**5.1 The Parkland formula**

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

women with large breasts, and gravid women (**Table 2**) [71, 75].

**5. Burn shock**

tem organ failure (MOF) [81].

tion is preferred [88, 89].

considered to be the most accurate and reliable method of determining TBSA, with only a few caveats. More specifically, patient populations that may not be accurately represented by Lund and Browder's chart include the morbidly obese, amputees,

When burns cover <10% of the TBSA, the associated inflammatory response and vascular leakage tend to remain localized within the immediate proximity of the injured tissue. However, as the TBSA approaches 15–20%, the overall quantity of cytokines released systemically into the circulatory system increases dramatically, contributing to systemic inflammatory response whereby uninjured anatomically distant body regions experience various deleterious downstream manifestations such as vasoactive changes, increased capillary permeability, and tissue edema [3, 76, 77]. In the setting of such more severe burns, abrupt fluid shifts from vasculature into the interstitial space quickly lead to clinically apparent hypovolemic shock. In the setting of severe burn injury, this type of shock is appropriately termed "burn shock" [78, 79]. The state of hypovolemic shock during the acute, or "ebb," phase can be further exacerbated by the copresence of low cardiac output from decreased effective circulating blood volume, increased blood viscosity, and depressed cardiac contractility [77, 79, 80]. Most severely affected patients may experience multisys-

From a clinical management standpoint, the initiation of appropriate fluid resuscitation immediately upon the completion of BPE is imperative to providing (and maintaining) the necessary cardiovascular support. Every additional hour from time of injury that resuscitative fluid administration is delayed increases the risk of mortality [82]. Under resuscitation can lead to tissue hypoperfusion, acute renal injury, and death. Over-resuscitating, however, can cause increased tissue edema, compartment syndromes, acute respiratory distress syndrome (ARDS), infections (e.g., pneumonia), and MOF [83–85]. Therefore, proper resuscitation of burn patients requires individually tailored fluid administration and close monitor-

Initiating appropriate intravenous fluid resuscitation requires establishing and maintaining dependable vascular access [3]. Short, large bore peripheral intravenous catheters placed through unburned skin are ideal because this approach avoids potentially thrombosed superficial veins underlying full thickness burn areas. That said, venous access through burned skin is preferred over no venous access, and in most situations may be more rapidly available then central venous access. Central venous access is reliable but comes with increased risk of complications compared to other available options such as saphenous venous cut-down or intraosseous route [86, 87]. Once adequate vascular access is established, fluid resuscitation should be initiated immediately. Optimally, a protocol-driven approach to fluid administra-

The rate of clinical failure (defined as patient deterioration or mortality) with prompt and adequate resuscitation is relatively low (e.g., <5% even for patients with burned TBSA >85%) [90]. As a general guideline, patients who benefit the most from formula-based, calculated fluid resuscitation include adults between 15 and 50 years of age with ≥20% TBSA involving second and third degree burns; children ≤15 years old and adults ≥50 years of age with ≥ 10% TBSA involving second and third degree burns. In practice, many institutions will consider initiating resuscitative fluids when adult burn victim presents with injuries involving ≥15% TBSA [91]. A significant body of research regarding modern fluid resuscitation protocols

ing in order to prevent secondary, mostly iatrogenic injuries.

**148**

The Parkland formula is among the most widely used and studied burn patient resuscitation paradigms [91, 96–98]. When originally published, this resuscitation approach advocated total crystalloid infusion of 4 mL/kg for each percent of body surface area burned [96–98]. The equation estimates the total amount of Ringer's lactate to be given in the initial 24-h post-burn period. Half of the calculated total fluid amount is to be given in the first 8 h and the remaining over the following 16 h [91, 98]. At the same time, certain limitations inherent to formula-based resuscitative approaches do exist. For example, the Parkland formula has been noted to underestimate the total volume of Ringer's lactate needed during the first 24 h in severe burns (>40% TBSA) [91, 99]. This tendency to need larger than estimated fluid volume is referred to as "fluid creep" [84, 100]. Although the exact factors responsible for this phenomenon are still being debated, one effective way of addressing it involves frequent urine output monitoring with hourly adjustments in fluid rates [84]. Goal urine output for adults is 0.5 mL/kg/h and for children ≤30 kg is 1 mL/kg/h. Some institutions have developed protocols that incorporate hourly fluid infusion rate adjustments of 10–30% depending on whether urine output is above or below goal [84]. As an example, we will consider using an hourly rate adjustment of 20% in an adult burn victim. In such scenario, if urine output decreased to <0.5 mL/kg/h, then the current fluid rate would be increased by 20%. If urine output was maintained at 0.5–1 mL/kg/h, then no rate adjustments are made. Finally, if urine output was measured to be >1 mL/kg/h, then the current fluid rate would be reduced by 20%.

### **5.2 The Galveston formula**

Children have larger surface/volume ratios compared to adults, which translates to disproportionately higher infusion rates. The Galveston formula is designed to account for this difference, whereby during the first 24 h, patients receive fluids based on 5000 mL/m2 × %TBSA +2000 mL/m2 daily maintenance [101]. Similar to Parkland formula, half of the calculated total is given in the first 8 h and the rest over the remaining 16 h [102]. Children have lower glycogen stores than adults and consequently should have 5% dextrose added to the primary resuscitative crystalloid solution [103, 104]. As the formula indicates, children require greater amount of resuscitation fluid per kilogram than adults. Unfortunately, children also have lower physiologic reserves, which may predispose them to side effects of more aggressive fluid resuscitation approaches [105]. For example, it has been shown that the cardiac output of pediatric burn victims may not return to pre-burn levels for 24–48 h post-injury, even with complete intravascular status restoration. Furthermore, excessive secretion of antidiuretic hormone may lead to oliguria that extends beyond 48–72 h post-burn [105]. Taking the above parameters into consideration, it is recommended that urine output surveillance and fluid rate adjustments be made on a more frequent basis than adults.

#### **5.3 Post-acute resuscitation period**

Following the initial 24 h of resuscitation, both Parkland and Galveston and some derived formulae provide for a transition to reflect the changing vascular environment as hemodynamic and vascular homeostasis returns. The so-called Baxter formula—a derivation of the Parkland method—introduces a fourth "8-h period" during which plasma is given at 0.3–0.5 mL/kg/%TBSA in order to complete resuscitation [106]. The Galveston formula for pediatric patients calls for Ringer's lactate with dextrose at a rate of 3750 mL/m<sup>2</sup> burned area + 1500 mL/m2 total area over a 24-h period [107]. It is important to remember that these formulae, like the many other proposed paradigms, should be considered within the overall context of a multifaceted approach to manage the burn patient. Once appropriate initial resuscitation has been completed, subsequent fluid administration should be tailored to maintain post-resuscitation stability while avoiding any secondary/ iatrogenic injury.

An important question arises regarding the course of action in cases where resuscitation formulae are followed appropriately yet the patient fails to meet the intended resuscitation endpoints. Such an occurrence may indicate that a secondary diagnosis (or a complication) is present, including inhalation injury, infection/ sepsis, compartment syndrome, or an acute cardiovascular event (e.g., pulmonary embolism) [108]. There is no single perfect marker for determining when a patient is adequately resuscitated. Traditionally, monitoring urine output has been considered as the gold standard for ongoing assessment of resuscitative adequacy. This is because it is a convenient, practical, and inexpensive way to determine if tissues are being adequately perfused in near real-time [109]. The ability to maintain urine output of ≥ 0.5 mL/kg/h in adults and older children (>50 kg) may guide appropriate resuscitation in most patients, but relying on urine output alone can be both challenging and potentially misleading. For example, a recent systematic review showed that when compared to hourly urine output measurements, hemodynamic monitoring appeared to provide some degree of survival benefit, with no associated effect on renal failure [109]. At the same time, heterogeneity of data quality within that same review was problematic, and when only randomized controlled trials were examined in isolation, the mortality benefit of hemodynamic monitoring over hourly urine outputs was no longer present [109].

In practice, a patient whose cumulative fluid resuscitation approaches 250 mL/ kg during the initial 24 h post-injury period should place the treating clinician on high alert for complications related to excessive or over-resuscitation [100, 108]. Careful evaluation of the patient's extremities for signs and symptoms of compartment syndrome should be performed. In particular, burned extremities in which escharotomies may not have been indicated initially may develop the need for escharotomy as increased tissue edema underlying the burned skin further exacerbates venous flow disruption and eventually leads to compromised arterial flow [3]. The emergence of compartment syndrome may be associated with the symptoms of numbness, tingling, or pain with passive movement of the involved extremity [110]. Assessment of capillary refill as well as Doppler signals of digital arteries, palmar arches, and plantar arches of affected limbs should be performed frequently as part of clinical surveillance [50, 111]. Finally, tissue pressure measurements can be checked, and if found to be >30–40 mmHg, this would also be an indication for urgent escharotomy [112, 113]. Burn care providers must remember that the determination to perform an escharotomy can (and often should) be made using clinical exam as the primary decision tool.

When performing escharotomy, areas of constrictive eschar are incised longitudinally along medial and lateral aspects of the affected body region/extremity

**151**

tioned complications.

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

[114, 115]. Even after escharotomy, severely injured limbs continue to be at risk for developing compartment syndrome requiring fasciotomy [116]. Although uncommon, sudden restoration of perfusion to muscle compartments after prolonged ischemia can potentiate the swelling within an already edematous muscle tissue and

Intraabdominal organs and tissues are not excluded from the widespread edema

When indicated, abdominal compartment pressures are fairly easy to measure. Abdominal compartment pressures are most accurately obtained in patients who are ventilated, sedated, and paralyzed (however, this is rarely the case). Placed in the supine position, the patient should be completely flat and level with the ground. Through a Foley catheter, approximately 50–100 mL of normal saline is instilled into the empty bladder, and a pressure transducer is connected to the port at the proximal end of the catheter [126, 127]. Patients with abdominal pressures approaching 30 mmHg in the setting of end organ dysfunction should be consid-

In the absence of chronic kidney disease and abdominal compartment syndrome, low urine output and depressed cardiac indices, especially in the setting of large volume fluid administration could indicate ongoing under-resuscitation and/ or the presence of cardiac dysfunction. Key factors associated with the presence of clinical under-resuscitation include significant delays in initiating resuscitative fluids, underestimation of partial and full thickness burn %TBSA, or concurrent lung injury requiring mechanical ventilation [85, 88, 128]. Burn injuries have been shown to increase cardiac stress and cause myocardial dysfunction [1, 129]. Myocardial dysfunction, in turn, leads to decreased contractility and cardiac output [130]. Dedicated evaluation consisting of a clinical exam, an electrocardiogram (EKG), and bedside echocardiography may be indicated. Advanced hemodynamic

Overly aggressive intravenous fluid resuscitation has also been reported to lead to abnormal intraocular pressure elevations [84, 133]. Similar to other "compartment syndromes," sustained intraocular pressures of ≥20–30 mmHg may lead to permanent injury and vision loss [133–135]. Any unexpected or unexplained symptoms of vision changes or ocular pain should prompt a thorough reevaluation for changes in the patient's clinical exam, fluid balance, and any other aforemen-

*Colloid-based resuscitation*. If the patient appears to be under-resuscitated despite ongoing administration of large volumes of crystalloids, the resuscitating provider should strongly consider transitioning the resuscitative efforts to incorporate colloid-based fluid administration [83, 136]. Although there is still some

resulting from the combination of physiologic changes due to initial injury and subsequent resuscitation. Development of abdominal compartment syndrome in a burn patient undergoing massive fluid resuscitation can be difficult to identify [119, 120]. Due to high sensitivity of the renal system to increased intraabdominal pressures, decreased urine output from diminished kidney perfusion is one of the earlier signs of abdominal compartment syndrome [121–123]. Of note, in a burn patient undergoing massive fluid resuscitation, observed decrease in urine output may be erroneously interpreted as insufficient resuscitation, thus prompting the clinician to inappropriately increase fluid administration [124, 125]. One important consideration is the performance of relevant clinical cross-checks, where additional clinical variables are examined concurrently, including elevated peak airway pressures and decreased tidal volumes in mechanically ventilated patients. Patients who develop abdominal compartment syndrome will become increasingly difficult to ventilate due to increased abdominal pressures being transmitted across the dia-

cause limb-threatening compartment pressure elevations [117, 118].

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

phragms into the thoracic cavity.

ered for decompressive laparotomy [126].

monitoring may be of benefit in selected cases [99, 131, 132].

*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*

Following the initial 24 h of resuscitation, both Parkland and Galveston and some derived formulae provide for a transition to reflect the changing vascular environment as hemodynamic and vascular homeostasis returns. The so-called Baxter formula—a derivation of the Parkland method—introduces a fourth "8-h period" during which plasma is given at 0.3–0.5 mL/kg/%TBSA in order to complete resuscitation [106]. The Galveston formula for pediatric patients calls for

total area over a 24-h period [107]. It is important to remember that these formulae, like the many other proposed paradigms, should be considered within the overall context of a multifaceted approach to manage the burn patient. Once appropriate initial resuscitation has been completed, subsequent fluid administration should be tailored to maintain post-resuscitation stability while avoiding any secondary/

An important question arises regarding the course of action in cases where resuscitation formulae are followed appropriately yet the patient fails to meet the intended resuscitation endpoints. Such an occurrence may indicate that a secondary diagnosis (or a complication) is present, including inhalation injury, infection/ sepsis, compartment syndrome, or an acute cardiovascular event (e.g., pulmonary embolism) [108]. There is no single perfect marker for determining when a patient is adequately resuscitated. Traditionally, monitoring urine output has been considered as the gold standard for ongoing assessment of resuscitative adequacy. This is because it is a convenient, practical, and inexpensive way to determine if tissues are being adequately perfused in near real-time [109]. The ability to maintain urine output of ≥ 0.5 mL/kg/h in adults and older children (>50 kg) may guide appropriate resuscitation in most patients, but relying on urine output alone can be both challenging and potentially misleading. For example, a recent systematic review showed that when compared to hourly urine output measurements, hemodynamic monitoring appeared to provide some degree of survival benefit, with no associated effect on renal failure [109]. At the same time, heterogeneity of data quality within that same review was problematic, and when only randomized controlled trials were examined in isolation, the mortality benefit of hemodynamic monitoring over

In practice, a patient whose cumulative fluid resuscitation approaches 250 mL/ kg during the initial 24 h post-injury period should place the treating clinician on high alert for complications related to excessive or over-resuscitation [100, 108]. Careful evaluation of the patient's extremities for signs and symptoms of compartment syndrome should be performed. In particular, burned extremities in which escharotomies may not have been indicated initially may develop the need for escharotomy as increased tissue edema underlying the burned skin further exacerbates venous flow disruption and eventually leads to compromised arterial flow [3]. The emergence of compartment syndrome may be associated with the symptoms of numbness, tingling, or pain with passive movement of the involved extremity [110]. Assessment of capillary refill as well as Doppler signals of digital arteries, palmar arches, and plantar arches of affected limbs should be performed frequently as part of clinical surveillance [50, 111]. Finally, tissue pressure measurements can be checked, and if found to be >30–40 mmHg, this would also be an indication for urgent escharotomy [112, 113]. Burn care providers must remember that the determination to perform an escharotomy can (and often should) be made using

When performing escharotomy, areas of constrictive eschar are incised longitudinally along medial and lateral aspects of the affected body region/extremity

burned area + 1500 mL/m2

**5.3 Post-acute resuscitation period**

iatrogenic injury.

Ringer's lactate with dextrose at a rate of 3750 mL/m2

hourly urine outputs was no longer present [109].

clinical exam as the primary decision tool.

**150**

[114, 115]. Even after escharotomy, severely injured limbs continue to be at risk for developing compartment syndrome requiring fasciotomy [116]. Although uncommon, sudden restoration of perfusion to muscle compartments after prolonged ischemia can potentiate the swelling within an already edematous muscle tissue and cause limb-threatening compartment pressure elevations [117, 118].

Intraabdominal organs and tissues are not excluded from the widespread edema resulting from the combination of physiologic changes due to initial injury and subsequent resuscitation. Development of abdominal compartment syndrome in a burn patient undergoing massive fluid resuscitation can be difficult to identify [119, 120]. Due to high sensitivity of the renal system to increased intraabdominal pressures, decreased urine output from diminished kidney perfusion is one of the earlier signs of abdominal compartment syndrome [121–123]. Of note, in a burn patient undergoing massive fluid resuscitation, observed decrease in urine output may be erroneously interpreted as insufficient resuscitation, thus prompting the clinician to inappropriately increase fluid administration [124, 125]. One important consideration is the performance of relevant clinical cross-checks, where additional clinical variables are examined concurrently, including elevated peak airway pressures and decreased tidal volumes in mechanically ventilated patients. Patients who develop abdominal compartment syndrome will become increasingly difficult to ventilate due to increased abdominal pressures being transmitted across the diaphragms into the thoracic cavity.

When indicated, abdominal compartment pressures are fairly easy to measure. Abdominal compartment pressures are most accurately obtained in patients who are ventilated, sedated, and paralyzed (however, this is rarely the case). Placed in the supine position, the patient should be completely flat and level with the ground. Through a Foley catheter, approximately 50–100 mL of normal saline is instilled into the empty bladder, and a pressure transducer is connected to the port at the proximal end of the catheter [126, 127]. Patients with abdominal pressures approaching 30 mmHg in the setting of end organ dysfunction should be considered for decompressive laparotomy [126].

In the absence of chronic kidney disease and abdominal compartment syndrome, low urine output and depressed cardiac indices, especially in the setting of large volume fluid administration could indicate ongoing under-resuscitation and/ or the presence of cardiac dysfunction. Key factors associated with the presence of clinical under-resuscitation include significant delays in initiating resuscitative fluids, underestimation of partial and full thickness burn %TBSA, or concurrent lung injury requiring mechanical ventilation [85, 88, 128]. Burn injuries have been shown to increase cardiac stress and cause myocardial dysfunction [1, 129]. Myocardial dysfunction, in turn, leads to decreased contractility and cardiac output [130]. Dedicated evaluation consisting of a clinical exam, an electrocardiogram (EKG), and bedside echocardiography may be indicated. Advanced hemodynamic monitoring may be of benefit in selected cases [99, 131, 132].

Overly aggressive intravenous fluid resuscitation has also been reported to lead to abnormal intraocular pressure elevations [84, 133]. Similar to other "compartment syndromes," sustained intraocular pressures of ≥20–30 mmHg may lead to permanent injury and vision loss [133–135]. Any unexpected or unexplained symptoms of vision changes or ocular pain should prompt a thorough reevaluation for changes in the patient's clinical exam, fluid balance, and any other aforementioned complications.

*Colloid-based resuscitation*. If the patient appears to be under-resuscitated despite ongoing administration of large volumes of crystalloids, the resuscitating provider should strongly consider transitioning the resuscitative efforts to incorporate colloid-based fluid administration [83, 136]. Although there is still some

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 continues to be elusive.

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].
