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BURNS - COMPREHENSIVE MD ANAESTHESIA PG EXAM ANSWER

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SECTION 1: BURNS BASICS, CLASSIFICATION & PATHOPHYSIOLOGY

Epidemiology

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Classification of Burns

By Depth:

Severity Classification (ABA):

• Minor: Partial-thickness <5% TBSA (children/elderly) or <10% TBSA (adults), or full-thickness <2% TBSA
• Moderate/Major: Greater TBSA, burns to face, hands, feet, perineum, high-voltage electrical, inhalation injury, or associated major trauma

TBSA Estimation:

• Rule of Nines (Adults): Head = 9%, each arm = 9%, chest = 9%, abdomen = 9%, each thigh = 9%, each leg = 9%, perineum = 1%
• Lund & Browder chart - more accurate, especially in children (adjusts for changing head:leg ratio with age)
• Palm Rule: Patient's palm (including fingers) = 1% TBSA - useful for small, scattered burns
• Note: First-degree burns are NOT counted in TBSA for fluid resuscitation

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Pathophysiology of Burns

Local (Jackson's Zones):

1. Zone of Coagulation - central area of maximal damage; irreversible cell death
2. Zone of Stasis - surrounding ischemic tissue; potentially salvageable (may progress to necrosis without proper resuscitation)
3. Zone of Hyperemia - outermost zone; inflammatory vasodilatation; recovers within 7-10 days

Systemic Pathophysiology:

• Massive capillary leak - occurs at burn site AND (in burns >20% TBSA) systemically
• Hypovolaemia, haemoconcentration, reduced cardiac output
• Mediators: histamine, serotonin, bradykinin, prostaglandins, oxygen free radicals
• Protein-rich fluid leaks into interstitium → oedema

• Initial: reduced cardiac output, elevated SVR (due to hypovolaemia + catecholamines)
• After 24-48 hrs: hyperdynamic state - elevated CO, reduced SVR (hypermetabolism)
• Myocardial depressant factor (MDF) may contribute to early cardiac dysfunction

• Hypermetabolism peaks at 5-7 days; can persist for 1-2 years
• Catabolic state: elevated cortisol, catecholamines, glucagon; muscle wasting
• Temperature dysregulation - inability to conserve heat; core temperature set-point rises by ~2°C

• Impaired neutrophil function, reduced complement activity
• Increased susceptibility to sepsis (leading cause of mortality after the first 48 hrs)
• Loss of skin barrier function

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SECTION 2: INHALATION BURNS - PATHOPHYSIOLOGY, DIAGNOSIS & TREATMENT

Epidemiology

Classification of Inhalation Injury:

1. Upper airway injury - supraglottic; mainly thermal
2. Lower airway & pulmonary parenchymal injury - chemical; subglottic
3. Systemic toxicity - CO, cyanide

Pathophysiology:

• Smoke loses heat rapidly traversing the upper airway; direct thermal injury usually limited to supraglottic mucosa
• Exception: steam inhalation - can cause thermal injury throughout the entire airway
• Mucosal oedema - can cause laryngeal oedema within minutes to 12-24 hours → airway compromise
• External burns to face/neck further distort airway structures

• Chemical injury from toxic components of smoke (aldehydes, acids, ammonia, phosgene, nitrogen oxides)
• Water-soluble irritants (acrolein, aldehydes, HCl) - damage proximal airways → intense bronchitis/bronchorrhea
• Less water-soluble agents (phosgene, chlorine, NO₂) - penetrate deeper → insidious parenchymal damage
• Inflammatory cascade: neutrophil recruitment, mucosal oedema, ulceration, increased capillary permeability → capillary leak → ARDS
• Loss of mucociliary clearance → inspissated secretions, plugging → atelectasis, pneumonia (3-5 days post-injury)

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SECTION 3: COMPONENTS OF SMOKE

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Diagnosis of Inhalation Injury:

• Enclosed space exposure
• Singed nasal vibrissae, singed eyebrows/facial hair
• Carbonaceous sputum (soot in airway/secretions)
• Hoarse voice, stridor
• Erythematous/edematous oropharyngeal mucosa
• Altered consciousness, confusion

• ABG with co-oximetry - essential; pulse oximetry is unreliable (cannot distinguish HbO₂ from HbCO; gives falsely normal reading)
• Carboxyhemoglobin (HbCO) level
• Fiberoptic bronchoscopy - gold standard for diagnosis; shows mucosal erythema, edema, ulceration, carbonaceous deposits, cast formation
• Chest X-ray (initially often normal; useful for serial monitoring)
• Xenon-133 ventilation scan - demonstrates areas of ventilation-perfusion mismatch

Treatment:

1. 100% humidified O₂ via tight-fitting mask - first priority; competes with CO for Hb binding
2. Early intubation - do not delay; laryngeal oedema progresses rapidly; surgical airway (cricothyrotomy/tracheostomy) if intubation fails
3. Mechanical ventilation - lung-protective strategy: tidal volume 4-6 mL/kg ideal body weight, PEEP as needed
4. Bronchodilators - nebulised salbutamol for bronchospasm
5. Pulmonary toilet - aggressive; N-acetylcysteine nebulisation, heparin nebulisation (reduces cast formation)
6. Treat underlying causes - CO poisoning with HBO₂; cyanide with hydroxycobalamin (Cyanokit)
7. ECMO - occasional lifesaving role in refractory respiratory failure
8. Surveillance for ventilator-associated pneumonia

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SECTION 4: BURNS PATIENT RESUSCITATION - FLUID FORMULAS

Principles:

• Begin resuscitation immediately (pre-hospital)
• Only second- and third-degree burns (partial and full thickness) are counted for TBSA
• First-degree burns are excluded
• Time of burn (not time of arrival to hospital) is the reference point for the 8-hour period
• Goal urine output: 0.5-1.0 mL/kg/hr (adults); 1.0 mL/kg/hr (children <30 kg)
• Fluid of choice: Lactated Ringer's (Hartmann's) solution - closest to physiological wound exudate

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Commonly Used Formulas (First 24 Hours):

• Total = 4 × 70 × 40 = 11,200 mL LR
• First 8 hrs: 5,600 mL (700 mL/hr)
• Next 16 hrs: 5,600 mL (350 mL/hr)
• Do not forget to add maintenance fluids (most online calculators omit this!)

• Switch to colloid (albumin 5%) at 0.3-0.5 mL/kg/% TBSA
• Reduce crystalloid; add D5W to maintain free water
• Goal: maintain euvolaemia while minimising further oedema

Paediatric Modifications:

• Use Galveston formula or modified Parkland (3 mL × kg × % TBSA + maintenance)
• Add 5% dextrose to maintenance in children <20 kg (lower glycogen stores)
• Goal urine output: 1 mL/kg/hr

Pitfalls:

Endpoints of Resuscitation:

• Urine output (0.5-1 mL/kg/hr)
• MAP >65 mmHg
• Heart rate trending down
• Serum lactate normalising
• Base deficit improving

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SECTION 5: CARBON MONOXIDE POISONING

Causes / Sources:

• Incomplete combustion of carbon-based fuels (wood, coal, charcoal, paper, gasoline, LPG)
• House fires, enclosed space fires
• Faulty/unvented heaters, stoves, combustion motors
• Car exhaust in closed garage
• Suicide attempts (deliberate inhalation)
• CO is produced from cellulolytic materials (wood, paper, cotton) and PVC

Mechanism of Toxicity:

1. Competitive Hb binding: CO has ~200-250x greater affinity for haemoglobin than O₂ → forms carboxyhaemoglobin (HbCO) → reduced O₂-carrying capacity
2. Left shift of O₂-Hb dissociation curve: Allosteric change → bound O₂ cannot dissociate at tissues → impaired tissue O₂ delivery
3. Intracellular cytochrome inhibition: CO binds cytochrome oxidase (cytochromes a and P-450) → blocks mitochondrial electron transport → cellular hypoxia despite normal O₂ delivery
4. Myocardial binding: CO binds cardiac myoglobin → direct myocardial depression
5. Lipid peroxidation & neuronal damage: Delayed neuropsychiatric sequelae

Symptoms by HbCO Level:

Diagnosis:

• High index of suspicion
• ABG with co-oximetry (gold standard) - directly measures HbCO
• Metabolic acidosis (lactic acidosis)
• ECG (arrhythmias, ST changes mimicking MI)
• Echocardiography if cardiac involvement suspected

Treatment:

• HBO₂ indications: HbCO >25%, LOC, seizures, cardiac dysfunction, pregnancy, severe metabolic acidosis
• Concurrent cyanide poisoning must always be considered in enclosed-space fires → treat with hydroxocobalamin (Cyanokit) 5g IV

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SECTION 6: PREOPERATIVE ANAESTHETIC CONSIDERATIONS & INTRAOPERATIVE MANAGEMENT - BURNS EXCISION & GRAFTING

Preoperative Assessment:

Airway:

• Most critical consideration
• Burns to face, oropharynx, neck → distortion of anatomy; progressive oedema
• Singed nasal vibrissae, hoarse voice, stridor = urgent intubation; do not delay
• Assess mouth opening (scar contracture in late presentation), cervical mobility
• Have surgical airway (cricothyrotomy/tracheostomy) immediately available
• ABG to assess HbCO, oxygenation, ventilatory status

Cardiovascular:

• Early phase: hypovolaemia, low CO → assess fluid status carefully
• Late phase (after 48 hrs): hyperdynamic; high CO, low SVR
• ECG (arrhythmias from CO, electrolyte disturbances)
• Assess adequacy of fluid resuscitation; avoid over- and under-resuscitation

Respiratory:

• Pre-existing inhalation injury → lung-protective strategy
• Circumferential chest burns → escharotomy may be needed pre-op for adequate ventilation

Metabolic:

• Electrolytes: hypernatraemia, hyperkalaemia (haemolysis, tissue necrosis)
• Anaemia: haemolysis + repeated surgical bleeding
• Coagulopathy: dilutional, DIC
• Hypoglycaemia risk in children
• Temperature regulation impaired - warm OT to 28-32°C

Infection/Sepsis:

• Assess for signs of sepsis (burns infection is a major post-burn mortality cause)
• Optimise antibiotics perioperatively

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Intraoperative Management:

Environment:

• OT temperature: 28-32°C (burns patients cannot thermoregulate; hypothermia worsens coagulopathy, increases mortality)
• Warm IV fluids; forced-air warming blankets; radiant heaters
• Minimise exposure of uninvolved areas

Monitoring (challenging in extensive burns):

• Pulse oximetry: finger/toe may not be usable → nose, ear, tongue, cheek
• NIBP: Apply to unburnt areas; arterial line preferred for continuous monitoring (radial, femoral, or through burned tissue if necessary)
• Temperature: oesophageal, tympanic, or rectal (depending on burn areas)
• ECG electrodes: adhesive pads may not stick; needle electrodes may be needed
• CVP/invasive monitoring for major procedures

Airway Management:

• Awake fibreoptic intubation - gold standard for anticipated difficult airway; always preferred in patients with known airway oedema
• Rapid sequence induction (RSI) when full stomach assumed
• Succinylcholine: SAFE within first 48 hours (AChR upregulation has not yet peaked)
• Succinylcholine: CONTRAINDICATED after 48 hours and up to 1-2 years post-injury → lethal hyperkalaemia from extrajunctional AChR proliferation (see Pharmacology section)
• Consider tracheostomy for prolonged ventilatory needs (neck burn, long-term ICU)

Induction Agents:

• Ketamine - preferred induction/analgesic agent in burns; maintains airway reflexes, bronchodilator, sympathomimetic (maintains BP); useful for repeated dressing changes
• Propofol - use with care in haemodynamically unstable patients; causes vasodilatation
• Etomidate - useful in haemodynamically compromised patients

Maintenance:

• Volatile agents (sevoflurane, isoflurane) can be used; note possible resistance to non-depolarising NMBAs
• TIVA (propofol + remifentanil/ketamine) - excellent choice; avoids post-op nausea, good analgesic coverage
• Avoid nitrous oxide (expands closed gas spaces; not ideal in patients with possible CO poisoning)

Fluid Management Intraoperatively:

• Burns surgery is haemorrhagic: tangential excision of 1% TBSA → ~1 mL/kg blood loss; major excisions can cause massive haemorrhage
• Anticipate and prepare blood products (PRBC, FFP, cryoprecipitate, platelets)
• Replace blood loss with RBC/colloid
• Continue crystalloid at maintenance + losses
• Cell salvage can be used
• Monitor: ABG, haematocrit, TEG/ROTEM for coagulopathy

Positioning:

• May require multiple position changes (donor sites on back, buttocks, thighs)
• Pressure injuries on non-burned areas
• Eyes must be protected

Post-op:

• Burns patients almost always require ICU post-op
• Continuation of ventilation common
• Pain management transition - opioids, ketamine infusion, regional where possible

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SECTION 7: PHARMACOLOGY OF DRUGS IN BURNS PATIENTS

Pharmacokinetic Changes:

Key Drug-Specific Changes:

Neuromuscular Blocking Agents (NMBA):

• Safe in first 24-48 hrs post-burn
• ABSOLUTELY CONTRAINDICATED after 48 hrs and up to 1-2 years post-burn
• Mechanism: Burn injury causes proliferation of extrajunctional (immature) acetylcholine receptors (AChR) throughout the muscle membrane. These immature receptors have an altered gamma subunit (vs epsilon in mature receptors), longer open-channel time, and efflux more K⁺ per depolarisation event. When succinylcholine is given, massively exaggerated K⁺ release → life-threatening hyperkalaemia → ventricular fibrillation and cardiac arrest.
• The extent of hyperkalaemia does not correlate with burn size; even small burns can cause this response

• Resistance - significantly increased doses required
• Mechanism: Extrajunctional AChRs have lower affinity for non-depolarising agents; more receptors present; the immature AChRs are resistant to blockade by non-depolarising drugs
• Rocuronium for RSI: 1.2-1.5 mg/kg (vs standard 0.6 mg/kg); onset ~90 seconds vs 60 seconds in non-burn patients
• Atracurium: slight advantage as metabolism is Hofmann elimination (independent of organ function)
• Sugammadex can reverse rocuronium normally; doses may need adjustment

Opioids:

• Increased requirements due to hypermetabolism, tolerance, altered PK (increased Vd), psychological sensitisation
• Methadone - useful for burns pain due to long half-life, N-methyl-D-aspartate (NMDA) receptor antagonism, useful for chronic pain component
• Remifentanil infusion - excellent for intraoperative use; short context-sensitive half-life useful for repeated procedures
• Risk of opioid tolerance and dependence must be monitored

Inhalational Agents:

• Isoflurane - MAC unchanged; volatile agents provide good background anaesthesia
• Sevoflurane - preferred for smooth induction (especially paediatric burns)

Ketamine:

• Agent of choice in burns
• Sympathomimetic - maintains haemodynamics in hypovolaemic patients
• Bronchodilator - useful with inhalation injury
• Provides analgesia AND anaesthesia; useful for repeated dressing changes
• Combine with a benzodiazepine to reduce emergence phenomena

Propofol:

• Altered Vd → higher loading doses needed
• Short duration - good for TIVA
• Caution in haemodynamic instability

Antibiotics:

• Increased Vd and augmented renal clearance → higher doses needed (especially aminoglycosides, vancomycin, beta-lactams)
• Therapeutic drug monitoring (TDM) essential for aminoglycosides and vancomycin

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SECTION 8: BURNS PAIN & ITS MANAGEMENT

Types of Burns Pain:

1. Background pain - continuous resting pain from damaged tissue; moderate to severe
2. Procedural pain - acute, intense pain from dressing changes, debridement, physiotherapy, venepuncture; often undertreated
3. Operative/post-operative pain - from excision and donor sites (donor sites are often more painful than the burn)
4. Neuropathic pain - from direct nerve damage, inflammatory neuropathy; burning, dysaesthetic quality; often persistent
5. Chronic pain - scarring, contracture, phantom limb (in amputations); can persist for years

Multimodal Analgesia - The Framework:

Step 1: Opioids

• Morphine/Oxycodone - moderate-severe background pain; IV, oral, PCA
• Fentanyl - procedural analgesia; intranasal fentanyl for dressing changes in children; IV for intraoperative
• Remifentanil infusion - ideal intraoperative (short procedures, repeated surgeries)
• Methadone - chronic burns pain; NMDA receptor antagonism limits central sensitisation; helps with opioid rotation

Step 2: NMDA Antagonists

• Ketamine - reduces opioid requirements; prevents central sensitisation; sub-anaesthetic infusion (0.1-0.3 mg/kg/hr) effective for background and procedural pain; also prevents opioid-induced hyperalgesia
• Evidence supports ketamine as a key adjunct in burns pain management

Step 3: Non-Opioid Adjuncts

• Paracetamol - routine; opioid-sparing
• NSAIDs - use with caution (GI bleeding risk, renal impairment in the acute phase); useful in rehabilitation phase
• Gabapentinoids (Gabapentin, Pregabalin) - for neuropathic component; helps reduce opioid requirements
• Lignocaine (Lidocaine) IV infusion - reduces central sensitisation; anti-nociceptive; used intraoperatively and in ICU settings
• Clonidine - alpha-2 agonist; reduces opioid requirements; analgesic, anxiolytic, reduces catecholamine-driven hypermetabolism; can be given IV, oral, or epidurally
• Dexmedetomidine - alpha-2 agonist; useful in ICU sedation/analgesia; reduces opioid requirements

Step 4: Regional Anaesthesia

• Extremely valuable when applicable; reduces systemic opioid requirements
• Peripheral nerve blocks: excellent for limb burns/donor sites (femoral, saphenous, brachial plexus blocks)
• Epidural analgesia: for large truncal burns/donor sites; thoracic epidural for chest wall donors
• Limitations in acute phase: may mask compartment syndrome symptoms - use with caution in first 24-48 hrs; skin infections at block site; coagulopathy

Step 5: Non-Pharmacological

• Distraction techniques - virtual reality (VR) distraction during dressing changes (good evidence)
• Anxiolytics (midazolam/lorazepam) before procedures
• Music therapy, hypnosis, psychological support
• Physiotherapy and occupational therapy early

Dressing Changes:

• Anticipate as a high-pain event; pre-medicate 30-60 min before
• Oral morphine/oxycodone + midazolam/lorazepam + paracetamol
• For children: intranasal fentanyl (1.5 mcg/kg) + oral midazolam (0.5 mg/kg)
• For large dressing changes: GA with ketamine ± propofol

Long-term Concerns:

• Opioid tolerance and dependence: plan opioid rotation, gradual taper in rehabilitation
• Neuropathic pain: gabapentinoids, tricyclic antidepressants (amitriptyline), SNRIs
• Psychological comorbidities (PTSD, depression, body dysmorphia) require concurrent management

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SUMMARY TABLE: Key Anaesthetic Pearls for Burns Patients (MD Exam Quick Reference)

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