The worldwide incidence of fire-related injuries was estimated to be 1.1 per 100000 populations in 2004 (Forjuoh, 2006). The most vulnerable groups for burn injuries are children, women and the elderly. Lack of supervision of children, frailty and co-morbid illnesses of the elderly, clothing made of flammable materials, parental illiteracy, congested housing, preexisting impairment of a child and low socioeconomic status are important risk factors for burn injuries (Atiyeh et al., 2009a; Parbhoo et al., 2010; Peck, 2011; Balan and Lingam, 2012).

The majority of burn injuries worldwide are unintentional. Less than 5% are deliberate self-burnings or the result of abuse, with regional exceptions (Peck, 2012). Assault, usually by a spouse, is most often caused by throwing caustic chemicals or flammable liquids at the victim’s face or genitalia or by the ignition of clothing (e.g. dowry deaths in India) (Shaha and Mohanthy, 2006; Kumar et al., 2013). In locations with seasonal variations of temperature, burns occur more frequently in the colder winter months. Clothing ignition, such as bedclothes and loose-fitting cotton garments, is a common cause of unintentional and intentional severe flame burns. Work-related injuries account for 20–25% of all serious burns, with the most common being fire or flame and scald. Food service industries (e.g. restaurants that use deep fryers) are responsible for 12% of work-related injuries (Dissanaike and Rahimi, 2009; Dissanaike et al., 2009; Teo et al., 2012).

Infants in Africa have an incidence of fire-related burns that is three times the world average for this age group (Peck, 2011). In children younger than three years, scalds are responsible for most of the burns (Lowell et al., 2008). Scald burns usually occur when a child accidentally pulls a container with hot liquid onto themselves. It may also result from bathtub submersion injuries, usually by an unattended child. In older children, flame burns are more common. Young children are particularly vulnerable to thermal injury, partly due to a lack of discernment about what could be hazardous. In addition, the relative immobility of infants means that they may not be able to move away from the hot substance or surface, which can result in a deeper burn (Birchenough et al., 2008). Burns account for 10% of all cases of child abuse (Parbhoo et al., 2010). Contact with heated objects including cigarettes, irons, curling irons, hair dryers and heated kitchen utensils are commonly used in abuse cases (Van Niekerk et al., 2004; Parbhoo et al., 2010).

A burn is a traumatic injury to the skin or other organic tissue primarily caused by thermal or other acute exposures. Burns occur when some or all of the cells in the skin or other tissues are destroyed by heat, cold, electricity or caustic chemicals. Burns are acute wounds caused by an isolated, non-recurring insult and the majority of burn injuries progress rapidly through an orderly series of healing steps. Flame injuries are the most common causes of burns. This is followed by scalding, contact with a hot object, electrical and chemical injuries (Sheridan, 2002).

The following types of burn injuries are discussed in this section:

Chemical burn injuries may occur as a result of assault, attempted suicide or may be work-related. In work-related injuries the extremities are mostly involved, whereas in the case of assault or attempted suicide the head, neck and trunk are mostly affected (Olaitan and Jiburum, 2008; Tahir et al., 2012; Li et al., 2013). Injury to the skin and underlying structures is caused by a wide range of corrosive reactions. This includes alteration of pH, disruption of cellular membranes and direct toxic effects on metabolic processes. Injury severity is determined by the duration of exposure and the nature of the agent. Tissue coagulation will result from acid contact, while alkaline burns results in liquefactive necrosis. Systemic absorption of some chemicals is life threatening (Palao et al., 2010). Complications associated with chemical burns include respiratory failure, septicaemia, renal failure, blindness, axillary contractures and hypertrophic scarring, to name a few, and often lead to a prolonged hospital stay (Olaitan and Jiburum, 2008).

Inhalation injury is defined as the aspiration of superheated gasses, steam, hot liquid and toxic products of incomplete combustion. Inhalation burns are a predictor of injury severity, need for ventilation and mortality (Osler et al., 2010; Kasten et al., 2011). Inhalation injuries will increase the risk of death by 20% irrespective of the victim’s age and the extent of the burn injury (Osler et al., 2010). There are three phases of inhalation injury (upper airway thermal injury, lower airway and lung parenchyma chemical injury and systemic toxicity), which are discussed below.

Thermal injury is usually limited to the oropharyngeal area due to the poor conductivity of dry air, rapid heat dissipation of the smoke-filled air and reflex closure of the glottis. Animal experiments have shown that at 142°C, inhaled air cools to 38°C by the time it reaches the carina. The thermal injury results in mucosal oedema; this peaks at 24 hours after the initial insult and resolves within the first week. This oedema can cause upper airway obstruction and will develop independent of fluid resuscitation. Steam can burn the airway below the glottis due to the high conductivity of moist air (Mlcak et al., 2007). Because the paediatric airway is much smaller than that of an adult, it may be more rapidly and readily occluded as a result of oedema after thermal injury (Sheridan, 2002).

The lower respiratory tract is mostly damaged by steam inhalation, but toxic chemicals (aldehides, oxides of sulphur and nitrogen) produced in fires may also injure the lower airways with chemical burns. Inhalation of the toxic products resulting from incomplete combustion destroys the epithelial layer of the airways, resulting in airway sloughing. In reaction to the damaged epithelium, mucosal oedema develops, causing airway obstruction. The release of oxygen free radicals and inflammatory mediators contribute to the development of pulmonary oedema, which may occur within two days after injury (Church et al., 2006). In addition, hyper-secretion of mucus and epithelial ciliary damage decreases the effectiveness of the mucociliary clearance system. As a result, patients present with excessive amounts of secretions which further increase airways obstruction. This, coupled with surfactant inactivation due to destruction of type II pneumocytes, could result in atelectasis. Ultimately, ventilation/perfusion (V/Q) mismatch develops as the alveolar injury progresses, while there is an increase in lung and bronchial blood flow (Demling, 2008). A clinical picture consisting of a decrease in lung compliance, hypoxia and hypercarbia develops. If not managed effectively, pneumonia may develop any time between four days and four weeks after inhalation injury (Demling, 2008).

Combustion of plastics, polyurethane, wool, silk, nylon, rubber and paper products can all lead to the production of cyanide gas. Cyanide interferes with cellular metabolism by binding the ferric ion in cytochrome a3. Anaerobic metabolism ensues, with the development of lactic acidosis and decreased oxygen utilisation. Cyanide poisoning should be suspected in burn patients who present with persistent lactic acidosis despite adequate fluid resuscitation (Huzar et al., 2013). The extent of the damage caused during inhalation injury is related to duration of exposure and the nature of the materials aspirated.

The thermoregulatory system resets to a higher baseline temperature of around 38.5ºC after burn injury. Adult patients suffer from hyperthermia due to the metabolic response to systemic inflammation or an infective process. Cellular injury and death may ensue if hyperthermia is sustained above 40ºC (Nachiappan et al., 2012).

The large BSA to body mass ratio of the child, in addition to the thinner skin and subcutaneous layers, predisposes the child to hypothermia, which is important to avoid. In very young children, temperature regulation is partially based on non-shivering thermogenesis, which further increases metabolic rate, oxygen consumption and lactate production. The thin skin in young children may make the initial burn depth assessment difficult (Sharma and Parashar, 2010).

Burn wounds are not usually uniform in depth and many have a mixture of deep and superficial components. A precise classification of the burn wound may be difficult and may require up to three weeks for a final determination. Thin skin, particularly on the volar surfaces of the forearms, medial thighs, perineum and ears, sustains deeper burn injuries than suggested by initial appearance. It is best to assume there are no shallow burns in these areas. Children under the age of five and adults over the age of 55 are also more susceptible to deeper burns because of thinner skin.

The traditional classification of burns as first, second, third or fourth degree is now replaced by a system that reflects the need for surgical intervention. Current designations of burn depth are superficial, superficial partial thickness, deep partial thickness and full thickness. The term fourth degree is still used to describe the most severe burns. These are burns that extend into the muscle, bone and joints.

Superficial or epidermal burns involve only the epidermal layer of the skin. They do not blister but are dry, painful, red and blanch with pressure. Over the following two to three days the pain and erythema subside. By day four, the injured epithelium peels away from the newly healed epidermis. Such injuries are generally healed in six days without scarring. This process is commonly seen with sunburns (Rice and Orgill, 2012).

Partial thickness burns involve the epidermis and portions of the dermis. They are characterised as either superficial or deep (Kasten et al., 2011; Rice and Orgill, 2012).

These burns characteristically form blisters between the epidermis and dermis within 24 hours and are painful, red, weeping and blanch with pressure. Burns that initially appear to be only epidermal in depth may be determined to be partial thickness 12–24 hours later. These burns generally heal in seven to 21 days; scarring is unusual, although pigment changes may occur. A layer of fibrinous exudates and necrotic debris may accumulate on the surface, which may predispose the burn wound to heavy bacterial colonisation and delayed healing. These burns typically heal without functional impairment or hypertrophic scarring.

The eschar eventually separates from the underlying tissue and reveals an unhealed bed of granulation tissue. Without surgery, these wounds heal by wound contracture with epithelialisation around the wound edges. Scarring is severe with contractures and complete spontaneous healing is not possible (Rice and Orgill, 2012).

Advances in the medical and surgical management of patients with burn injury have improved the mortality and morbidity. The medical and surgical management of patients with burn injuries is divided into:

The secondary survey may take place in the emergency department or in the burn unit. It is a ‘head-to-toe’ evaluation of the patient, which involves taking a detailed history of the patient as well as a complete neurological and physical examination including the abdomen, cornea, ears (especially with explosion trauma), genital region, lower and upper limbs. The history should include mechanism of injury, time of injury, consideration of abuse (especially if the patient is a child) and lastly, possibility of carbon monoxide intoxication (based on presence of soot in the mouth and nose and on a history of burns in a closed area) (Alharbi et al., 2012).

Definitive care is initiated after completion of the primary and secondary surveys. Definitive care has been broken down into care provided over the first 24 hours, surgery and wound management. Each of these is discussed below.

Ringer lactate, ringer acitate or balanced electrolyte solutions may be used for fluid replacement therapy over the first 24 hours of admission. The use of colloids and other blood products is not recommended during this time period as these have been shown to prolong tissue oedema and increase the risk for mortality (Latenser, 2009; Alharbi et al., 2012).

Patients with burns have a markedly increased caloric requirement because of the development of a hypermetabolic response after injury as a result of the burn itself, catecholamine release, pain and anxiety, surgical interventions and tissue metabolic demands. Delivery of appropriate nutrition (including protein and carbohydrate) to a patient with burn injuries is vital for wound healing, management of inflammation, suppression of the hypermetabolic response and reduction of sepsis-related morbidity and mortality (Kasten et al., 2011). The patient’s caloric needs are determined using the Harris Benedict equation or the Curreri formula (Alharbi et al., 2012). Adult patients with 20% TBSA burn or greater will be fed through enteral feeding tubes (nasojejunal or orojejunal) to ensure adequate nutrition is supplied to meet the patient’s energy needs (Hall et al., 2012). In general, a child with a burn greater than 20-30% TBSA will require placement of a nasoduodenal feeding tube to provide the required caloric supplementation (Sharma and Parashar, 2010).

Routine interventions include screening for bacterial colonisation. This is done using cotton swabs that are swiped over different bodily areas such as the mouth, nose, burn and inguinal areas. Re-evaluation of the TBSA and depth of burn wounds is performed after the patient is washed. At this stage determination of indications for emergent surgery (debridement, escharotomy or skin grafting) is done. Circumferential burns over the abdomen may lead to organ hypoperfusion and could lead to burn-induced compartment syndrome. Abdominal compartment syndrome can lead to impairment in renal function, gastrointestinal ischaemia, and poor perfusion of the cardiac and pulmonary systems (Latenser, 2009). Compartment syndrome may also develop in extremities with circumferential burns. Intra-abdominal pressure should be monitored regularly for the early identification of the development of compartment syndrome.

Pain originates from various sources in patients with burn injury. Pain management for patients with burn injury therefore becomes quite complex. Pain originates from the site of injury as a direct result of injury to and stimulation of nociceptors in the dermis and epidermis (De Castro et al., 2013). Pain is also generated from the local inflammatory response to injury, which is activated a few minutes after injury. Numerous chemical irritants are released into the area and sensitise and stimulate the nociceptors. This leads to primary hyperalgesia, which means the injured area remains painful and sensitive to mechanical and thermal stimuli (De Castro et al., 2013). Secondary hyperalgesia develops in the tissues that surround the burn site. As the inflammatory response subsides over time, a change in pain quality is observed. Where nociceptors are destroyed as a result of severe burn injury, insensitivity to pain may be noted initially; however, neuropathic pain may develop in these areas as nerve tissue regenerates in a disorderly fashion. Neuropathic pain develops in over half of patients with severe burn injury and is chronic in nature (De Castro et al., 2013). Pain also originates from procedures such as placement of lines or cleaning of wounds. Effective pain management is crucial for the successful management of patients following burn injuries. Ineffective pain management may result in the patient distrusting the interdisciplinary team and has a negative impact on early patient rehabilitation. It may also lead to the development of psychiatric disorders such as depression and post-traumatic stress disorder (De Castro et al., 2013).

Dead tissue is an excellent medium for the growth of bacteria, so it needs to be removed as quickly and thoroughly as possible in patients who have sustained burn injury. Evidence shows that early burn wound excision (between days two and seven of admission) leads to decreased mortality and length of hospital stay in patients aged 30 years or younger (Kasten et al., 2011).

Deep cleaning and removal of dead tissue and contaminants from burn wounds is called debridement. Some units make use of burns baths or shower the patient in the cubicle even in the ICU setting. Autolytic, enzymatic or surgical means can be used to perform debridement and are discussed below (Alharbi et al., 2012).

Severely burnt tissue can be tense, firm and leathery in appearance. It is immobile, rigid and constrictive in nature. This type of tissue is called eschar. If eschar is circumferential around a limb or the thorax it can restrict movement, circulation or respiration. In this situation the eschar must be cut to prevent damage. The surgical cutting of eschar is called escharotomy. If escharotomy is necessary, it is usually quite evident soon after admission or within the first few hours. Escharotomy is usually a surgical emergency to prevent death of tissue or limb loss. If eschar is affecting the limbs, longitudinal incisions are generally used, starting, if possible, on unburned tissue, cutting through the eschar to expose the fatty tissue below and ending in unburned tissue. These incisions can be very extensive and in multiple sites simultaneously (Alharbi et al., 2012). Due to the amount of tension in the tissues, this longitudinal incision often widens substantially after the procedure. This is in direct proportion to the amount of pressure the tissues were under prior to the escharotomy being carried out. The site may require grafting at a later stage for skin closure.

The main aims of burn wound management are to prevent wound infection and facilitate the closure of wounds. This can generally be achieved spontaneously in superficial burns. After any of the abovementioned surgical procedures, the open wound will require coverage. The various methods of wound closure are discussed below.