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Burns: History, Physical Examination & Pathophysiology

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PART I — HISTORY IN A CASE OF BURNS

1. Presenting Complaint

• Burn wound with pain, blistering, or skin loss
• Associated symptoms: shortness of breath, hoarseness, altered consciousness

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2. History of the Burn Injury (AMPLE + Burn-Specific)

A. Circumstances of the Injury

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

• 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

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PART II — PHYSICAL EXAMINATION IN BURNS

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

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SECONDARY SURVEY — Burn Assessment

1. Burn Depth Classification

Superficial burns (1st degree) are not included in TBSA calculations.

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2. Burn Size — Total Body Surface Area (TBSA)

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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)

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4. Special Sites

• 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

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5. Associated Injuries

• Examine for fractures (especially in explosions, falls)
• Check for blast injuries, lacerations

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INVESTIGATIONS ORDERED AFTER EXAMINATION

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PART III — PATHOPHYSIOLOGY OF BURNS

1. Local Injury — Jackson's Zones of Burn Injury

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2. Local Inflammatory Response

• 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

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3. Systemic Effects — Burn Shock

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

• 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

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4. Inhalation Injury

• 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)

• 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

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5. Metabolic Response — Hypermetabolism

• 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

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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

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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

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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

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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

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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

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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

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• 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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ACE Inhibitors in Hypertension: Rationale for Use

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1. Background: Why Target the RAAS?

• Systemic vasoconstriction via angiotensin II (Ang II)
• Sodium and water retention via aldosterone
• Cardiac and vascular remodelling (hypertrophy, fibrosis)
• Glomerular hypertension and proteinuria
• Endothelial dysfunction

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2. The RAAS Cascade and Site of ACE Inhibitor Action

Angiotensinogen (α₂-globulin)
        ↓  [Renin — released by juxtaglomerular cells in response to ↓BP, ↓Na⁺, ↑SNS]
Angiotensin I (inactive decapeptide)
        ↓  [ACE — enzyme in lung endothelium] ← ACE INHIBITORS BLOCK HERE
Angiotensin II (potent vasoconstrictor octapeptide)
        ↓
 ├─ AT₁ receptor → Vasoconstriction, ↑aldosterone, ↑SNS activity, cardiac hypertrophy, renal efferent constriction
 └─ Aldosterone → ↑Na⁺ + H₂O retention by kidneys

• Block Ang I → Ang II conversion
• Prevent bradykinin breakdown → bradykinin accumulates → stimulates bradykinin B₂ receptors → release of nitric oxide and prostacyclin (potent vasodilators)

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3. Mechanisms by Which ACE Inhibitors Lower Blood Pressure

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4. Therapeutic Rationale — Why ACE Inhibitors Are Preferred in Hypertension

4.1 Blood Pressure Lowering Efficacy

• All ACE inhibitors are equally effective in reducing blood pressure at equivalent doses
• Achieve sustained BP reduction with chronic treatment
• Relatively flat dose-response curve; efficacy similar to ARBs
• Less effective as monotherapy in Black patients (low-renin hypertension predominates), but efficacy equalises with combination therapy

4.2 Cardiac Benefits

• Regression of left ventricular hypertrophy (LVH): Ang II directly drives cardiac myocyte hypertrophy and fibrosis via AT₁ receptors and TGF-β; ACE inhibitor use causes measurable regression of LVH
• Post-MI ventricular remodelling: ACE inhibitors improve ventricular remodelling after myocardial infarction, reducing dilatation and progression to systolic heart failure; they are a standard of care post-MI
• Heart failure: ACE inhibitors are first-line agents in heart failure with reduced ejection fraction (HFrEF) — reduce morbidity and mortality; improve endothelial dysfunction and vascular remodelling
• Coronary artery disease risk: ACE inhibitors are first-line drugs in hypertensive patients at increased risk of coronary artery disease

4.3 Renal Benefits — A Key Differentiating Rationale

• Ang II preferentially constricts the efferent arteriole of the glomerulus → raises intraglomerular pressure → promotes proteinuria and glomerulosclerosis
• ACE inhibitors cause efferent arteriolar vasodilation → ↓ intraglomerular pressure → ↓ proteinuria → slow progression of CKD
• Diabetic nephropathy: ACE inhibitors slow progression and decrease albuminuria — a compelling, evidence-based indication independent of blood pressure effect
• Indicated in CKD when urine albumin:creatinine ratio >300 mg/g (Goldman-Cecil)

4.4 Metabolic Neutrality

• Unlike thiazide diuretics and beta-blockers, ACE inhibitors do not cause:
  • Hypokalemia
  • Hyperglycaemia / insulin resistance
  • Dyslipidaemia
  • Hyperuricaemia
• They are therefore particularly appropriate in patients with diabetes mellitus and metabolic syndrome

4.5 Endothelial Protection

• Bradykinin accumulation → ↑ NO release → improved endothelial function
• Potential anti-atherosclerotic effects via reduced oxidative stress and inflammation

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5. Compelling Indications for ACE Inhibitors in Hypertension

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6. Pharmacokinetics — Clinically Relevant Points

Common ACE Inhibitors

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7. Adverse Effects — Mechanism and Management

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8. Contraindications

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9. ACE Inhibitors vs Other First-Line Antihypertensive Classes

Note: ACE inhibitors provide equal protection against coronary events, lesser protection against stroke (compared to CCBs), but better protection against heart failure than calcium-channel blockers. - Goldman-Cecil Medicine

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10. Summary: The Rationale in Brief

1. Directly target the RAAS - the core neurohormonal driver of hypertension and its end-organ consequences
2. Lower BP via dual mechanisms - reducing vasoconstriction (↓ Ang II) and enhancing vasodilation (↑ bradykinin → ↑ NO + prostacyclin)
3. Reduce cardiac preload AND afterload - lessening myocardial workload
4. Reverse hypertensive end-organ damage - LVH regression, improved ventricular remodelling, reduced proteinuria
5. Are metabolically neutral - no adverse effects on glucose, lipids, or uric acid
6. Carry special benefits in high-risk populations - diabetes, CKD, post-MI, heart failure, CAD
7. Are well tolerated - with a predictable, manageable side-effect profile

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• Lippincott Illustrated Reviews: Pharmacology, Ch. 8 (Antihypertensives)
• Goldman-Cecil Medicine, Ch. 463 (Hypertension)
• Textbook of Family Medicine, 9th Ed., Ch. 27 (Hypertension Management)
• Brenner and Rector's The Kidney, 2-Vol Set (RAAS Physiology)