LOCAL EFFECTS

Thermal injury produces complex local and systemic responses. The local inflammatory response results in vasodilatation and an increase in vascular permeability. The changes are immediate and combine to produce extravasation of fluid and plasma protein at the site of injury. In extensive burns, oedema becomes generalised. The greatest rate of oedema formation occurs in the first few hours, but further extravasation occurs up to 24 hours post burn.² The total amount of oedema formed depends on the extent of injury and the volume and rate of fluid administration. Without fluid replacement, hypovolaemic shock occurs, limiting the extent of extravasation. On the other hand, excessive fluid administration will produce excessive oedema. By 24 hours post burn, oedema formation is largely complete and vascular integrity restored.

The process of deepening of the burn wound beyond the area of heat necrosis following injury is at least partly due to microvascular stasis. Events occurring within minutes and hours of injury that contribute to stasis include microthrombus formation, neutrophil adherence, fibrin deposition and endothelial swelling. Diverse agents, including antioxidants and anti-inflammatory drugs, have been shown to attenuate this process in experimental settings, but none is yet established in clinical practice. Empirically, it is assumed that maintenance of good tissue oxygenation, avoidance of overresuscitation and prevention of wound dehydration all contribute to wound healing by preventing undue extension of necrosis in the wound bed.

CIRCULATORY EFFECTS

Circulatory effects of burn injury become significant in burns of over 15% TBSA. Changes are rapid and the magnitude is roughly proportional to the extent of burn injury. Cardiac output is reduced immediately following injury. Secretion of adrenaline (epinephrine), noradrenaline (norepinephrine), vasopressin and angiotensin cause an increase in systemic and pulmonary vascular resistance. Circulating levels of agents with myocardial depressant properties, such as interleukin-1 and TNF-α, are increased following burn injury, but developing hypovolaemia and increased blood viscosity may be equally important.³

Cardiac output recovers gradually during the second post-burn day, reaching supranormal levels by day 3 as the hypermetabolic response to burn injury becomes manifest. Circulatory dynamics are complicated by resorption of oedema fluid and by continuing evaporative fluid loss from the wounds. Prolonged elevation of renin/angiotensin and antidiuretic hormone (ADH) has been well documented and circulating blood volume may remain subnormal into the second week post burn.⁴

METABOLIC EFFECTS

The hypermetabolic state, which ensues from around the third post-burn day until the wounds are substantially healed, is a manifestation of the systemic inflammatory response syndrome. The state is partly sustained by evaporative and radiant heat loss through the wounds, and energy expenditure can be reduced by increasing the ambient temperature and by the use of occlusive dressings.^5,6 Other factors known to influence the metabolic rate include pain, fear and anxiety. There is also a suggestion that bacterial colonisation may aggravate hypermetabolism.^7,8 Burn patients often develop moderate pyrexia, even when all microbial cultures are negative.

PHARMACOLOGICAL EFFECTS

The pharmacokinetics and pharmacodynamics of many drugs are markedly altered in burn patients. During the first 24 hours, when the cardiac output is depressed, absorption and distribution of administered drugs are delayed. Thereafter, increased cardiac output leads to accelerated drug absorption and distribution, while oedema fluid acts as an ill-defined third space. At the same time, renal blood flow and creatinine clearance are increased, particularly in younger patients. Drugs excreted via this route, such as the quinolone and aminoglycoside antibiotics, may therefore fail to reach effective levels at conventional dosages.⁹ On the other hand, toxic levels may ensue if renal failure supervenes. If possible, therefore, antibiotic administration should be guided by measurement of plasma concentrations.

Serum albumin levels are low in burn patients, and drugs bound to this protein, including some benzodiazepines, will show increased bioavailability. On the other hand, α₁-glycoprotein levels, which bind fentanyl, are increased. Detoxification via redox pathways, such as cytochrome P-450, is depressed, lengthening the half-life of drugs such as diazepam.¹⁰ Accumulation of benzodiazepine derivatives may be increased.

The pharmacodynamics of muscle relaxants are significantly altered due to an increase in peri-junctional acetylcholine receptors.¹¹ Patients become relatively insensitive to non-depolarising agents, while administration of succinylcholine may give rise to excessive release of potassium, and cardiac arrest.

The burn wound is a significant route of drug absorption as well as drug loss. For example, the topical sulfonamide agent, mafenide, may cause metabolic acidosis through inhibition of renal carbonic anhydrase; deafness has been reported following the topical use of gentamicin.

FIRST AID

Immediate aid comprises stopping the burn process, followed by the removal of clothing and cooling the wound, preferably with tepid, running water, for 10–20 minutes. This provides pain relief and may prevent deepening of the wound.¹² Hypothermia should be avoided. Oxygen should be given, if available, and patients with burns to head and neck should be kept in a semi-upright position. Burn injury can only be assessed properly in hospital conditions, and priority should be given to early evacuation of the victim.

GENERAL MANAGEMENT: 0–24 HOURS

On admission, a careful history should be taken of the circumstances of the injury, and to elucidate past medical history. The patient should be undressed, weighed, and carefully examined to exclude additional traumatic injury. The extent and depth of injury is assessed with the aid of printed Lund and Browder charts, or by using the ‘rule of nines’ (Figure 73.1). The rule of nines is modified for children (Figure 73.2). A nasogastric tube and urinary catheter should be inserted in patients requiring resuscitation therapy. Escharotomies may be required for circular burns of the trunk and limbs.

Figure 73.1 Rule of nine to estimate body surface area burns in adults.

Figure 73.2 Surface area percentages by age.

FLUID THERAPY: 0–24 HOURS

Fluid therapy is required for injuries exceeding 15% of body surface area (10% in children and the elderly), preferably via a wide-bore peripheral i.v. cannula (preferably not in a burned area). The aim is to provide sufficient salt and water to preserve normal organ function, while minimising oedema formation. Excessive fluid administration increases the risk of circulatory overload in the days following the resuscitation period. Potentially fatal complications of excessive fluid administration include the abdominal compartment syndrome in adults¹³ and the occurrence of cerebral oedema in children.¹⁴ An increasing tendency in recent years to overresuscitate burn patients has been signalled.^15,16 In contrast to other traumatic injuries, burn hypovolaemia is gradual, obligatory and predictable. Aggressive fluid administration will not restore the circulating volume¹⁷ and in the absence of frank shock, bolus fluids should not be given.

Various resuscitation formulae have been published in the past to guide initial fluid therapy. These formulae are entirely experience-based and many are of historical interest only, but all comprise a fluid intake of 2–4 ml/kg body weight per % burn in 24 hours, and a sodium intake of approximately 0.5 mmol/kg per % burn.¹⁸ These findings have led some to employ resuscitation regimens based on the administration of hypertonic sodium solutions, which require a smaller volume of fluid. However, the solute load may be excessive, requiring extra water administration in subsequent days, with an increased risk of fluid overload. The use of isotonic saline solutions is therefore preferred by those without experience of burns resuscitation.

The most widely used resuscitation formula for adults is based on the Parkland Formula, which has been adopted by major training programmes, such as the Advanced Trauma Life Support and the Emergency Medicine for Severe Burns:

The formula thus incorporates a faster rate of administration if initial treatment has been delayed.

Children require extra fluid to compensate for basal needs. For children under 30 kg, the resuscitation formula of Carvajal¹⁹ is useful:

where TBSA is the total body surface area (m²) and TBSAB is total body surface area burned (m²). Again half of the calculated amount is given in the first 8 hours.

These formulae are to be regarded as guidelines only. The actual amount of fluid given depends on the clinical condition and the actual amount of fluid administered can vary widely from that predicted. Adequacy of resuscitation is monitored by vital signs and a targeted urine output of 0.5–1 ml/kg per hour in adults and 1–2 ml/kg per hour in children. Other indicators include warm extremities and return of gut peristalsis. Fluid intake may be adjusted to maintain urine output at the desired range. Requirements are increased in the presence of mechanical ventilation, additional traumatic injury and dehydration (e.g. fire-fighters).

Invasive monitoring is not essential in uncomplicated burns and the results may be misleading, as central pressures are invariably low. Hypoalbuminaemia develops rapidly and may be extreme. The extent to which burn patients will tolerate hypoalbuminaemia is unknown and clinical studies into best practice are awaited. In our unit at present, albumin is given to maintain serum albumin above 15 g/l, commencing 12 hours post burn when capillary integrity has been largely restored.

Thirst is common, but unrestricted oral fluids will increase oedema formation. Controlled quantities of nutritional liquids are recommended to protect gut integrity.²⁰ In patients with extensive injuries, tube feeding at a low rate can be commenced within a few hours of injury.

FLUID THERAPY AFTER 24 HOURS

During the second 24 hours, enteral nutritional intake is increased, while the total rate of fluid administration is gradually reduced. At the end of the second day, fluid intake should allow for generous urine production, while compensating for evaporative losses through the wounds.

The actual fluid loss through wounds varies widely, and depends on the type of burn and topical wound treatment. A useful formula to obtain a rough estimate for insensible fluid loss is:

Electrolyte disturbance is common following burn injury and requires treatment. Hypernatraemia is often a sign of hypovolaemia, confirmed if urine sodium is low. The condition is perilous, especially in the first week post burn, as oliguria and renal failure may develop unexpectedly. The amount of free water given should be increased gradually, particularly in the elderly, to avoid fluid overload. Patients who are in fluid balance may require sodium supplementation to compensate for solute loss in wound exudates.

HAEMOGLOBINUREA/MYOGLOBINUREA

Tissue injury from deep burns, particularly electrical injury, causes the release of myoglobin and haemoglobin from damaged cells. Diagnosis is made on observing discoloration of the urine, from faint pink in mild cases to almost black. Fluid administration should be increased; additional measures such as mannitol (12.5 g/l resuscitation fluid) to encourage diuresis, and bicarbonate to alkalinise the urine pH and increase the rate of pigment excretion may be considered.

PAIN THERAPY

During the first 24 hours, pain management is best achieved by incremental doses of i.v. morphine, or equivalent opiate. Thereafter, the pain suffered by burn patients may be divided into background pain, which is continuous, and procedural pain caused by interventions.²¹ The recurring ordeal of dressing changes, physiotherapy exercises and surgical procedures generates apprehension and anxiety, which compound distress.

Regular pain therapy is required to counter background pain, topped up by extra analgesics prior to procedures. In recent years, the advent of slow-release oral opiate medication has greatly improved the administration of analgesia. Procedural pain is best treated with continuous i.v. morphine or fentanyl, with titrated incremental boluses as required. Patient-controlled analgesia is effective, although modification of the control button may be necessary for those with bandaged hands. Ketamine in subanaesthetic doses is extremely useful for procedural pain in children. The influence of anxiety and depression on pain perception suggests additional avenues of therapy.²² Non-pharmacological interventions, such as hypnosis and other distraction techniques, are an effective adjunct in susceptible patients.²³ Many burn patients may develop posttraumatic distress syndrome, and the emergence of symptoms may require additional support. Above all, an attitude of reassurance and understanding by all carers is indispensable.

NUTRITION

The hypermetabolic response is roughly proportional to the extent of injury. In young adults and children with extensive burns, energy expenditure may be doubled. In addition, protein and substantial amounts of trace elements, such as zinc, copper and selenium are lost in wound exudate.²⁴

There is no doubt that burn patients require additional calories and proteins, but traditional formulae for calculating requirements produce overestimates in the context of current burn care.²⁵ In the absence of direct metabolic measurements we currently use an empirical formula for estimating caloric intake:

where REE is the resting energy expenditure calculated from the Harris and Benedict equation.

Patients with extensive burns will require tube feeds, which are generally well tolerated. If gastric emptying is problematic, a post-pyloric tube is usually effective. A high-protein proprietary feed is usually adequate, but should be supplemented by extra trace elements and vitamins. The possible benefit of glutamine supplements in burns has recently been reviewed.²⁶ Adequacy of feeding is best assessed by monitoring body weight. Adjunctive therapy aimed at promoting anabolism includes the use of insulin to maintain normoglycaemia, the administration of oxandrolone (10 mg twice daily for adults),²⁷ and the use of β-blockers to control tachycardia and extensive catabolism.²⁸

WOUND HEALING

Treatment of extensive, full-thickness burn wounds by early excision and grafting has been firmly linked to survival.²⁹ Wound excision should be completed within the first week, before bacterial colonisation and neovascular infiltration of the wound bed develop. These operations are therefore urgent. Successfully grafted wounds will heal within 5 weeks, reducing the time available for bacterial infection to develop, and shortening the period of physiological disturbance. Wounds covered with widely meshed autografts lose large amounts of fluid, unless protected by a semipermeable layer, such as allograft skin. Autograft donor sites are a further source of fluid loss.

For wounds treated conservatively, the main effort is devoted to the prevention of infection. Topical antimicrobial agents are commonly used, but may have potential side-effects (Table 73.1). These compounds change the appearance of the wound and should never be applied until expert wound inspection is complete. A number of biosynthetic materials are currently available, which are designed to improve cosmetic and functional outcome. Despite the use of antiseptic dressings or biosynthetic coverings there is still a risk of microbial infection developing and unexplained signs of sepsis may necessitate urgent wound revision.

Table 73.1 Commonly used topical antimicrobial agents

PREVENTION OF WOUND INFECTION

Bacterial infection is still the most common cause of death in burns. Depression of the immune system is well documented.³⁰ At the same time, the burn wound presents a favourable medium for bacterial growth.

HEAT INJURY TO THE UPPER AIRWAY

Burns due to the inhalation of hot gases (steam excepted) rarely extend beyond the larynx. The development of mucosal and facial oedema can cause respiratory obstruction, particularly in children.

EFFECTS OF SMOKE ON THE RESPIRATORY SYSTEM

Many of the chemicals that are contained in smoke are highly reactive and produce damage to the tracheobronchial tree. Detachment of epithelial cells and the development of tracheobronchial oedema cause airway narrowing and cast formation. Small airway closure leads to hypoxaemia and respiratory failure. Later, bronchorrhoea and mucosal sloughing may cause atelectasis and provide a focus for infection. In the absence of a cutaneous injury the clinical course is usually benign. However, the presence of an extensive skin burn increases the likelihood of acute respiratory distress syndrome (ARDS); respiratory infection may follow.

INHALATION OF TOXIC GASES

Of the many toxic compounds³⁸ in smoke (Table 73.2), carbon monoxide (CO) deserves special mention. The affinity of CO for haemoglobin is 240 times that of oxygen. The loss of oxygen transport capacity is dependent on the concentration of inhaled CO and the duration of exposure. In addition, CO binds to cytochrome systems, inhibiting cellular oxidative processes. The half-life of COHb is 4 hours when breathing air, compared with 45 minutes when breathing 100% oxygen.

Table 73.2 Common inhaled toxic gases