Thermal burn injuries can be some of the most challenging wounds to treat in small animal practice. They commonly occur as a result of scalding, fire or iatrogenic injury from inappropriate patient warming. Successful management of these cases depends on treatment of the patient as a whole, not just the wound.
Local and systemic effects
Profound hypovolaemia can occur within hours of a severe burn, due to systemic extravasation of fluid combined with local vascular leakage and evaporative fluid loss from the burn surface (Ravage et al., 1998). Intense pain stimulates a massive sympathetic response, which promotes the cardiovascular effects of shock.
The systemic inflammatory response to severe burns negatively impacts a number of organ systems, even affecting gastrointestinal barrier function with subsequent translocation of gut bacteria, endotoxin and cytokines, leading to septic shock (Gosain and Gamelli, 2005). Negative effects on leucocyte production and function are also seen, further increasing susceptibility to sepsis. Burn victims experience major changes in energy and protein metabolism, with basal energy expenditure increasing by more than 100 percent (Williams et al., 2009). These factors highlight the importance of stabilisation and supportive care for burn patients.
Successful management requires intensive fluid resuscitation, surgical debridement and comprehensive supportive care. Burn severity can be described as a percentage of total body surface area (TBSA), with major burns affecting greater than 10 percent TBSA, and severe burns affecting greater than 20 percent TBSA, leading to life-threatening systemic complications (Pavletic and Trout, 2006). Burns may be partial-thickness (first and second degree) or full-thickness with loss of the dermis (third degree), muscle or bone (fourth or fifth degree respectively).
Immediate first aid should be provided through applying cool to cold running water (2 to 15°C) directly to the burn wound. Cooling is analgesic and improves long-term wound healing; these beneficial effects are seen as long as cooling is within three hours of injury (Cuttle et al., 2008). The burn should subsequently be covered with a sterile, occlusive, non-adherent dressing to reduce pain, limit contamination and prevent further trauma.
Smoke inhalation significantly influences prognosis and the full effect of this injury may not be seen for 24 to 36 hours. Immediate clinical signs (hypoxia and respiratory crackles/ wheezes) are usually only seen in severe cases. The majority of pulmonary damage and systemic pathophysiology is caused by inhalation of toxic chemicals, including carbon monoxide and hydrogen cyanide (Vaughn and Beckel, 2012).
Treatment protocols for inhalation injury must include bronchial hygiene therapy and oxygen supplementation. Success of treatment can be monitored with pulse oximetry, serial thoracic radiography or simply clinical response. Nebulisation of sterile saline can be combined with oxygen therapy (5 to 10l/min of 100 percent oxygen), to hydrate and loosen mucous prior to chest coupage (Bohling, 2017).
Lactated Ringer’s solution remains the standard crystalloid for resuscitation. In practice, the easiest approach is to calculate an appropriate initial fluid rate, then make adjustments to achieve acceptable values for basic physiologic parameters. In particular, fluid administration should be sufficient to maintain a urine output of approximately 1ml/ kg/hr and mean arterial pressure above 70mmHg (Vaughn et al., 2012). Administration of colloid or albumin should be delayed for 24 hours following injury, as increased vascular permeability can exacerbate oedema (Pham et al., 2008).
Neuroleptanalgesia with opioid and alpha-2 agonist combinations is particularly useful in managing the acute pain associated with burn treatment (Slingsby and Taylor, 2008). Local anaesthetic agents may also be delivered topically before removal of the bandage contact layer; a solution of lidocaine (2 percent) and sodium bicarbonate in a 9:1 ratio has been described (Bohling, 2017). Non-steroidal antiinflammatory drugs, opioids and other analgesics, such as ketamine, delivered as constant rate infusions are then used for managing background pain. Chronic pain can occur due to wound contracture, particularly over high-motion areas, and surgical scar revision may be required.
Nutritional and metabolic management
Major burns cause a hypermetabolic state characterised by hyperglycemia and catabolism of body protein stores. A high-energy critical care diet is therefore recommended, with some evidence suggesting that additional vitamin E supplementation may improve clinical outcomes, particularly for smoke inhalation injury (Morita et al., 2006). Adequate analgesia, sedation and provision for sleep all reduce stress-associated catecholamine release and associated hypermetabolism (Herndon and Tompkins, 2004).
Small partial-thickness burns often heal well by second intention because the dermis is partially intact. Small full-thickness burns can also be managed in this way, but healing will result in scar formation and contracture. Priorities for treatment are adequate analgesia, and protecting the wound from further trauma and infection. The bandage should include a moist (semi-occlusive or occlusive) contact layer to minimise pain, reduce fluid loss and promote autolytic debridement and re-epithelialisation. Topical antimicrobial (silver sulphadiazine) is advised and is preferable to systemic treatment unless this is specifically indicated (Pavletic and Trout, 2006).
Large burns (both deep partial-thickness and full-thickness) should be surgically debrided to remove the eschar (thick, leathery necrotic tissue) and other devitalised tissue (see Figures 1 to 4). Left untreated, infection and systemic inflammatory response syndrome may occur. Sharp surgical debridement of deep burns (excluding muscle and bone) is performed with tangential debridement, where affected tissue is sliced off in very thin layers until viable bleeding tissue is reached. Deeper burns extending to the muscle and bone require layered debridement, starting at the perimeter of the burn where damage is more superficial, progressing inward to debride deeper layers (Bohling, 2017).
Subsequent autolytic debridement with moisture retentive dressings, enzymatic or chemical debridement agents, have all been reported for the removal of residual nonvital tissue (Campbell, 2006). Similarly, negative pressure wound therapy, in conjunction with nanocrystalline silver dressings, has been used, although patients may experience significant discomfort with this treatment (Mullally et al., 2010). Once a healthy granulation bed is established, definitive skin reconstruction with skin grafts or flaps can be performed.
While immediate surgical debridement is strongly recommended, some circumstances may preclude this. Cerium nitrate combined with silver sulphadiazine has been used for over 40 years to treat burn wounds, with results comparable to acute escharectomy and grafting (Vehmeyer-Heeman et al., 2006). Cerium binds to the eschar making it tough, impermeable and firmly adherent to the wound bed for several weeks, before delayed escharectomy and skin reconstruction is performed.
Burn injuries and associated systemic complications pose significant challenges for case management. An understanding of the pathophysiology involved is necessary to provide both effective emergency treatment and ongoing wound management.