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ANESTHETIC MANAGEMENT OF THE BURNS PATIENT

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1. CLASSIFICATION OF BURNS

Depth

Extent — TBSA Estimation

• Rule of Nines (adults): Head 9%, each arm 9%, chest 18%, back 18%, each leg 18%, perineum 1%
• Lund–Browder chart: More accurate, especially in children (accounts for age-related body proportion changes)
• Palmar surface method: Patient's palm = ~1% TBSA — useful for scattered burns
• Children: Head proportionally larger, legs smaller than adults

American Burn Association — Major Burn Criteria (Box 83.1)

• Partial thickness burns >25% TBSA (adults), >20% (children/elderly)
• Full thickness burns >10% TBSA
• Burns involving face, hands, feet, genitalia, perineum, major joints
• Electrical/chemical burns
• Inhalation injury
• Circumferential extremity/chest burns
• Burns in patients with significant pre-existing disease

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2. PATHOPHYSIOLOGY OF BURN INJURY

Biphasic Cardiovascular Response (Ebb and Flow)

• Massive capillary leak → fluid shifts from intravascular to interstitial compartment
• ↓ Cardiac output, ↓ stroke volume, ↑ SVR
• Hypovolemia, hemoconcentration
• Decreased organ perfusion (kidney, liver, gut)
• Cause: DAMPs, histamine, prostaglandins, complement activation → ↑ capillary permeability
• Burn wound protein: strongly negative interstitial fluid pressure draws water in

• Begins after successful resuscitation when capillary integrity is partially restored
• ↑ Cardiac output (2–3× normal), ↑ HR, ↑ temperature (38–39°C set-point reset)
• Hyperglycemia, ↑ protein catabolism, muscle wasting
• Increased hepatic and renal blood flow → ↑ drug clearance
• This phase persists until wounds are healed (months)

Local Burn Pathophysiology (Jackson's Zones)

• Zone of coagulation: Central, irreversible cell death
• Zone of stasis: Potentially salvageable with adequate resuscitation
• Zone of hyperemia: Peripheral, will recover

Systemic Effects

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3. INHALATION INJURY

Types

1. Supraglottic (upper airway) injury: Due to heat — steam or hot gases. Direct thermal injury to mucosa → edema, obstruction. Carbon particles rarely reach below vocal cords.
2. Subglottic (lower airway) injury: Due to toxic products of combustion (aldehydes, HCl, cyanide, CO) — NOT heat. Chemical tracheobronchitis, mucosal sloughing, cast formation, bronchospasm, ARDS.
3. Systemic toxins:
   • Carbon monoxide (CO): Binds hemoglobin with 250× affinity of O₂. SpO₂ falsely normal on pulse oximetry. Tx: 100% O₂ (reduces half-life from 4–5h to 60–90 min). If severe: hyperbaric O₂.
   • Cyanide (HCN): From burning plastics/synthetics. Inhibits cytochrome oxidase → histotoxic hypoxia. Treat with hydroxocobalamin.

Diagnosis of Inhalation Injury

• History: closed-space fire, steam, facial burns, singed nasal hairs
• Clinical: hoarseness, stridor, carbonaceous sputum, dyspnea
• Flexible bronchoscopy (FOB): Gold standard — soot, mucosal edema, hyperemia, ulceration, exudation, narrowing of laryngeal inlet
• PaO₂/FiO₂ ratio after resuscitation: most reliable indicator of impact
• Other: xenon-133 scanning, CT, pulmonary function tests

Treatment

• Observation and monitoring
• Upright positioning (reduces edema)
• Early intubation if: anticipated airway swelling, impaired oxygenation/ventilation, neurologic impairment from CO, circumferential chest burns
• Rule: Intubate early rather than risk difficult intubation after swelling
• Patients with inhalation injury require ~30–50% MORE fluid than burns formulae predict

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4. FLUID RESUSCITATION

Principles

• Goal: maintain organ perfusion, UO 0.5–1 mL/kg/h adults; 1 mL/kg/h children
• Commence within 2–6 hours of injury
• All formulae are guides only — titrate to physiologic endpoints

Parkland (Baxter) Formula (most widely used)

• 4 mL × weight (kg) × %TBSA of crystalloid (Ringer's lactate) in first 24 hours
• Half in first 8 hours from TIME OF BURN (not time of arrival)
• Remaining half over next 16 hours
• Day 2 onward: colloid (albumin) to maintain plasma proteins, reduce crystalloid

Modified Brooke Formula

• 2 mL × weight (kg) × %TBSA RL in first 24 hours
• Same distribution as Parkland

Colloid Resuscitation

• Colloid rescue: albumin (5%) started at 12–24h after injury (when capillary integrity is partly restored) to limit total fluid volume
• Fresh frozen plasma: used in some protocols for very large burns

"Fluid Creep"

• Trend of over-resuscitation → pulmonary edema, abdominal compartment syndrome (ACS), MOF, infection, extension of burn injury
• Causes: overestimated burn size, supra-physiologic targets, opioid creep
• Monitor intra-abdominal pressure via intravesical catheter:
  • Normal: <12 mmHg
  • Intra-abdominal hypertension: 12–25 mmHg → monitor closely
  • ACS: >25 mmHg with new organ dysfunction → intervention (paracentesis/laparotomy)

Hypertonic Saline / Ascorbic Acid

• Hypertonic saline: reduces fluid volumes, but hypernatremia → risk of ARF
• Vitamin C (high-dose): may reduce resuscitation volumes, but risks osmotic diuresis, pseudohyperglycemia

Monitoring Resuscitation

• Standard: urine output
• For fluids >6 mL/kg/%TBSA/24h — obtain more information:
  • TEE/TTE, stroke volume variation, ITBVI, PAWP, ScvO₂, lactate, base deficit

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5. PREOPERATIVE ASSESSMENT

Box 83.3 — Major Perioperative Concerns for Burn Patient

• Age of patient
• Extent of burn (TBSA, depth, location)
• Mechanism of injury
• Elapsed time from injury (phase of response)
• Associated injuries (treat as polytrauma — missed injuries → mortality)
• Inhalation injury and lung dysfunction
• Adequacy of resuscitation
• Coexisting diseases
• Airway patency
• Difficult vascular access
• Gastric stasis (risk of aspiration)
• Altered drug responses
• Altered mental state, pain, anxiety
• Presence of infection
• Hematologic issues (anemia, coagulopathy)
• Magnitude of planned procedure

Anemia and Coagulation

• Hemolysis at wound site, bone marrow suppression, phlebotomy losses
• Blood transfusion trigger: Hb <7 g/dL generally (higher threshold if hemodynamically unstable)
• Coagulopathy worsens with massive transfusion and hemodilution

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6. AIRWAY MANAGEMENT

Challenges by Phase

Assessment

• Preoperative: palpate neck and submandibular space for tightness
• Assess mouth opening, neck mobility, nasal patency, nares scarring
• Dressings/NGT can impair mask seal

Techniques

• Early intubation is preferred: if any sign of inhalation injury or impending obstruction
• Video laryngoscopy: useful to assess hypopharyngeal and glottic anatomy
• Fiberoptic intubation: for known/anticipated difficult airway — perform awake with topical lidocaine (nebulized or spray) if cooperative; use ketamine in uncooperative patients/children
• LMA: useful as alternative to intubation or as rescue/conduit; limited in microstomia and fixed neck flexion
• Tracheostomy: for prolonged mechanical ventilation; early tracheostomy if large burns, inhalation injury, elderly, COPD, large burn size; surgeon should be available when difficult airway anticipated

Key Adjuncts

• Awake fiberoptic: nebulized lidocaine, trans-tracheal block, superior laryngeal nerve block
• Inhalational induction: if unable to place IV and SPONTANEOUS VENTILATION must be maintained
• Ketamine IV: preserves airway reflexes and spontaneous breathing — ideal in children and for short procedures

ETT Fixation in Facial Burns

• Adhesive tape — AVOID on facial burns (damages graft/wound)
• Use: circumferential tie, dental wire, arch bars

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7. VASCULAR ACCESS

• Can be extremely difficult (burned/edematous skin, hypovolemia)
• May need to place IV through burned tissue
• Intraosseous access: for any age in emergencies — obviates venous cutdown
• Ultrasound guidance: for peripheral and central access
• Central venous catheter (multi-port): essential in major burns — for simultaneous drug/fluid infusion, pressure monitoring, hyperalimentation
• CVC can remain in situ for 7–14 days with strict aseptic technique; rotate sites (internal jugular → subclavian → femoral)
• In excision/grafting procedures: ensure adequate access before knife to skin (blood loss can be rapid)

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8. INTRAOPERATIVE MONITORING

• ECG: needle electrodes or staples if gel electrodes don't stick; place on back/dependent areas
• SpO₂: alternative sites — ear, nose, tongue, lip (unreliable in CO poisoning!)
• NIBP: cuff over burned/grafted area if necessary — sterile cuff, protect underlying tissue
• Arterial line: for extensive procedures with expected significant blood loss; waveform guides fluid responsiveness
• Temperature: imperative — hypothermia common and poorly tolerated; also used to detect transfusion reactions (>2°C rise)
• Neuromuscular monitoring: mandatory when using NMBDs — dose requirements markedly altered
• Central venous pressure/hemodynamic monitoring: for large procedures

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9. PHARMACOLOGIC CONSIDERATIONS

General Principles

1. Altered plasma protein binding
2. Changed volume of distribution (Vd)
3. Altered organ blood flow (renal and hepatic clearance)
4. Receptor plasticity

Plasma Protein Changes

• Albumin (binds acidic/neutral drugs): DECREASED after burns
  • ↑ Free fraction of acidic drugs (phenytoin, barbiturates, diazepam)
• α₁-Acid glycoprotein (AAG) (binds cationic drugs): INCREASED 2× or more (acute-phase reactant)
  • ↓ Free fraction of cationic drugs: lidocaine, propranolol, muscle relaxants, some opioids

Phase-dependent Drug Changes

• Volume of distribution increased for virtually all drugs studied (propofol, fentanyl, muscle relaxants) — due to ↓ albumin, fluid leak, resuscitation fluids

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10. DRUG-SPECIFIC CONSIDERATIONS

Succinylcholine — ABSOLUTELY CONTRAINDICATED after 24–72 hours

• Burn injury causes upregulation of extra-junctional acetylcholine receptors (nAChR) throughout skeletal muscle
• Succinylcholine → massive K⁺ efflux from all these receptors → life-threatening hyperkalemia → cardiac arrest
• Risk begins 24–72 hours post-burn and persists until wounds are completely healed (months)
• Safe in the first 24 hours only
• Extra-junctional receptor upregulation affects all denervation/immobilization states (crush injury, prolonged immobility, UMN/LMN lesions)

Non-Depolarizing Muscle Relaxants (NDMRs)

• Markedly increased resistance from approximately 1–2 weeks post-burn
• Mechanism:
  1. Upregulated extra-junctional nAChRs with reduced sensitivity to NDMRs
  2. Increased Vd
  3. Increased AAG → ↓ free fraction
• Dose requirement may be 2–5× normal
• This resistance increases progressively and is proportional to burn size
• Duration also shortened due to increased clearance in hyperdynamic phase
• Neuromuscular monitoring is mandatory

Opioids

• Early: reduced clearance (↓ hepatic flow), sedation with normal doses
• Late (hyperdynamic phase): opioid tolerance develops, often within 1 week of continuous use
• μ-receptor desensitization and downregulation; ↑ NMDA receptor activity
• Dosage requirements can far exceed standard recommendations
• Adjuncts for opioid tolerance: ketamine, dexmedetomidine, clonidine, methadone

Propofol

• Increased Vd → larger loading doses needed
• Induction: can cause hypotension especially in hypovolemic phase

Ketamine (agent of choice in burns)

• Advantages:
  • Hemodynamic stability (sympathomimetic)
  • Preserves airway reflexes and muscle tone
  • Preserves spontaneous ventilation
  • Bronchodilator
  • Analgesic + amnestic
  • Anti-inflammatory effects
  • Peripheral vasoconstriction → reduces hypothermia risk
  • NMDA antagonist → prevents central sensitization and opioid tolerance
  • Metabolite norketamine has antidepressant effect
• Caution: in late burns, catecholamine desensitization and β-receptor downregulation → direct myocardial depressant effect of ketamine can manifest → bolus doses may cause hypotension
• Side effects: emergence delirium, hallucinations, nausea — attenuated by co-administration of benzodiazepines
• NMDA and ketamine requirements also increased after burns (↑ NMDA receptor expression)
• Indications: induction, maintenance, analgesia, procedural sedation (dressing changes, line placement)

Volatile Agents

• Isoflurane, sevoflurane: increased MAC? — not clearly defined, but hypermetabolic state increases metabolic demand
• Nitrous oxide: used as adjunct for dressing changes

NSAIDs

• Useful first-line for minor burns
• Avoided in major burns: bleeding risk, renal complications, GI complications, CVS risk

α₂-Agonists (Clonidine, Dexmedetomidine)

• Useful adjuncts — analgesia without respiratory depression
• Dexmedetomidine reduces opioid requirements, reduces delirium (vs. benzodiazepines)
• Caution: hypotension in hypovolemic/hemodynamically unstable patients

Gabapentin/Pregabalin

• Useful adjuncts — modulate central sensitization and opioid-induced hyperalgesia
• Beneficial additions to opioid regimens

Benzodiazepines

• Used for anxiolysis before procedures
• Combination with opioids useful for dressing changes (reduces anticipatory anxiety)
• Caution: long-term midazolam may exacerbate opioid tolerance

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11. SURGICAL PROCEDURES & INTRAOPERATIVE MANAGEMENT

Types of Burn Surgery

1. Escharotomy: for circumferential full-thickness burns to relieve compartment syndrome (chest, extremities)
2. Fasciotomy: deeper, for electrical burns with deep muscle involvement
3. Burn wound excision: tangential or fascial excision — ideally within 48–72h for burns >20% TBSA
4. Skin grafting: split-thickness skin graft (STSG) from donor sites
5. Reconstructive procedures: contracture release, scar revision

Intraoperative Concerns

• Blood loss: major concern — tangential excision can cause 100–200 mL blood loss per %TBSA excised
  • Strategies: tumescent infiltration (adrenaline solution), tourniquets for limb burns, topical thrombin, surgical positioning
• Hypothermia: major threat — expose only area being operated, warm IV fluids, forced warm air blanket, warm operating room (>30°C), warm irrigating fluids
• Positioning: frequent position changes, protect eyes, pressure points, nerves
• Infection control: strict aseptic technique for all catheters and procedures

Ventilation

• Lung-protective strategy: Vt 6–8 mL/kg IBW, plateau pressure <30 cmH₂O
• In hypermetabolic phase: ↑ O₂ consumption, ↑ CO₂ production → minute ventilation may exceed 20 L/min
• Faster desaturation during apnea → pre-oxygenate thoroughly
• Post-op mechanical ventilation may be needed after major excision/grafting (tumescent fluid reabsorption + cytokine release → lung dysfunction)

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12. PAIN MANAGEMENT IN BURNS

Types of Burn Pain

Multimodal Analgesia Strategy

• Opioids: morphine, fentanyl, hydromorphone — dose-escalation needed; IV/PCA
• Ketamine: IV bolus or infusion for procedures; prevents central sensitization
• Paracetamol: first-line for mild-moderate; ceiling effect
• NSAIDs: avoid in major burns
• Gabapentin/Pregabalin: neuropathic and opioid-sparing
• α₂-agonists (dexmedetomidine, clonidine): opioid-sparing, sedation
• Benzodiazepines: anxiolysis
• Regional anesthesia: tumescent, peripheral nerve blocks, neuraxial (when anatomy permits)
• Non-pharmacological: distraction, virtual reality, hypnotherapy

Regional Anesthesia

• Advantages: opioid-sparing, superior analgesia for donor sites and grafts
• Techniques: tumescent local anesthesia for donor sites, peripheral nerve blocks, epidural (when feasible)
• Limitation: difficult in burn areas, infection risk, coagulopathy

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13. SPECIAL SITUATIONS

Pediatric Burns

• Higher surface area-to-volume ratio → more hypothermia and fluid loss
• Lund–Browder chart mandatory for TBSA estimation
• Cuffed ETTs are safe and recommended regardless of age
• Ketamine-based anesthesia preferred
• Awake fiberoptic intubation not practical — use ketamine for fiberoptic in children
• IO access valuable in emergencies

Electrical Burns

• High-voltage injury (>1000V): loss of consciousness, arrhythmias (ECG monitoring mandatory), myoglobinuria, rhabdomyolysis, extensive deep tissue injury, compartment syndrome
• Morbidity far exceeds burn-size estimate
• Evaluate: ECG, CK, myoglobin, renal function, associated traumatic injury
• Fasciotomy within 24h may be required
• Urinary output target ↑ to 1–2 mL/kg/h until myoglobinuria clears
• Alkalinization of urine (sodium bicarbonate) to prevent renal tubular damage

Chemical Burns

• Acid: coagulative necrosis (self-limiting eschar)
• Alkali: liquefactive necrosis (deeper, ongoing penetration)
• Hydrofluoric acid: systemic fluoride toxicity → hypocalcemia → cardiac arrhythmias → treat with calcium gluconate
• Phenol: systemic absorption → CNS and cardiac toxicity

CO Poisoning

• SpO₂ unreliable — use co-oximetry (ABG)
• Treatment: 100% O₂; hyperbaric O₂ for: COHb >25%, pregnancy, loss of consciousness, cardiac toxicity

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14. POSTOPERATIVE & ICU CONSIDERATIONS

• Intensive care often required after major burns
• Continue lung-protective ventilation
• Temperature management: nurse in warm environment; warming blankets
• Nutrition: early enteral nutrition (within 6h of injury) — reduces hypermetabolic response, prevents gut mucosal atrophy, reduces infection
• Glycemic control: insulin infusion for hyperglycemia (target 110–150 mg/dL in ICU)
• Stress ulcer prophylaxis: H₂ blocker/PPI
• DVT prophylaxis: early mobilization, LMWH when safe
• Sepsis monitoring: burns patients are profoundly immunocompromised; surveillance cultures, early antibiotic therapy for confirmed infection
• Psychological support: PTSD, depression common in survivors; early psychiatric assessment

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15. SUMMARY TABLE — KEY PHARMACOLOGICAL CHANGES

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HIGH-YIELD EXAM POINTS

1. Succinylcholine is contraindicated 24–72h post-burn — extrajunctional nAChR → hyperkalemia
2. Parkland formula: 4 mL × kg × %TBSA — ½ in first 8h, ½ in next 16h (from time of burn)
3. Inhalation injury: FOB is gold standard; early intubation is safer than late
4. Biphasic response: ebb (hypodynamic, 0–48h) → flow (hyperdynamic, >48h)
5. Ketamine is the agent of choice — preserves airway, hemodynamically stable, analgesic, bronchodilator
6. NDMRs require 2–5× normal dose due to nAChR upregulation + pharmacokinetic changes
7. Albumin decreases, AAG increases — opposite effects on drug binding
8. Temperature protection is mandatory — hypothermia is dangerous and common
9. CO poisoning: SpO₂ normal on pulse oximetry — use ABG co-oximetry; treat with 100% O₂
10. Fluid creep — over-resuscitation causes ACS, pulmonary edema, MOF
11. Electrical burns — severity far exceeds surface appearance; ECG, CK, myoglobin mandatory
12. Blood loss during excision is rapid — 100–200 mL per %TBSA; ensure adequate IV access before starting

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1. Classification (depth, extent, TBSA methods)
2. Pathophysiology (ebb/flow phases, Jackson's zones, systemic effects)
3. Inhalation injury (types, CO/HCN toxicity, diagnosis, treatment)
4. Fluid resuscitation (Parkland formula, fluid creep, ACS monitoring)
5. Preoperative assessment (Box 83.3 checklist)
6. Airway management (phases, techniques, ETT fixation)
7. Vascular access
8. Intraoperative monitoring
9. Pharmacokinetic principles (protein binding, phase-dependent changes)
10. Drug-specific considerations (succinylcholine contraindication, NDMR resistance, ketamine)
11. Surgical procedures and intraoperative management (blood loss, hypothermia)
12. Pain management (multimodal, regional)
13. Special situations (pediatric, electrical, chemical, CO poisoning)
14. Post-op/ICU care
15. Summary pharmacology table + 12 high-yield exam points