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July/August 2010
Clinical Pharmacist
CLINICAL FOCUS
There are many causes of burns. Patients with complex
burns should be referred to a specialist burns unit
Nils Oskar Johansen | Dreamstime.com
Burns
clinical features
and prognosis
By Nicola Rudall, MSc, MRPharmS, and
Andy Green, DipClinPharm, MRPharmS
E
ach year, around 175,000 cases of burns, of varying
severity and cause, present for treatment at UK
accident and emergency departments.1 Severe burns
can be fatal, with 378 deaths from exposure to smoke, fire
or contact with heat or hot substances reported in England
and Wales in 2008.2 Patients who survive are likely to stay
in hospital for lengthy periods.
Types of burn
There are several causes of burns, ranging from direct heat
(including flames and hot liquids) to chemical or electrical
injury.3 Presentations differ depending on the cause, and
severity is dependent on both contact time and the
temperature to which the skin has been exposed.
Flame burns account for approximately 50% of adult
cases, whereas in children scalding predominates,
accounting for 70% of injuries.4 Flame burns can be
associated with other injuries, including airway trauma.
Electrical burns may present with an entry and exit point
where the current has passed through the body. Internal
damage, following the path of electricity, can occur along
with the external burns. Cardiac involvement, particularly
arrhythmias, may be present; damage is voltage-dependent.
Chemical burns can be caused either by household
products or, more usually, by an industrial accident; wet
cement is a common cause. With the exception of
hydrofluoric acid, alkaline substances generally cause
more damage than acids, although pain is often minimal in
the initial stages. Alkali damage is due to saponification of
fat, creating further heat and damage.
Other causes of burns or burn-like injuries include
direct contact thermal burns (from radiators, motorbike
❝
SEVERE BURNS CAN
BE FATAL, WITH 378
DEATHS FROM
EXPOSURE TO
SMOKE, FIRE OR
CONTACT WITH HEAT
OR HOT SUBSTANCES
REPORTED IN
ENGLAND AND
WALES IN 2008
❞
exhausts, etc) friction burns and prolonged exposure to
ultraviolet radiation (eg, sunburn).
Clinical features
Burn injuries can be divided into primary and secondary
injuries, with the former being the immediate damage
caused by the burn and the latter the morbidity resulting
from the initial injury.5
Large burns present with local as well as systemic
symptoms.4–6 Locally, there may be redness, blistering,
swelling and pain or altered sensation. Systemic effects
such as hypovolaemic shock, hypothermia, deranged blood
test results and metabolic changes may occur as discussed
below. Compartment syndrome (see below) can be a
problem depending on the burn site.
Hypovolaemic shock may be seen in patients with
burns greater than 25% of body surface area (BSA) and is
caused by increased vascular permeability that continues
for at least the first 36 hours following the burn. Proteins,
including albumin, leak out into the interstitial space
pulling fluid with them leading to oedema and
dehydration. Additionally, the body loses fluid via the burn
area, which compounds dehydration. To compensate, the
peripheral and splanchnic vessels vasoconstrict and this
can lead to hypoperfusion. In the initial phase, cardiac
output also decreases because of reduced myocardial
contractility, increased afterload and reduced plasma
volume. Tumour necrosis factor-α, released as part of the
inflammatory response, appears to play a role in the
SUMMARY
Burns are sustained by approximately 175,000 people in the UK each
year and vary widely in severity and cause.
The presentation depends of the cause of the burn (eg, from heat,
chemicals, electricity or other miscellaneous causes such as friction) and
the severity of the burn (which depends on percentage of body surface
area burnt and thickness of the burn). Sequelae of large burns include
hypovolaemic shock, hypothermia, deranged blood test results, metabolic
abnormalities and compartment syndrome.
245
Nicola Rudall is senior lead clinical pharmacist for
perioperative and critical care and Andy Green is
senior lead clinical pharmacist for surgical services,
both at Newcastle upon Tyne Hospitals NHS
Foundation Trust.
E: nicola.rudall@nuth.nhs.uk
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reduction of myocardial contractility. Early fluid
resuscitation is essential to minimise the effects of shock.
Initially, core body temperature is substantially
reduced with large burns. This is a result of heat loss from
the burn (caused by high skin temperatures around the
area of the burn leading to evaporation of fluids) and
hypovolaemic shock. Because of this, patients should be
kept in a warm, humid room.
Blood test results are often deranged, with high
potassium (caused by damage to cells), low calcium
(caused by hypoalbuminaemia), and abnormal clotting
(resulting from disseminated intravascular coagulopathy).
About 48 hours after the burn injury, a patient with
large burns will become hypermetabolic (the metabolic
rate can increase up to threefold). The patient’s cardiac
output, and therefore organ perfusion, will increase. The
baseline temperature will increase to 38.5C as part of the
systemic inflammatory response associated with burns.6
Compartment syndrome is characterised by muscle
and tissue damage and reduced blood flow, caused by the
compression of nerves and blood vessels in an enclosed
space (eg, as a result of swelling). For patients with burns,
compartment syndrome, particularly in the abdomen,
can lead to renal impairment, gut ischaemia and cardiac
and pulmonary complications. In the extremities,
compartment syndrome can cause pain, reduced capillary
refill and paraesthesia.
The patient’s immune response is reduced because of
receptor downregulation, increasing the risk of infection
(which may already be high due to damage to the body’s
natural shield, the skin).
Inhalational injuries may accompany flame burns,
creating problems such as bronchoconstriction or adult
respiratory distress syndrome. Patients with inhalational
injuries may present with wheezing, hoarseness, increased
respiratory secretions, tachypnoea, stridor and
hypoxaemia. Carboxyhaemoglobin should be checked to
assess the degree of carbon monoxide exposure and
patients should receive 100% oxygen. Airway tissues may
become inflamed leading to obstruction, so a secure
airway is vital.
Full-thickness burn
Epidermis
Dermis
Subcutaneous
tissue
Nucleus Medical Art, Visuals Unlimited | SPL
CLINICAL FOCUS
246
Muscle
Figure 1: Illustration of a full-thickness burn
endings growing back into healing tissue can cause altered
sensations and neuropathic pain. It is estimated that 52%
of burn survivors suffer from long-term or chronic pain.7
Assessment
There are two common methods used to assess the extent
of a patient’s burns: Wallace’s “rule of nines” and the Lund
and Browder chart (see Figure 2).1,3,5 The rule of nines
splits the body into 12 sections: 11 of the areas are each
allocated 9% and the groin region is given 1%. The
percentage of the BSA that has been burnt can then be
estimated. The Lund and Browder chart is the more
accurate of the two methods because it takes into account
the change in body proportion relating to age (eg, children
have relatively larger heads than adults). Erythematous
regions should not be included in BSA estimations.5
Burn depths can be classified by degree. They can also
be described as superficial, partial thickness or full
Figure 2: Lund and Browder chart
Percentage of total body surface area burnt
PERCENTAGE
Pain Burn-associated pain comes from a variety of
Region
sources including the burn itself, surrounding tissue,
dressing changes and donor graft sites. Following a burn,
the inflammatory response leads to the release of
mediators, such as bradykinin and histamine, which
trigger pain signals.7 A full-thickness burn (Figure 1) may
damage the nerve to the extent where the pain signal
cannot be felt. However, the surrounding tissue may not
have been burnt to the same depth, meaning that pain is
still present. Primary hyperalgesia is the heightened
response to pain at the burn site. Secondary hyperalgesia
develops minutes later and is caused by nerve
transmission from the surrounding undamaged skin.
Hyperalgesia may last for days. Pain alters during the
treatment period but tends to be worst at donor sites or
areas of upper- or mid-dermal skin loss.
Once the burn site is covered with either a graft or
appropriate dressing the pain usually reduces. Donor site
pain may persist for 10–14 days after harvesting. Five to
six weeks post-burn, nerve regeneration occurs, and nerve
Head
PT
FT
Neck
Anterior trunk
Posterior trunk
Right arm
Left arm
Buttocks
Genitalia
Right leg
Left leg
PT = partial thickness FT = full thickness
Relative percentage of areas dependent on growth
Age (years)
0
1
5
10
15
Adult
A = 1/2 of head
9 1/2
8 1/2
6 1/2
5 1/2
4 1/2
3 1/2
B = 1/2 of one thigh
2 3/4
3 1/4
4
4 1/4
4 1/2
4 3/4
C = 1/2 of one lower leg
2 1/2
2 1/2
2 3/4
3
3 1/4
3 1/2
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Box 1: Burn damage according to depth1,3,5
DEPTH
DEGREE
EXTENT OF DAMAGE
APPEARANCE
HEALING TIME
Superficial
First
Epidermis
Pink, moist,
bleeding,
painful
Pink, blistering,
moist, bleeding,
painful
Patchy red and
white, dry, no
bleeding,
reduced
sensation
White/black,
dry and
leathery, no
bleeding, lack
of sensation
Days
Partial thickness: Second
superficial
Epidermis to
papillary dermis
Partial thickness: Second
deep dermal
Epidermis to
reticular dermis
Full thickness
Third
Whole thickness
of skin
Fourth
Skin plus
tendons, tissue,
muscle and bone
Figure 3: Jackson’s burn model
Zone of
hyperaemia
Zone of stasis
Epidermis
One to two
weeks
Zone of
coagulation
Dermis
> Four weeks
Subcutaneous
tissue
> Four weeks
disadvantage of LDI is that it is expensive and requires a
high level of expertise to interpret the results (so is not
routinely available in many centres that treat burns).
Admission criteria
thickness (see Box 1).1,3,5 First-degree burns are classed as
superficial. Second-degree, partial-thickness burns are
subdivided into superficial and deep dermal. Thirddegree burns are full-thickness. Fourth-degree burns, also
full-thickness, can occur and these affect the tendons,
subcutaneous tissue or bones as well as the skin. It is
possible for there to be a mixture of burn depths in one
patient, although reassessment should be made in the first
few days after the burn since depth may increase
depending on the treatment received.
Patients with first-degree or second-degree superficial
burns usually respond well to treatment and heal within
two weeks; these types of burns are typically pink or red,
painful and have a good blood supply. Patients with deep
dermal or full-thickness burns can take months to recover
and have significant scarring without surgical treatment
and skin grafting. These types of burns tend to have a poor
blood supply so will appear less red.
Jackson’s burn model splits the burn into three distinct
zones: the zone of coagulation, the zone of stasis and the
zone of hyperaemia (see Figure 3).4,5 The zone of
coagulation is at the centre of the burn and is an area of
severe damage resulting in irreversible tissue loss.
Although the zone of stasis contains less damaged tissue,
perfusion is affected and the correct treatment must be
provided to prevent progression to necrosis and allow full
recovery. The zone of hyperaemia contains tissue that is
well perfused and this usually recovers well.
Assessment techniques
In the first few days after injury it is often difficult to
determine the depth of a burn and, thus, the prognosis and
need for surgery to aid recovery. Various methods have
been employed to supplement visual inspection of the
burn.1,8,9 Techniques that assess tissue perfusion in the
injured area give a more objective assessment of prognosis.
Increasingly, a technique called laser Doppler imaging
(LDI) is being used and appears to give the most accurate
measurement of burn depth among the available
techniques. Depth is assessed by taking a thermal image of
the burn area which correlates with skin blood flow. The
To ensure that treatment is appropriate, the British Burn
Association has published criteria for complex burn injury.
(see Box 2).1 Patients meeting these criteria should be
referred to a specialist unit within six hours of injury since
swift assessment and treatment of burns is crucial to
optimise patient outcomes. The very young and the
elderly are particularly at risk of complex burn injuries.
References
1
Enoch S, Roshan A, Shah M. Emergency and early management of burns
and scalds. BMJ 2009;338:937–41.
2
Mortality Statistics: Deaths registered in 2008. Office of National
Statistics.www.statistics.gov.uk/downloads/theme_health/DR2008/
DR_08.pdf (accessed 18 June 2010).
3
Benson A, Dickson WA, Boyce DE. ABC of wound healing: Burns. BMJ
2006;332:649–52.
4
Hettiaratchy S, Dziewulski P. ABC of burns: Pathophysiology and types of
burns. BMJ 2004;328:1427–9.
5
Duncan RT, Dunn KW. Immediate management of burns. Surgery
2006;24:9–14.
6
Latenser BA. Critical care of the burn patient: The first 48 hours. Critical
Care Medicine 2009;37:2819–26.
7
Richardson P, Mustard L. The management of pain in the burns unit.
Burns 2009;35:921–36.
8
Shelley OP, Dziewulski P. Late management of burns. Surgery
2006;24:15–7.
9
Orgill DP. Excision and skin grafting of thermal burns. New England
Journal of Medicine 2009;360:893.
Box 2: Specialist burns unit admission criteria
All patients with complex burns should be referred to a specialist burns unit.
A burn injury is more likely to be complex if associated with the following:
● Inhalational injury
● Deep burn
● High tension electrical
●
●
●
●
●
Circumferential burns
High pressure steam burn
Chemical burn >5% BSA
burn
Suspicion of non-accidental burn
● Hydrofluoric acid burn
Dermal or full-thickness burns >10%
>1% BSA
of BSA (>5% if over 16 years old)
● Existing medical conditions ● Dermal or full-thickness burns to
(eg, pregnancy, cirrhosis or
face, hands, perineum, feet or
immunosuppression)
flexures
● Other injury or major
● Age under five or over 60 years old
trauma (eg, crush injuries) ● Exposure to ionising radiation
BSA = body surface area