Despite advances in wound care and critical care medicine, the outcomes of severe burn injuries is still poor. The clinical impact of the injury is often underestimated. Severe burns are followed by a complex catabolic, hypermetabolic response nearly proportional to the size of the injury.1 The response is mediated by a deluge of catecholamines, cortisol, and glucagon to levels up to 10-fold of normal values.2 These elevations persist months to years postinjury, while the clinical manifestations may persist much longer.3,4 The hypermetabolic response to severe burn is associated with increased energy expenditure and energy substrate release from both fat and protein storage leading to profound and persistent whole body catabolism.
The skin is the largest organ in the human body. It is primarily composed of two layers: the epidermis and the dermis, which can be of variable thickness. For example, the thickness of the epidermis varies among different parts of the body, from 0.05 mm on the eyelids to over 1 mm on the soles of the feet.5,6 The variability of dermal thickness is dependent on gender, age, and location. The skin protects against fluid and electrolyte loss, radiation, infection, and provides thermal regulation. Skin provides perception of temperature and pain to the surrounding environment via touch.5
The epidermis is derived from ectoderm and is comprised principally of keratinocytes. Keratinocytes divide and differentiate at the basal layer and move progressively outward over 4 weeks along the outer four layers of the epidermis: the stratum spinosum, the stratum granulosum, the stratum lucidum, and the stratum corneum. Other important cells of the epidermis include melanocytes and Langerhans cells. Melanocytes produce the melanin pigment essential for protection against ultraviolet radiation. Langerhans cells protect against pathogens by performing phagocytosis and presentation of foreign antigens. Because the epidermis is derived from ectoderm, it is capable of regeneration. Pure epidermal injuries (first degree or superficial burns) heal by regeneration and without scarring. Keratinocytes achieve re-epithelialization by proliferating from dermal appendages (hair follicles, sweat glands) and the edges of the wound. Depleted melanocytes regenerate as well but at a much slower rate. This may lead to permanent pigment changes within the healed wound.5,7,8
The epidermis connects to the dermis via rete ridges (or epidermal projections) that interdigitate into papillae (or dermal projections). Keratinocyte-derived collagen VII anchoring fibrils that extend into the dermis stabilize the epidermal-dermal junction. Thermal injuries to these keratinocyte-derived anchoring fibrils can take up to weeks to heal during burn wound healing.5,9
The dermis provides stretching and tensile strength. The bulk of the dermal structure is composed of collagen. It is derived from mesoderm and divided into two layers: superficial papillary dermis and the deeper reticular dermis. Elastic fibers in the dermis impart the elastic recoil properties of skin. Protein turnover ...