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) | Epidermal |
| Superficial partial thickness (Second degree) | Superficial dermal |
| Deep partial thickness (Second degree) | Deep dermal |
| Full thickness (Third degree) | Complete dermal destruction |
| Fourth degree | Involvement of underlying soft tissue |
Pathophysiology
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 1st 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)
Management
A+B
Features of inhalational injury (heat or toxic products of incomplete combustion)
History
Enclosed space
CNS altered
Steam burn
Signs
Facial burns
Naso/Oropharyngeal burn
Stridor, wheeze, dysphonia
Indications for intubation
Full thickness burns to lips/nose/neck
Facial burns with ↓GCS
Oropharyngeal oedema
Stridor
↓O2, ↑CO2
Investigations
CO >20%
↓O2, ↑CO2
Bronchoscopy
- 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.
Cyanide
Older furnishings can release cyanide.
Suspect if severe unexplained acidosis (↑ lactate).
Other
Sux safe in 1st 24h. After that will cause ↑↑K+.
Leave ETT long or uncut to allow for facial swelling.
C
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.
pastedGraphic
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.
Analgesia.
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.
Infection
↑ susceptibility.
Immunosuppression.
Loss of cutaneous barrier.
Multiple invasive and surgical procedures.
Difficult to distinguish SIRS from infection.
No role for prophylactic ABX.
Nutrition
Important
Enteral best
Establish ASAP