Burns in the ICU

Contents

Overview

Severe burns represent one of the most physiologically demanding injuries managed in critical care. Burns causing more than 20% total body surface area (TBSA) injury, or any burn with inhalation injury, require ICU admission. Management involves coordinated burn-specific care, critical care support, and close collaboration with burn surgery teams. Major burn centres provide the optimal environment for complex burn injuries.

Assessment

Burn Size

Rule of Nines (adults):

Region % TBSA
Head and neck 9%
Each arm 9%
Anterior trunk 18%
Posterior trunk 18%
Each leg 18%
Perineum 1%

The Lund-Browder chart is preferred in children, as the head is proportionately larger and the legs smaller relative to adults.

Superficial burns (erythema only, no blistering) are excluded from TBSA calculations. The patient's palmar surface (including fingers) represents approximately 1% TBSA and can be used to estimate irregular burns.

Burn Depth

  • Superficial: Erythema, intact blisters, painful; heals in 5–10 days without scarring
  • Superficial partial-thickness: Blisters, moist, very painful; heals in 14–21 days, may scar
  • Deep partial-thickness: Pale or mottled, reduced pain sensation, slow to heal, high scarring risk; often requires grafting
  • Full-thickness: Leathery, insensate, avascular; requires surgical excision and grafting

Burn Centre Referral Criteria (British Burn Association)

  • 10% TBSA in children, >15% in adults

  • Full-thickness burns >5% TBSA
  • Burns involving face, hands, genitalia, feet, or major joints
  • Inhalation injury
  • Circumferential burns
  • Chemical or electrical burns
  • Burns with significant comorbidities or extremes of age
  • Suspected non-accidental injury

Airway Assessment

Inhalation injury must be actively sought:

  • Facial burns, singed nasal hair, eyebrows, or eyelashes
  • Carbonaceous (soot-stained) sputum
  • Hoarse voice, stridor, or progressive oropharyngeal oedema
  • History of exposure in an enclosed space

Early intubation is essential — delay allows airway oedema to develop to the point where intubation becomes impossible and surgical airway is required. If in doubt, intubate.

Pathophysiology

Burn Shock

Major burns trigger a massive inflammatory response within minutes. Cytokine release (TNF-α, interleukins) causes systemic endothelial activation and capillary leak. In the first 24–48 hours, extensive fluid shifts from the intravascular to interstitial compartment occur, both locally at the burn wound and systemically. Hypovolaemia from capillary leak combines with a distributive component to produce burn shock, reaching its nadir at 12–24 hours.

Hypermetabolism

After the initial shock phase, burns produce a sustained hypermetabolic state lasting weeks to months. Metabolic rate may double above baseline. Features include:

  • Increased oxygen consumption and CO2 production
  • Elevated catecholamine and cortisol levels
  • Muscle protein catabolism
  • Impaired insulin sensitivity and hyperglycaemia

This hypermetabolic state is the primary driver of the high nutritional requirements in burn patients and contributes to ICU-acquired weakness.

Immunosuppression

The combination of disrupted skin barrier, systemic inflammation, and hypermetabolism profoundly impairs immune function. Wound colonisation and systemic infection are the leading cause of death in burns patients after the initial resuscitation phase. MRSA, Pseudomonas aeruginosa, and Candida species are particularly common pathogens.

Fluid Resuscitation

Parkland Formula

The most widely used formula for guiding burn fluid resuscitation:

4 mL × weight (kg) × %TBSA burned over the first 24 hours using Hartmann's solution.

  • Half given in the first 8 hours from the time of burn (not from time of presentation)
  • Half given over the remaining 16 hours

Example: A 70 kg patient with 40% TBSA burns requires 4 × 70 × 40 = 11,200 mL over 24 hours. Half (5,600 mL) is given in the first 8 hours from the time of burn.

Modified Approaches

The Parkland formula is a starting point, not a prescription. Ongoing resuscitation is guided by:

  • Urine output: target 0.5–1.0 mL/kg/hour in adults; 1.0 mL/kg/hour in children
  • Clinical signs of adequate perfusion
  • Lactate trends

Colloid (albumin 5%) may be introduced after the first 12–24 hours once the capillary leak phase begins to resolve, to reduce the volume of crystalloid required and limit tissue oedema.

Risks of Over-Resuscitation

Excessive fluid administration — particularly in the first 24–48 hours — causes:

  • Pulmonary oedema and abdominal compartment syndrome
  • Worsening burn wound oedema and conversion of partial-thickness to full-thickness injury
  • Compartment syndrome in limbs and abdomen

The concept of 'fluid creep' — systematic over-resuscitation relative to the Parkland formula — is well recognised and associated with worse outcomes. Resuscitation volumes should be frequently reassessed and adjusted downward if urine output targets are met at lower volumes.

Inhalation Injury

Inhalation injury encompasses three distinct components:

Upper airway thermal injury: Heat damages the supraglottic airway, causing oedema that may be progressive over 12–24 hours. Steam causes deeper injury than dry heat. The lower airway is generally protected by the efficient heat exchange of the nasopharynx — thermal injury to the trachea and bronchi is rare except with steam inhalation.

Lower airway chemical injury: Toxic combustion products — acrolein, hydrochloric acid, carbon particles — cause bronchospasm, bronchorrhoea, and mucosal ulceration. Ciliary dysfunction impairs secretion clearance, increasing the risk of ventilator-associated pneumonia (VAP), which is the most common infectious complication in mechanically ventilated burns patients.

Systemic CO and cyanide toxicity: Carbon monoxide toxicity is managed as per standard CO poisoning protocols. Hydrogen cyanide is produced by combustion of synthetic materials and nitrogen-containing compounds; it causes cellular hypoxia by inhibiting cytochrome oxidase. Hydroxocobalamin 5 g IV is given empirically in patients with a high index of suspicion (house fire, persistent metabolic acidosis, clinical features of systemic toxicity disproportionate to COHb).

Ventilation Strategy

Burns patients with inhalation injury have increased bronchospasm and secretions, requiring aggressive suction regimens and nebulised bronchodilators. Prone positioning may be used for ARDS complicating inhalation injury. High-frequency percussive ventilation (HFPV) is used in some burn centres to improve secretion clearance.

Infection and Wound Management

Infection is the most common cause of death after the first 48 hours. The burn wound is not sterile and rapidly becomes colonised. Key organisms include Pseudomonas aeruginosa, Staphylococcus aureus (including MRSA), Acinetobacter species, and Candida.

Wound management:

  • Regular wound debridement and dressing changes under appropriate analgesia and sedation
  • Topical antimicrobials: silver sulfadiazine, cerium nitrate-silver sulfadiazine (Flammacerium), and silver-containing dressings reduce bacterial load
  • Early surgical excision and skin grafting of deep partial-thickness and full-thickness burns within 24–72 hours reduces infection risk, systemic inflammation, and length of stay
  • Temporary coverage with biological dressings (allograft, xenograft) or synthetic skin substitutes (e.g., Integra) bridges the period before autografting

Antibiotic use: Prophylactic antibiotics are not recommended. Targeted treatment based on wound and blood cultures guides antibiotic selection. Broad empirical therapy is appropriate for suspected sepsis, with de-escalation on microbiological results.

Nutritional Support

Burns cause the most extreme nutritional requirements of any ICU condition. Early and aggressive enteral nutrition is essential.

Energy requirements: Calculated using the Toronto formula or Curreri formula in major burns. Target 25–35 kcal/kg/day as a starting point, adjusted by indirect calorimetry in specialist centres.

Protein requirements: 1.5–2.5 g/kg/day — substantially higher than standard ICU recommendations. Muscle catabolism from hypermetabolism must be offset by high protein intake.

Route: Enteral feeding via nasogastric or nasojejunal tube should begin within 6 hours of admission. Parenteral nutrition is a last resort — it is associated with worse infection outcomes in burns.

Anabolic agents: Oxandrolone (anabolic steroid) has been shown to reduce muscle catabolism in major burns. Propranolol reduces hypermetabolic response by blocking catecholamine-driven protein catabolism.

Viva Questions

How do you calculate fluid resuscitation requirements for a 70 kg adult with 40% TBSA burns?

Using the Parkland formula: 4 mL × weight (kg) × %TBSA = 4 × 70 × 40 = 11,200 mL over the first 24 hours, using Hartmann's solution. Half of this volume — 5,600 mL — is given in the first 8 hours from the time of the burn (not from the time of arrival). The remaining 5,600 mL is administered over the following 16 hours. It is essential to calculate from the time of the burn injury, not the time of arrival, as the first phase of resuscitation may have been partially completed before the patient reaches hospital. The Parkland formula is a guide; actual infusion rates should be adjusted continuously against a target urine output of 0.5–1.0 mL/kg/hour. Over-resuscitation causing pulmonary oedema or abdominal compartment syndrome is a recognised complication of formulaic fluid administration without clinical titration.

What are the indications for early intubation in a burn patient and why is it important to act promptly?

Early intubation is indicated in any burn patient with evidence of inhalation injury or impending airway compromise. Specific indications include facial and oropharyngeal burns, singed nasal hair, a hoarse voice, stridor, carbonaceous sputum, respiratory distress, or a history of enclosed-space exposure. The urgency of early intubation relates to the progressive nature of airway oedema: thermal injury to the supraglottis causes oedema that may be mild at initial presentation but progresses substantially over the first 6–12 hours. If intubation is deferred, the anatomy becomes increasingly distorted, the cords become difficult to visualise, and what was a straightforward intubation at hour one becomes a surgical airway at hour eight. Once the airway is lost, bag-mask ventilation may be impossible. A difficult airway approach — awake fibreoptic technique or videolaryngoscopy — should be considered when facial burns or oropharyngeal oedema are present. The threshold for intubation should therefore be low when clinical signs suggest impending compromise.

What is the most common cause of death after the first 48 hours in burn patients and how do you reduce the risk?

After the initial resuscitation phase, infection is the most common cause of death in major burns. The combination of a disrupted skin barrier (the primary physical defence against pathogens), systemic immunosuppression from the burn injury itself, the presence of devitalised wound tissue that is an ideal culture medium, and the prolonged ICU admission creates extreme susceptibility to infection. Wound colonisation is inevitable; the challenge is to prevent invasive wound sepsis and systemic infection. The key strategies are early surgical excision and skin grafting of deep burns — preferably within 24–72 hours — to remove the devitalised tissue before it becomes a source of systemic sepsis; appropriate topical antimicrobial wound dressings; a strict hand hygiene and infection control programme; and avoidance of prophylactic systemic antibiotics (which select for resistant organisms). Inhalation injury markedly increases VAP risk, so an aggressive ventilator care bundle and regular chest physiotherapy are important. Nutritional support is also protective — malnourished burn patients have higher infection rates and worse wound healing.