**11.3 Toxic epidermal necrolysis (TEN)**

TEN is a severe, life-threatening disorder (with a mortality rate approaching 40%) characterized by generalized loss of epidermis and mucosa (**Figure 3**), typically involving more than 30% of the skin [215]. A tell-tale clinical finding that is almost always present in TEN is the phenomenon in which intact superficial epidermis can, via a pushing or shearing force, be dislodged and slid over underlying layers of skin; this indicates a plane of cleavage in the skin at the epidermal-dermal junction and is referred to as Nikolsky's sign [216]. TEN is almost always medication-induced and involves a cytotoxic T-cell reaction with apoptosis of keratinocytes mediated by Fas ligand [217]. Consequently, the first step in treatment is similar to that of a burn injury—stop the underlying causative agent (i.e., discontinue all medications that are not essential). The next step is to confirm the diagnosis through a careful medication history and skin biopsy with frozen section. The finding of full-thickness epidermal involvement distinguishes TEN from other conditions such as staphylococcal scalded skin syndrome (see

**157**

**Figure 4.**

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

**11.4 Staphylococcal scalded skin syndrome (SSSS)**

below), which may appear similar but are treated very differently. In addition to the more controversial therapeutic roles that systemic steroids, intravenous immunoglobulins, and plasmapheresis may play, the mainstay clinical TEN management is excellent "burn care," ideally in a burn center with careful attention to pain management, electrolyte balance, topical disinfection, access to burn beds and nonadherent dressings, and prompt treatment of secondary infections. An ophthalmologic consultation is also required because of the risk of corneal

The SSSS is typically characterized by fever and rapid onset of diffuse, painful erythema progressing to widespread formation of thin-walled, easily ruptured, fluid-filled vesicles and bullae (**Figure 4**). Newborns and small infants tend to be most susceptible, though adults may certainly be affected. Nikolsky's sign is almost always present [216]. The clinical presentation of SSSS is the result of specific exotoxins that cleave desmoglein-1 (i.e., disrupt the connection between keratinocytes) and cause cellular detachment within the epidermis. While exotoxins are released by S. aureus, cultures to isolate these bacteria, however, are often negative. More helpful is a skin biopsy with frozen section that should demonstrate a very superficial epidermal split (in contrast to TEN where there is full-thickness epidermal necrosis). Differentiating SSSS from similar clinical presentations is critical because treatment typically involves the addition of medications (i.e., antibiotics) rather than the cessation of them. SSSS patients may require topical disinfection and careful placement on a burn bed covered with nonadherent sheeting. Attention to fluid replacement, pain management, electrolyte balance, and temperature and humidity control are paramount. Less urgent but just as important, the diagnosis of SSSS should prompt a search for staphylococcal "carriers" among close contacts of the affected patient. Healing is usually rapid with correct therapy and vigilant

Necrotizing fasciitis refers to the severe and rapid destruction of skin, subcutaneous fat, and muscle caused by bacterial infection (e.g., group A streptococci,

*Typical appearance of staphylococcal scalded skin syndrome (SSSS). Left—face; right—abdomen.*

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

erosions and scarring [218].

wound care [219].

**11.5 Necrotizing fasciitis**

**Figure 3.** *Typical appearance of toxic epidermal necrolysis (TEN).*

*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*

**11.2 Dermatologic conditions that require burn center management**

that closely resembles a large thermal burn.

**11.3 Toxic epidermal necrolysis (TEN)**

Historically, the spheres of the dermatologist and the burn surgeon have failed to overlap as much as the associated anatomic and physiologic considerations might lead one to believe they should. Reasons for this lack of collegiality and collaboration have included training bias (i.e., an "elixir" versus "cold steel" approach), lack of awareness of the other's expertise, and good old fashioned egos and turf wars. Thankfully, a new era of cooperation between these specialties has begun to emerge based on large part around the understanding that a multimodal, multidisciplinary approach may lead to more optimal clinical outcomes. The intersection of these two specialties may perhaps be best illustrated through several devastating dermatological conditions that involve the acute and extensive necrosis of cutaneous tissue, leading to catastrophic deterioration of the affected patient and a clinical picture

TEN is a severe, life-threatening disorder (with a mortality rate approaching 40%) characterized by generalized loss of epidermis and mucosa (**Figure 3**), typically involving more than 30% of the skin [215]. A tell-tale clinical finding that is almost always present in TEN is the phenomenon in which intact superficial epidermis can, via a pushing or shearing force, be dislodged and slid over underlying layers of skin; this indicates a plane of cleavage in the skin at the epidermal-dermal junction and is referred to as Nikolsky's sign [216]. TEN is almost always medication-induced and involves a cytotoxic T-cell reaction with apoptosis of keratinocytes mediated by Fas ligand [217]. Consequently, the first step in treatment is similar to that of a burn injury—stop the underlying causative agent (i.e., discontinue all medications that are not essential). The next step is to confirm the diagnosis through a careful medication history and skin biopsy with frozen section. The finding of full-thickness epidermal involvement distinguishes TEN from other conditions such as staphylococcal scalded skin syndrome (see

**156**

**Figure 3.**

*Typical appearance of toxic epidermal necrolysis (TEN).*

below), which may appear similar but are treated very differently. In addition to the more controversial therapeutic roles that systemic steroids, intravenous immunoglobulins, and plasmapheresis may play, the mainstay clinical TEN management is excellent "burn care," ideally in a burn center with careful attention to pain management, electrolyte balance, topical disinfection, access to burn beds and nonadherent dressings, and prompt treatment of secondary infections. An ophthalmologic consultation is also required because of the risk of corneal erosions and scarring [218].
