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Burns: History, Physical Examination & Pathophysiology
PART I — HISTORY IN A CASE OF BURNS
A thorough history is essential for assessing burn severity, anticipating complications, and guiding management.
1. Presenting Complaint
- Burn wound with pain, blistering, or skin loss
- Associated symptoms: shortness of breath, hoarseness, altered consciousness
2. History of the Burn Injury (AMPLE + Burn-Specific)
A. Circumstances of the Injury
| Question | Clinical Relevance |
|---|
| When did the burn occur? | Time since injury → guide fluid resuscitation timing; delays raise concern for non-accidental injury |
| Where did it occur? | Enclosed space → high risk of inhalation injury + carbon monoxide (CO) poisoning |
| How did it occur? | Mechanism determines burn type and depth (see below) |
| Duration of exposure? | Longer exposure = greater depth |
| Was the patient trapped? | Trapped in a car, room → inhalation injury until proven otherwise |
B. Mechanism of Injury
- Thermal (flame/scald): Most common; scalds predominant in children <5 yrs (kettles, hot drinks, bath water); flame burns more common in adults
- Chemical: Alkali burns penetrate deeper than acid burns; occupational history crucial
- Electrical: Document voltage (high vs. low); risk of rhabdomyolysis, cardiac arrhythmia, internal injury out of proportion to skin wound
- Radiation: Sunburn, arc-welding, radiation therapy
- Contact burns: Common in elderly (falls against radiators)
C. First Aid Administered
- Was the burn cooled? (Cool running water ≥20 min within 1 hour of injury — reduces depth and pain)
- Any creams, toothpaste, or traditional remedies applied? (Can obscure depth assessment and introduce infection)
- Clothing removed? (Retained hot clothing continues to burn)
D. Associated Injuries
- Burns from explosions, house fires, or road traffic crashes may have concurrent fractures, blast injuries, or blunt trauma
- Screen for loss of consciousness (CO poisoning, head injury)
E. Symptoms Suggesting Inhalation Injury
- Hoarseness, voice change, stridor
- Cough, soot in sputum
- Shortness of breath, wheezing
- Headache, confusion (CO poisoning — cherry-red lips are a late sign)
- History of being in a burning building/vehicle
F. Past Medical History
- Epilepsy, cardiovascular disease, diabetes, immunosuppression (alter resuscitation targets and healing)
- Psychiatric illness, substance abuse, suicidal intent (up to 80% of admitted burn patients in some populations have an underlying factor such as epilepsy, alcohol/drug use, or mental illness)
- Previous burns or hospital admissions
G. Medications & Allergies
- Anticoagulants, immunosuppressants, beta-blockers (affect wound healing and haemodynamic response)
- Drug allergies (especially to antibiotics, silver-containing dressings)
H. Tetanus Immunisation Status
- Burns are tetanus-prone wounds
I. Nutritional & Social History
- Pre-injury nutritional status (critical for wound healing)
- Living situation, support network, occupational exposures
J. Safeguarding / Non-Accidental Injury (NAI) Screen
Always screen in children and vulnerable adults. Raise concern if:
- Delay in presentation
- Inconsistent history between caregivers
- Unexpected burn pattern or depth (e.g., stocking/glove distribution in a child — suggests deliberate immersion)
- Other unexplained injuries (bruises, fractures)
- Frequent hospital attendances
PART II — PHYSICAL EXAMINATION IN BURNS
Follow ATLS primary and secondary survey principles.
PRIMARY SURVEY (ABCDE)
A — Airway
- Inspect oropharynx: singed nasal/facial hairs, soot in mouth, mucosal erythema or blistering
- Note hoarseness, stridor, drooling — early intubation if airway compromise is imminent (oedema progresses rapidly)
- Perioral burns alone don't confirm airway injury but mandate pharyngeal inspection
B — Breathing
- Respiratory rate, SpO₂ (note: pulse oximetry is falsely normal in CO poisoning — check ABG + carboxyhaemoglobin)
- Listen for wheeze (chemical pneumonitis from inhaled smoke particles), stridor, or reduced air entry
- Observe chest expansion — full-thickness circumferential chest burns can mechanically restrict rib movement
- Chest auscultation: bronchospasm, crepitations
C — Circulation
- Heart rate, blood pressure, capillary refill time
- IV access: two large-bore cannulae (avoid burned tissue if possible)
- Insert urinary catheter — urine output target: 0.5 mL/kg/hr (adults); 1 mL/kg/hr (children <30 kg)
- Signs of haemodynamic shock in burns >15% TBSA
D — Disability
- Glasgow Coma Scale (GCS), AVPU
- Pupil responses
- Blood glucose
- CO poisoning → confusion, agitation, coma
E — Exposure
- Fully expose the patient to assess all burn surfaces
- Maintain temperature (cover with dry clean sheet — prevent hypothermia, especially in children and elderly)
- Check all body surfaces including perineum, intertriginous areas, back
SECONDARY SURVEY — Burn Assessment
1. Burn Depth Classification
| Degree | Layer Involved | Appearance | Sensation | Blistering | Healing |
|---|
| Superficial (1st degree) | Epidermis only | Erythema, dry, no blisters | Painful | None | 3–5 days, no scarring |
| Superficial partial-thickness (2nd degree) | Epidermis + superficial papillary dermis | Moist, erythematous, blistered, blanches | Very painful | Present, clear fluid | 10–14 days, minimal scarring |
| Deep partial-thickness (2nd degree) | Epidermis + reticular dermis | Mottled red/white, less wet, may not blanch | Reduced sensation | May be present | >21 days, scarring likely; may need grafting |
| Full-thickness (3rd degree) | All skin layers | Leathery, white/brown/black eschar, dry | Painless (nerve destruction) | None | Cannot self-heal; requires grafting |
| 4th degree | Skin + underlying fascia/muscle/bone | Charred, necrotic | None | None | Major reconstruction |
Superficial burns (1st degree) are not included in TBSA calculations.
Burn depth progression from 1st degree (a) to 4th degree (e). — PMC Clinical VQA
2. Burn Size — Total Body Surface Area (TBSA)
Rule of Nines (Adults):
| Body Part | % TBSA |
|---|
| Head & neck | 9% |
| Each arm | 9% |
| Anterior trunk | 18% |
| Posterior trunk | 18% |
| Each leg | 18% |
| Perineum | 1% |
Lund & Browder Chart — preferred in children (adjusts for age-related head:leg ratio differences)
Palmar surface rule: Patient's palm (including fingers) ≈ 1% TBSA — useful for irregular/scattered burns
3. Circumferential Burns
- Check all limbs, chest, and neck for circumferential full-thickness burns
- Signs of compartment syndrome: tense swelling, loss of distal pulses, parasthesia, pain on passive stretch
- Chest: note whether rib expansion is restricted
- Escharotomy indicated for circumferential full-thickness limb or chest burns (incisions placed on lateral aspects of extremities to avoid neurovascular structures)
4. Special Sites
Assess burns involving:
- Face: Airway threat, eyelid/corneal involvement
- Hands/feet: Functional implications — require specialist unit
- Genitalia/perineum: Urinary catheter mandatory
- Major joints: Risk of contracture
- Circumferential limb/chest: Risk of ischaemia/ventilatory compromise
5. Associated Injuries
- Examine for fractures (especially in explosions, falls)
- Check for blast injuries, lacerations
INVESTIGATIONS ORDERED AFTER EXAMINATION
| Investigation | Purpose |
|---|
| ABG + carboxyhaemoglobin | Inhalation injury, CO poisoning (SpO₂ misleading) |
| FBC, U&E, creatinine | Baseline, rhabdomyolysis (electrical burns) |
| Blood glucose, coagulation | Baseline |
| CK, myoglobin | Electrical burns → rhabdomyolysis |
| Urine myoglobin | Electrical burns |
| ECG | Electrical burns → arrhythmia |
| CXR | Inhalation injury, baseline |
| Lactate | Cyanide poisoning, shock |
PART III — PATHOPHYSIOLOGY OF BURNS
1. Local Injury — Jackson's Zones of Burn Injury
Jackson (1947) described three concentric zones radiating outward from the point of maximum heat application:
| Zone | Description | Clinical Implication |
|---|
| Zone of Coagulation (central) | Maximal thermal damage; irreversible cell necrosis; protein coagulation | Full-thickness destruction; cannot be salvaged |
| Zone of Stasis (middle) | Decreased perfusion; cells viable but at risk; capillary endothelial damage with microvascular sludging | Target of resuscitation — can be saved or lost depending on management |
| Zone of Hyperaemia (peripheral) | Increased blood flow, minimal cell injury, inflammatory vasodilation | Heals spontaneously |
Clinical relevance: The zone of stasis can progress to coagulation if resuscitation is inadequate, infection supervenes, or cooling is delayed — this is why 20 minutes of cool water is effective up to 1 hour post-burn.
2. Local Inflammatory Response
Thermal injury triggers an intense local inflammatory cascade:
- Stimulation of pain fibres → release of neuropeptides (substance P, CGRP) → local vasodilation
- Activation of Hageman factor (Factor XII) → initiates the kinin, coagulation, complement, and fibrinolytic cascades
- Arachidonic acid pathway → prostaglandins and leukotrienes → vasodilation + increased vascular permeability
- Complement activation → anaphylatoxins (C3a, C5a) → mast cell degranulation → histamine release → further capillary leak
- Kallikrein–kinin pathway → bradykinin → vasodilatation + increased permeability
Result: Massive capillary leak → oedema formation both locally and systemically (in burns >30% TBSA)
3. Systemic Effects — Burn Shock
In burns involving >15% TBSA (adults), fluid losses become haemodynamically significant:
Haemodynamic sequence:
- Increased vascular permeability → loss of plasma proteins + fluid into interstitium
- Intravascular volume depletion → decreased cardiac preload → decreased cardiac output
- Hypotension → compensatory vasoconstriction → increased afterload → further ↓ cardiac output
- A myocardial depressant factor (MDF) released early post-burn directly impairs myocardial contractility — cardiac output may fall to 30% of baseline within 30 minutes
- Organ hypoperfusion → metabolic acidosis
Fluid kinetics:
- Maximum fluid loss: first 6–8 hours post-burn
- The volume lost is directly proportional to the burn surface area
- Oedema continues to form for 18–24 hours
4. Inhalation Injury
Three distinct mechanisms — can occur alone or together:
| Mechanism | Injury | Cause |
|---|
| Upper airway injury | Supraglottic oedema, laryngeal oedema | Direct thermal injury from hot gases |
| Lower airway injury | Chemical tracheobronchitis, loss of respiratory epithelium, bronchospasm | Inhaled smoke particles → chemical pneumonitis |
| Metabolic poisoning | Tissue hypoxia | Carbon monoxide (CO) or hydrogen cyanide (HCN) |
Carbon monoxide poisoning:
- CO binds haemoglobin with 250× greater affinity than O₂ → carboxyhaemoglobin (COHb) → impaired O₂ carrying capacity
- CO also competes with O₂ at cytochrome oxidase → disrupts aerobic metabolism → cellular hypoxia even if PaO₂ is normal
- Treatment: High-flow 100% oxygen (reduces CO half-life from 4–5 hours to ~90 minutes)
Cyanide (HCN):
- From combustion of nitrogen-containing polymers (plastics, wool, silk)
- Binds trivalent iron in mitochondrial cytochrome A3 complex → inhibits electron transport → histotoxic hypoxia
- Treatment: hydroxocobalamin (preferred) or sodium thiosulfate
5. Metabolic Response — Hypermetabolism
Burns >30–40% TBSA trigger the most profound hypermetabolic response of any injury:
- Metabolic rate increases to 150–200% of basal (peaks at 2–3 weeks post-burn)
- Driven by: catecholamines, cortisol, glucagon, cytokines (TNF-α, IL-1, IL-6)
- Features: marked catabolism, muscle wasting, impaired wound healing, immunosuppression
- Persistent hypermetabolism can last up to 2 years post-injury
6. Immunological Effects
- Burns produce a biphasic immune response: initial pro-inflammatory phase (SIRS) followed by compensatory anti-inflammatory response (CARS)
- Cell-mediated immunity is significantly reduced
- Depressed neutrophil function, impaired T-cell activity
- Loss of skin barrier → entry point for bacteria
- Sources of infection: burn wound, lungs (pneumonia), central venous catheters, urinary catheters
- Translocation of gut bacteria (impaired gut mucosal barrier) → another infection source in large burns
7. Gastrointestinal Effects
- Inflammatory stimulus + hypovolaemic shock → gut mucosal ischaemia
- ↓ Gut motility, impaired absorption
- Bacterial translocation → systemic sepsis
- Curling's ulcer — acute gastric ulceration in major burns (prevented by enteral feeding and H₂ blockers/PPIs)
- Gut mucosal swelling + peritoneal oedema → abdominal compartment syndrome → splints the diaphragm → ↑ airway pressures
8. Peripheral Circulation and Compartment Syndrome
- Full-thickness burns → collagen coagulation → skin loses elasticity → leathery eschar
- Circumferential full-thickness limb burns: as oedema forms, inelastic eschar acts as a tourniquet → compartment syndrome → limb-threatening ischaemia
- Escharotomy releases this pressure
9. Renal Effects
- Hypovolaemia → ↓ renal perfusion → acute tubular necrosis (ATN)
- In electrical burns: myoglobin + haemoglobin released → tubular precipitation → acute kidney injury
- Adequate fluid resuscitation (urine output target 0.5 mL/kg/hr in adults) is essential
Summary: Pathophysiology at a Glance
BURN INJURY
│
├─► Local: Zones of coagulation / stasis / hyperaemia
│
├─► Inflammatory cascade (Hageman factor, arachidonic acid, complement, kallikrein)
│ └─► Massive capillary leak → oedema → BURN SHOCK (>15% TBSA)
│
├─► Inhalation injury (upper airway, lower airway, CO/CN poisoning)
│
├─► Hypermetabolism + catabolism (peaks week 2–3)
│
├─► Immunosuppression → infection (wound, lung, gut, lines)
│
├─► Gut mucosal ischaemia → ileus, bacterial translocation, Curling's ulcer
│
├─► Circumferential burns → compartment syndrome → escharotomy
│
└─► Renal: ATN from hypovolaemia or myoglobinuria
ABA Burn Center Referral Criteria (Memorise)
-
10% TBSA partial- or full-thickness burns
- Burns involving face, hands, feet, genitalia, perineum, or major joints
- Any full-thickness burn
- Electrical burns (including lightning)
- Chemical burns
- Inhalation injury
- Burns in patients with pre-existing medical conditions
- Burns + concomitant trauma
- Burned children without specialist paediatric facilities
- Burns requiring special social/emotional/rehabilitative intervention
Sources:
- Bailey and Love's Short Practice of Surgery, 28th Ed., Ch. 46 (Burns)
- Schwartz's Principles of Surgery, 11th Ed., Ch. 8 (Burns)
- Mulholland & Greenfield's Surgery, 7th Ed., Ch. 12 (Burns)
- Sabiston Textbook of Surgery (Burns, Paediatric Burns)