• It is important to remember a burned patient is also a trauma patient with the potential for other injuries beyond those related to the burn.
• Morbidity and mortality increases with increased BSA % of burn, in the very young or very old, and when pre-existing diseases are present such as cardiovascular, renal or pulmonary disorders. 
• Standard approach to trauma is followed including assessment for C-spine and head injuries, pulmonary and abdominal trauma, fractures etc.
  

• Carbon Monoxide Poisoning
  
  
• PaO2 may be elevated with a low oxygen saturation (carbon monoxide preferentially combines with hemoglobin instead of oxygen)
• pulse oximetry cannot distinguish between oxyhemoglobin and carboxyhemoglobin, resulting in falsely elevated SpO2 reading 
• carbon monoxide toxicity contributes to the metabolic acidosis by limiting oxygen transport to tissues
• carbon monoxide levels are measured as carboxyhemoglobin
  
  
• Upper Airway Obstruction Secondary to Edema
  
  
• superheated air typically causes injury to structures above the vocal cords; lower respiratory tract is not usually affected
• airway burns should be suspected if carboxyhemoglobin is high or burns occurred in an enclosed space
• edema with impaired upper airway patency may not occur for 12 to 18 hrs
• edema is progressive during the first 18 to 24 hrs - if airway burn is suspected, prophylactic intubation should be done early 
• soot in the nares or mouth, or burned/swollen lips indicate that intubation is warranted
• a deep neck burn may cause external compression of the airway as the skin lacks the elasticity needed to accommodate tissue edema (compartment syndrome); escharotomy may be required
  
  
• Chemical Burn to Upper and Lower Airways
  
  
• water soluble gases found in smoke from burning plastics or rubber reacts with water in mucous membranes to produce strong acids and alkalies
• may cause bronchospasm, ulceration, edema and damage to ciliary mechanism
• lipid soluble compounds are transported to lower airways on carbon particles and produce cell membrane damage and alveolar flooding
• pulmonary infections are common
• corticosteroids increase mortality and are contraindicated
• only treat infections documented on culture (to reduce chance of developing infections with resistant organisms)
• pulmonary edema may develop as a consequence of profound hyponatremia associated with burns, excessive fluid resuscitation or renal failure
  
  
• Impaired Chest Wall Compliance
  
  
• present with full thickness burns to thorax due to loss of elasticity of skin
• full thickness burns to abdomen can impair ventilation due to abdominal compartment syndrome
• increased chest wall resistance from burned skin can lead to laboured breathing and rapid respiratory deterioration
• increased CVP secondary to raised intrathoracic pressures can accelerate the rate of protein and fluid loss into the burn tissue and increase the chest wall edema
• urgent escharotomy is required on admission, and should extend into fat and possibly through the fascia 

 
Monitoring and Management


• maintain 100% oxygen therapy to enhance oxygen binding with hemoglobin (100% oxygen decreases the half life of carbon monoxide to 45 minutes)
• monitor carboxyhemoglobin and blood gases (the pulmonary lab at SSC measures true oxygen saturation; calculated values will not be reliable)
• pulse oximetry is unreliable - it overestimates oxygen saturation if carbon monoxide or methemoglobin levels are increased
• monitor for metabolic acidosis or lactic acidosis - can develop as a result of carbon monoxide poisoning or cardiovascular shock
• assess for evidence of inhalational injury (suspect if burn occurs in enclosed space or if carboxyhemoglobin is elevated)
• soot, singed airways, stridor, hoarseness or wheeze indicates need for intubation - AIRWAY EDEMA WILL GET WORSE OVER INITIAL 24 HRS - PROPHYLACTIC INTUBATION IS INDICATED IF EVIDENCE OF AIRWAY BURNS ARE PRESENT ON ADMISSION! 
• bronchoscopy may be performed to assess airway for injury
• be careful not to cut the endotracheal tube too short - leave several inches of endotracheal tube beyond the mouth to allow for facial and lip swelling (which can be extensive!) 
• observe for neck burns that could further compromise airway
• monitor respiratory status for increased RR rate, effort, minute volume and blood gases  - monitor closely for need to mechanically ventilate
• depolarizing agents such as succinylcholine are CONTRAINDICATED if neuromuscular blockade is required for intubation - use non-depolarizing agents such vecuronium if required (deplolarizing agents may worsen hyperkalemia)
• increased effort, peak airway pressures or CVP could indicate compartment syndrome secondary to thoracic or abdominal burns, hemo/pneumothorax or pulmonary edema
• difficulty with clearance of secretions increases risk for secretion retention; PEEP, Bronchodilators, frequent suctioning and chest physiotherapy important
• monitor for signs of pulmonary infection
  
  

• Burn Shock
  
  
• the result of massive fluid shifts where intravascular volume is lost into burned and nonburned tissue
• increased vascular permeability, raised tissue osmotic forces and cellular swelling contribute to the loss of intravascular volume
• myocardial depressant factor may contribute to shock by decreasing myocardial contractility
  
  
• Burn Edema
  
  
• during the first 6 to 8 hours, there is a large loss of protein rich fluid from the intravascular compartment to the interstitial fluid, due to vascular permeability
• intravascular protein loss results in a loss of the protein gradient between the plasma and interstitium
• interstitial edema fluid forms a gel after approximately 12 hrs and leads to obstruction of local lymphatics
• tissue oxygen tension decreases with edema as distance for oxygen delivery increases
• the increased permeability gradually returns to normal by 24 hrs
  
  
• Changes in Nonburned Tissue
  
  
• fall in intravascular colloid pressure drives fluid into interstitium 
• vascular permeability is only minimally affected
• impairment of Na/K ATPase leads to a shift of sodium and water from the extracellular space into the cell
• ATPase is normalized by 24 hrs if fluid resuscitation is adequate 
  
  
• Hypermetabolic State
  
  
• beginning at day 5, there is a gradual increase in the metabolic rate to levels ranging from 2 to 2.5 X normal at day 10
• characterized by increased oxygen consumption (cardiac output and minute volume), heat production, body temperature, hyperglycemia and protein catabolism
• cardiac output and CO2 production can double
• augmented enteral feedings should be initiated within 48 hrs of the burn injuries
• inflammatory mediators generate SIRS (systemic inflammatory response syndrome), increasing the potential for circulatory failure

 
Monitoring and Management


• Fluid Management
  
  
• monitor BP, HR and urine output closely (as evidence of adequate fluid resuscitation)
• monitor electrolytes, especially potassium and sodium
• fluid resuscitation is the cardiovascular priority in burn management
• the larger the area of burn, the more significant the fluid deficit
• the goal is to achieve a balance between the restoration of adequate tissue perfusion while minimizing edema formation
• administer Lactated Ringers as per the Parkland Formula (one guide for fluid replacement) - lactated ringers is preferred as it matches extracellular fluid more closely than normal saline 

Caution: Ringers Lactate contains potassium; if renal failure develops, ringers lactate can contribute to hypekalemia
• 4mL/kg/% BSA of burn - give 50% in first 8 hrs and remaining volume over next 16 hrs (serves only as a guideline and should be modified according to hemodynamic parameters)

Caution: trauma victims with other injuries may require higher replacement volumes
• rapid boluses are discouraged as they transiently increase pressure and increase the rate of fluid loss into the burn
• at 8 to 10 hrs, the rate should be decreased to the lowest level needed to maintain adequate perfusion
• colloid (5% Albumin) may be introduced at 8 to 24 hrs as a drip at the rate of 0.5 cc to 1.0 mL/kg/% BSA burn 
• large fluid and/or blood products may be required following surgical debridement
  
  

Pharmacological Support



• inadequate volume resuscitation should be considered as the main cause for hypotension in the first 3 days, and following debridement of wounds
• inotropes may be required if hypotension persists despite fluid replacement
• beyond 3 days, increasing need for inotropes or vasoconstrictors may indicate development of septic shock
• monitor for signs of infection or sepsis 
  
  

• Secondary to Burn Shock
  
  
• renal blood flow should be monitored closely to reflect the adequacy of systemic perfusion during the early phase of injury; the target urine output is 0.5 to 1.0 mL/kg/hr
  
  
• Secondary to Rhabdomyolysis
  
  
• compartment syndrome can develop as a result of loss of tissue elasticity
• compartment syndrome requires early escharotomy to preserve tissue perfusion (late escharotomy can result in the release of lactic acid, potassium and other metabolites from dead tissue, with subsequent cardiovascular collapse)
• rhabdomyolysis (or breakdown of skeletal muscle) can occur as a result of compartment syndrome or burn injury
• rhabdomyolysis is diagnosed by elevated serum myoglobin and myoglobinuria
• to prevent renal failure if rhabdomyolysis occurs, increased fluid resuscitation, aggressive diuresis and alkalinization of the urine with a bicarbonate infusion is required

 

Preferred Sites for Escharotomy

Monitoring and Management

• monitor urine output, creatinine and BUN
• hyperkalemia can develop early in the burn injury as a result of metabolic acidosis and the release of potassium from damaged cells
• kayexalate or insulin/dextrose to treat early hyperkalemia is not recommended; hyperkalemia will usually resolve with fluid resuscitation and correction of acidosis
• hypokalemia is common during resuscitation and can be exaggerated by nasal gastric loss or diarrhea
• hyponatremia is common due to loss of sodium through the burn wound and dilution during fluid administration
• monitor for compartment syndrome and treat early with escharotomies
• monitor urine myoglobin and treat rhabdomyolysis 
  
  

• with a deep burn, the barrier to evaporative water loss is impaired, promoting heat loss 
• heat loss can lead to an increased metabolic rate as the burn victim attempts to maintain body temperature
• heat loss is decreased by covering the wounds and maintaining high room temperatures
  
  

Cleansing 

• keep wounds covered to minimize infection
• avoid prophylactic systemic antibiotics - not useful because wounds are avascular and antibiotics may promote the growth of resistant organisms
• topical antibiotic creams such as Flamazine control bacterial counts and increase comfort
• aggressive wound debridement is essential to the removal of potential sources for infection such as bacteria and necrotic tissue
• eschar (dead tissue) must be removed with scissors and forceps or scalpels; small areas can be debrided during routine burn dressing changes
• wet to dry dressings and scrubbing of wounds during dressing changes can enhance mechanical debridement
• enzymatic debriding agents may be ordered to loosen eschar and promote removal, particularly in patients unable to go to the OR
• frequent surgical debridement is optimal to remove non-viable tissue; bleeding and fluid loss is generally significant after debridements
• monitor all wounds for purulent drainage or signs of infection
  
  

Grafts and Dressings

• polyurethane film is useful for simple partial thickness burns or donor sites
• hydrocolloid dressings may be used on donor sites, but they limit the ability to observe the site and are not recommended for burned sites 
• deep partial thickness and very small full thickness burns will heal spontaneously; should be dressed with bacitracin and adaptic dressing
• autografts (from an uninjured area of the patient's own skin or from an identical twin) provide the only permanent graft material; grafting shortens healing time and improves the cosmetic appearance of deep partial burns, and is mandatory for the healing of full thickness burns (decision to graft may be based on the total % BSA burn and the need to conserve donor sites for full thickness injuries)
• in large area burns, the same graft donor site may need to be used repeatedly as the only source for graft material; protection of this donor site from infection is critical
• when autograft sites are sparse, donor skin can be minced and placed into a growth medium to increase the number of epithelial cells or small pieces of donor skin can be dropped across a large burn (in an attempt to increase the benefit from a small donor area)
• cadaver skin (allograft or homograft) can be used as a temporary dressings - allografts will promote vascular ingrowth to seal the wound against bacterial invasion, however, they will be rejected within about 2 weeks
• xenografts/heterographs (from other species) such as porcine grafts can also provide temporary wound dressings - place pigskin dermal side onto the wound (the dermal side faces the centre of the roll - the graft will roll towards the dermal side) 
• porcine grafts should be removed in 3 - 4 days or if purulent discharge is noted (porcine grafts may be digested by the wound, becoming a source for bacterial growth)
• scarlet red or xeroform dressings are used to protect the donor site; as the site heals, the edges of the dressing dry and curl - trim the loosened edges gradually until the entire wound heals (do not forcefully remove donor dressings or wound healing will be disrupted)
• tubular support dressings provide pressure in the range of 10 - 20 mmHg and are applied 5 - 7 days after grafting to minimize contracture formation
  
  

Dressing Routines

• pain management is a priority
• coordinate physiotherapy with dressing changes
• splint limbs to minimize contractures and maintain functional position of joints
  
  

• gastric dilation and ileus is common in burns > 20% BSA
• GI function should return in 24 - 48 hours
• increased stress hormone output increases the risk for Curling's ulcer

Monitoring and Management


• gastric drainage on admission minimizes gastric distention, emesis and risk for aspiration
• feeding should be initiated as soon as possible; burned patients have high caloric requirements due to wound healing and the increased catabolic state
• careful nutritional assessment is needed to ensure adequate caloric intake
• metabolic rate calculations with the metabolic cart can assist in providing appropriate nutritional support while monitoring for excessive carbohydrate loading (which increases demands on the cardiorespiratory system)
• GI prophylaxis with H2 blockade is important due to high risk for stress ulceration
• monitor for return of bowel function
• monitor for evidence of GI bleeding, anemia or occult rectal blood