Burns and smoke inhalation

Scalding (children), flame (adults), electrical, chemical, sun.

Classified by
% of total body surface area (TBSA) burnt
Depth of tissue injury
Whether accompanied by smoke inhalation
Location of damage
Associated injuries and co-morbidity

Depth of burn
Tissue damage
Superficial (First degree)
Superficial partial thickness (Second degree)
Superficial dermal
Deep partial thickness (Second degree)
Deep dermal
Full thickness (Third degree)
Complete dermal destruction
Fourth degreeInvolvement of underlying soft tissue


Local response
Dead tissue caused by heat damage
A zone of surrounding ischaemia which is viable but at risk
A zone of inflammatory tissue not directly injured but which drives the systemic response

Systemic response
Cytokines (esp IL 6 and 8) released activating the acute phase response resulting in loss of intravascular fluid, protein catabolism, hypoalbuminaemia (loss from vessels and formation of acute phase proteins)
Hypovolaemia and oedema reduce DO2 to vulnerable injured areas
In the 1
st 24h there is SVR and myocardial depression (burn shock)
This is followed by a SIRS response with
SVR and CO
Hypercatabolism much greater than other forms of trauma. Muscle breakdown, hyperglycaemia, lipolysis and
osteoclast activity causing osteopenia ( # susceptibility)


Features of inhalational injury (heat or toxic products of incomplete combustion)
Enclosed space
CNS altered
Steam burn
Facial burns
Naso/Oropharyngeal burn
Stridor, wheeze, dysphonia
Indications for intubation
Full thickness burns to lips/nose/neck
Facial burns with
Oropharyngeal oedema
O2, CO2
CO >20%
O2, CO2
  • Carbonaceous deposits below glottis
  • Airway oedema
  • Bronchial erythema, haemorrhage, ulceration
  • Small airway casts

Carbon Monoxide
>20% indicate a significant inhalational injury and >60% is life threatening.
Symptoms include nausea and vomiting, headache, hyperventilation, hypotension, increased muscle tone and coma.
100% oxygen reduces the half-life of HbCO from 240 min to 60 min.
Hyperbaric O2 at 300 kPa
T1/2 23 min and should be considered in pregnant or comatose patients, those with initial HbCO levels >40%, or failure to respond to conventional therapy.

Older furnishings can release cyanide.
Suspect if severe unexplained acidosis (

Sux safe in 1st 24h. After that will cause ↑↑K+.
Leave ETT long or uncut to allow for facial swelling.

Fluid resus based on total body surface area (TBSA) of burn
Quick assessment made by rule of 9s until can be more accurate with Lund and Browder chart.


Capillary permeability changes with time predictable allowing calculations for 1st 24h.
Guide only – adjust to response.
Most common formula used in UK is the Parkland formula (4 ml/kg/% burn of Hartmann’s solution, half given in the first 8 hours and the rest in the following 16 hours).
Also need additional 2ml/kg water.
>20% burns often need blood transfusion.

Pain from damaged nociceptors and chemical release from damaged cells
Hyperalgesia later develops.
Frequent dressing changes and trips to theatre.
Simple + opiates (beware SEs NSAIDs).
PCA if hands OK.
Can use short acting opioids or N2O for dressing changes.
Regional anaesthesia of no proven benefit.
Often later develop chronic pain.

Wound management
Removal of dead tissue to reduce inflammatory response and covering with temporary dressings or skin grafts.
Escharotomies if circumferential burns to limbs, neck or thorax.
Burns usually dressed with silver sulfadiazine cream.

Loss of cutaneous barrier.
Multiple invasive and surgical procedures.
Difficult to distinguish SIRS from infection.
No role for prophylactic ABX.

Enteral best
Establish ASAP