Burns Flashcards
(47 cards)
Define a burn
A coagulative destruction of the skin and its structures
What are the main mechanisms of a burn?
Thermal (note, scalding confers greater thermal energy than dry heat)
Electrical
Chemical
Mechanical
At what total body surface area (TBSA) is a burn considered “Major”?
15%
At what total body surface area (TBSA) is a burn likely to produce a SIRS response
25%
What are the main determinants of survival in burns?
%TBSA
Age
Inhalation injury
These are packaged into the modified Baux score
What is the name given to the pathological model of burns. Please describe it.
Jackson’s burn wound model. Describes 3 zones: 1) zone of coagulation, 2) Zone of stasis, 3) zone of hyperaemia and vasodilatation
How are burns classified?
Epidermal (no involvement of the dermis, red and painful, self limiting)
Superficial partial thickness (upper dermis)
Deep partial thickness (lower dermis)
Full thickness (extends through the dermis into underlying tissue)
Note: this is the UK model of description.
What is the modified Baux Score
Age + %TBSA + (17 x inhalation injury)
What is the current limit of survivability of the Baux score
160
List some burns prognostication scores other than the Baux score
Belgian outcome in burn injury score
Abbreviated burn severity index
Rockwood clinical frailty score (this last one isn’t burns specific, but may be helpful in contextualising the prognostication of burns patients)
Describe the appearance and sensation of a superficial partial thickness burn
Pale, pink and moist
Blisters form with fluid leak from blood vessel damage
They are very painful because of exposed nerve endings
Describe the appearance and sensation of a deep partial thickness burn
Drier than a superficial partial thickness burn. Tend to be red and non-blanching as the dermal plexus is coagulated by the heat
Less painful than superficial partial thickness
Describe the appearance and sensation of a
full thickness burn
Waxy and white
Not painful
Describe the main features of the “Zone of coagulation” in the Jackson burn model
Irreversibly dead tissue that acts as a nidus of infection and a reservoir of inflammatory products that can lead to systemic injury
Describe the main features of the “Zone of stasis” in the Jackson burn model
Hypoperfused, vasocontricted, alive but at risk tissue in proximity to the zone of coagulation. This tissue is at high risk of ischaemia, infection and necrosis. For this reason, burns may widen and deepen if this zone dies
Describe the main features of the “Zone of hyperaemia” in the Jackson burn model
Inflammatory mediators released from the zone of coagulation cause local vasodilatation, increased vascular permeability and oedema within this zone. When %TBSA exceeds 25%, the whole body effectively becomes the zone of hyperaemia and a profound SIRS response occurs
What is a key early surgical priority in the management of burns?
Early burn excision is aimed at reducing the nectrotic tissue load, infection risk and SIRS response. It is associated with improve survival
Burns is often described in two phases. What are these phases, and over what time frame do they occur?
The Acute Phase: occurs over the first 48 hours following burn during which vasodilatation, hypovolaemia and myocardial depression contribute to burns shock.
The Hypermetabolic Phase: occurs from 48 hours to around 1 year
If a burns patient is hypotensive at presentation to hospital, what is the most likely cause
It is almost certainly not from the burn itself; burns shock takes some time to manifest. If there are no overt other injuries, consider inhalation injury (carbon monoxide/Hydrogen Cyanide poisoning). Otherwise look for other trauma related injuries on the secondary survey and consider blood loss.
Which poisons should one always consider in tandem with Burns?
Carbon monoxide
Hydrogen cyanide
One might also argue that you could consider recreational drugs or paracetamol if there is a suspicion that a depressed conscious level led to the injury
At what level of COHb should you be concerned?
At 10% COHb patients are symptomatic
At 50% COHb patients generally enter coma
Levels over 30% are unambiguously considered “severe”
What is the mechanism of action of carbon monoxide toxicity?
There are three mechanisms:
1) CO binds to Hb with x250 greater affinity than O2, blocking the binding of O2
2) CO causes a left shift of the OHDC inhibiting oxygen delivery at the tissues
3) CO causes competitive inhibition of michondrial cytochrome oxidase, inhibiting cellular utilisation of oxygen
What are the indicators of severe CO poisoning?
New objective neurological signs (increased muscle tone, up-going planters)
Coma
ECG indications of ischaemia
Clinically significant acidosis
Initial COHb > 30%
What is the half life of COHb at an FiO2 of 0.21?
6 hours