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.