I now have comprehensive content from three major anesthesia textbooks. Let me now compile the full, detailed MD Anaesthesiology exam notes.---
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
| Degree | Depth | Features | Fluid Replacement |
|---|
| First | Epidermis only | Erythema (sunburn); insensate | Not required; exclude from TBSA calc |
| Second (Superficial partial) | Into superficial dermis | Blistering; painful; heals in <3 wk without scarring | Required if >20% TBSA |
| Second (Deep partial) | Deep dermis | Less painful; requires debridement + grafting | Required |
| Third (Full thickness) | Entire dermis; nerves/vessels destroyed | Insensate wound; surrounding tissue very painful; always needs grafting | Required |
| Fourth | Subcutaneous fat, fascia, bone | Char; devastating; escharotomy/amputation | Required |
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)
| Type | Mechanism | Features |
|---|
| Supraglottic (thermal) | Heat exchange limits injury to upper airway | Mucosal 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 toxicity | CO and cyanide | Impaired 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 Level | Clinical 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
| Indicator | Significance |
|---|
| Hoarse voice / stridor | Supraglottic oedema in progress |
| Dyspnoea / tachypnoea | Respiratory compromise |
| Altered consciousness | CO poisoning, hypoxia |
| HbCO >20% | Requires mechanical ventilation |
| Facial + oral burns with oedema | Airway may become impassable within hours |
| Burns >40% TBSA | Resuscitation 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 Burn | Safety |
|---|
| 0–24 (–48) hours | SAFE to use |
| After 48 hours | CONTRAINDICATED — risk of lethal hyperkalaemia |
| Duration of risk | Up 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
| Investigation | Relevance |
|---|
| ABG + Co-oximetry | HbCO, SpO₂, pH, lactate (cyanide?), PaO₂ |
| FBC | Haematocrit (elevated in ebb phase), anaemia (flow phase) |
| Serum electrolytes | K⁺ (hyperkalaemia risk), Na⁺ |
| Urea/creatinine | AKI monitoring |
| Coagulation (PT, APTT, fibrinogen) | DIC possible in major burns |
| Blood glucose | Hyperglycaemia in stress response |
| CXR | Inhalation injury, pulmonary oedema |
| ECG | Cardiac arrhythmias (CO poisoning, hyperkalaemia, electrical burns) |
| Flexible bronchoscopy | If 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
| Monitor | Indication |
|---|
| Standard (ECG, NIBP, SpO₂, EtCO₂, temperature) | All cases — note SpO₂ unreliable in CO poisoning |
| Invasive arterial line | Major burns, haemodynamic instability, repeat ABG needed |
| Central venous pressure | Guide fluid resuscitation |
| Cardiac output monitoring | Major haemodynamic instability; "fluid creep" prevention |
| Temperature (core + peripheral) | Hypothermia prevention — critical |
| Urinary catheter + UO hourly | Guide fluid resuscitation (0.5–1 mL/kg/h) |
| TOF monitoring | Mandatory with NDNMBs |
| Intravesical pressure | If ACS suspected |
| Blood glucose | Hyperglycaemia, 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
| Complication | Timing | Mechanism |
|---|
| Burn shock | 0–48 h | Vasoconstriction, capillary leak, reduced CO |
| Inhalation injury/ARDS | Early | Chemical bronchial injury, surfactant loss |
| CO / cyanide poisoning | Immediate | Histotoxic hypoxia |
| Hyperkalemia with succinylcholine | >48 h | nAChR upregulation |
| Fluid creep / ACS | 24–72 h | Excessive fluid resuscitation |
| AKI | Early | Hypovolemia, myoglobinuria (electrical burns) |
| Sepsis / MODS | Days–weeks | Immune compromise, wound contamination |
| Hypermetabolism | 48 h–months | Cytokine-driven hyperdynamic state |
| Coagulopathy / DIC | Variable | Massive tissue injury, dilution, consumption |
| Hypothermia | Intraoperative | Loss of skin barrier + cold environment |
| Difficult airway | Any time | Progressive 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)
| Topic | Key Fact |
|---|
| CO affinity for Hb | ~250× that of O₂ |
| Pulse oximetry in CO poisoning | Falsely normal |
| Parkland formula | 4 mL × kg × %TBSA; half in first 8 h |
| Target UO (adults) | 0.5–1.0 mL/kg/h |
| Succinylcholine safe window | First 24–48 hours only |
| Succinylcholine risk duration | Up to 2 years |
| K⁺ level with sux in burns | Up 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 Rx | 100% O₂ → HBO if significant |
| Lethal HbCO | >60% |
| Fluid creep complication | ACS, pulmonary oedema |
| ACS diagnosis | Bladder pressure >20 mmHg |
| Inhalation injury gold standard | Flexible bronchoscopy |
| Phase 1 (ebb) duration | 0–48 hours |
| Phase 2 (flow) onset | 48–72 hours |
| First-degree burns and fluids | Excluded from TBSA calc; no resuscitation |
| Neuromuscular monitoring | Mandatory (quantitative TOF) in burns |
| Hypermetabolic phase duration | Months to years |
| Cyanide antidotes | Hydroxocobalamin + 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:
- Epidemiology & Classification — degrees of burns, Rule of Nines, Lund-Browder for children
- Pathophysiology — two-phase model (ebb/burn shock vs. hypermetabolic/flow phase), local burn zones
- Inhalation Injury — three types, diagnosis (flexible bronchoscopy gold standard), clinical indicators
- CO & Cyanide Poisoning — HbCO levels/effects, unreliable pulse oximetry, management with HBO
- Fluid Resuscitation — Parkland formula (4 mL/kg/%TBSA), fluid creep, ACS (bladder pressure >20 mmHg), colloid vs. crystalloid
- Airway Management — early vs. delayed intubation, AFOI, RSI technique, protective ventilation
- 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
- Pharmacokinetics — altered Vd, hypoalbuminaemia, hypermetabolic clearance
- Preoperative Assessment — history, examination, investigations
- Intraoperative Management — temperature (OR at 40°C), ketamine as drug of choice, monitoring, muscle relaxant protocol
- Special Situations — escharotomy, excision/grafting, dressing changes
- Paediatric Considerations — dextrose supplementation, higher UO target
- Postoperative/ICU Care — ventilation, nutrition, infection control
- Electrical Burns — rhabdomyolysis, cardiac arrhythmias
- High-Yield Exam Summary Table — all key numbers and facts in one place