**6. Ambient temperature control**

Over the past several decades, major advances have been made in our understanding of the complex physiologic changes that occur as a result of severe burn injury. While burn shock, as outlined in previous sections of this chapter, is historically compartmentalized as a form of "hypovolemic shock," we now know that "fluids alone do not cure burn shock" [143]. Consequently, there are various strategies that may be employed to help counteract or "blunt" the cascading physiologic response to burn injury. For example, even simple measures such as increasing the ambient temperature (up to 33°C) have been shown to reduce the hypermetabolic response focused on maintaining elevated body core temperatures during the acute injury phase [144].

## **7. Nutritional support**

Delays in nutritional support can have devastating effects on patient outcomes [145]. The post-burn hypermetabolic state that begins immediately after injury can approach 200% of normal resting energy expenditure [146]. This can naturally lead to rapid depletion of energy stores, loss of muscle tissue, and further worsening of any pre-existing or acquired malnutrition. Malnutrition itself contributes to alterations in cell membrane transport, organ dysfunction, immune compromise, and delayed/abnormal wound healing [147]. Ideally, nutritional support is initiated within 6 h of injury. Due to the tremendous increase in metabolic demand, severely

**153**

*Burn Shock and Resuscitation: Many Priorities, One Goal*

burned patients are simply unable to fully meet the caloric demands on their own accord. For this reason, it is recommended that a post-pyloric feeding access be placed on admission, with prompt (preferably protocol-driven) initiation of tube feeding formulae specifically tailored to meet individual patient requirements [148, 149]. For gastric tube feeds, the choice of continuous versus bolus administration may be a secondary consideration [150]. For post-pyloric feeding, continuous

Unfortunately, the gastrointestinal tract itself is affected adversely by severe

Adequate and prompt nutritional support is critical to the overall management of burn patients, and its importance parallels the severity (e.g., %TBSA) and complexity (e.g., inhalation component) of the injury [148, 156, 157]. In addition to ensuring adequate caloric provision, it may be important to consider supplementing the patient's enteral intake with specific vitamins and minerals. For example, there has been increasing support in the literature for administration of high dose vitamin C (a.k.a., ascorbic acid) during the acute phase of burn injury [158, 159]. Cellular oxidative stress from reactive oxygen species generated immediately after burn injury appears to play a significant role in cardiovascular dysfunction of burn shock. Vitamin C is a powerful antioxidant, and it has been suggested that high dose ascorbic acid administration during the acute phase of burn shock may be protective to microvascular circulation, beneficial to cardiac output, help optimize fluid resuscitation, and may enhance wound healing [159, 160]. Other proposed components of the so-called "pharmacological" nutritional supplementation after burn injury include glutamine, arginine, n-3 (polyunsaturated) fatty acids, as well as various other vitamins and trace

Patients who develop burn shock and remain hemodynamically labile despite large volume resuscitation may require additional cardiovascular support. Low cardiac output during the acute post-injury phase is a common component of early "burn shock" [162, 163] and may be more pronounced among geriatric patients [164]. In some cases, inotropic support with dobutamine may be required to maintain adequate systemic perfusion [165, 166]. Vasopressors should be avoided if possible as their vasoconstrictive properties can lead to decreased end-organ perfusion, including skin (and thus elevated risk of the propagation of primary injury or impaired healing of skin grafts) and bowel (e.g., contribution to potential bowel ischemia). This is especially applicable to patients with initial low cardiac output and early multiple organ dysfunction [167]. Patients who do require vasopressor support should undergo close hemodynamic monitoring (MAP, CVP, echocardiography, SvO2). As the patient transitions from the "ebb phase" to the "flow phase" (typically around the 48–72 h mark) of the post-burn state, hemodynamic behavior evolves toward the hyperdynamic profile [168]. As the

burn injury, and varied degrees of ileus may develop in the acute post-burn timeframe [151]. In the setting of complete intolerance to enteral feeding, total parenteral nutrition may be considered on highly selective basis [152]. Total parenteral nutrition is generally not recommended due to associated increases in rates of complications and mortality compared to enteral feeding, and the latter should be started as soon as the gastrointestinal dysfunction resolves [152]. A commonly used formula for calculating caloric requirements is the Curreri formula (including its variants) which calls for 25 kcal/kg/day maintenance plus additional

administration requires the presence of intact intestinal function.

*DOI: http://dx.doi.org/10.5772/intechopen.85646*

40 kcal/%TBSA/day [153–155].

minerals [149, 161].

**8. Special hemodynamic considerations**

#### *Burn Shock and Resuscitation: Many Priorities, One Goal DOI: http://dx.doi.org/10.5772/intechopen.85646*

*Clinical Management of Shock - The Science and Art of Physiological Restoration*

continues to be elusive.

**6. Ambient temperature control**

injury phase [144].

**7. Nutritional support**

controversy regarding the optimal application and timing of various colloids during burn patient resuscitation, especially in the setting of severe burns, there is clear evidence in support of colloid use in general [83, 136, 137]. Research suggests that the use of colloids in resuscitation of severe burns (>40% TBSA or > 30% TBSA with inhalation injury) may decrease the total resuscitation volume, reduce the incidence of abdominal compartment syndrome, number of days spent on a ventilator, and potentially even mortality [138–140]. The majority of historically important formulae include some form of colloids administered at various timeframes within the first 48 h post-burn. The presence of this general theme throughout the literature corroborates the importance of colloids for resuscitation of severe burns, especially in the management of burn shock in the most severely injured population. Despite this, definitive evidence regarding the efficacy of either approach

The Parkland formula does not call for the transition to colloids prior to the first 24-h mark. If earlier administration of colloids is desired, one might consider transitioning to the Brooke Formula or West Penn formula [88, 93]. During the initial 24-h post-burn period, the Brooke Formula can be delivered as a combination of crystalloid and colloid fluids, including 1.5 mL/kg/%TBSA of Ringer's lactate plus 0.5 mL/kg/%TBSA of a colloid and 2000 mL of 5% dextrose in water [81, 141, 142]. After the first 24-h period, the formula mandates reducing the crystalloid and colloid fluid rates by 50–75% and repeating the 2000 mL of 5% dextrose in water [81, 141, 142]. The West Penn formula—first published in the early 1990s—is the most recently proposed derivation of colloid-based burn resuscitation formulae. The West Penn formula calls for Ringer's lactate at a set rate of 83 mL/h and fresh frozen plasma (FFP) at an initial rate of 75 mL/kg/36 h. The rate of FFP administration is then titrated on an hourly basis to a urine output of 0.5–1 mL/kg/h and both fluids are continued for until the 48-h mark after burn injury is reached [88, 143].

Over the past several decades, major advances have been made in our understanding of the complex physiologic changes that occur as a result of severe burn injury. While burn shock, as outlined in previous sections of this chapter, is historically compartmentalized as a form of "hypovolemic shock," we now know that "fluids alone do not cure burn shock" [143]. Consequently, there are various strategies that may be employed to help counteract or "blunt" the cascading physiologic response to burn injury. For example, even simple measures such as increasing the ambient temperature (up to 33°C) have been shown to reduce the hypermetabolic response focused on maintaining elevated body core temperatures during the acute

Delays in nutritional support can have devastating effects on patient outcomes [145]. The post-burn hypermetabolic state that begins immediately after injury can approach 200% of normal resting energy expenditure [146]. This can naturally lead to rapid depletion of energy stores, loss of muscle tissue, and further worsening of any pre-existing or acquired malnutrition. Malnutrition itself contributes to alterations in cell membrane transport, organ dysfunction, immune compromise, and delayed/abnormal wound healing [147]. Ideally, nutritional support is initiated within 6 h of injury. Due to the tremendous increase in metabolic demand, severely

**152**

burned patients are simply unable to fully meet the caloric demands on their own accord. For this reason, it is recommended that a post-pyloric feeding access be placed on admission, with prompt (preferably protocol-driven) initiation of tube feeding formulae specifically tailored to meet individual patient requirements [148, 149]. For gastric tube feeds, the choice of continuous versus bolus administration may be a secondary consideration [150]. For post-pyloric feeding, continuous administration requires the presence of intact intestinal function.

Unfortunately, the gastrointestinal tract itself is affected adversely by severe burn injury, and varied degrees of ileus may develop in the acute post-burn timeframe [151]. In the setting of complete intolerance to enteral feeding, total parenteral nutrition may be considered on highly selective basis [152]. Total parenteral nutrition is generally not recommended due to associated increases in rates of complications and mortality compared to enteral feeding, and the latter should be started as soon as the gastrointestinal dysfunction resolves [152]. A commonly used formula for calculating caloric requirements is the Curreri formula (including its variants) which calls for 25 kcal/kg/day maintenance plus additional 40 kcal/%TBSA/day [153–155].

Adequate and prompt nutritional support is critical to the overall management of burn patients, and its importance parallels the severity (e.g., %TBSA) and complexity (e.g., inhalation component) of the injury [148, 156, 157]. In addition to ensuring adequate caloric provision, it may be important to consider supplementing the patient's enteral intake with specific vitamins and minerals. For example, there has been increasing support in the literature for administration of high dose vitamin C (a.k.a., ascorbic acid) during the acute phase of burn injury [158, 159]. Cellular oxidative stress from reactive oxygen species generated immediately after burn injury appears to play a significant role in cardiovascular dysfunction of burn shock. Vitamin C is a powerful antioxidant, and it has been suggested that high dose ascorbic acid administration during the acute phase of burn shock may be protective to microvascular circulation, beneficial to cardiac output, help optimize fluid resuscitation, and may enhance wound healing [159, 160]. Other proposed components of the so-called "pharmacological" nutritional supplementation after burn injury include glutamine, arginine, n-3 (polyunsaturated) fatty acids, as well as various other vitamins and trace minerals [149, 161].
