Thermal injury to the oral cavity and throat can cause oedema of the supraglottic airway, leading to airway obstruction and difficulties with intubation. Patients with burns to the neck are also at risk of airway obstruction due to external compression from oedema and eschar. Maximal oedema typically occurs 8–36 h after the burn injury [7, 8].

Indicators of upper airway burn injury include hoarse voice, carbonaceous sputum, singed nasal hairs, facial burns and/or history of confinement in a burning environment; however, these signs are not sensitive or specific [7]. Clinicians tend to have a low threshold for early tracheal intubation in patients with possible upper airway burn injury, due to valid concerns about impending airway obstruction. It is important to remember, however, that tracheal intubation is not risk free and the majority of patients who are intubated for suspected upper airway burn injury do not actually have it [7]. Intubation should not be performed solely for facial burns [4, 7].

Continuous assessment (especially with regard to voice quality), serial examinations of the intra-oral mucosa (looking for evidence of oedema or blistering) and serial fibreoptic nasendoscopies may be the most accurate way of detecting those at risk of airway obstruction [7, 8]. Upright positioning and avoidance of over-zealous fluid resuscitation will minimize facial and airway oedema [7–9]. The regional burn centre is always available to advise about the management of patients with suspected upper airway burn injury [6].

If tracheal intubation is performed, it is important to leave the endotracheal tube uncut, as massive facial oedema can develop. The initial intubation should be with a size 8.0 mm internal diameter endotracheal tube or larger, as this allows passage of a standard bronchoscope and facilitates investigation and treatment of inhalation injury [9]. Once facial and airway oedema occur, it can be difficult and risky to upsize a small endotracheal tube.

Smoke inhalation is a major cause of morbidity and mortality in burn patients. A dose dependent relationship between degree of smoke exposure and severity of airway injury has been described [10].

Smoke inhalation directly damages the airways, causing exfoliation of the epithelial lining, mucus secretion, inflammatory cell influx and plasma exudation. Intra-airway coagulation and fibrin deposition occurs, which admixes with cellular debris and mucin to form obstructive airway casts. The obstructive airway casts partially or totally obstruct the lower airways leading to gas trapping, alveolar barotrauma, ventilation/perfusion mismatch and the development of pneumonia [10].

Care for patients with inhalation injury includes a lung protective ventilation strategy, serial bronchoalveolar lavage (BAL) to clear soot, casts and mucus plugs, and attention to preventing and treating pneumonia. BAL samples can be subjected to quantitative microscopy, with 10⁴ CFU/mL diagnostic for pneumonia [11].

Treatment with inhaled heparin potentiates anti-thrombin III and prevents the formation of fibrin. It should be initiated as soon as possible, and administered every 4h for 48 h. Adding mucolytic oral carbocisteine and nebulized N-acetylcysteine further minimizes the formation of obstructive airway casts. Inhaled dornase alfa, which cleaves DNA in mucus, might augment the breakdown of cellular debris [10, 11].

Patients with inhalation injury are at risk of systemic toxicity from inhaled carbon monoxide or hydrogen cyanide. These molecules impair the delivery and utilization of oxygen leading to tissue hypoxia. Patients with carboxyhaemoglobin levels above 10 % should be treated with 100 % oxygen. Whilst hyperbaric oxygen therapy may be beneficial, it is logistically difficult to achieve. Treatments for cyanide poisoning include sodium thiosuphate and sodium nitrite [8].

Patients with burns of >15 % TBSA require fluid resuscitation to avoid hypovolaemic shock [5, 12, 13]. Burns involving >30 % TBSA are only partially responsive to fluid therapy as the systemic inflammatory response causes microvascular injury, fluid shifts, vasodilatation, decreased cardiac contractility and decreased cardiac output [5, 14]. Inotropic/vasopressor support may be required if hypotension persists despite fluid replacement [15], although vasoconstriction may extend the burn injury.

There is no consensus on the most effective fluid resuscitation solution or volume. Worldwide, the Parkland Formula is the most commonly used formula and Ringer’s Lactate solution the most commonly used fluid, although colloid is often initiated within the first 24 h of injury [16]. Colloids, including albumin, may reduce oedema-related complications and be warranted in patients with the most severe burns (>40%TBSA) [5, 16].

There is a tendency for patients to receive more fluid than they require, both in the initial resuscitation and ongoing management phases [16–18]. Common problems are for medical staff to inaccurately assess the size of the burn [19], lose track of the amount of fluid delivered or neglect to reduce fluid input in the face of a high urine output. Over-resuscitation is not benign, causing coagulopathy [18, 20], oedema, compartment syndromes and ARDS [15, 16]. It also impacts on the success of skin grafting.

Whilst the Parkland Formula is a useful initial guide, fluid therapy should ideally be ‘goal directed’. The most commonly used parameter to guide fluid therapy is urine output, aiming for 0.5–1 mL/kg/h [16]. Computer controlled feedback technology that automatically controls infusion rates in response to urine output has been developed [21]. This technology may reduce crystalloid infusion volumes [22].

Other units use invasive and non-invasive cardiac output monitoring to dictate fluid and inotrope/vasopressor therapy [16]. In a small study, LiDCO reduced fluid administration and decreased cumulative fluid balance compared with standard monitoring [23].

Oxidative stress is a key component of the systemic inflammatory response and contributes to burn shock. Antioxidant vitamin C has been investigated as a treatment. Matsuda and Tanaka administered high-dose vitamin C to animals and humans and found a decrease in volume of resuscitation and compartment syndromes. Further studies are needed to evaluate efficacy and determine the optimum dose and route of administration, and whether any side effects occur [24].

Other researchers are investigating the use of extra-corporal blood circuits to modulate the inflammatory response in the early post-burn period, either with cytokine removing membranes or continuous venovenous haemofiltration. Both have shown promising results in terms of reducing cytokine levels, catecholamine requirements, ARDS and mortality, albeit in small studies. Further evaluation is warranted [25].

After the first 24–48 h of injury, patients with severe burns enter a hypermetabolic and catabolic state, characterized by hyperdynamic circulation, hyperthermia, hyperglycaemia and rapid muscle wasting. These responses are seen in all surgical and trauma patients, however, the severity and persistence is unique to burn patients. The response is driven by marked and sustained sympathetic stimulation and inflammation, causing catecholamine, glucocorticoid, glucagon, dopamine and cytokine release, particularly IL-6, IL-8, G-CSF and MCP-1. This hypermetabolic state persists for many years after the initial burn injury [26].

Loss of lean body mass after burn injury impairs immune function and wound healing, contributes to the hyperglycaemic state, increases the risk of pressure sores, prolongs mechanical ventilation and increases mortality [26].

Alongside good nutritional support, physiotherapy and early wound closure, some pharmacological therapies may be beneficial in blunting this hypermetabolic and catabolic response, and may preserve muscle mass [5, 26]. Oxandrolone is a testosterone analogue, which enhances protein synthesis and reduces lean mass catabolism. It has been shown to reduce length of stay (LOS) in patients with >20 % TBSA burns [27, 28]. The non-selective beta-blocker propranolol blocks the effects of the catecholamine surge and has been shown to suppress lipolysis, decrease resting energy expenditure, preserve lean body mass and decrease LOS [29].

Hyperglycemia in burn patient populations is associated with stimulation of a persistent inflammatory state, poor wound healing, increased skin graft loss, protein catabolism, infection and death [26, 29]. Studies in both children and adults have shown that controlling blood glucose to a target range of 4–7.5 mmol/L improves morbidity and mortality [30, 31].

Burn injury induces excruciating pain, which is poorly understood and challenging to control. Poorly controlled pain in the acute setting causes distress and lack of engagement with treatment, and leads to chronic pain and post-traumatic stress disorder [32].

Burn tissue damage is caused by direct thermal injury, ischaemia and the inflammatory response. Sensory and sympathetic neurons are activated, sensitized and/or directly injured causing a combination of nociceptive and neuropathic pain [32–34]. Repeated painful insults, such as dressing changes or surgery, cause central sensitization and promote chronic pain development [33, 34].

Burn patients experience background pain, breakthrough pain, procedural pain and post-operative pain [32, 33]. The analgesic regimen should be multimodal, continuously assessed and flexible to meet patients’ varying needs. Early involvement of the pain team is crucial [35].

The usual mainstay of treatment is opioids, but opioids alone are not sufficient [32, 33, 35]. The prolonged requirement for opioids by burn patients leads to tolerance and significantly increased doses. Paracetamol, ketamine and clonidine are useful adjuncts to opioids. Pregabalin and amitriptyline should be initiated early for the neuropathic pain component [35]. Regional anaesthetic techniques can be considered, but are often not useful due to coagulopathy, concerns about infection and the extent of the wounds [33, 35]. General anaesthesia, or deep sedation by an anaesthetist, is often warranted for procedures such as dressing changes [33].

Alterations in the magnitude or type of pain should be fully assessed, as they may indicate the development of burn complications such as wound infection, compartment syndrome or intra-abdominal pathology [33].

Nutritional support is an essential component of burn care. Failure to meet the nutritional requirements of the catabolic burn patient leads to impaired wound healing, susceptibility to infection, development of pressure sores, organ failure and death [5, 26, 36].

The evidence favours enteral over parenteral feeding [5] and it should be commenced as soon as practical. Improved outcomes have been seen when enteral nutrition is initiated <24 h after burn injury [37, 38]. At our institution, a nasogastric tube for enteral nutrition is inserted at the earliest opportunity and converted to a nasojejunal (NJ) tube when trained staff are available. Feeding via the NJ tube removes the requirement for ‘starvation periods’ prior to theatre and significantly increases the amount of nutrition delivered. As NJ tubes easily become blocked, it is useful to deliver medication via an NG tube and use the NJ tube solely for feed. Parenteral nutrition should be considered if patients are not tolerating enteral feed despite aggressive attempts to maximize gastrointestinal motility.