventilation if in arrest

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REFRACTORY ANAPHYLAXIS (3+ doses of IM adrenaline)

• IV adrenaline infusion: 1-20 mcg/min (titrate to BP)
• Glucagon 1-2 mg IV - for patients on beta-blockers (blocks normal adrenaline response; glucagon bypasses beta-receptor and directly activates cardiac adenylyl cyclase)
• Vasopressors: Noradrenaline, vasopressin
• ICU admission

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Observation After Anaphylaxis

• Clinically stable
• No adrenaline required for at least 4 hours
• Patient educated + prescribed EpiPen + follow-up arranged

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Discharge - Mandatory Steps

1. EpiPen (adrenaline auto-injector) prescribed - 2 pens
2. Written anaphylaxis action plan
3. Education on trigger avoidance
4. Medic alert bracelet
5. Referral to allergist/immunologist
6. Advise: steroids / antihistamines for 3-5 days to reduce late-phase reaction

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Summary: Priority Order in Anaphylaxis

1. ADRENALINE 0.5 mg IM (outer mid-thigh) ← FIRST, ALWAYS
2. Remove trigger
3. Position (flat + legs up / upright if dyspnoeic)
4. 100% O2
5. IV access + Fluid bolus (NS 500 mL-1L)
6. Repeat adrenaline every 5-15 min if needed
7. Antihistamine (chlorpheniramine 10 mg IV)
8. Hydrocortisone (200 mg IV)
9. Salbutamol nebulisation (if bronchospasm)
10. Observe ≥4 hours

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Key Points for OHC/CMO Interview

• Washington Manual of Medical Therapeutics - Anaphylaxis, p. 425
• Harrison's Principles of Internal Medicine 22E (2025) - Chapter 364
• GA²LEN Consensus Report 2024: Anaphylaxis Definition & Clinical Support Tool

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Snake Bite Management

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Epidemiology (India Context)

• India reports ~58,000 snake bite deaths/year - highest in the world
• Big 4 of India (responsible for >95% of deaths):

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Types of Venom & Effects

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Clinical Assessment on Arrival

History

• Time of bite, site, description of snake
• Symptoms since bite (local vs systemic)
• Any first aid given (tourniquets, incisions, herbal remedies)
• Nocturnal bite while sleeping on floor = suspect Krait even without visible fang marks

Local Signs

• Fang marks (1 or 2 puncture wounds)
• Pain, swelling, erythema, blistering
• Local necrosis
• Painful tender lymphadenopathy
• Swelling >half the bitten limb = indication for ASV

Systemic Signs to Look For

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Key Bedside Test: 20-Minute Whole Blood Clotting Test (20WBCT)

1. Draw 2-3 mL of blood into a clean, dry, ordinary glass tube (NOT plastic - false positive)
2. Leave undisturbed at room temperature for 20 minutes
3. Tilt the tube at the end of 20 minutes

• Repeat every hour for first 3 hours, then every 6 hours
• Use GLASS only - plastic/polystyrene gives false positive non-clotting result

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Investigations

---

First Aid: WHAT TO DO

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First Aid: WHAT NOT TO DO

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Indications for Anti-Snake Venom (ASV) - WHO / India MoHFW

Systemic Envenomation Indicators:

1. Haemostatic abnormalities: spontaneous bleeding (gums, nose, IV sites), positive 20WBCT (non-clotting blood), INR >1.2, thrombocytopenia <1 lakh/µL
2. Neurotoxic signs: ptosis, external ophthalmoplegia, descending paralysis
3. Cardiovascular: hypotension, shock, arrhythmia
4. Acute kidney injury: oliguria/anuria, rising creatinine
5. Haemoglobin/myoglobinuria: dark brown/black urine

Local Envenomation Indicators:

1. Swelling involving >half the bitten limb within 48 hours
2. Rapid progression of local swelling

ASV is NOT indicated for dry bites (no venom injected) or purely local reactions not meeting above criteria.

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Anti-Snake Venom (ASV) Administration

Indian Polyvalent ASV

• Raised against venom of all Big 4 species
• Each vial = 10 mL reconstituted ASV
• Neutralises 0.6 mg of cobra or Russell's viper venom per mL

Initial Dose (India MoHFW / SCTIMST Guidelines):

How to Give ASV:

• Reconstitute in 100-200 mL of normal saline
• Infuse over 30-60 minutes with close monitoring
• DO NOT give ASV test dose - test doses have no predictive value for anaphylaxis (India guidelines)
• Keep adrenaline 0.5 mL (1:1000) drawn and ready for ASV reactions

Repeat Dosing:

• Repeat 20WBCT every 6 hours
• If still non-clotting → repeat ASV every 6 hours until blood clots
• Maximum 30 vials

• Reassess at 1-2 hours after initial dose
• If worsening or no improvement → give second dose of 10 vials
• Maximum 20 vials (then assume all circulating venom is neutralised)
• If respiratory failure despite 20 vials → assisted ventilation, stop ASV

• May require 50+ vials (injects massive venom)

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Management of ASV Reactions

Early Anaphylactic Reaction (within 30-60 min)

• Stop ASV infusion
• Adrenaline 0.25-0.3 mg SC immediately
• Antihistamine + hydrocortisone IV
• Restart ASV infusion at slower rate once stabilised

Pyrogenic/Febrile Reaction (within 1-2 hours)

• Rigors, fever, hypotension
• Adrenaline + paracetamol
• Slow down infusion

Late Serum Sickness (5-10 days)

• Fever, urticaria, arthralgia, lymphadenopathy
• Treat with prednisolone + antihistamine for 5-7 days

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Specific Management by Type

Neurotoxic Envenomation (Cobra / Krait)

For post-synaptic blockade (Cobra) - neostigmine reverses paralysis For pre-synaptic blockade (Krait) - neostigmine does NOT work (venom destroys NMJ)

• Atropine 0.6 mg IV → then immediately Neostigmine 1.5 mg IV
• Repeat neostigmine 0.5 mg (with atropine) every 30 minutes for 5 doses
• Children: Atropine 0.05 mg/kg + Neostigmine 0.04 mg/kg, repeat 0.01 mg/kg every 30 min

• Monitor for descending paralysis
• Watch neck flexor strength (unable to lift head = impending respiratory failure)
• Early intubation and mechanical ventilation if respiratory muscles weaken
• Ventilate until paralysis resolves (may take days to weeks)

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Hemotoxic Envenomation (Russell's Viper / Saw-scaled Viper)

1. ASV 10 vials IV - repeat every 6 hours until 20WBCT clots
2. Fresh Whole Blood or Fresh Frozen Plasma (FFP) if severe bleeding persists after full ASV dose
3. Platelet concentrate if severe thrombocytopenia with bleeding
4. Monitor urine output hourly (AKI risk)
5. IV fluids to maintain urine output >0.5 mL/kg/hour
6. Dialysis (haemodialysis) if AKI with oliguria/anuria
7. Do NOT give heparin (not recommended in India for OP-VICC)
8. Analgesia: Tramadol 50 mg IV (avoid morphine/pethidine in neurotoxic cases)

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Management Flow Summary

PATIENT WITH SNAKE BITE
         ↓
FIRST AID: Immobilise, reassure, transport (no tourniquet, no incision)
         ↓
AT HOSPITAL:
• ABCDE
• IV access x2
• 20WBCT in glass tube
• Baseline investigations
• Observe minimum 24 hours
         ↓
SYSTEMIC ENVENOMATION? (20WBCT non-clotting / ptosis / bleeding / AKI)
         YES → ASV 10 vials IV over 30-60 min
         NO  → Observe, repeat 20WBCT every hour x3 hours, then 6 hourly
         ↓
NEUROTOXIC?          HEMOTOXIC?
↓                    ↓
AN test              Repeat ASV every 6h if 20WBCT non-clotting
(Atropine +          FFP/Blood if bleeding
Neostigmine)         Monitor AKI → dialysis if needed
↓
Ventilate if
respiratory
failure

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Complications to Monitor

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Key Points for OHC / CMO Interview

• WHO Guidelines for Management of Snakebites, South-East Asia Region
• India MoHFW Standard Treatment Guidelines for Snake Bite
• SCTIMST Snake Bite Indian Guidelines & Protocol

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Chemical Splash Management in OHC

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Overview

• Eyes (most urgent - risk of permanent blindness)
• Skin (burns, systemic absorption)
• Inhalation (fumes, vapours, mists)
• Ingestion (accidental or suicidal)

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First Priority: MSDS / SDS (Safety Data Sheet)

• Identify the chemical from the Material Safety Data Sheet (MSDS) / Safety Data Sheet (SDS)
• Know: acid vs alkali, concentration, systemic toxicity, specific antidotes
• Section 4 of SDS = First Aid Measures (by route of exposure)
• Contact Poison Control Centre if uncertain

In India: National Poison Information Centre (NPIC), AIIMS - 24h helpline: 1800-116-117 / 011-26593677

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GENERAL PRINCIPLES FOR ALL CHEMICAL EXPOSURES

Step 1: Rescuer Safety

• Wear PPE: nitrile gloves, gown, eye protection, face shield
• Chemical-contaminated patients can cause secondary contamination to healthcare workers
• Do not enter confined spaces with hazardous fumes without SCBA (Self-Contained Breathing Apparatus)

Step 2: Remove from Exposure

• Move patient to fresh air / clean area
• Stop ongoing exposure

Step 3: Remove Contaminated Clothing

• Cut off all contaminated clothing, shoes, jewellery
• Double-bag contaminated items (do NOT put in regular waste)
• Avoid contaminating unaffected areas while removing clothing

Step 4: Irrigate, Irrigate, Irrigate

• Water is the universal first decontaminant
• Do NOT waste time looking for specific antidotes before washing
• Begin irrigation within seconds of exposure

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A. CHEMICAL SPLASH TO THE EYE

Why Eyes Are Most Urgent

• Chemical eye burns are the second most common occupational eye injury (after foreign bodies)
• Alkali burns can penetrate the anterior chamber within minutes
• Risk of permanent corneal scarring, blindness, and loss of the eye

Acid vs Alkali Eye Burns

Immediate First Aid (Eye Wash Station)

1. Flush immediately - every second counts
2. Remove contact lenses right away (if easily removable without trauma)
3. Use eye wash station - hold eyelids open forcibly
4. Do NOT rub the eye - causes further mechanical damage
5. Direct flow from inner canthus (nose side) outward to prevent washing chemical into other eye
6. Flush with clean lukewarm tap water or saline - at least 20-30 minutes
7. For alkali burns: extend irrigation to 60 minutes minimum (deeper penetration)

At OHC - Medical Management

• Use pH litmus paper / strip on the conjunctival sac
• Normal eye pH = 7.0-7.4
• Continue irrigation until pH reaches neutral (7.0-7.4)
• Recheck pH 5-10 min after stopping (chemical can re-leach from tissues)

• Proparacaine 0.5% or tetracaine eye drops
• Makes irrigation tolerable and allows proper examination

• Visual acuity (document baseline)
• Fluorescein staining - identifies corneal epithelial defects (shows green under cobalt blue light)
• Slit-lamp examination - assess depth of damage
• Intraocular pressure - elevated IOP can indicate penetrating injury
• Limbal assessment - ischaemic limbus = poor prognosis (limbal stem cells destroyed)

Roper-Hall Grading of Chemical Eye Burns

Treatment After Irrigation (OHC or Hospital)

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B. CHEMICAL SPLASH TO SKIN

Immediate First Aid

1. Brush off any dry/solid chemical first (before water - water can activate dry chemical)
2. Remove all contaminated clothing and jewellery immediately
3. Irrigate with copious water - use safety shower if available
   • Acid burns: ≥15-20 minutes
   • Alkali burns: ≥30 minutes (deeper penetration, longer irrigation needed)
4. Do NOT neutralise acid with alkali or vice versa - exothermic reaction generates heat and worsens burn
5. Protect from hypothermia (especially large body surface area irrigation)

Assessment of Chemical Skin Burns

Treatment at OHC

• Wound cleaning - gentle debridement of loose tissue/blisters (burst blisters to prevent chemical sequestration in fluid)
• Dressing - non-adherent dressings (paraffin gauze)
• Analgesia - paracetamol, NSAIDs, tramadol/morphine for severe pain
• Tetanus prophylaxis - if not up to date
• IV fluids (Parkland Formula) - for burns >15% BSA in adults (>10% in children):
  • 4 mL × Weight (kg) × % BSA burned = Total fluid in first 24h
  • Give half in first 8 hours, half in next 16 hours
  • Use Ringer's Lactate (Hartmann's)
• Refer to Burns Unit if: >10% BSA, full thickness, hands/face/feet/genitals/joints involved

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C. CHEMICAL INHALATION (Fumes/Vapours)

Types of Chemical Lung Injury

Management

1. Remove from exposure - fresh air immediately
2. Assess ABCDE
3. 100% O2 via non-rebreather mask - even if SpO2 appears normal (especially for CO)
4. Bronchodilators (salbutamol 2.5-5 mg nebulised) for wheeze/bronchospasm
5. Steroids (hydrocortisone 100-200 mg IV) for severe bronchospasm or ARDS risk
6. Observe for minimum 24 hours even if initially asymptomatic after low-solubility agent exposure (NOx, phosgene)
7. Serial CXR, ABG, SpO2 monitoring
8. Intubation if respiratory failure develops
9. Diuretics (frusemide 40 mg IV) if pulmonary oedema develops

Critical point for OHC interview: "The absence of initial symptoms after phosgene or NOx exposure is DECEPTIVE - pulmonary oedema develops 4-24 hours later. Mandatory 24-hour observation."

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D. CHEMICAL INGESTION

1. Do NOT induce vomiting - corrosives cause equal damage coming back up
2. Do NOT give activated charcoal for corrosives (obscures endoscopy view)
3. Do NOT attempt to neutralise (acid + alkali = exothermic reaction)
4. Dilute with water - small sips (4-8 oz water or milk) if patient conscious and swallowing
5. Keep NPO after initial dilution
6. IV access, supportive care
7. Urgent endoscopy to assess oesophageal/gastric damage
8. Call Poison Control

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E. SPECIAL CHEMICALS - Important for OHC

Hydrofluoric (HF) Acid Burns - Most Dangerous Industrial Acid

• Irrigate 15-30 min with water
• Calcium gluconate 2.5% gel topically - apply and massage into burn (neutralises fluoride ion)
• If pain persists: Calcium gluconate 10% subcutaneous injection (0.5 mL/cm² via 27-30G needle)
• Monitor electrolytes - K⁺, Mg²⁺, Ca²⁺
• ECG monitoring (QTc prolongation = systemic toxicity)
• IV Calcium gluconate for systemic toxicity
• Do NOT use calcium chloride topically (tissue irritant)

Cement/Lime Burns (Alkali - Common in Construction)

• Slow onset - workers may not notice until significant damage
• Prolonged irrigation essential (60+ min)
• Remove all cement from skin/boots before irrigating

Phenol Burns

• Irrigate with water, then polyethylene glycol (PEG) solution
• Systemic absorption causes: CNS depression, hepatotoxicity, renal failure
• Monitor LFT, RFT, CNS status

Tar Burns

• Do NOT pull off tar - causes skin avulsion
• Cool with cold water, then dissolve with petroleum jelly or mineral oil

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OHC Facility Requirements for Chemical Emergencies

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Quick Reference Summary

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Key Points for OHC/CMO Interview

1. Water first, always - do not waste time finding specific antidotes before irrigating
2. Do NOT neutralise acid with alkali or vice versa on skin/eyes
3. Alkali burns are worse than acid burns - deeper penetration, longer irrigation
4. pH 7.0-7.4 = irrigation endpoint for eye burns
5. HF acid = calcium gluconate - specific antidote; monitor for systemic hypocalcaemia
6. NOx/phosgene = no early symptoms, delayed pulmonary oedema - observe 24h
7. MSDS must be checked for every chemical involved
8. PPE for rescuer before approaching contaminated patient

• Rosen's Emergency Medicine, Chemical Burns chapter
• Fitzpatrick's Dermatology - Chemical Burn section
• PMC: Emergency Treatment of Chemical Eye Burns in Workplaces
• Mayo Clinic: Chemical Burns First Aid (2024)

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Types of Chemical Splash in OHC - Complete Classification

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Why Classification Matters in OHC

• Duration and method of irrigation
• Specific antidotes needed
• Systemic toxicity to watch for
• Which specialist to refer to
• What to document in the health record

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Master Classification: 8 Types of Chemical Hazards

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1. ACIDS (Corrosive - Proton Donors)

Common Industrial Acids

Signs of Acid Splash

• Immediate pain and burning
• White/grey/brown coagulum on skin
• Bleached appearance
• Eye: immediate tearing, redness, photophobia

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2. ALKALIS / BASES (Corrosive - Hydroxyl Donors)

Alkali burns are MORE DANGEROUS than acid burns of equal concentration

Common Industrial Alkalis

Specific Rule for Cement/Lime Burns

• Workers often do not feel the burn initially (cement in wet boots/gloves)
• Burns discovered hours later when severe
• Require longer irrigation (60+ min)

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3. ORGANIC SOLVENTS

Common Solvents in Industry

Solvent Splash Specific Management

• Flush skin with water
• Do NOT use other solvents to clean (increases absorption)
• Systemic absorption can occur even from skin - monitor CNS, LFT, RFT
• Benzene: CBC monitoring for haematological effects (long-term)
• Methanol exposure: check blood methanol level, give fomepizole or ethanol as antidote if systemically absorbed

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4. OXIDISING AGENTS

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5. TOXIC GASES & VAPOURS (Inhalation Hazard - No Direct Splash but OHC Encounters)

Highly Soluble (Upper Airway - Immediate Symptoms)

Low Solubility (Deep Lung - Delayed Pulmonary Oedema 4-24h)

Asphyxiant Gases

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6. PESTICIDES & ORGANOPHOSPHATES

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7. HEAVY METALS & METAL COMPOUNDS

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8. BIOLOGICAL/INFECTIOUS CHEMICAL HAZARDS

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Industry-Wise Chemical Splash Profile (For CMO Interview)

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Quick Reference: Chemical Type vs Key Management

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Key Points for CMO Interview

1. Acids = coagulative necrosis (self-limiting) vs Alkalis = liquefactive necrosis (deeper, more dangerous)
2. HF acid = unique - not just a burn; fluoride ion causes systemic hypocalcaemia and cardiac arrest
3. NOx and phosgene = minimal early symptoms, fatal delayed pulmonary oedema at 4-24h - mandatory 24h admission
4. CO = 100% O₂; CO-oximetry (NOT pulse oximetry - it reads falsely normal)
5. HCN = hydroxocobalamin (Cyanokit) - "cherry-red" appearance, sudden collapse in enclosed space
6. Paraquat = DO NOT give O₂ (hyperoxia accelerates lung destruction); no antidote
7. Mixing bleach (NaOCl) + acid = chlorine gas - common accidental exposure in cleaning
8. Chromium VI = carcinogen - requires long-term surveillance and cancer screening

• Rosen's Emergency Medicine - Chemical Injury chapter
• ILO: Exposure to Hazardous Chemicals at Work
• OSHA: Types of Chemical Hazards in the Workplace (2024)
• CCOHS: First Aid for Chemical Exposures (2024)

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Cyanide Poisoning - Management in OHC

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What is Cyanide Poisoning?

"Cyanide binds readily to the ferric iron (Fe³⁺) in cytochrome oxidase, inhibiting oxygen utilization within the cell mitochondria and leading to cellular hypoxia and lactic acidosis."

• Katzung's Basic & Clinical Pharmacology, 16th Ed.

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Mechanism of Toxicity

Normal:
O₂ → Mitochondrial ETC → ATP production (aerobic respiration)
                ↓
         Complex IV (Cytochrome c oxidase)

Cyanide Poisoning:
CN⁻ binds Fe³⁺ in Cytochrome c oxidase → BLOCKS ETC
                ↓
Cells CANNOT use O₂ (even though blood O₂ is NORMAL/HIGH)
                ↓
Forced into ANAEROBIC metabolism
                ↓
Massive LACTIC ACIDOSIS
                ↓
Cellular energy failure → seizures → cardiac arrest → DEATH

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Sources of Cyanide in OHC / Industrial Settings

Occupational (High relevance for OHC medical officer)

Non-Occupational

• Cyanogenic plants: cassava, bitter almonds, apple/peach/apricot seeds, lima beans
• Smoke inhalation in enclosed space fires (always suspect CN + CO together)
• Accidental ingestion of nail polish remover (acetonitrile - metabolised to CN⁻)

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Routes of Exposure

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Clinical Features

The Stages of Cyanide Poisoning

• Headache, dizziness, anxiety
• Nausea, vomiting
• Tachycardia, tachypnoea
• Flushed/cherry-red skin (venous blood stays oxygenated - cells can't use O₂)
• Bitter almond odour on breath (not everyone can smell this - genetic variation)

• Confusion, agitation
• Hypertension → hypotension
• Bradycardia
• Seizures

• Coma
• Cardiovascular collapse
• Respiratory arrest
• Death within minutes to hours if untreated

Classic Triad to Remember:

🔴 Sudden collapse in industrial/enclosed space setting 🔴 Bitter almond smell (detectable by only ~60% of people genetically) 🔴 Venous blood appears bright red (not dark - paradox of histotoxic hypoxia)

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Diagnosis

Investigations

Diagnostic Key: Lactate ≥8 mmol/L + metabolic acidosis + known/suspected cyanide exposure = TREAT IMMEDIATELY

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Management - Step by Step

STEP 1: RESCUER SAFETY FIRST

• Do NOT enter a cyanide-contaminated environment without SCBA (Self-Contained Breathing Apparatus)
• HCN gas is invisible, odourless in high concentrations, and can kill a rescuer in seconds
• Use nitrile/neoprene gloves (not latex)
• Protect airway of staff during decontamination

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STEP 2: REMOVE FROM EXPOSURE + DECONTAMINATION

---

STEP 3: STABILISE - ABCDE

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STEP 4: ANTIDOTES - THE DEFINITIVE TREATMENT

---

ANTIDOTE 1: HYDROXOCOBALAMIN (Cyanokit) - FIRST LINE ✅

• Does NOT cause methemoglobinemia (safe if CO poisoning coexists)
• Does NOT cause hypotension
• Safe in haemodynamically unstable patients
• Safe in fire victims (where CO + CN coexist)
• Only significant side effect: red/pink discolouration of skin and urine (transient, harmless - warn staff not to confuse with haemoglobin)

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ANTIDOTE 2: SODIUM NITRITE + SODIUM THIOSULFATE (Nithiodote) - SECOND LINE

---

Antidote Comparison Summary

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STEP 5: SUPPORTIVE CARE

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Management Flow Chart

Worker found collapsed / confused in industrial area
(cyanide suspected - gold mine, electroplating, fire)
             ↓
RESCUER SAFETY - PPE, SCBA before entry
             ↓
Remove from exposure
Decontaminate (skin wash, eye wash, remove clothing)
             ↓
         ABCDE
Airway secured + 100% O₂ non-rebreather mask
IV access x2, ECG, cardiac monitor
             ↓
Is hydroxocobalamin available?
    YES → HYDROXOCOBALAMIN 5g IV over 15 min
    NO  → Sodium Nitrite 300mg IV over 2-4 min
           THEN Sodium Thiosulfate 12.5g IV over 10 min
             ↓
Serum lactate, ABG, ECG, blood glucose
             ↓
Supportive care (seizure control, vasopressors, bicarbonate)
             ↓
Transfer to ICU for monitoring

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Special Scenarios

Scenario 1: Fire Victim (CO + CN coexist)

• Both CO and CN poisoning common in enclosed space fires
• Use Hydroxocobalamin ONLY - sodium nitrite would add methemoglobin to carboxyhaemoglobin = fatal
• 100% O₂ treats both (competes with CO on haemoglobin + aids CN detoxification)

Scenario 2: Sodium Nitroprusside Toxicity

• Long IV infusions of SNP → CN⁻ accumulation
• Sodium Thiosulfate infusion prevents/treats this
• Monitor thiocyanate levels in ICU

Scenario 3: Mass Casualty / Multiple Workers Exposed

• Hydroxocobalamin has limited supply
• Triage: treat unconscious/critically ill first
• For conscious patients with mild symptoms: 100% O₂ + sodium thiosulfate alone
• Activate on-site emergency plan, call ambulances for all exposed workers

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OHC Preparedness for Cyanide-Risk Industries

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Key Points for CMO Interview

• Katzung's Basic & Clinical Pharmacology, 16th Ed. - Cyanide section
• Lippincott Illustrated Reviews: Pharmacology - Chapter Summary
• OSHA: Cyanide Antidotes Standard Interpretation (2020)
• StatPearls: Cyanide Toxicity - Evaluation (NCBI)
• Medscape: Cyanide Toxicity Treatment & Management