Nursing patients with burn injuries can be hugely challenging as the individual may have severe metabolic, cardiovascular and pulmonary derangements, not to mention large tissue deficits. A range of systems have been developed to classify burn wounds including percentage of body surface involved, through to depth of tissue involved and the use of these systems may help in giving a prognosis of the extent of the injury.The treatment of burn wounds can start at home by the owner and appropriate early therapy can make a huge difference to the extent of the injury. All major body systems may be affected due to the nature of the injury and so early fluid therapy, analgesia, respiratory derangements, including carbon monoxide toxicity, wound management and analgesia need to be addressed appropriately. The close monitoring of these patients is vital in order to achieve a good outcome and so these cases rely heavily on good nursing care and attention to detail, so a good background knowledge of these considerations is essential.
It has been said that the burn patient is the ultimate or universal trauma model (Pruitt, 1985). The response to a major burn injury affects all organ systems of the body, and the severity of the response seems to be proportional to the magnitude of the injury. In addition to the age of the patient and the extent of the burn, the depth of the burn injury is of major concern and is one of the most predictable factors influencing mortality following thermal injury. Burn depth is the primary determinant of the patient’s short-term, long-term, functional and cosmetic outcome.
Burn injuries in animals can result in severe metabolic, cardiovascular and pulmonary derangements. The four main types of burn injuries in small animals include thermal, radiation, chemical and electrical, e.g. chewing through electrical wires (Keck et al, 2009; Johnson and Richard, 2003). This article will look specifically at thermal burns. Thermal injuries may be further complicated by smoke inhalation and carbon monoxide poisoning.
Extent of burns
Historically burn wounds have been classified according to the extent of body surface involved and the depth of injury to the skin. Extent of injury is initially estimated in human burn patients using ‘the rule of nines’. This rule divides the adult human body into areas corresponding to 9% of the total body surface area, or multiples of 9%. For example, each forelimb comprises approximately 9% of total body surface area; each hind limb, 18%; head and neck, 9%; chest and abdomen, 18%; back, 18%; and perineum, 1% (Johnson and Richard, 2003; Pavletic and Trout, 2006). The modern burn classification system classifies burns by increasing depth: superficial, superficial partial-thickness, deep partial-thickness, and full thickness (Johnson and Richard, 2003; Paveletic and Trout, 2006) (Table 1).
Table 1.Classification of burn wounds (Vaughan and Beckel, 2012)
| Superficial | Epidermis only | Erythematous desquamation Dry flaky appearance | Heals in 3–5 days via re-epithelialization Minimal scar formation |
| Superficial partial-thickness (Figure 1a, b, and c) | Epidermis Upper 1/3 dermis (papillary layer) | Painful blisters may be present Minimal scar formation Oedema may be present Eschar(thick leathery surface of dead tissue) formation | Minimal scar formation (Figure 1c) Heals in 1–2 weeks |
| Deep partial- thickness | Epidermis All dermis | Red-waxy white appearance Reduced pain sensation Blisters present Eschar formation | Heals in 2–3 weeks Requires surgical intervention to prevent significant scar formation |
| Full thickness (Figure 3a–c) | Epidermis Dermis Subcutaneous tissue | Bloodless pear-white (Figure 2) Requires Eschar formation (Figure 3a, b) Hair easily plucked | surgical intervention |
The depth of injury can be difficult to assess initially, and usually requires repeated evaluation over the first 24 hours for accurate determination. Local burn injuries may take approximately 24–48 hours to become readily apparent to owners and veterinary staff (Paveletic and Trout, 2006; Saxon and Kirby, 1992).
Pre hospital treatment of the burned patient
The first consideration in treatment of the burned patient is to stop the burning process. Because the skin is slow to cool, the burning process may continue for some time after the patient is removed from the heat source. For this reason burned areas should be cooled with running water for up to 30 minutes. Current recommended first aid treatment includes cooling the wounds with cold tap water (15°C (59°F)) for 20–30 minutes (Cuttle et al, 2008). The utilization of wet compress towels (Yuan et al, 2007) are not as effective as water at reducing burn depth. Ice water should not be used as this can rapidly decrease the patient’s body temperature and may contribute to increased wound depth by inducing vasoconstriction, reducing circulation to the immediate area. To avoid hypothermia during transport, the patient should be wrapped in several clean, dry sheets or blankets (Cuttle et al, 2008; Yuan et al, 2007). The temperature of the patient should be monitored closely while cooling burn wounds to avoid hypothermia.
Initial treatment
Since these patients are at such a high risk of sepsis all personnel must wear examination gloves when handling the patient and must use strict aseptic technique (sterile gloves, sterile prep etc) when performing any invasive procedures (placing catheters, collecting blood etc). Analgesia is essential as burns are usually extremely painful.
Pain management
A multimodal analgesic regimen is most effective for management of pain in people and animals (Montgomery, 2004; Richardson and Mustard, 2009). During the acute phase of burn injury, intravenous opioids should be the primary method of analgesia. The degree of pain associated with burn wounds is incredibly varied. Pure agonists such as fentanyl constant rate infusion (CRI: 3-5 μg/kg/hour), methadone (0.1–0.25 mg/kg every 2–4–6 hourly dependent on dosage and patient’s pain score) or morphine (0.1–0.5 mg/kg subcutaneously every 2–4–6 hours) are recommended for patients (cats and dogs) with moderate to severe pain. Ketamine can be useful for the relief of somatic pain, and may be used in conjunction with opioids at a constant rate infusion of 0.15–0.6 mg/kg/hour, or ketamine orally at 8–12 mg/kg per os every 6 hours (Pascoe, 2000). Lidocaine may provide adjunctive analgesia in addition to free radical scavenging properties (Cassutto and Gfeller, 2003), and may also be added at a rate of 1.5–3 mg/kg/hour. Intravenous lidocaine should be used with caution in feline patients. If using CRIs, a loading dose equal to the hourly rate should initially be administered. Each patient should be evaluated individually for optimal analgesia.
Assessment of pain in veterinary medicine can be challenging. Physiologic parameters such as heart rate, blood pressure, and respiratory rate are considered the least accurate when assessing for pain in human patients and behavioural pain indicators have been assessed in both people and animals (Montgomery, 2004). In people able to communicate after burn injury, pain assessment tools including ‘0 to 10’ numeric rating scale, visual analog, descriptor words (e.g. adjectives), face, and colour scales are frequently utilized (Montgomery, 2004; Summer et al, 2007). The Glasgow Composite Measure Pain Scale is a behaviour-based composite scale that is used to assess pain in small animals and could be considered for use in burn patients (Morton et al, 2005; Murrell et al, 2008).
Primary survey
As with all emergency patients, a primary survey should be performed to determine the extent of injury and to institute treatment as needed. Ensuring a patent airway and supporting breathing should be the first priority, followed by fluid therapy to treat hypovolaemic shock. 100% oxygen should be administered to any patient suspected of having smoke inhalation injury to hasten the elimination of carbon monoxide. Intubation or emergency tracheostomy may be required if airway oedema is severe. In the event of orotracheal intubation, tubes should be carefully secured, as worsening oedema may make re-intubation more difficult.
The effects of smoke inhalation injury on the upper respiratory tract are seen within the first 24 hours (Saxon and Kirby, 1992; Fitzgerald and Flood, 2006; Sheridan, 2005). Soot, the principal product of most fires, adheres to the respiratory mucosa allowing other irritants to bind to the mucosa (Fitzgerald and Flood, 2006). Direct thermal injury and adherence of irritants to the upper respiratory tract results in the release of inflammatory mediators and reactive oxygen species (ROS) (by-products of respiration which can cause damage to cell DNA), increased vascular permeability and oedema formation (Fitzgerald and Flood, 2006; Mlcak et al, 2007). The formation of oedema in the upper respiratory tract can progress to airway obstruction and bronchospasm that peaks at 24 hours and subsequently resolves over a few days (Saxon and Kirby, 1992; Cochran, 2009). Haemorrhage, mucosal congestion, ulceration and laryngospasm may also occur within the first 24 hours (Saxon and Kirby, 1992).
Vascular access may be difficult in hypovolemic, burned patients. Ideally, short peripheral catheters should be placed in non-burned areas, though burned areas may be used in the first 24 hours. If burned sites are used for catheterization, the catheters should be removed within 24–48 hours due to bacterial colonization of these areas. Intraosseous catheters are another good alternative for patients in whom vascular access is limited. Central lines may be required in patients with large burns, those needing parenteral nutrition, or those requiring central venous pressure monitoring, their use however should be avoided whenever possible due to the risks associated with hypercoagulability in burned patients.
Fluid therapy
Fluid resuscitation is the single most important treatment for severe burn patients. The goal of fluid resuscitation is to maintain organ perfusion and avoid tissue ischaemia with the least amount of fluid required. Within the first 1–2 hours of injury burn patients experience little change in intravascular volume or haemodynamics. However, a delay in fluid resuscitation beyond 2 hours of burn injury reportedly complicates resuscitation and increases mortality (Latenser, 2009). After the initial 1–2 hour window haemodynamic instability ensues for approximately 24–48 hours after severe burn injury despite fluid resuscitation. Neither preload nor cardiac output is able to be normalized with fluid resuscitation until 24 hours after injury (Pham et al, 2008). In severe burn injury patients with concurrent inhalation injury a marked increase in haemodynamic instability and a 30–50% increase in initial fluid requirement are seen when compared with patients with burn injury alone (Demling, 2005; Saffle, 2007).
‘Consensus formula’ (formerly referred to as the ‘Parkland formula’) has become the most widely used resuscitation guideline in humans and is utilized to calculate the volume of crystalloid required within the first 24 hours after severe burn injury (Latenser, 2009). The formula recommends administering isotonic crystalloids at 4 ml/kg per percentage total body surface area affected in the first 24 hours, with half of this amount administered in the first 8 hours (Saxon and Kirby, 1992; Pham et al, 2008; Latenser, 2009). The remainder of the calculated fluid volume is administered over the remaining 16 hours (Saffle, 2007).
The use of colloids, both natural (e.g. albumin) and synthetic (e.g. hydroxyethyl starches (HES)), in resuscitation of burn patients is controversial. This is due to the concern regarding the leakage of proteins and large molecules through compromised capillary membranes. The recommendations are to wait at least 8–12 hours post burn injury before utilizing colloids (Grunwald and Garner, 2008; Pham et al, 2008). The use of colloids augments colloid osmotic pressure (COP) which has been documented to reduce oedema formation in non-burned tissue (but not in the burn wound itself) (Pham et al, 2008).
The use of hypertonic saline is controversial in the resuscitation of human burn victims (Ipaktchi and Arbabi, 2006; Tricklebank, 2009). Administration of hypertonic saline creates a hyperosmolarity that results in plasma volume expansion due to the shift of fluid into the vascular space (Tricklebank, 2009). Fluid may also be mobilized from the interstitial space by osmotic action which may limit burn oedema (Tricklebank, 2009), but administration of large quantities of hypertonic saline can lead to hypernatremia. Hypernatremia and hyperosmolarity can result in brain shrinkage, intracranial vessel detachment, kidney failure, fluid overload, cerebral oedema, and seizures (Ahrns, 2004).
Secondary survey
Following initial stabilization, a secondary survey should be performed to identify concurrent injuries. Patients should be assessed for neurologic injuries secondary to trauma, hypoxemia, or carbon monoxide poisoning. The abdomen should be assessed for compartment syndrome (increased intra-abdominal pressure due to underlying disease processes), gastric distension, or other traumatic injuries. The airways and thorax should be carefully ausculted for stridor, crackles, or wheezes, and adequacy of ventilation should be assessed. The face, oral cavity, and pharynx should be examined for the presence of burns or particulate debris that may indicate inhalation injury. Baseline radiographs should be obtained to evaluate for changes related to smoke inhalation or traumatic injury. Chest radiographs may be normal initially, although bronchial markings may be present. The development of pulmonary infiltrates or lobar consolidation may suggest pneumonia. Arterial blood gas evaluation is useful for determination of parameters related to oxygenation and perfusion. However, because both partial pressure of oxygen (pO2) and oxygen saturation can be misleading in the presence of carbon monoxide (pulse oximetry will misread carboxyhaemoglobin (CO-Hgb) as oxyhaemoglobin), co-oximetry should also be performed if available to determine carboxyhaemoglobin levels (as co-oximeters allow the direct measurement of carboxyhaemoglobin and oxyhaemoglobin) (Ayres, 2012). Baseline complete blood count, serum biochemistry panel, and urinalysis should be obtained on admission. The presence of myoglobinuria may indicate a need for higher fluid rates to avoid renal tubular damage. Coagulation testing should be performed, as burned patients may suffer from hyper- or hypocoagulable states. The eyes should be evaluated for the presence of conjunctivitis, particulate material, or corneal ulceration. Corneal ulcers are common secondary to thermal injury or abrasion by particulate material, so fluorescein staining should always be performed (Fitzgerald and Flood, 2006). A topical anaesthetic such as proparacaine may be used to facilitate examination behind the third eyelids for foreign material, and the eyes should be copiously flushed with sterile saline (Fitzgerald and Flood, 2006).
Carbon monoxide toxicity
As previously mentioned, carbon monoxide is the most common inhaled agent producing complications in smoke inhalation victims (Fitzgerald and Flood, 2006). The extent of injury secondary to carbon monoxide toxicity is directly dependent on the concentration of inhaled carbon monoxide, the duration of exposure, and the underlying health status of the patient (Kealey, 2009). Carbon monoxide, the product of combustion of organic material in the presence of insufficient oxygen, is rapidly absorbed across the alveolar membrane (Mariani, 2003). Carbon monoxide binds haemoglobin with an affinity 200–250 × that of oxygen (Mariani, 2003; Cochran et al, 2007). This binding of carbon monoxide prevents the binding of oxygen to haemoglobin molecules producing a ‘functional anaemia’ (Mariani, 2003; Duffy et al, 2006; Fitzgerald and Flood, 2006; Kealey, 2009). Carbon monoxide inhibits the release of oxygen and produces cellular hypoxia and thus shifts the oxygen– haemoglobin dissociation curve to the left (Berent et al, 2005; Mlcak et al, 2007). Additional detrimental effects of carbon monoxide toxicity include induction of lipid peroxidation, direct cellular damage, reperfusion injury, and central nervous system demyelination (Mariani, 2003; Fitzgerald and Flood, 2006). The use of supplemental oxygen administration improves SpO2 and decreases the half life of CO-Hgb (Duffy et al, 2006). The elimination half life of carbon monoxide is 5 hours at 21% oxygen, 1 hour at 100% oxygen (Fitzgerald and Flood, 2006), therefore supplementation with increased oxygen concentrations is recommended. Oxygen may be delivered via a face mask, nasal cannula, oxygen hood, oxygen cage, or via intubation. Nasopharyngeal burns can hinder oxygen supplementation via nasal cannula, and so techniques such as oxygen or Crowe collars would be recommended.
Monitoring
Severe burn patients require continuous electrocardiogram (ECG), direct blood pressure (BP), pulse oximetry, frequent arterial blood gases, electrolytes and lactate (to monitor perfusion), biochemical profiles (to check liver, kidney parameters) and complete blood count (to look for infection, anaemia, low platelets etc), coagulation profiles, and a closed urinary collection system with urinary catheter placed aseptically (sterile gloves, sterile technique) (Vaughn et al, 2012). Urine output is routinely measured in patients with severe burn injuries to guide fluid therapy and resuscitation (Latenser, 2009; Tricklebank, 2009).
Placement of a central venous catheter is often associated with a high incidence of thrombosis and infection in burn patients (O’Dwyer, 2011/12). An aseptic peripheral intravenous catheter should be placed as the first choice. When central venous pressure (CVP) cannot be used serum lactate can help guide therapy. It will increase as anaerobic metabolism increases, and as it is a marker of perfusion, will decrease as perfusion increases. The advantage of monitoring CVP is that it tells you how the right side of the heart is handling the fluid load delivered to it (O’Dwyer, 2011/2012). If a central line must be placed it should be removed as soon as possible.
Wound management
Early priority in the management of burn wounds is lavage and debridement. A flush should be set up using a litre of warm lactated Ringer’s solution (LRS), an extension set and a stopcock with a 35 ml syringe and an 18 g needle attached. This allows for the optimal pressure (~8psi) to irrigate the wound. Higher pressures are more likely to drive bacteria deeper into the wound, while lower pressures do not adequately remove debris (O’Dwyer, 2007). The area around the wound is scrubbed with chlorhexidine solution and flushed with the warm LRS. The wound itself is only flushed with warm LRS as chlorhexidine and iodine are both lethal to fibroblasts in vitro, and therefore are likely to inhibit wound healing (Sanchez et al, 1988). Flushing should be continued until all debris is removed.
Once adequate lavage has been performed topical treatments are generally applied to the wound. Topical antimicrobial agents should be instituted after initial decontamination to prevent bacterial colonization of the burn wound (Sheridan, 2005; Duffy et al, 2006). Systemic agents are less successful in treating local infections because they do not reach the burn wounds in large concentrations due to microthombosis of vessels and wound oedema causing compression of the vessels that supply the area (Honari, 2004). An antimicrobial agent should be applied directly to the burn wound. The area should then be covered with a non-adherent dressing, e.g. foam type dressing. The most common topical agents used in the UK for treatment of burn wounds include silver sulfadiazine and honey (Pavletic and Trout, 2006; Latenser, 2009). Silver sulfadiazine (SSD), a water-soluble cream base synthesized from silver nitrate and sodium sulfadiazine, has long been considered the gold standard in topical burn treatment (Pavletic and Trout, 2006; Latenser, 2009). SSD has a broad antimicrobial spectrum and fair to good eschar penetration with minimal adverse side effects in people (Duffy et al, 2006; Atiyeh et al, 2009). Recently, sustained silver releasing products have been developed combining a silver agent with a ‘carrier’ dressing, e.g. foam dressing. Such products can be applied to partial thickness burns and can remain in place for 3–7 days (Duffy et al, 2006) (Figures 1a, b and c). This eliminates manipulation of the burn site and the pain associated with dressing changes (Latenser, 2009; Atiyeh et al, 2009). SSD should not be used in patients with kidney or liver failure and has been shown to cause a transient leukopenia in human burn patients, which resolves with discontinuation. It is recommended to change to another topical medication if the patient’s white blood count begins to fall.
Figure 1a. Partial thickness burn, only the epidermis and part of the dermis has been lost.
Figure 1b. Partial thickness burn, 5 days following injury, healing is beginning to occur.
Figure 1c. Complete healing, and regrowth of hair 13 days later.
Figure 2. Shih Tzu puppy with full thickness burns to ventral neck after getting stuck behind a radiator. The classic ‘pear white’ colour to the burn can be seen.
The use of honey for treatment of wounds has been employed for many years due to its antimicrobial properties, but limited information is available regarding its utility in burn wounds (Langemo et al, 2009). Antimicrobial properties include a high osmolarity, a low pH and the production of hydrogen peroxide (Kwakman et al, 2008; Langemo et al, 2009). Non-standardized honey, from the natural environment, has a variable antimicrobial spectrum whereas a medical grade honey has a broad spectrum of action that is highly reproducible (Kwakman et al, 2008). Honey not only provides a physical barrier to invading organisms but it also provides a moist environment for wound healing (Wijesinghe et al, 2009). Honey results in a greater healing rate, less contracture, decreased over-granulation, increased wound strength and a more sterile environment when compared with SSD (Wijesinghe et al, 2009) (Figures 3a, b and c). Manuka honey is the author’s topical treatment of choice for burn wounds.
Figure 3a. Eschar formation on a German Shepherd Dog involved in a house fire.
Figure 3b. Escharectomy being performed on the German Shepherd Dog in Figure 3a.
Figure 3c. The same German Shepherd Dog after several weeks’ treatment with manuka honey. Epithelialization is occurring from the multiple ‘islands’ of skin. This meant surgical intervention was not required.
Debridement is the next stage of wound manage and this is frequently performed via sharp or surgical debridement once the patient is deemed stable enough to tolerate general anaesthesia. Research has indicated that an earlier and more aggressive surgical approach leads to attenuation of the hypermet response and decreased infection rates (Saxon and Kirby, 1992; Pavletic and Trout, 2006; Williams et al, 2009). Early burn wound excision decreases re of proinflammatory mediators (Williams et al, 2009; Chang et al, 2010). The increased permeability of the burn eschar causes excessive fluid, protein, immunoglobulin, and electrolyte loss (Bishop, 2004). In addition, the eschar promotes bacterial growth. Escharectomy is the best means of preventing bacterial infections and sepsis and exposes a viable bed of tissue for skin grafting or permanent wound closure this is generally carried out as part of a surgical debridement process (Orgill, 2009).
Nutritional support and the hypermetabolic response
Nutritional support is an important component of burn care, and should ideally be provided as soon after fluid resuscitation as possible. During the hy phase, burn patients experience in muscle catabolism and a negative nitrogen balance resulting in the loss of lean body mass and severe muscle wasting. Accurate caloric and protein requirement estimation and appropriate supplementation are necessary to support metabolic energy requirements (Chinkes et al, 2009). Institution of enteral feeding within 24–48 hours post burn injury is recommended (Saxon and Kirby, 1992; Pavletic and Trout, 2006; Williams et al, 2009). Enteral nutrient is superior to parenteral nutrition because it maintains gut motility, decreases plasma endotoxin and inflammatory mediators, preserves ‘first pass’ nutrient delivery to the liver and decreases intestinal ischaemia and reperfusion injury (Chen et al, 2007). Parenteral nutrition should be administered only when patients do not tolerate enteral nutrition due to vomiting, oral ulceration, prolonged ileus, or during the perioperative period (Latenser, 2009; Chen et al, 2007). Even in these situations enteral nutrition may be provided via oesophogostomy or gastrostomy tubes.
Resting energy requirements (RER) may be calculated using the formula: RER = (weight (kg) x 30) + 70. Calculation has largely fallen by the wayside in veterinary medicine, however, multiplying RER by an illness energy requirement (IER) of 1.3–1.7 (Newton and Heimburger, 2006) may be appropriate in the burn patient to compensate for the anticipated hypermetabolic response. The use of such formulas has been shown to correlate poorly with actual energy requirements in both human and veterinary patients O’Toole et al, 2004).
Conclusion
Burn patients can be incredibly difficult to deal with and challenging patients to nurse in terms of the complexity of their multifactorial effects on the major body systems. However they can be highly rewarding as they allow veterinary nurses to carry out holistic nursing of the patient and put all their knowledge into action. Almost every aspect of ‘nursing needs to be considered from analgesia, nutrition, wound management, fluid therapy through to respiratory and cardiovascular considerations. This means these cases can be very demanding from beginning to end, but with good nursing and appropriate treatment these cases should have a rewardingoutcome.
Key Points
Honey results in a greater healing rate, less contracture, decreased over-granula, increased wound strength and a more sterile environment when compared with SSD.
The depth of injury can be difficult to assess initially, and usually requires re evaluation over the first 24 hours for accurate determination.
The burn patient is the ultimate or universal trauma model.
Burn injuries in animals can result in severe metabolic, cardiovascular and pul derangements.
Since these patients are at such a high risk of sepsis all personnel must wear examination gloves when handling the patient.
Fluid resuscitation is the single most important treatment for severe burn patients.
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