Flap lacerations: Relatively minor trauma to the tibia commonly produces a V-shaped flap laceration (Fig. 17.2) particularly in older patients or in patients on long-term corticosteroids. If untreated, this injury habitually fails to heal because of poor blood supply to flap and underlying tissue. Attempting to suture or tape a flap into place increases tension, causing ischaemia, tissue loss and ulceration. The most effective management is early excision and immediate split skin grafting. This can be performed under local anaesthesia and takes an average of 2 weeks to heal.

Fig. 17.2 Flap laceration
This wound was caused by a fall in which the patient’s shin was scraped on a stone step. It is tempting to suture such a wound, but if this is done the flap will invariably undergo necrosis

Facial lacerations: Minor facial lacerations heal well and can be primarily sutured in the accident department after careful cleaning. Infection is rare because of the excellent blood supply. Even ragged skin edges do not become devitalised and trimming is rarely necessary. The main consideration is the cosmetic outcome, so great care should be taken with technique, employing general anaesthesia if necessary. Complex lacerations, lacerations across the lip margin or eyelid and areas of substantial skin loss, especially on children and young people, should ideally be managed by plastic surgeons (see next section).

Scalp lacerations: With scalp lacerations, brain injury and skull fracture must be excluded and then determine whether the aponeurotic layer (galea) has been breached. Haemostasis must also be achieved; it is easy to underestimate blood loss from scalp lacerations, sometimes sufficient to cause hypovolaemic shock in the elderly. Assessment and thorough exploration is made easier by shaving the wound edges; large lacerations may need exploring under general anaesthesia. If the aponeurosis is breached, it should be repaired separately to prevent a subaponeurotic haematoma vulnerable to infection. Care should be paid to haemostasis from major scalp blood vessels lying in the superficial fascia between dermis and aponeurosis. Dense collagenous bands cross the area and can prevent torn vessels contracting, hindering the spontaneous arrest of bleeding. Torn vessels need to be individually ligated or sutured.

Major soft tissue injuries

Major injuries of soft tissues alone requiring hospital treatment are uncommon and can be classified as in Box 17.1. A primary survey (Ch. 15) determines the order injuries are managed, with life-threatening injuries treated first. For other injuries, the urgency depends on the potential for deterioration (e.g. blood loss, ischaemia or loss of an eye), the risk of infection and the availability of the necessary specialists. Contused or contaminated wounds need early cleansing and excision of all devitalised tissue (debridement), usually under GA. If substantially contaminated, wounds are often left unsutured to prevent wound infection and are then sutured a few days later by delayed primary closure. Less commonly, wounds are left open and are allowed to heal by secondary intention (see Ch. 3, p. 36). Wounds involving skin loss may need early skin grafting.

Injury to a vital part of the body

Eye: Injuries greater than ‘sand in the eye’ are best managed by ophthalmic specialists who require a slit lamp and other instruments to assess the injury. Typical injuries include abrasions to the cornea, penetrating injuries (dart or pellets) and firework injuries.

Neck: Penetrating injuries to the neck must be treated with respect. Vital structures are concentrated here and may be injured. These include major arteries and veins (carotid, jugular, subclavian, vertebral), the brachial plexus, some cranial nerves, the cervical sympathetic chain (see Fig. 17.3), and lung and pleura.

Case History

Fig. 17.3 Horner’s syndrome caused by stab wound in the neck
This 19-year-old was stabbed in the neck: the knife missed the great vessels but succeeded in damaging the cervical sympathetic chain, causing miosis (constriction) of the pupil as a result of unopposed parasympathetic activity

Lacerations to the limbs and hands: (for Traumatic amputation, see p. 236)

The main considerations with this type of injury are:

• Possible nerve, tendon or vascular injury—assessment includes testing sensation, movement, peripheral pulses and tissue perfusion (i.e. pulses, warmth, colour, capillary refilling after blanching). Tendon and nerve injuries are covered below

• Tissue viability—particularly important in crush injuries and flap lacerations such as in the pretibial area (see above)

• Risk of infection—the fingers and hands are vulnerable to infection of pulp spaces and the deep palmar space. Wounds need antibiotic prophylaxis against staphylococci and streptococci (e.g. flucloxacillin plus amoxicillin). They also need meticulous cleansing and exploration, if possible by a specialist hand or plastic surgeon. Injuries from bites (especially by dogs or humans) and bones (usually in meat workers) almost invariably become infected (see below).

Extensive facial lacerations: Facial injuries should be thoroughly cleaned and examined under local or general anaesthesia to determine the extent of the damage before repair; ideally within 12 hours of injury. Facial wound edges need minimal trimming. Important anatomical boundaries should be aligned first; these include the vermilion border of the lip, the rim of the eyelid and the eyebrow. Tissue layers should then be approximated individually—mucosa, muscle, cartilage and skin. Parotid duct injury should be considered in deep lacerations of the cheek and the duct repaired if possible. Photographic documentation is useful to help the patient appreciate the extent of injury and to provide an accurate record of progress.

Facial nerve integrity should be determined before anaesthesia is given. Nerve branches should be repaired (usually by a plastic surgeon with microsurgical skills). Those caused by a laceration posterior to a vertical line from the lateral canthus of the eye do better than those anterior to this. Nerve repair should be performed no more than 72 hours after injury.

At the scene of the injury, the severed digit should be washed gently to remove obvious dirt and placed in a plastic bag which is then placed inside a second plastic bag containing ice or frozen peas. In this way it can be successfully preserved for up to 12 hours.

Contamination with soil and road dirt

Superficial wounds such as grazes caused by motorcycle injuries and lack of protective clothing often become widely impregnated with road debris. These need to be scrubbed clean, often under general anaesthesia. In the case of large contaminated and contused wounds involving muscle, the potential for gas gangrene must be considered. Dead tissue must be thoroughly excised, benzylpenicillin given prophylactically, and primary closure avoided in favour of delayed primary closure. Note that hydrogen peroxide must NOT be used in any wounds other than purely superficial ones because of the dangers of oxygen embolism causing brain damage.

Crush injuries

Crush injuries occur most commonly in earthquakes and during wars after buildings have collapsed on people. Rhabdomyolysis follows prolonged heavy continuous pressure on muscle and crush syndrome is caused by reperfusion injury when the damaged muscle revascularises on removing compression. Damaged cells release potassium and potentially toxic substances such as myoglobin, phosphate and urate into the circulation. Water and extracellular electrolytes enter the damaged muscle. The net result is hypovolaemic shock with electrolyte disturbances leading to prerenal and toxic renal failure.

Following earthquakes, the incidence of crush syndrome is 2–5% of those buried under rubble. About half develop acute renal failure, and half of those need dialysis. Crush syndrome is also seen following industrial incidents, particularly in mining, and in road traffic collisions.

Diagnostic criteria for crush syndrome include:

• A crushing injury to a large mass of skeletal muscle

• Sensory and motor disturbances in the compressed limb

• Swelling and tenseness of the limb a few hours later

• Myoglobinuria and/or haematuria

• Elevated serum creatine kinase (CK) with a peak greater than 1000 U/L

• Renal insufficiency hours or days later. This may manifest with oliguria (urine output less than 400 ml in 24 hours), decreased plasma calcium concentration and elevated plasma urea, creatinine, uric acid, potassium and phosphate

Presentation: Crush syndrome presents with profound shock. A limb trapped will be pulseless on release; later it becomes red, swollen and blistered with loss of sensation and muscle power. Reperfusion injury causes compartment syndrome after release of compression. Once the compartment pressure exceeds capillary perfusion pressure (about 30 mmHg), tissues in the compartment become ischaemic.

Management: At the accident scene, after substantial crush injury, limb amputation on site will prevent crush syndrome. This takes fine judgement but a severely damaged limb may not be salvageable. Venous access should be obtained early, and saline infused at 1000–1500 ml/h during extrication.

Once urine flow is established, a mannitol-forced diuresis of up to 8 L/day should be maintained. Allopurinol can be given to reduce urate levels and protect the myocardium. If compartment syndrome seems likely, fasciotomy should be performed early.

Hyperkalaemia and infection are common complications and may lead to death. Intractable hyperkalaemia may benefit from dialysis. Disseminated intravascular coagulation can occur with massive tissue damage, and established acute renal failure requires appropriate management.

The earthquake in Marmara, northern Turkey, in 1999 was well documented and had a mortality rate for crush syndrome of 15%. Peak levels of CK give useful prognostic information: levels greater than 100 000 U/L virtually always signify that haemodialysis will be needed or that the patient is likely to die. Children with extensive injuries do very poorly.

Peripheral nerve injuries

Anatomy: In a peripheral nerve trunk, individual axons are sheathed in endoneurium and groups are bundled into fascicles. Each fascicle is covered in tough perineurium composed of collagen and elastin and may contain sensory and motor axons. A peripheral nerve trunk consists of a number of fascicles in a matrix of epineurium which also coats the nerve. Fascicles divide repeatedly along the course of a nerve, communicating with each other and intermixing rather than running neatly in parallel. This means the arrangement and type of axons and fascicles in one cross-section of the nerve may be very different from that in an adjoining cross-section. The difficulty of aligning the proximal with the distal arrangement is an important reason why functional recovery is poor if a segment of nerve is lost and has to be replaced with a nerve graft.

Types of injury: Nerve injuries were classified by Seddon in 1943:

• Neuropraxia is the mildest injury, where nerve continuity is preserved and only transient functional loss occurs. Recovery occurs within 6–8 weeks, without Wallerian axonal degeneration. The lesion is caused by compression, blunt impact or nearby low-velocity missile injuries and the injury is probably biochemical. Motor nerves are more sensitive to damage than sensory nerves and autonomic function is often retained

• Axontmesis occurs when there is interruption of axon and its myelin, but perineurium and epineurium are preserved. Axontmesis results from more severe crush injury or contusion; axonal continuity is lost and complete denervation occurs but supporting structures remain intact. Electromyography (EMG) confirms muscle denervation distal to the injury. Recovery eventually takes place by axon regeneration and is likely to be complete

• Neurontmesis involves complete functional disconnection and occurs with severe contusion, stretching or laceration of a nerve. Axons and encapsulating connective tissues lose continuity and motor, sensory and autonomic functions are completely lost, and rarely recover without surgical intervention. The nerve is not usually completely severed but suffers internal structural disruption. In such cases, axonal regeneration causes fusiform swelling of the injured segment. If the nerve is divided, fibroblast proliferation produces dense fibrous scarring which inhibits sprouting axons from entering distal tubules; this seriously impairs nerve regeneration

Nerve regeneration: In axontmesis, calcium-mediated Wallerian (or antegrade) degeneration of the distal axon and myelin occurs early on. Within a few days, sprouting begins from the ends of proximal axons. Regenerating fibres eventually cross the injury site and then progress distally at 1–2 mm a day through undamaged tubules which provide a precise path for reinnervation of target organs.

In neurontmesis, nerve lesions close to the parent cell often lead to death of the cell body. If cell death does not occur, axons sprout (as in axontmesis) but the first barriers are the scar and any gap in the nerve. A neuroma forms on the proximal nerve end and no functional recovery occurs without operative repair. The most favourable injury for repair is a clean wound without segmental nerve loss.

Denervated muscle becomes irreversibly damaged after 18 months. Axons regenerate at about 2.5 cm per month provided they have an uninterrupted route, thus the distance between the injury and target muscle must be under 45 cm for any hope of functional recovery. As an example, if the ulnar nerve is injured in the brachial plexus, the wrist and finger flexors in the forearm may recover, but the intrinsic muscles of the hand may not. A further period is needed to achieve functional recovery because the new axon needs to mature, the synapse has to be reconstituted, the end-organ must recover from trophic changes, and a critical number of axons must reach the target end-organs to accomplish neural control.

Clinical types of nerve injury:

Compression: Compression affects the largest myelinated fibres most. Motor control is lost first and discrete sensation follows. The underlying cause is probably ischaemia; large myelinated fibres are more susceptible to this than smaller unmyelinated ones. In partial injuries, smaller pain-bearing and sympathetic fibres are often preserved, causing pain and hyperaesthesia in the nerve distribution. Compression injuries include so-called ‘Saturday night palsy’, where the radial nerve becomes compressed over the back of a seat in a patient who passes out under the influence of alcohol. Total loss of motor and sensory function is likely to occur. Adverse effects are spontaneously reversible unless ischaemia persists for more than 8 hours.

Traction: Traction is the most common mechanism of nerve injury and is often associated with fracture or dislocation. Nerves have little elasticity and can only stretch 4% without injury. Luckily, most traction injuries are self-limiting and have a good prognosis; as many as 90% achieve good or fair recovery. The prognosis is worse when vascular trauma or open fractures are present, with only 65% recovering useful function.

Laceration: Lacerations such as those caused by a knife blade comprise up to 30% of serious nerve injuries. Exploration and repair is recommended in most cases.

Missile injury: Low-velocity gunshot missiles are less likely to sever nerves than sharp lacerations. However, about 70% of missile wounds that require exploration for other reasons demonstrate complete or partial transsection of a nerve. In high-velocity missile injuries, cavitation of soft tissues can produce nerve stretch injuries.

Repair of nerve injury:

Direct repair: A clean sharp division of a nerve by a knife wound should be repaired by primary anastomosis within 24 hours of injury. Simple epineural repair involves re-approximation of the nerve ends using a circumferential line of sutures. This is technically easier than fascicular repair which involves microsurgical anastomosis of fascicles or groups of fascicles. Results of epineural repair are often good if the fascicular patterns at the cut ends are similar and where anatomic distortion is minimal. Even for proximal nerve trunk repair where a plexiform layout of fibres is more likely, the chances of the correct type of axons passing down the proper fascicles appear to be as good as in fascicular repair. Epineural repair is also stronger and resists tension better. With compression, stretching or contusion injuries, repair should be undertaken between 8 weeks, and 3 months of injury if there is no evidence of natural recovery.

Cable grafting: Autologous nerve grafting is needed if there is a large gap in a nerve. The most commonly used donor nerve is the sural, a large sensory nerve running down the posterior calf to the lateral dorsum of the foot. Several ‘cables’ are usually fashioned and attempts made to match proximal and distal fascicles. The plexiform and mixed nature of fascicles makes full recovery difficult to achieve.

Results of nerve repair: Assuming good technique, the following factors improve the prognosis for recovery after nerve repair:

• The repair involves purely sensory or motor nerves, e.g. the functional result of a severed peroneal nerve repair (motor) is likely to be better than an equivalent median nerve repair (mixed)

• The lesion is distal rather than proximal because distal trunks have a more linear arrangement

• The patient is younger; children have better results than adults, and younger adults better than older adults

• The repair is undertaken soon after injury

Burns

Introduction

Burns affect everyone—young or old, rich or poor, in the developing or developed world—but the poor and underprivileged are more at risk and generally receive worse treatment. Burns cause devastating injuries. Initially there is severe pain and distress, but soon there is a massive assault on both physical and psychological aspects of those affected. There are visible physical scars and invisible psychological scars which together cause severe and long lasting disability.

Epidemiology

Thermal injury is common. Burns are the fourth most common trauma worldwide (after traffic collisions, falls and personal violence). Most burns are caused by flame injuries and many of the rest by scalds. Electrocution and chemical injuries are uncommon. In the UK, about 250 000 people are burnt each year; 112 000 attend accident departments and 13 000 are admitted to hospital. About 1000 have burns severe enough to need fluid resuscitation and, sadly, half of these are children under 12. In an average year, burns cause 250 deaths in the UK, although the incidence has decreased owing to prophylactic measures, e.g. curly cables on kettles; abandonment of open fires; and flameproof sofas and clothing. The incidence in the USA is higher, and is even more of a problem in the developing world, with 90% occurring in low to middle income countries. India alone has over 2 million burns a year. Mortality in the developing world is also much higher, e.g. Nepal has 1700 burn deaths annually in a population of 20 million, proportionately 17 times higher than in the UK.

Two-thirds of burns occur in the home and one third largely in industrial accidents. Around 60% of domestic burns are associated with cooking. Half of all deaths in domestic fires occur between 10 p.m. and 8 a.m. and excess alcohol often plays a role. Fireworks and bonfires are frequent causes of domestic burns. Most burns are preventable. Young children and the elderly are at greatest risk and also suffer disproportionate mortality. There is a male predominance except in the elderly; 10% of those burnt are over 65, often as a result of immobility, slowed reactions and decreased dexterity placing them at risk from scalds, contact burns and flame burns. Twenty per cent of all burns occur in children under the age of 4; 70% are scalds caused by spilling hot liquids or by exposure to hot bath water. Toddlers frequently pull containers or cups of hot liquid over themselves from cookers and tables which burn the outstretched arm, face, neck and front of the chest and can cover a large area (see Fig. 17.4).

Fig. 17.4 Typical pattern of burns in a young child
The child pulls a teapot or cup of hot liquid from a table or when being held by a seated adult. The area shaded pink is typically burnt

Teenagers are often burnt as a result of illicit activities, e.g. with petrol, explosives or high tension electricity. Overall, 60% of burns occur between the ages of 15 and 64, of which half are flame burns, often with inhalational injury; burns tend to be deep dermal or full thickness (see Fig. 17.5).

Fig. 17.5 Classification of depth of burns
Erythema—red, dry skin that easily blanches then rapidly refills (not illustrated here)
Superficial—red, moist wound that blanches and rapidly refills
Superficial dermal—pale, dry, blanching wound that regains colour slowly
Deep dermal—mottled cherry red and does not blanch (fixed capillary staining). The blood is thrombosed and fixed in damaged capillaries in the deep dermal plexus
Full thickness—dry, leathery or waxy, hard wound that does not blanch. In extensive burns, full thickness burns can be mistaken for unburnt skin

Pathophysiology of burns

In thermal skin burns, the depth of destruction determines the local outcome. Skin burns are broadly divided into partial or full thickness. In partial thickness burns, epidermal elements are spared, eventually allowing spontaneous healing without skin grafting. In deep partial thickness burns, the only epithelial remnants may be hair follicles and sweat glands extending into the hypodermis, making regeneration slower. In full thickness burns, all the epidermis has been destroyed. Skin grafting is needed because epithelialisation from the margins is slow and prone to complications, in particular infection, fibrotic scarring and contractures.

The depth of damage is a function of the temperature and duration of exposure as well as the thickness of the skin (important in the very young and very old where the dermis is thinner). If applied for long enough, water at a temperature of only 45°C will cause full thickness destruction and is often the mechanism of tragic burns in childhood. Note that the area of a major burn will not be uniformly deep.

Three zones of a major burn were described by Jackson in 1947. There is a central zone of coagulation where skin cells are irreversibly damaged. This is surrounded by a zone of stasis characterised by decreased tissue perfusion in which injured cells can survive or die according to the effectiveness of treatment. These zones extend deeply but the outer zone of erythema is superficial. Here the cells are minimally injured and recover in 7 days. This erythematous zone should not be included in calculating the burnt area.

Systemic effects (Box 17.2)

Extensive burns cause large fluid losses. Epidermal destruction removes the barrier that normally prevents evaporation of body water. In addition, inflammation causes exudation of protein-rich fluid into the extracellular space causing oedema and blisters. The large volumes lost need to be replaced urgently (see Fig. 17.7, below), with the amount lost depending on burn area rather than depth. Once 30% of the body surface area is burnt, particularly if there is necrotic tissue, inflammatory mediators and cytokines spill into the circulation, causing a systemic inflammatory response. This provokes a generalised rise in capillary permeability, escalating the volume of plasma leaving the circulation into the ‘third space’. Fluid losses are greatest in the first few hours but continue for at least 36 hours.

Epidermal loss and necrotic tissue place the patient at high risk of infection. The main organisms are Streptococcus pyogenes during the first week and Pseudomonas aeruginosa thereafter. If burns become infected, the risk of sepsis and organ failure increases and leads to substantial mortality, even in this antibiotic era.

Electrocution burns

Electrical burns result from the conversion of electrical energy into heat; electrocution is responsible for around 3% of admissions to burns units. The voltage is the key determinant of severity. Low domestic voltages just cause small but deep contact burns at exit and entry sites. High-tension injuries occur at voltages over 1000 V and cause large amounts of necrosis of bone and soft tissues and often limb loss. Muscle damage gives rise to rhabdomyolysis and renal failure. Contact with voltages greater than 70 000 V is invariably fatal.

The extent of burning is proportional to the electrical resistance of the tissue through which the current is transmitted. Bone offers the highest resistance; if current passes through a limb, the bones become heated and adjoining muscle is injured. Fasciotomy is likely to become necessary to decompress muscle compartments. Blood vessels also sustain intimal damage and thrombose. Deep tissue necrosis may not become clinically apparent until some days afterwards and the extent of damage is often much greater than suspected.

Chemical burns

Chemical burns usually result from industrial accidents but may be caused by household chemicals. The severity depends on the agent, the concentration and quantity, and the duration of contact. Chemical burns tend to be deep because corrosives continue to act until fully removed. Alkalis such as cement tend to penetrate more deeply and cause worse burns than acids. Hydrofluoric acid is widely used in glass etching and circuit board construction and is a common cause of industrial chemical burns. It must be neutralised with topical or locally injected calcium gluconate to prevent the burning continuing. The initial management of chemical burns is similar for all agents, i.e. remove all contaminated clothing and dilute or wash away the chemical by thoroughly irrigating the area, often by showering the patient.

Early appraisal of the burnt area is important, not least because it helps determine the fluid volume required for resuscitation. Area estimation is often badly done even by experts and is complicated by the fact that erythema must be excluded to avoid overestimates. Preliminary evaluation can be done immediately but definitive assessment should be deferred for a few hours until erythema settles.

All of the burnt area needs to be exposed sequentially, ensuring the patient is kept warm. For adults, Wallace’s rule of nines (Fig. 17.6) is fairly reliable for medium to large areas and is quick, but is inaccurate in children. Another method is to use the patient’s palm and finger area to indicate 1% of body surface area. This is useful for small burns, and in very large burns where the unburnt area is measured. The most accurate method is to use Lund and Browder charts which compensate for variations in body shape with age; the charts are also accurate in children.

Fig. 17.6 Rule of nines
Wallace’s rule for estimating the percentage of the skin surface area burnt. A useful alternative estimate is that the area of the patient’s own palm plus fingers is approximately 1% of the total skin area.

Early assessment of burn depth is difficult, not least because most large burns are a mixture of different depths. Burns are dynamic wounds where the eventual depth is influenced by the effectiveness of resuscitation and by inflammatory mediators, as well as external factors such as bacterial proliferation, dehydration and cooling. Thus it is essential to re-appraise the burn regularly until it heals.

Depth assessment is not relevant for calculating fluid resuscitation but is important for management of the burn. Figure 17.5 (p. 240) explains a widely used classification of depth, detailed below. In essence, partial thickness burns are capable of regenerating skin from preserved dermal adnexae whereas full thickness burns regenerate slowly from the edges and are likely to need skin grafting. By way of preliminary assessment, if the burnt area is erythematous, blanches on pressure and retains pinprick sensation, it is partial thickness; charred skin or thrombosed skin vessels invariably indicate a full thickness burn.

Partial thickness burns may be classified as follows:

• Superficial burns—affect the epidermis but not the dermis, e.g. sunburn

• Superficial dermal burns—destroy the epidermis and upper dermal layers; blistering usually occurs. The burn may be covered with soot or dirt, which needs removing, and blisters should be deroofed so that the base can be checked. Capillary refill can be tested by pressure from a sterile cotton bud. A 21 gauge needle is used to test sensation and bleeding; in superficial dermal burns, pain is felt normally and bleeding is brisk. Scalds tend to cause ‘superficial’ to ‘superficial dermal’ burns

• Deep dermal burns—these destroy all the epidermis and most of the dermis, leaving only the deepest skin adnexae, sweat glands and some hair follicles, all of which are scanty. Accurate depth estimation can be difficult. On needle testing, bleeding is delayed and only non-painful sensation is experienced

• Full thickness burns are insensate and do not bleed on needling

Principles of management of burns

Optimal treatment reduces the morbidity of burns as well as mortality in large burns. Effective treatment shortens the period of healing, speeds return of function and reduces the need for secondary reconstruction.

First aid: The first priority at the scene is to stop the burning process. The heat source must be removed and any flames doused. Clothing is removed unless stuck to the burn, and active cooling employed to remove heat and arrest progression. Ideally this is achieved by immersing the burnt area in tepid water (~15°C) for 15–20 minutes. This can cause hypothermia, especially in children.

Analgesia: Burns are very painful, with pain being greatest in superficial burns. Pain relief is best achieved by cooling and covering burns in addition to analgesic drugs. In larger burns, opioids are given initially and NSAIDs later.

Dressings: Cling film (PVC) is ideal as an initial burn dressing. It is essentially sterile and forms a pliable, non-adherent, impermeable barrier which is transparent to allow inspection. It should be laid on rather than wrapped around and covered with a blanket to keep the wound warm. Burnt hands are enclosed in plastic bags. Prepacked cooling hydrogels, e.g. Burnshield®, are available for applying at the scene of the burn.

Where should burns be managed?: Very small or erythema-only burns can be managed in primary care but all other patients should be assessed and resuscitated in an emergency unit. Initial assessment then determines whether treatment can continue as an outpatient in a general hospital, whether admission is required or whether transfer to a specialist burns unit is needed. Patients with extensive burns involving more than 30% of body surface should be transferred to a specialist burns unit right after initial treatment and resuscitation. Facial burns should also be referred after covering with bland paraffin ointment (repeated every 1–4 hours to minimise crust). Other referral criteria are summarised in Box 17.3.

Outpatient management of minor burns

Patients appropriate for outpatient management are adults without inhalation injury or significant co-morbidity, with partial thickness burns affecting less than 10% of body surface area. Children with less than 5% burns are also suitably managed in this way. Patients with full thickness burns of up to 1% can also be managed as outpatients.

Immediate care involves analgesia and reassurance. Fluid resuscitation is not needed. The main objective of local treatment is to prevent dehydration and infection of the burn site; epithelialisation progresses faster in a moist environment. The burnt area is cleaned of soot and debris with soap and water or weak chlorhexidine if necessary. Larger blisters are de-roofed and covered with a non-stick impregnated gauze dressing. Tulle gras (paraffin gauze) has long been used but it soon dries out and adheres to the wound. A better, more expensive alternative is a soft silicone-coated net such as Mepitel. A generous layer of silver sulfadiazine cream (Flamazine) can be used instead; this antibacterial cream covers Gram-negative organisms including the common infecting organism, Pseudomonas. Either dressing is then covered by a thick absorbent layer of gauze and wool (Gamgee). Burns on the fingers and hands are best treated with a liberal coating of silver sulfadiazine cream and enclosing the hand in a plastic bag. Burnt areas should be checked at 24 hours and the dressing changed at 48 hours, by which time the depth should be evident and the treatment plan can be reviewed. Silver sulfadiazine cream can then be applied every 24–48 hours and skin slough excised as it separates. Partial thickness burns re-epithelialise within 14–21 days. If the burn has failed to heal within 3 weeks, the burn must be assumed to be full thickness and requires referral to a specialist unit.

Managing burns of specific depth

Superficial burns, typically sunburn, require only supportive therapy with regular analgesia and dressings for moist areas. Healing takes place within a week by regeneration from undamaged keratinocytes.

Superficial dermal burns. Blistering is common and exposed superficial nerves make these burns painful. Progression to a deeper burn is unlikely. Healing is expected within 2 weeks from keratinocytes within sweat glands and hair follicles. The rate depends on the density of adnexae, i.e. thin hairless skin on the inner arm or eyelid heals more slowly than thick or hairy skin of the back, scalp or face. Treatment is as above although Hypafix is a special dressing that preserves mobility and allows washing with the dressing in place. It is applied directly to hand burns, for example. This dressing needs changing at least weekly by soaking in oil. Awkward facial burns are left open but liberally coated with antimicrobial creams or ointment. If burns are still unhealed after 2 weeks, depth assessment was incorrect and the patient should be referred to a burns unit.

Deep dermal burns. These are the most difficult to assess as superficial dermal burns may progress to deep dermal burns (with fixed capillary staining) within 48 hours. The density of skin adnexae is less at this depth and healing is slower and subject to contractures. Some of these burns heal spontaneously if kept warm, moist and free of infection, but if deep dermal burns are extensive or are in functionally or cosmetically sensitive areas, they are better treated in a burns unit by excision to a viable depth and skin grafting within 5 days. This can reduce morbidity and accelerate return to normal function.

Full thickness burns. All regenerative elements have been destroyed; without grafting, wound contraction and distortion would be substantial. Ideally all full thickness burns need excision and grafting unless they are sited where function would not be compromised and are less than 1 cm in diameter.

Management of extensive burns

Major burns are those affecting more than 20% of the body surface area. Survival depends crucially on accurate assessment, prompt and effective resuscitation, also the premorbid condition of the patient and whether there has been smoke inhalation. The main early aspects of management are fluid replacement, assessment and treatment of inhalational respiratory problems and local management of the burns.

It is difficult to give an early prognosis. Clearly, aggressive treatment of someone who definitely will not survive is inhumane but victims of severe yet potentially survivable burns must be treated rapidly and effectively. The risk of dying is greater with increasing area, with inhalational injury and in children under 3 and adults over 60. Very high voltage electrical burns are particularly lethal. Other medical conditions also increase the risk, e.g. alcoholism, epilepsy, diabetes, atherosclerosis and drug abuse.

Resuscitation and fluid management: Adults with 15% and children with 10% body surface burns lose sufficient fluid to be at risk of hypovolaemic shock. Fluid replacement depends on the area of the burn and the patient’s weight. Hypovolaemia in the presence of myoglobinaemia readily precipitates acute renal failure. Effective resuscitation maintains tissue perfusion in the zone of stasis, inhibiting depth progression. Most fluid is lost in the first 8–12 hours, during which there is a general shift of fluid from intravascular to interstitial. Substantial fluid losses continue for at least another 36 hours. Rapid boluses of fluid should not be given early on as raised intravascular hydrostatic pressure drives it rapidly out of the circulation.

Fluid requirements should be calculated from the time of injury, not the time of arrival in the emergency department. Colloids appear to offer no advantage over crystalloids and the volume required is estimated by referring to well-tried formulae such as that of Muir and Barclay shown in Figure 17.7, or the Parkland formula, Box 17.4. The Parkland formula has the advantage that it uses only crystalloids, it is easy to calculate and the rate can be adjusted by titrating against urine output.

Box 17.4 The Parkland formula for fluid resuscitation in the first 24 hours in major burns

• For adults, the total volume to be given over 24 hours is 3–4 ml Hartmann solution per kg body weight for each per cent surface area burnt

• For children, the calculation is the same as for adults plus normal maintenance fluids

• For all cases, half the estimated volume is given in the first 8 hours and the rest over the next 16 hours

Fig. 17.7 Serious burns—a method for estimating fluid requirements over the first 36 hours (after Muir and Barclay)
The lower panel shows an example of a fluid replacement regimen for a 70 kg man with 20% burns. Each block represents one unit of fluid volume and is calculated as follows:

These formulae are only a guide, however, and fluid balance must also be monitored according to pulse, blood pressure and urine output via a urinary catheter. Patients should also have 4–6-hourly estimations of packed cell volume, serum sodium, base excess and lactate. Note that patients with high-tension electrocution injuries need substantially more fluid than estimated by these formulae. In extensive full thickness burns, widespread red cell destruction occurs and blood transfusion may be needed.

Local management of the burns: All wounds should achieve epithelial cover within 3 weeks to minimise scarring. Partial thickness burns re-epithelialise spontaneously given proper care, but full thickness burns require excision and skin grafting. Fingers, eyelids, limb flexures and genitalia nearly always require primary grafting soon after injury. For optimal care, grafting should be performed within 5 days of injury and patients needing transfer to a burns unit should reach there within a maximum of 10 days.

The best covering for excised areas is autograft split skin from unburnt areas, ideally harvested near the recipient area to ensure best colour match. Sheets rather than postage stamp grafts should be used for hands and face. Wounds to be grafted must be free of infection; large areas of deep burns need excising and grafting early to prevent infection and systemic sepsis. With extensive burns, skin grafting usually has to be performed in several stages because of a shortage of donor sites. Sites already used can be reused (donor site rotation) after 3 weeks or so; burnt areas can be primarily excised and covered with temporary covering until donor sites become mature. Temporary coverings include cadaveric allograft skin, xenograft skin (e.g. pigskin), specially developed synthetic products or cultured epithelial autografts (sheets can be available in 3 weeks, skin cell suspensions in 1 week).

Deep circumferential burns of the limbs and thorax begin to contract early and may restrict blood flow and respiratory movements. If excision and grafting is not done early, and if these signs develop, escharotomy is performed, involving incision of the eschar longitudinally down to bleeding tissue (Fig. 17.8).

Fig. 17.8 Sites for performing escharotomy in deep circumferential burns

Inhalational injuries

Respiratory and systemic damage from inhalation of hot air, smoke and toxic gases (e.g. carbon monoxide or cyanides from burning upholstery) is a major cause of death and complications even if skin burns are insignificant (Box 17.5). The heat of inhaled gases is often sufficient to cause inflammatory oedema of the oral, nasal and laryngeal mucosa or even serious burns. Blackening by smoke or burnt skin around the nasal or oral cavities warns of inhalation injury. In addition, noxious gases can injure the lung parenchyma, resulting in pulmonary oedema, atelectasis and secondary pneumonias a day or two later.

Box 17.5 Clinical indications of likely inhalational injury that may prompt endotracheal intubation and ventilation

• A history of flame burns or burns in an enclosed space

• Stridor, tachypnoea or dyspnoea

• Singed nasal hair

• Full thickness or deep dermal burns to face, neck or upper torso

• Changes in the voice with hoarseness or a harsh cough

• Carbonaceous sputum or carbon particles visible in oropharynx

• Erythema or swelling of the oropharynx on direct inspection

Investigations include chest X-ray, blood gas and carbon monoxide estimations and upper respiratory tract examination with flexible pharyngoscopy and bronchoscopy.

Initial treatment involves administration of humidified air by mask and antibiotics to prevent chest infection. More severe cases require oxygen by mask, progressing to endotracheal intubation and intermittent positive pressure ventilation if blood gases deteriorate or pulmonary oedema develops.