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CLINICAL FOCUS Vol 2 July/August 2010 Clinical Pharmacist 245 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 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 There are many causes of burns. Patients with complex burns should be referred to a specialist burns unit Burns clinical features and prognosis 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: [email protected] 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. 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 Nils Oskar Johansen | Dreamstime.com

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Page 1: Burns: Clinical features and prognosis · burns should be referred to a specialist burns unit Burns clinical features and prognosis ... Sequelae of large burns include hypovolaemic

CLINICAL FOCU

SVol 2 July/August 2010 Clinical Pharmacist 245

By Nicola Rudall, MSc, MRPharmS, and Andy Green, DipClinPharm, MRPharmS

Each year, around 175,000 cases of burns, of varyingseverity and cause, present for treatment at UKaccident and emergency departments.1 Severe burns

can be fatal, with 378 deaths from exposure to smoke, fireor contact with heat or hot substances reported in Englandand Wales in 2008.2 Patients who survive are likely to stayin hospital for lengthy periods.

Types of burnThere are several causes of burns, ranging from direct heat(including flames and hot liquids) to chemical or electricalinjury.3 Presentations differ depending on the cause, andseverity is dependent on both contact time and thetemperature to which the skin has been exposed.

Flame burns account for approximately 50% of adultcases, whereas in children scalding predominates,accounting for 70% of injuries.4 Flame burns can beassociated with other injuries, including airway trauma.

Electrical burns may present with an entry and exit pointwhere the current has passed through the body. Internaldamage, following the path of electricity, can occur alongwith the external burns. Cardiac involvement, particularlyarrhythmias, may be present; damage is voltage-dependent.

Chemical burns can be caused either by householdproducts or, more usually, by an industrial accident; wetcement is a common cause. With the exception ofhydrofluoric acid, alkaline substances generally causemore damage than acids, although pain is often minimal inthe initial stages. Alkali damage is due to saponification offat, creating further heat and damage.

Other causes of burns or burn-like injuries includedirect contact thermal burns (from radiators, motorbike

exhausts, etc) friction burns and prolonged exposure toultraviolet radiation (eg, sunburn).

Clinical features Burn injuries can be divided into primary and secondaryinjuries, with the former being the immediate damagecaused by the burn and the latter the morbidity resultingfrom the initial injury.5

Large burns present with local as well as systemicsymptoms.4–6 Locally, there may be redness, blistering,swelling and pain or altered sensation. Systemic effectssuch as hypovolaemic shock, hypothermia, deranged bloodtest results and metabolic changes may occur as discussedbelow. Compartment syndrome (see below) can be aproblem depending on the burn site.

Hypovolaemic shock may be seen in patients withburns greater than 25% of body surface area (BSA) and iscaused by increased vascular permeability that continuesfor at least the first 36 hours following the burn. Proteins,including albumin, leak out into the interstitial spacepulling fluid with them leading to oedema anddehydration. Additionally, the body loses fluid via the burnarea, which compounds dehydration. To compensate, theperipheral and splanchnic vessels vasoconstrict and thiscan lead to hypoperfusion. In the initial phase, cardiacoutput also decreases because of reduced myocardialcontractility, increased afterload and reduced plasmavolume. Tumour necrosis factor-α, released as part of theinflammatory response, appears to play a role in the

There are many causes of burns. Patients with complexburns should be referred to a specialist burns unit

Burnsclinical featuresand prognosis

Nicola Rudall is senior lead clinical pharmacist forperioperative and critical care and Andy Green issenior lead clinical pharmacist for surgical services,both at Newcastle upon Tyne Hospitals NHSFoundation Trust.E: [email protected]

SUMMARYBurns are sustained by approximately 175,000 people in the UK eachyear 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) andthe severity of the burn (which depends on percentage of body surfacearea burnt and thickness of the burn). Sequelae of large burns includehypovolaemic shock, hypothermia, deranged blood test results, metabolicabnormalities and compartment syndrome.

�SEVERE BURNS CANBE FATAL, WITH 378DEATHS FROMEXPOSURE TOSMOKE, FIRE ORCONTACT WITH HEATOR HOT SUBSTANCESREPORTED INENGLAND ANDWALES IN 2008

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246 Clinical Pharmacist July/August 2010 Vol 2

reduction of myocardial contractility. Early fluidresuscitation 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 fromthe burn (caused by high skin temperatures around thearea of the burn leading to evaporation of fluids) andhypovolaemic shock. Because of this, patients should bekept 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 metabolicrate can increase up to threefold). The patient’s cardiacoutput, and therefore organ perfusion, will increase. Thebaseline temperature will increase to 38.5C as part of thesystemic inflammatory response associated with burns.6

Compartment syndrome is characterised by muscleand tissue damage and reduced blood flow, caused by thecompression of nerves and blood vessels in an enclosedspace (eg, as a result of swelling). For patients with burns,compartment syndrome, particularly in the abdomen, can lead to renal impairment, gut ischaemia and cardiacand pulmonary complications. In the extremities,compartment syndrome can cause pain, reduced capillaryrefill 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’snatural shield, the skin).Inhalational injuries may accompany flame burns,

creating problems such as bronchoconstriction or adultrespiratory distress syndrome. Patients with inhalationalinjuries may present with wheezing, hoarseness, increasedrespiratory secretions, tachypnoea, stridor andhypoxaemia. Carboxyhaemoglobin should be checked toassess the degree of carbon monoxide exposure andpatients should receive 100% oxygen. Airway tissues maybecome inflamed leading to obstruction, so a secureairway is vital.

Pain Burn-associated pain comes from a variety ofsources including the burn itself, surrounding tissue,dressing changes and donor graft sites. Following a burn,the inflammatory response leads to the release ofmediators, such as bradykinin and histamine, whichtrigger pain signals.7 A full-thickness burn (Figure 1) maydamage the nerve to the extent where the pain signalcannot be felt. However, the surrounding tissue may nothave been burnt to the same depth, meaning that pain isstill present. Primary hyperalgesia is the heightenedresponse to pain at the burn site. Secondary hyperalgesiadevelops minutes later and is caused by nervetransmission from the surrounding undamaged skin.Hyperalgesia may last for days. Pain alters during thetreatment period but tends to be worst at donor sites orareas 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 sitepain may persist for 10–14 days after harvesting. Five tosix weeks post-burn, nerve regeneration occurs, and nerve

endings growing back into healing tissue can cause alteredsensations and neuropathic pain. It is estimated that 52%of burn survivors suffer from long-term or chronic pain.7

AssessmentThere are two common methods used to assess the extentof a patient’s burns: Wallace’s “rule of nines” and the Lundand Browder chart (see Figure 2).1,3,5 The rule of ninessplits the body into 12 sections: 11 of the areas are eachallocated 9% and the groin region is given 1%. Thepercentage of the BSA that has been burnt can then beestimated. The Lund and Browder chart is the moreaccurate of the two methods because it takes into accountthe change in body proportion relating to age (eg, childrenhave relatively larger heads than adults). Erythematousregions should not be included in BSA estimations.5

Burn depths can be classified by degree. They can alsobe described as superficial, partial thickness or full

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

PERCENTAGE

Region PT FT

Head

Neck

Anterior trunk

Posterior trunk

Right arm

Left arm

Buttocks

Genitalia

Right leg

Left leg

Relative percentage of areas dependent on growth

Percentage of total body surface area burnt

PT = partial thickness FT = full thickness

Figure 2: Lund and Browder chart

Figure 1: Illustration of a full-thickness burn

Full-thickness burn

Epidermis

Dermis

Subcutaneous tissue

Muscle

Nucl

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ical

Art,

Vis

uals

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disadvantage of LDI is that it is expensive and requires ahigh level of expertise to interpret the results (so is notroutinely available in many centres that treat burns).

Admission criteriaTo ensure that treatment is appropriate, the British BurnAssociation has published criteria for complex burn injury.(see Box 2).1 Patients meeting these criteria should bereferred to a specialist unit within six hours of injury sinceswift assessment and treatment of burns is crucial tooptimise patient outcomes. The very young and theelderly are particularly at risk of complex burn injuries.

References1 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 NationalStatistics.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. BMJ2006;332:649–52.

4 Hettiaratchy S, Dziewulski P. ABC of burns: Pathophysiology and types ofburns. BMJ 2004;328:1427–9.

5 Duncan RT, Dunn KW. Immediate management of burns. Surgery2006;24:9–14.

6 Latenser BA. Critical care of the burn patient: The first 48 hours. CriticalCare 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. Surgery2006;24:15–7.

9 Orgill DP. Excision and skin grafting of thermal burns. New EnglandJournal of Medicine 2009;360:893.

thickness (see Box 1).1,3,5 First-degree burns are classed assuperficial. Second-degree, partial-thickness burns aresubdivided into superficial and deep dermal. Third-degree burns are full-thickness. Fourth-degree burns, alsofull-thickness, can occur and these affect the tendons,subcutaneous tissue or bones as well as the skin. It ispossible for there to be a mixture of burn depths in onepatient, although reassessment should be made in the firstfew days after the burn since depth may increasedepending on the treatment received.

Patients with first-degree or second-degree superficialburns usually respond well to treatment and heal withintwo weeks; these types of burns are typically pink or red,painful and have a good blood supply. Patients with deepdermal or full-thickness burns can take months to recoverand have significant scarring without surgical treatmentand skin grafting. These types of burns tend to have a poorblood supply so will appear less red.

Jackson’s burn model splits the burn into three distinctzones: the zone of coagulation, the zone of stasis and thezone of hyperaemia (see Figure 3).4,5 The zone ofcoagulation is at the centre of the burn and is an area ofsevere damage resulting in irreversible tissue loss.Although the zone of stasis contains less damaged tissue,perfusion is affected and the correct treatment must beprovided to prevent progression to necrosis and allow fullrecovery. The zone of hyperaemia contains tissue that iswell perfused and this usually recovers well.

Assessment techniquesIn the first few days after injury it is often difficult todetermine the depth of a burn and, thus, the prognosis andneed for surgery to aid recovery. Various methods havebeen employed to supplement visual inspection of theburn.1,8,9 Techniques that assess tissue perfusion in theinjured 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 accuratemeasurement of burn depth among the availabletechniques. Depth is assessed by taking a thermal image ofthe burn area which correlates with skin blood flow. The

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 � Circumferential burns� Deep burn � High pressure steam burn� High tension electrical � 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 orimmunosuppression) flexures

� Other injury or major � Age under five or over 60 years oldtrauma (eg, crush injuries) � Exposure to ionising radiation

BSA = body surface area

248 Clinical Pharmacist July/August 2010 Vol 2CL

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S Box 1: Burn damage according to depth1,3,5

DEPTH

Superficial

Partial thickness:superficial

Partial thickness:deep dermal

Full thickness

DEGREE

First

Second

Second

Third

Fourth

EXTENT OF DAMAGE

Epidermis

Epidermis topapillary dermis

Epidermis toreticular dermis

Whole thicknessof skin

Skin plustendons, tissue,muscle and bone

APPEARANCE

Pink, moist,bleeding,painfulPink, blistering,moist, bleeding,painfulPatchy red andwhite, dry, nobleeding,reducedsensationWhite/black,dry andleathery, nobleeding, lackof sensation

HEALING TIME

Days

One to twoweeks

> Four weeks

> Four weeks

Zone of coagulation

Zone of hyperaemia

Zone of stasisEpidermis

Dermis

Subcutaneoustissue

Figure 3: Jackson’s burn model

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