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ANESTHETIC MANAGEMENT OF BURNS PATIENT

MD Anaesthesiology Exam Notes


1. EPIDEMIOLOGY & SIGNIFICANCE

  • Burns are the second most common cause of accidental death, after motor vehicle accidents
  • 11 million new burns annually worldwide; ~180,000 deaths per year
  • Children (high BSA:mass ratio) and elderly (thinner skin) are at greatest risk for major burns
  • Second- or third-degree burns involving >20% TBSA require specialized burn center care
  • The anesthesiologist is involved at multiple stages: resuscitation, airway management, operative debridement/grafting, ICU care, and repeated dressing changes
Morgan & Mikhail's Clinical Anesthesiology, 7e; Barash Clinical Anesthesia, 9e

2. CLASSIFICATION OF BURNS

DegreeDepthFeaturesFluid Replacement
FirstEpidermis onlyErythema (sunburn); insensateNot required; exclude from TBSA calc
Second (Superficial partial)Into superficial dermisBlistering; painful; heals in <3 wk without scarringRequired if >20% TBSA
Second (Deep partial)Deep dermisLess painful; requires debridement + graftingRequired
Third (Full thickness)Entire dermis; nerves/vessels destroyedInsensate wound; surrounding tissue very painful; always needs graftingRequired
FourthSubcutaneous fat, fascia, boneChar; devastating; escharotomy/amputationRequired
Rule of Nines (adult TBSA estimation):
  • Head & neck: 9%
  • Each upper limb: 9%
  • Chest (anterior): 9%; Abdomen (anterior): 9%
  • Upper back: 9%; Lower back: 9%
  • Each thigh: 9%; Each lower leg + foot: 9%
  • Perineum: 1%
In children: head = 18%, each leg = 14% (Lund-Browder chart preferred for <10 years)
Morgan & Mikhail's Clinical Anesthesiology, 7e

3. PATHOPHYSIOLOGY OF MAJOR BURNS

3.1 Two Temporal Phases

Phase 1: Burn Shock / Ebb Phase (0–48 hours)

  • Massive release of inflammatory mediators (histamine, prostaglandins, reactive oxygen species, cytokines, DAMPs)
  • Capillary leak with loss of plasma proteins into interstitium — both injured and non-injured tissue
  • Hypovolemia, hemoconcentration, raised haematocrit
  • Cardiac output falls up to 50–60% within 30 minutes (normovolemic hypoperfusion = "burn shock")
  • Massive vasoconstriction
  • Reduced urine output; risk of acute kidney injury
  • Loss of endothelial barrier function → transcapillary fluid loss + evaporative loss through broken skin

Phase 2: Hypermetabolic State / Flow Phase (48–72 hours onward)

  • Inflammatory cytokines drive systemic vasodilation
  • Hyperdynamic circulation: raised CO, tachycardia
  • Elevated basal body temperature; markedly increased O₂ consumption
  • Muscle protein catabolism; severe negative nitrogen balance
  • Impaired immune function; risk of sepsis
  • This phase can persist for months to years after injury — highlighting need for aggressive nutritional support
Barash Clinical Anesthesia, 9e; Morgan & Mikhail's Clinical Anesthesiology, 7e; Miller's Anesthesia, 10e

3.2 Local Burn Wound

  • Zone of coagulation (central, irreversible)
  • Zone of stasis (potentially salvageable)
  • Zone of hyperaemia (peripheral, recovers)
Early excision and grafting reduces SIRS and mortality.

4. INHALATION INJURY

Present in 2–14% of admitted burn patients; significantly increases mortality beyond that predicted by TBSA alone.

4.1 Three Types (may coexist)

TypeMechanismFeatures
Supraglottic (thermal)Heat exchange limits injury to upper airwayMucosal oedema, epiglottic swelling, upper airway obstruction; rapidly progressive during fluid resuscitation
Tracheobronchial/alveolar (chemical)Combustion products (aldehydes, HCl, acids)Loss of surfactant; ciliary dysfunction; epithelial sloughing; inflammatory mediators; bronchoconstriction; ARDS
Systemic toxicityCO and cyanideImpaired cellular respiration

4.2 Diagnosis of Inhalation Injury

Clinical indicators:
  • Burns in an enclosed space
  • Unconsciousness at scene
  • Singed nasal vibrissae / facial hair
  • Carbonaceous (sooty) sputum
  • Hoarse voice, stridor
  • Soot/erythema in oropharynx
  • Facial/neck burns
Investigations:
  • Flexible bronchoscopy — gold standard (diagnoses and grades severity, predicts mortality/ICU LOS)
  • ABG: PaO₂, HbCO level, carboxyhemoglobin, methemoglobin
  • Pulse oximetry is unreliable (cannot distinguish HbO₂ from HbCO)
  • CXR, CT thorax
Barash Clinical Anesthesia, 9e

5. CARBON MONOXIDE AND CYANIDE POISONING

5.1 Carbon Monoxide (CO) Poisoning

HbCO LevelClinical Features
<10%Usually asymptomatic (smokers may be at 10%)
10–20%Headache, nausea, dizziness
20–40%Confusion, syncope — intubation indicated
40–60%Convulsions, coma
>60%Death
Mechanism:
  • CO binds haemoglobin with affinity ~250× greater than O₂ → reduces O₂ carrying capacity
  • Shifts oxyhaemoglobin dissociation curve to the left → impairs O₂ release to tissues
  • Pulse oximetry is falsely normal — SpO₂ reads HbCO as oxyhaemoglobin
Management:
  • 100% O₂ via tight-fitting non-rebreather mask (t½ of HbCO falls from 5 hours in room air → 60–90 min on 100% O₂)
  • If HbCO >20%: intubate + mechanically ventilate with FiO₂ 1.0
  • Hyperbaric oxygen (HBO) therapy — indicated for significant CO poisoning; multiple sessions needed

5.2 Cyanide Poisoning

  • From combustion of plastics, synthetics (polyurethane, nylon)
  • Blocks cytochrome c oxidase → histotoxic hypoxia
  • Suspect when: lactic acidosis, altered consciousness despite normal SpO₂/PaO₂
  • Treatment: sodium thiosulphate + hydroxocobalamin (or dicobalt edetate)
Morgan & Mikhail's Clinical Anesthesiology, 7e

6. FLUID RESUSCITATION

6.1 Indications

  • Adults: burns >15% TBSA
  • Children: burns >10% TBSA
  • First-degree burns are excluded from TBSA calculation

6.2 Standard Formulas

Parkland Formula (most widely used)

  • Total volume in first 24h = 4 mL × kg × % TBSA (Lactated Ringer's / Plasmalyte)
  • Half given in first 8 h (from time of burn, not hospital arrival)
  • Remaining half over next 16 h
  • Second 24 hours: 0.8 mL/kg/% TBSA (5% dextrose) + 0.015 mL/kg/% TBSA (5% albumin)

Modified Brooke Formula

  • 2 mL × kg × % TBSA in first 24 h
  • Half in first 8 h, remainder over next 16 h
  • Second 24 h: colloid added

Muir & Barclay Formula (UK)

  • Colloid-based (fresh frozen plasma or albumin)
Barash Clinical Anesthesia, 9e; Miller's Anesthesia, 10e

6.3 Monitoring Adequacy of Resuscitation

  • Target urine output: 0.5–1.0 mL/kg/h (adults), 1.0 mL/kg/h (children)
  • If UO >1 mL/kg/h → slow infusion rate
  • Adjuncts: invasive arterial monitoring, CVP, cardiac output monitoring

6.4 Fluid Creep

  • Phenomenon where administered volumes exceed calculated goals (often >6 mL/kg/% TBSA in 24 h vs. Parkland's 4 mL/kg)
  • Occurs due to: miscalculating TBSA (including first-degree), sedation-related hypotension treated with fluids, pressure to respond to any hemodynamic change
  • Consequences of fluid creep:
    • Pulmonary oedema / ARDS
    • Abdominal compartment syndrome (ACS)
    • Conversion of partial to full-thickness burns
    • Raised intraocular pressure
    • Muscle compartment syndromes requiring fasciotomy

6.5 Choice of Fluid

  • Balanced crystalloids (Ringer's Lactate / Plasmalyte) are preferred for initial resuscitation
  • Avoid:
    • Normal saline (hyperchloraemic acidosis)
    • Hypertonic saline (increased AKI risk)
    • Blood transfusion in early phase (increased mortality)
    • Albumin/colloid in early phase — controversial (capillary leak may allow oncotically active molecules to extravasate)
  • Colloids may be used after 12–24 h to reduce total fluid load

6.6 Abdominal Compartment Syndrome (ACS)

  • Risk when: circumferential abdominal burns OR >6 mL/kg/% TBSA administered
  • Monitor: intravesical (bladder) pressure via Foley catheter connected to pressure transducer
    • Zero at pelvic brim; instil 20 mL fluid; measure after 60 s
    • IAP >20 mmHg = ACS → abdominal decompression
  • Risk of Pseudomonas infection if laparotomy near burned tissue
Morgan & Mikhail's Clinical Anesthesiology, 7e; Miller's Anesthesia, 10e

7. AIRWAY MANAGEMENT IN BURNS

7.1 Indications for Early Intubation

IndicatorSignificance
Hoarse voice / stridorSupraglottic oedema in progress
Dyspnoea / tachypnoeaRespiratory compromise
Altered consciousnessCO poisoning, hypoxia
HbCO >20%Requires mechanical ventilation
Facial + oral burns with oedemaAirway may become impassable within hours
Burns >40% TBSAResuscitation oedema will worsen airway
Critical principle: Upper airway oedema progresses relentlessly during fluid resuscitation. Early intubation is safer than delayed; a patent airway today may be impassable in 4–6 hours.

7.2 Approach to Intubation

  • Awake fibreoptic intubation (AFOI) is technique of choice for anticipated difficult airway (facial burns, oropharyngeal oedema, limited neck mobility)
  • Rapid sequence induction (RSI) appropriate for early presentations (<48 h) without oedema
  • Use succinylcholine only within first 24–48 hours (see muscle relaxant section)
  • Have surgical airway (cricothyrotomy kit / tracheostomy) immediately available
  • Video laryngoscopy as alternative
  • Document airway carefully — multiple providers will manage over time

7.3 Tube Choice and Ventilation

  • Use uncut ETT (swelling makes tube shortening dangerous)
  • Secure tube carefully (circumferential burns make adhesive tape unreliable — use ties)
  • Tracheostomy may be necessary for long-term ventilation (>2 weeks)
  • Protective ventilation:
    • Tidal volume 6 mL/kg ideal body weight
    • PEEP 5–8 cmH₂O (higher if inhalation injury + ARDS)
    • Permissive hypercapnia if needed
    • Target SpO₂ >95% based on co-oximetry, not pulse oximetry
Barash Clinical Anesthesia, 9e; Morgan & Mikhail's Clinical Anesthesiology, 7e

8. MUSCLE RELAXANTS IN BURNS

8.1 Mechanism of Altered Response

After burn injury and immobilisation, there is upregulation of nicotinic acetylcholine receptors (nAChRs):
  • Both fetal (α₂βγδ) and mature (α₂βεδ) subtype isoforms proliferate
  • Increased quantal content of evoked ACh release (noted by 72 hours post-injury)
  • Changes in diaphragm acetylcholinesterase content and molecular forms
Consequence:
  • Resistance to non-depolarising neuromuscular blockers (NDNMBs)
  • Hypersensitivity / exaggerated response to succinylcholine

8.2 Succinylcholine

Time After BurnSafety
0–24 (–48) hoursSAFE to use
After 48 hoursCONTRAINDICATED — risk of lethal hyperkalaemia
Duration of riskUp to 2 years after burn injury
  • Mechanism: Upregulated extrajunctional receptors release massive K⁺ on depolarisation
  • Serum K⁺ may reach 13 mEq/L → ventricular tachycardia, ventricular fibrillation, cardiac arrest
  • Magnitude of hyperkalaemia does not correlate with burn size (lethal hyperkalaemia reported with as little as 8% TBSA burn)
  • Burns involve >25% TBSA typically to show clear resistance; but CONTRAINDICATION applies to ALL burns after 48 h
Other conditions causing nAChR upregulation (same succinylcholine risk): spinal cord injury, prolonged immobility, stroke, Guillain-Barré syndrome, multiple sclerosis, prolonged NDNMB exposure
Miller's Anesthesia, 10e; Morgan & Mikhail's Clinical Anesthesiology, 7e

8.3 Non-Depolarising Neuromuscular Blockers

  • Resistance typically seen when burns involve >25% TBSA
  • May require 2–5× normal dose to achieve adequate relaxation
  • Recovery to pre-burn neuromuscular function can take months to years
  • Mandatory quantitative neuromuscular monitoring (TOF ratio, PTC) — wide inter-individual variation
  • Drug choice: rocuronium (high-dose for RSI if sux contraindicated: 1.2 mg/kg), vecuronium, cisatracurium (useful in multi-organ failure — Hofmann elimination)

9. PHARMACOKINETICS IN BURNS

Major burns cause profound changes in drug pharmacokinetics affecting all phases (ADME):

9.1 Absorption

  • Delayed gastric emptying (early phase)
  • Increased skin absorption of topical agents

9.2 Distribution

  • Increased volume of distribution (Vd) for hydrophilic drugs (oedema expands extracellular space)
  • Hypoalbuminaemia (capillary leak, catabolism) → increased free fraction of protein-bound drugs
  • Raised α₁-acid glycoprotein → increased binding of basic drugs (e.g., lidocaine)
  • Anaemia in later phases

9.3 Metabolism

  • Phase 1 (ebb): reduced hepatic blood flow → reduced drug metabolism
  • Phase 2 (flow): hypermetabolic state → markedly increased hepatic blood flow and enzyme activity → increased clearance of many drugs
  • Induction of CYP450 enzymes

9.4 Elimination

  • AKI (early) reduces renal clearance
  • Polyuria (later hypermetabolic phase) increases renal drug clearance
  • Altered morphine pharmacokinetics confirmed in burns patients during surgery
Practical implications:
  • Opioids: may need higher doses in hypermetabolic phase; titrate carefully
  • Propofol: increased clearance in hypermetabolic phase
  • Ketamine: often drug of choice (see below) — maintains haemodynamic stability
  • Midazolam: increased Vd — higher loading doses

10. PREOPERATIVE ASSESSMENT

10.1 History

  • Time, mechanism (thermal/chemical/electrical), place (open vs. enclosed space)
  • Estimate % TBSA, depth of burns
  • Associated trauma (fall, blast, explosion)
  • CO/cyanide exposure history
  • Comorbidities (especially cardiac, respiratory, renal, diabetes)
  • Current medications, known allergies
  • Volume of fluid given so far; response; urine output

10.2 Examination

  • Airway: facial burns, singed vibrissae, oropharyngeal soot/oedema, mouth opening, neck mobility
  • Respiratory: RR, SpO₂, breath sounds, stridor
  • Cardiovascular: HR, BP, perfusion — signs of burn shock or hyperdynamic state
  • Neurological: GCS, orientation — CO poisoning?
  • Fluid status: UO, skin turgor, mucous membranes
  • Sites for vascular access: IV lines may need to be placed through or near burned skin

10.3 Investigations

InvestigationRelevance
ABG + Co-oximetryHbCO, SpO₂, pH, lactate (cyanide?), PaO₂
FBCHaematocrit (elevated in ebb phase), anaemia (flow phase)
Serum electrolytesK⁺ (hyperkalaemia risk), Na⁺
Urea/creatinineAKI monitoring
Coagulation (PT, APTT, fibrinogen)DIC possible in major burns
Blood glucoseHyperglycaemia in stress response
CXRInhalation injury, pulmonary oedema
ECGCardiac arrhythmias (CO poisoning, hyperkalaemia, electrical burns)
Flexible bronchoscopyIf inhalation injury suspected

11. INTRAOPERATIVE ANESTHETIC MANAGEMENT

11.1 Timing of Surgery

  • Emergency: escharotomy (circumferential burns causing compartment syndrome), airway burns, blast injuries
  • Early (days 1–5): early excision and grafting (EEG) — reduces SIRS, hospital stay, mortality
  • Repeated: multiple sequential grafting procedures often required for major burns
  • Burns patients may return to OR 5–20 times; cumulative pharmacological exposures matter

11.2 Temperature Management

  • Critical priority: burns patients cannot regulate temperature
  • OR temperature should be maintained at ≥37–40°C for all burn procedures
  • All IV fluids must be warmed
  • Forced-air warming blankets, radiant warmers
  • Wrap non-operative extremities
  • Hypothermia worsens: coagulopathy, cardiac dysfunction, drug metabolism, infection risk

11.3 Positioning and Access

  • Venous access through burned skin is acceptable in emergency (secure carefully)
  • Intra-osseous access if peripheral IV impossible
  • Central venous access may be required
  • Arterial line preferred for continuous BP monitoring + ABG sampling
  • Position carefully — pressure areas, padding (especially over bony prominences adjacent to grafted areas)

11.4 Choice of Anesthetic Technique

General Anaesthesia

  • Most common approach for operative procedures
  • Induction agents:
    • Ketamine — drug of choice in haemodynamically unstable burn patients
      • Sympathomimetic → maintains HR and BP
      • Bronchodilator → useful in inhalation injury
      • Good analgesic and amnestic
      • Combine with benzodiazepine to prevent emergence delirium
      • Dose: 1–2 mg/kg IV or 4–6 mg/kg IM (useful when IV access difficult)
    • Propofol — use cautiously in haemodynamically unstable patients; TIVA possible
    • Etomidate — useful in haemodynamically compromised patients; avoid repeated doses (adrenal suppression)
    • Thiopentone — used for rapid sequence induction; hypotension risk in hypovolaemia
  • Maintenance:
    • Volatile agents (sevoflurane, isoflurane, desflurane) — all acceptable
    • TIVA with propofol + remifentanil — useful to avoid volatile agent pollution in prolonged procedures
    • Ketamine infusion as adjunct
  • Analgesia:
    • Multimodal approach essential
    • Opioids: morphine, fentanyl, hydromorphone — titrate to effect; tolerance develops rapidly
    • Ketamine (sub-anaesthetic doses 0.1–0.5 mg/kg/h) — opioid-sparing
    • NSAIDs/COX inhibitors (with caution — AKI risk, gastric effects)
    • Paracetamol
    • Dexmedetomidine — sedation + analgesia, reduces opioid requirement

Regional Anaesthesia

  • Technically challenging (burned/scarred skin, oedema)
  • Useful for: limb procedures, donor site harvesting, dressing changes
  • May mask symptoms of compartment syndrome — caution in early post-burn period
  • Examples: peripheral nerve blocks (femoral, sciatic, brachial plexus), spinal/epidural

11.5 Muscle Relaxation Summary (Intraoperative)

  • <48 h from burn: succinylcholine acceptable for RSI
  • >48 h from burn: use rocuronium (1.2 mg/kg) for RSI; sugammadex available for reversal
  • Higher doses of NDNMBs required (>25% TBSA)
  • Quantitative TOF monitoring mandatory
  • Avoid vecuronium/pancuronium in hepatic/renal failure (accumulation)
  • Cisatracurium preferred in multi-organ failure

11.6 Monitoring

MonitorIndication
Standard (ECG, NIBP, SpO₂, EtCO₂, temperature)All cases — note SpO₂ unreliable in CO poisoning
Invasive arterial lineMajor burns, haemodynamic instability, repeat ABG needed
Central venous pressureGuide fluid resuscitation
Cardiac output monitoringMajor haemodynamic instability; "fluid creep" prevention
Temperature (core + peripheral)Hypothermia prevention — critical
Urinary catheter + UO hourlyGuide fluid resuscitation (0.5–1 mL/kg/h)
TOF monitoringMandatory with NDNMBs
Intravesical pressureIf ACS suspected
Blood glucoseHyperglycaemia, hypoglycaemia in children

12. SPECIAL OPERATIVE SITUATIONS IN BURNS

12.1 Escharotomy

  • Indicated for circumferential full-thickness burns causing compartment syndrome of limbs, chest, or abdomen
  • Full-thickness burns are insensate — no anesthesia needed for escharotomy of full-thickness burns
  • Deep partial-thickness burns may retain sensation — local anaesthesia/IV analgesia may be required
  • Chest escharotomy: releases respiratory restriction, improves compliance

12.2 Excision and Skin Grafting

  • Major surgical blood loss expected — have cross-matched blood immediately available
  • Blood transfusion threshold: Hb <7–8 g/dL (liberal in paediatrics, cardiac disease)
  • Tumescent epinephrine infiltration of donor/recipient sites reduces blood loss
  • Prone positioning for back/buttock grafts — airway access critical
  • Temperature management especially important during long procedures

12.3 Dressing Changes

  • Can be extremely painful — require sedation/analgesia/GA
  • Options: ketamine IM or IV, dexmedetomidine, nitrous oxide (Entonox), intranasal fentanyl/midazolam in children
  • Psychological preparation and distraction therapy adjuncts

13. PAEDIATRIC BURNS — SPECIAL CONSIDERATIONS

  • Use Lund-Browder chart (not Rule of Nines) for TBSA estimation
  • Children <30 kg: add 5% dextrose to IV fluids (hypoglycaemia risk)
  • Target UO: 1.0 mL/kg/h (vs 0.5 mL/kg/h in adults)
  • Maintenance fluids: 4-2-1 rule; avoid hypotonic solutions postoperatively (hyponatraemia risk from SIADH)
  • Greater risk of hypothermia (high BSA:mass ratio)
  • Succinylcholine restriction same as adults (>48 h post-burn)
  • Morphine remains first-line opioid in most burn centres for children with major burns

14. POSTOPERATIVE CARE

14.1 ICU Management

  • Most major burn patients go to burns ICU post-operatively
  • Continue temperature management — maintain normothermia
  • Mechanical ventilation: protective strategy (TV 6 mL/kg IBW, PEEP 5–8 cmH₂O)
  • Sedation and analgesia: opioid infusions (morphine/fentanyl), ketamine adjunct, dexmedetomidine
    • Opioid tolerance develops rapidly — dose escalation common
    • Avoid prolonged benzodiazepine use (delirium, withdrawal)
  • Nutritional support: critical in hypermetabolic phase — early enteral nutrition via NG tube
    • High protein (1.5–2 g/kg/day), high caloric (25–35 kcal/kg/day) requirements
    • Continue nutrition perioperatively when possible
  • Infection control: burns are a portal for sepsis
    • Regular wound inspection, cultures
    • Systemic antibiotics for confirmed sepsis — not prophylactically
    • Topical antimicrobials: silver sulfadiazine, mafenide acetate

14.2 Pain Management

  • Multimodal approach throughout hospitalisation
  • Background continuous pain + procedural pain (dressing changes, physiotherapy) — both must be addressed
  • Regional techniques where anatomically feasible
  • Psychological support integral to pain management

15. COMPLICATIONS OF BURNS AND ANESTHESIA

ComplicationTimingMechanism
Burn shock0–48 hVasoconstriction, capillary leak, reduced CO
Inhalation injury/ARDSEarlyChemical bronchial injury, surfactant loss
CO / cyanide poisoningImmediateHistotoxic hypoxia
Hyperkalemia with succinylcholine>48 hnAChR upregulation
Fluid creep / ACS24–72 hExcessive fluid resuscitation
AKIEarlyHypovolemia, myoglobinuria (electrical burns)
Sepsis / MODSDays–weeksImmune compromise, wound contamination
Hypermetabolism48 h–monthsCytokine-driven hyperdynamic state
Coagulopathy / DICVariableMassive tissue injury, dilution, consumption
HypothermiaIntraoperativeLoss of skin barrier + cold environment
Difficult airwayAny timeProgressive oedema, contractures, scarring

16. ELECTRICAL BURNS — SPECIAL CONSIDERATIONS

  • Entry and exit wounds may underestimate true extent of injury
  • Massive deep tissue destruction despite normal-appearing skin
  • Rhabdomyolysis and myoglobinuria → AKI → target UO 1–2 mL/kg/h + alkalinise urine
  • Cardiac arrhythmias (VF, heart block) — continuous ECG monitoring, 24-h observation post-exposure
  • Spinal cord injury risk (tetanic muscle contractions)
  • Cataracts (delayed)
  • Succinylcholine risk applies as with thermal burns >48 h

17. HIGH-YIELD EXAM POINTS (SUMMARY)

TopicKey Fact
CO affinity for Hb~250× that of O₂
Pulse oximetry in CO poisoningFalsely normal
Parkland formula4 mL × kg × %TBSA; half in first 8 h
Target UO (adults)0.5–1.0 mL/kg/h
Succinylcholine safe windowFirst 24–48 hours only
Succinylcholine risk durationUp to 2 years
K⁺ level with sux in burnsUp to 13 mEq/L (lethal)
Minimum TBSA for NDNMB resistance>25% TBSA
OR temperature for burns≥37–40°C
Induction drug of choice (unstable)Ketamine
CO poisoning Rx100% O₂ → HBO if significant
Lethal HbCO>60%
Fluid creep complicationACS, pulmonary oedema
ACS diagnosisBladder pressure >20 mmHg
Inhalation injury gold standardFlexible bronchoscopy
Phase 1 (ebb) duration0–48 hours
Phase 2 (flow) onset48–72 hours
First-degree burns and fluidsExcluded from TBSA calc; no resuscitation
Neuromuscular monitoringMandatory (quantitative TOF) in burns
Hypermetabolic phase durationMonths to years
Cyanide antidotesHydroxocobalamin + sodium thiosulphate

SOURCES

  • Miller's Anesthesia, 10th Edition (Miller et al.) — Chapters 24, 34
  • Morgan & Mikhail's Clinical Anesthesiology, 7th Edition — Chapter 39 (Burns)
  • Barash, Cullen & Stoelting's Clinical Anesthesia, 9th Edition — Chapter on Trauma/Burns
  • Miller's Anesthesia, 10e (Block 17) — Fluid Management in Burns
---These are comprehensive MD Anaesthesiology exam notes on anesthetic management of burns, drawn directly from Miller's Anesthesia (10e), Morgan & Mikhail's Clinical Anesthesiology (7e), and Barash Clinical Anesthesia (9e). Here's what's covered:
  1. Epidemiology & Classification — degrees of burns, Rule of Nines, Lund-Browder for children
  2. Pathophysiology — two-phase model (ebb/burn shock vs. hypermetabolic/flow phase), local burn zones
  3. Inhalation Injury — three types, diagnosis (flexible bronchoscopy gold standard), clinical indicators
  4. CO & Cyanide Poisoning — HbCO levels/effects, unreliable pulse oximetry, management with HBO
  5. Fluid Resuscitation — Parkland formula (4 mL/kg/%TBSA), fluid creep, ACS (bladder pressure >20 mmHg), colloid vs. crystalloid
  6. Airway Management — early vs. delayed intubation, AFOI, RSI technique, protective ventilation
  7. Muscle Relaxants — succinylcholine contraindicated after 48 h (lethal hyperkalaemia up to K⁺ 13 mEq/L), NDNMB resistance >25% TBSA, duration of risk up to 2 years
  8. Pharmacokinetics — altered Vd, hypoalbuminaemia, hypermetabolic clearance
  9. Preoperative Assessment — history, examination, investigations
  10. Intraoperative Management — temperature (OR at 40°C), ketamine as drug of choice, monitoring, muscle relaxant protocol
  11. Special Situations — escharotomy, excision/grafting, dressing changes
  12. Paediatric Considerations — dextrose supplementation, higher UO target
  13. Postoperative/ICU Care — ventilation, nutrition, infection control
  14. Electrical Burns — rhabdomyolysis, cardiac arrhythmias
  15. High-Yield Exam Summary Table — all key numbers and facts in one place
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