Elicit document and present history in a case of Burns and perform physical examination. Describe Pathophysiology of Burns.

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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

QuestionClinical 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

DegreeLayer InvolvedAppearanceSensationBlisteringHealing
Superficial (1st degree)Epidermis onlyErythema, dry, no blistersPainfulNone3–5 days, no scarring
Superficial partial-thickness (2nd degree)Epidermis + superficial papillary dermisMoist, erythematous, blistered, blanchesVery painfulPresent, clear fluid10–14 days, minimal scarring
Deep partial-thickness (2nd degree)Epidermis + reticular dermisMottled red/white, less wet, may not blanchReduced sensationMay be present>21 days, scarring likely; may need grafting
Full-thickness (3rd degree)All skin layersLeathery, white/brown/black eschar, dryPainless (nerve destruction)NoneCannot self-heal; requires grafting
4th degreeSkin + underlying fascia/muscle/boneCharred, necroticNoneNoneMajor reconstruction
Superficial burns (1st degree) are not included in TBSA calculations.
Burn depth classification: (a) 1st degree erythema, (b) superficial partial-thickness with clear blisters, (c) deep partial-thickness with mottled appearance, (d) full-thickness black eschar, (e) 4th degree with exposed muscle
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 & neck9%
Each arm9%
Anterior trunk18%
Posterior trunk18%
Each leg18%
Perineum1%
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

InvestigationPurpose
ABG + carboxyhaemoglobinInhalation injury, CO poisoning (SpO₂ misleading)
FBC, U&E, creatinineBaseline, rhabdomyolysis (electrical burns)
Blood glucose, coagulationBaseline
CK, myoglobinElectrical burns → rhabdomyolysis
Urine myoglobinElectrical burns
ECGElectrical burns → arrhythmia
CXRInhalation injury, baseline
LactateCyanide 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:
ZoneDescriptionClinical Implication
Zone of Coagulation (central)Maximal thermal damage; irreversible cell necrosis; protein coagulationFull-thickness destruction; cannot be salvaged
Zone of Stasis (middle)Decreased perfusion; cells viable but at risk; capillary endothelial damage with microvascular sludgingTarget of resuscitation — can be saved or lost depending on management
Zone of Hyperaemia (peripheral)Increased blood flow, minimal cell injury, inflammatory vasodilationHeals 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:
  1. Increased vascular permeability → loss of plasma proteins + fluid into interstitium
  2. Intravascular volume depletion → decreased cardiac preload → decreased cardiac output
  3. Hypotension → compensatory vasoconstriction → increased afterload → further ↓ cardiac output
  4. A myocardial depressant factor (MDF) released early post-burn directly impairs myocardial contractility — cardiac output may fall to 30% of baseline within 30 minutes
  5. 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:
MechanismInjuryCause
Upper airway injurySupraglottic oedema, laryngeal oedemaDirect thermal injury from hot gases
Lower airway injuryChemical tracheobronchitis, loss of respiratory epithelium, bronchospasmInhaled smoke particles → chemical pneumonitis
Metabolic poisoningTissue hypoxiaCarbon 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)

  1. 10% TBSA partial- or full-thickness burns
  2. Burns involving face, hands, feet, genitalia, perineum, or major joints
  3. Any full-thickness burn
  4. Electrical burns (including lightning)
  5. Chemical burns
  6. Inhalation injury
  7. Burns in patients with pre-existing medical conditions
  8. Burns + concomitant trauma
  9. Burned children without specialist paediatric facilities
  10. 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)
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