**3. Pathophysiology of burn injury**

The skin plays a crucial role in maintaining physiologic homeostasis through thermal regulation, sensory reception, synthesis of vitamins and hormones, maintaining fluid/electrolyte balance, and providing barrier protection to underlying tissues [31–34]. When exposed to excessive heat, human tissues develop clinical burn injury [35]. During thermal insult, the epidermis and dermis are able to limit the direct transfer of energy to underlying tissues [19]. Various pathophysiologic derangements occur including denaturation of macromolecular structures, cell membrane dysfunction or destruction, cytokine release, arrest of local blood flow, and eventually cell/tissue death [35]. Following the initial insult, the final depth of irreversible tissue injury may increase depending on how local tissues respond to the complex microvascular and inflammatory environment in their immediate surroundings [35–38]. Morphologically, the tissue environment at the location of burn injury has three physiologically distinct zones. Based on the immediate proximity (e.g., distance or depth) from the primary burn site, these zones are the zone of coagulation, zone of stasis, and zone of hyperemia (**Figure 1**) [12, 38].

The zone of coagulation refers to the area of tissue that has been irreversibly damaged at the time of injury and has undergone coagulative necrosis [39, 40].

**143**

**Figure 1.**

*injury.*

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

The zone of stasis, also known as the "watershed" region, represents the area of tissue injury that may be reversible under optimal resuscitative circumstances [40, 41]. This zone is characterized by vascular injury, capillary leakage, and high concentrations of thromboxane A2—a potent vasoconstrictor produced locally by platelets [1]. Catecholamines and serotonin also play an important role in modulating tissue responses within this zone [1]. The end effect is impaired tissue perfusion, and thus elevated risk of propagating the area of tissue necrosis during the initial 24–48 h following the index injury [1, 36, 42]. The zone of stasis is the area where early intervention with therapy directed at reducing vasoconstriction, optimizing perfusion, and controlling local inflammation may have the greatest effect at limiting the depth of injury. The zone of hyperemia is the most remote zone of cutaneous injury (relative to the primary burn site) where vasodilation is noted in viable tissue undergoing the healing process. This vasodilation is multifactorial and likely mediated through a combination of histamine- and kinin-related mechanisms [1, 43]. Accurate determination of burn wound depth is crucial for guiding clinical management (**Table 1**) [9, 44]. Some superficially limited burns may heal with local treatment alone, while deeper burns are more likely to require operative intervention. Although various tools are available to assist in this assessment [44–49], burn depth is usually determined during BPE through visual inspection by an experienced practitioner who then goes on to classify his or her findings in accordance to

*This schematic displays how resuscitation interacts with the pathophysiologic changes associated with burn* 

pre-established "degrees of injury severity" outlined below:

1.Superficial—commonly referred to as "first degree"—burns are generally limited to the epidermis. The burned skin is characterized by the presence of blanching erythema that tends to appear dry (without blistering) and is very tender on exam due to the proximity of sensory nerve endings. Common examples include sunburns or mild scalding from hot water [50]. Management of these burns is directed at reducing further injury, pain control, and provision of comfort measures. Within the first hour, exposing the injury to cool

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

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

**Figure 1.**

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

concluding with clinical management pearls.

**2. Overview of mechanistic considerations**

discussed herein also apply to other burn types.

injuries from falling or violent muscle contractions [26–30].

**3. Pathophysiology of burn injury**

out, the resuscitating team's focus can be directed toward managing the burn. Rapid initiation of therapy tailored to each burn patient during the initial 48 h from the time of burn injury is critical for preventing burn shock, secondary injuries, and other downstream sequelae [3]. In this chapter, we will discuss the fundamentals of burn shock, starting with pathophysiologic and mechanistic considerations and

Burn management begins with a complete history and physical examination, known as the "burn patient evaluation" (BPE), which is intended to quantify and classify the thermal injury [7, 8]. Burns are typically described and classified by etiologic cause, extent of body surface area involved, and depth [9–11]. There are three broad categories of etiologies associated with burn injuries—thermal, chemical, and electrical [12–14]. Thermal mechanisms can be further broken down into flame burns, scald burns, contact burns, steam burns, or flash burns [15, 16]. This chapter focuses primarily on thermal injuries, although many of the concepts

The understanding of mechanistic considerations and associated tissue injury patterns is of critical importance when evaluating and treating burn victims [17, 18]. For example, thermal injury causes coagulative necrosis of the affected tissue, and the depth of injury is directly dependent on temperature and duration of exposure, which will vary widely across different types of thermal exposures and injured tissue characteristics [19, 20]. The extent of chemical-induced tissue injury will vary with substance type (acids, alkalis, or hydrocarbon-based organic solvents), concentration, and duration of exposure, but all require expedited clinical management and lavage (when appropriate) of affected areas [21–25]. Electrical injuries will vary in nature between high and low voltage exposure, and depending on exact circumstances, involved victims may be at an increased risk of presenting with cardiovascular and neurologic manifestations, as well as associated traumatic

The skin plays a crucial role in maintaining physiologic homeostasis through thermal regulation, sensory reception, synthesis of vitamins and hormones, maintaining fluid/electrolyte balance, and providing barrier protection to underlying tissues [31–34]. When exposed to excessive heat, human tissues develop clinical burn injury [35]. During thermal insult, the epidermis and dermis are able to limit the direct transfer of energy to underlying tissues [19]. Various pathophysiologic derangements occur including denaturation of macromolecular structures, cell membrane dysfunction or destruction, cytokine release, arrest of local blood flow, and eventually cell/tissue death [35]. Following the initial insult, the final depth of irreversible tissue injury may increase depending on how local tissues respond to the complex microvascular and inflammatory environment in their immediate surroundings [35–38]. Morphologically, the tissue environment at the location of burn injury has three physiologically distinct zones. Based on the immediate proximity (e.g., distance or depth) from the primary burn site, these zones are the zone of

coagulation, zone of stasis, and zone of hyperemia (**Figure 1**) [12, 38].

The zone of coagulation refers to the area of tissue that has been irreversibly damaged at the time of injury and has undergone coagulative necrosis [39, 40].

**142**

*This schematic displays how resuscitation interacts with the pathophysiologic changes associated with burn injury.*

The zone of stasis, also known as the "watershed" region, represents the area of tissue injury that may be reversible under optimal resuscitative circumstances [40, 41]. This zone is characterized by vascular injury, capillary leakage, and high concentrations of thromboxane A2—a potent vasoconstrictor produced locally by platelets [1]. Catecholamines and serotonin also play an important role in modulating tissue responses within this zone [1]. The end effect is impaired tissue perfusion, and thus elevated risk of propagating the area of tissue necrosis during the initial 24–48 h following the index injury [1, 36, 42]. The zone of stasis is the area where early intervention with therapy directed at reducing vasoconstriction, optimizing perfusion, and controlling local inflammation may have the greatest effect at limiting the depth of injury. The zone of hyperemia is the most remote zone of cutaneous injury (relative to the primary burn site) where vasodilation is noted in viable tissue undergoing the healing process. This vasodilation is multifactorial and likely mediated through a combination of histamine- and kinin-related mechanisms [1, 43].

Accurate determination of burn wound depth is crucial for guiding clinical management (**Table 1**) [9, 44]. Some superficially limited burns may heal with local treatment alone, while deeper burns are more likely to require operative intervention. Although various tools are available to assist in this assessment [44–49], burn depth is usually determined during BPE through visual inspection by an experienced practitioner who then goes on to classify his or her findings in accordance to pre-established "degrees of injury severity" outlined below:

1.Superficial—commonly referred to as "first degree"—burns are generally limited to the epidermis. The burned skin is characterized by the presence of blanching erythema that tends to appear dry (without blistering) and is very tender on exam due to the proximity of sensory nerve endings. Common examples include sunburns or mild scalding from hot water [50]. Management of these burns is directed at reducing further injury, pain control, and provision of comfort measures. Within the first hour, exposing the injury to cool


#### **Table 1.**

*Description of clinical characteristics of burn wounds of various depths.*

water or applying a cold compress can help stop the burning process and relieve pain. Topical steroids, with their vasoconstrictive effects, are often considered "first-line" treatment for acute sunburn; however, their true efficacy remains controversial [51]. Topical applications such as menthol, camphor, pramoxine, lidocaine, and diclofenac gel, if available, may be useful for reducing pain, erythema, and edema. Soothing remedies such as aloe lotion (especially when refrigerated prior to application), baking soda, and oatmeal may provide additional relief. Oral nonsteroidal anti-inflammatory drugs (NSAIDs) help provide analgesia and may assist in reducing sunburn erythema. Healing of superficial burns occurs typically over a period of 3–7 days and will not result in scar formation [50, 52]. Of note, these burns are usually not included when estimating the total body surface area (TBSA) during the BPE, mainly because burns limited to the epidermis tend not to cause significant fluid shifts or losses.

2.Moderate partial thickness burns—also referred to as "superficial second degree" injuries—by definition involve the superficial layers of the dermis [50]. Partial thickness burns are further divided into two subtypes—superficial (focus of the current paragraph) and deep (discussed in next paragraph). Superficial partial thickness burns have similar appearance to first degree

**145**

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

level, as is the overall risk of infection.

next paragraph).

amputation [67, 68].

perfusion and limiting secondary injury.

burns but will additionally appear weepy and blistered [53]. Increased exposure of dermal nerve endings for pain, touch, temperature, and pressure contributes to these burns being very painful [54, 55]. Dermal blood vessels that carry oxygen and nutrients to the skin while removing metabolic waste products are also exposed giving the wound a blanching erythematous appearance. Exposure of sweat and sebaceous glands contributes to the wound's weepy appearance and the increase in evaporative losses [56]. Hair follicles, sweat glands, and rete ridges are typically spared allowing for reepithelialization to occur over the following 1–2 weeks post injury; however, alteration in cellular milieu at the site of the injury may result in permanent skin discoloration [56–58]. Finally, the risk of scarring is increased at this injury severity

3.Deep partial thickness burns—also known as "deep second degree burns" extend deeper into the dermis, resulting in a wound that appears pale and mottled [59, 60]. Since not all nerve endings have been destroyed in this type of burn, there may be considerable amounts of associated pain. Coagulative necrosis of the dermis from deep partial thickness burns is considered to have extended beyond the rete ridges, thus leaving behind only hair follicles and sweat glands to contribute to reepithelialization [61]. Without the rete ridges, the healing process is significantly slower and may result in more severe scarring. Ablative fractional laser resurfacing, excision, and skin grafting can improve both the healing time and scar quality. Consequently, the boundaries of clinical management tend to become blurry when approaching deep partial thickness and full thickness burns (discussed in

4.Full thickness burns—also known as "third degree burns"—extend beyond the epidermal and dermal tissues and into the subcutaneous fat [62, 63]. Full thickness burns are associated with complete destruction of all nerve endings, dermal glands, and hair follicles. In addition, thermal damage to superficial veins causes thrombosis [64, 65]. As a result of the above changes, the burn area is insensate and may appear charred, brown, and leathery, or at times white and waxy. Only the wound edges have retained the necessary components for reepithelialization of the wound, which is why full thickness burns

5.Fourth degree burns are defined as thermal injuries that involve tissues and structures deep to subcutaneous layer. This includes damage to muscle, tendon, or bone [67]. Patients who suffer from survivable fourth degree burns may require extensive limb-sparing efforts and reconstructive surgery to avoid

Determining the size, or total body surface area, of a burn is the cornerstone of the BPE and provides fundamental information to guide subsequent clinical management. Properly conducted BPE also provides insight into the burn victim's physiologic state and resuscitative fluid needs, as well as general prognostic information. It is important to remember that burn injuries have the potential to quickly evolve and progress if resuscitative conditions are not optimal [69, 70]. In other words, superficial and partial thickness burns can become deep partial thickness burns, and deep partial thickness burns have the potential to become full thickness burns. Optimizing the resuscitation effort can mitigate the tissue loss by enhancing

also require excision and grafting in order to heal [50, 66].

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

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

Epidermis only

Superficial (papillary) dermis

Deeper layer (reticular) dermis

Full skin thickness with extension into subcutaneous tissues

Involves tendon, muscle, or bone

*Description of clinical characteristics of burn wounds of various depths.*

**Etiology Tissue layer Appearance Pain Healing time**

Pink to red, moist, no blisters

Blister, red, moist, intact epidermal appendages, blanching on pressure

Dry, white, nonblanching, loss of all epidermal appendages

Leathery, dry, white or red with visibly thrombosed vessels

Skeletonizing of tissue, charring

Moderate– severe

3–7 days

Severe 1–3 weeks, long-

Minimal 3–6 weeks, with scars

No Does not heal

No Extensive

by primary intention, requires skin graft

reconstructive, limb salvage versus amputation

term pigment changes may occur

water or applying a cold compress can help stop the burning process and relieve pain. Topical steroids, with their vasoconstrictive effects, are often considered "first-line" treatment for acute sunburn; however, their true efficacy remains controversial [51]. Topical applications such as menthol, camphor, pramoxine, lidocaine, and diclofenac gel, if available, may be useful for reducing pain, erythema, and edema. Soothing remedies such as aloe lotion (especially when refrigerated prior to application), baking soda, and oatmeal may provide additional relief. Oral nonsteroidal anti-inflammatory drugs (NSAIDs) help provide analgesia and may assist in reducing sunburn erythema. Healing of superficial burns occurs typically over a period of 3–7 days and will not result in scar formation [50, 52]. Of note, these burns are usually not included when estimating the total body surface area (TBSA) during the BPE, mainly because burns limited to the epidermis tend not to cause significant fluid shifts

2.Moderate partial thickness burns—also referred to as "superficial second degree" injuries—by definition involve the superficial layers of the dermis [50]. Partial thickness burns are further divided into two subtypes—superficial (focus of the current paragraph) and deep (discussed in next paragraph). Superficial partial thickness burns have similar appearance to first degree

**144**

or losses.

**Depth/ degree**

Superficial I°

Superficial partial IIa°

Deep partial IIb°

Deep III°

**Table 1.**

Sunlight exposure, hot liquids with low viscosity and short exposure

Hot liquids, chemical burns with weak acid or alkali, flash

Flame, chemical, electrical, hot liquids with high viscosity

Flame, electrical, chemical, blast, selfimmolation

prolonged flame exposure

IV° Mostly

burns but will additionally appear weepy and blistered [53]. Increased exposure of dermal nerve endings for pain, touch, temperature, and pressure contributes to these burns being very painful [54, 55]. Dermal blood vessels that carry oxygen and nutrients to the skin while removing metabolic waste products are also exposed giving the wound a blanching erythematous appearance. Exposure of sweat and sebaceous glands contributes to the wound's weepy appearance and the increase in evaporative losses [56]. Hair follicles, sweat glands, and rete ridges are typically spared allowing for reepithelialization to occur over the following 1–2 weeks post injury; however, alteration in cellular milieu at the site of the injury may result in permanent skin discoloration [56–58]. Finally, the risk of scarring is increased at this injury severity level, as is the overall risk of infection.


Determining the size, or total body surface area, of a burn is the cornerstone of the BPE and provides fundamental information to guide subsequent clinical management. Properly conducted BPE also provides insight into the burn victim's physiologic state and resuscitative fluid needs, as well as general prognostic information. It is important to remember that burn injuries have the potential to quickly evolve and progress if resuscitative conditions are not optimal [69, 70]. In other words, superficial and partial thickness burns can become deep partial thickness burns, and deep partial thickness burns have the potential to become full thickness burns. Optimizing the resuscitation effort can mitigate the tissue loss by enhancing perfusion and limiting secondary injury.
