Teaching Material

C. Hall, C. Hardin, C. J. Corkins, A. Z. Jiwani, J. Fletcher, A. Carlsson, R. Chan. Pathophysiologic Mechanisms and Current Treatments for Cutaneous Sequelae of Burn Wounds. Compr Physiol. 8: 2018, 371-405.

Didactic Synopsis

Major Teaching Points:

• The skin or integumentary system provides protection to the underlying tissue, is composed of the superficial epidermis and the underlying dermis, and contains a wide range of adnexae such as hair, specialized glands, blood vessels, and sensory structures.
• Normal wound healing is characterized by four tightly regulated and temporally distinct phases: hemostasis, inflammation, cellular proliferation, and matrix remodeling.
• Burn injury is classified, in part, by the depth of tissue injury, where superficial and partial thickness burns may penetrate the epidermis and dermis, respectively, but do not cause extensive tissue damage, and usually heal without scarring. Deep-partial and full-thickness burns penetrate the deeper dermis and hypodermis, respectively, are slower to heal, and often result in scarring and contracture.
• Hypertrophic scarring is the most common morbidity associated with burn injury and is associated with delayed re-epithelialization.
• Debridement and grafting are the standard of care for deep-partial and full-thickness wounds.
• Topical and systemic pharmacotherapies developed to modulate wound healing, such as anti-inflammatories, antimicrobials, antifibrotics, beta blockers, and growth factors.
• Postburn scar treatments include pressure garments/dressings, silicone dressings, cryotherapy, intralesional steroid injections, nonsteroidal inralesional treatments, botulinum toxin, radiotherapy, laser therapy, and surgical intervention.
• Burn injuries are diverse, multifaceted, and unique to each individual patient thereby necessitating individualized care of acute wounds and late burn effects.

Didactic Legends

The figures—in a freely downloadable PowerPoint format—can be found on the Images tab along with the formal legends published in the article. The following legends to the same figures are written to be useful for teaching.

Figure 1. Teaching points: The integumentary system is the largest organ in the body and is comprised of the skin and associated appendages. The layers of the integument include the outermost epidermis, the middle dermal layer, and the deepest layer known as the hypodermis. The epidermis is further divided into layers or stratum: the stratum corneum (A), stratum spinosum (B), and stratum basale (C). The dermis is made up of dense connective tissue (J) and skin appendages such as sebacious glands (D), hair folicles (E), errector pili muscles (F), sweat glands (G), blood vessels (H), and nerves (I). The hypodermis contains subcutaneous fat and is located between the dermis and underlying muscle. The different layers of the skin, as well as the adnexal structures contained within, each have a unique functional role that together contributes to maintain homeostasis and provide protection to the body.

Figure 2. Teaching points: When the integrity of the skin is compromised, biochemical signals initiate the cell-mediated repair processes that mediate wound healing. Following hemostasis, normal wound healing occurs in a series of functional and temporally distinct phases. Inflammation typically begins within the first hour following injury and typically lasts from 2 to 5 days. The proliferative phase begins within a few days of injury and can last for several weeks. Tissue remodeling can last for weeks or months depending on the wound severity and healing conditions (size, depth, degree of inflammation, etc.). Notice the overlap of phases of healing. While wound healing is often thought of as a series of distinct phases, the entire process as a whole is complex and highly interdependent on the cellular and physiological events that take place during each wound healing stage.

Figure 3. Teaching points: Wound healing occurs in four defined phases: (A) hemostasis, (B) inflammation, (C) proliferation, and (D) remodeling. Hemostasis is the body's primary defense, taking place within the first few minutes following injury. Activated platelets and fibrin form a clot that slows bleeding. Inflammation begins within the first hour where white blood cells phagocytize damaged cells, debris, and any invading microbes. Cytokines released during this phase stimulate cell migration and growth. During the proliferative phase, angiogenesis, fibrobalst accumulation, granulation tissue formation, exptracellular matrix production, epithelialization, and wound contraction all occur. During the remodeling phase, newly formed collagen bundles are crosslinked and rearranged along tension lines. Following wound closure, cells that migrated to the wounded are and are no longer needed undergo apoptosis. The duration of this phase can last weeks, months, or even years, depending on the wound severity and quality of healing.

Figure 4. Teaching points: Burn injury is classified according to the depth of tissue injury or involvement. First degree burns (A) are superficial, penetrating no further than the epidermis and resolve on their own with no intervention. A sunburn is a classic example of this type of wound. Superficial-partial thickness burns (B), sometimes described as second-degree burns, penetrate the upper dermis without affecting adnexal structures. Injuries of this depth are often accompanied by blistering and blanching, but scarring is infrequent. Notice the bullae and sloughing of the epidermis. In more severe second-degree burn, or deep-partial thickness burns (C), the damage extends further into the dermis, often resulting in damage to hair follicles and sweat glands. As a result, these wounds typically heal with scarring and contracture occurring over several weeks. Full-thickness burns (D) or third degree burns are highly destructive, penetrating the epidermis and dermis completely, often extending into the subcutaneous tissue. These wounds also heal by scarring and contracture, but skin grafting is almost always required.

Figure 5. Teaching points: Example of a Lund-Brower chart used to estimate percent total body surface area burned (%TBSA).

Figure 6. Teaching points: Example of a hypertrophic burn scar involving the palmar aspect of the right hand.

Figure 7. Teaching points: Photographs of a 39-year-old male with keloids. (A) Linear and “dumbbell” or “butterfly” keloids on the upper back without any known previous trauma other than wearing football pads and military protective gear. (B) Close-up image of the left posterior shoulder. (C) Close-up image of the right posterior shoulder.

Figure 8. Teaching points: α-SMA staining in normal and scar tissue. (A) Shows α-SMA staining in normal skin. Positive staining can only be found in endothelial cells. (B) Shows α-SMA staining in burn scar tissue. Just as in the normal skin α-SMA positive cells can be seen in endothelial cells. However, the substantially thicker scar dermis shows α-SMA positive staining of myofibroblasts in a large streak in the middle of the dermis.

Figure 9. Teaching points: Contraction is a key component in the wound healing process. It tends to occur during the remodeling phase as a consequence of the contractile forces of the myofibroblasts. When there is excessive or unregulated myofibroblast activity, as often seen more severe burns (third and fourth degree), the wound tends to heal under increased tensile force resulting in wound contracture. When a contracture develops over cosmetically or functionally important areas, such as the face and joints, respectively, there is often associated cosmetic and functional sequela. For example, as seen in this figure, the contracture over the hand has resulted in a decreased ability of the patient to use his/her hand in a normal fashion. This can have significant impact on a patient's life and requires further interventions to include contracture release in attempt to restore function.

Figure 10. Teaching points: Example of an acute full-thickness burn wound of the right hand.

Figures 11 and 13. Teaching points: The standard treatment of burn injury depends on the depth of injury. If not infected, superficial burns often re-epithelialize with conservative treatment. On the other hand, deep burns require excision and grafting. This process involves removing all of the necrotic (dead), avascular tissue and then taking either a split- or full-thickness skin graft (STSG/FTSG) and placing it onto the vascularized wound bed. Often the skin graft is taken from the thighs or abdomen but can be removed from almost any large surface area where unburned skin is available. The choice of a split- versus full-thickness graft is largely dependent on the location and size of the wound. For example, a large surface area burn or an area that is not cosmetically or functionally important such as the chest, abdomen, or proximal extremities can be grafted with split-thickness grafts. Whereas, small burns in areas of cosmetic and functional importance (face, skin over joints, and ears) and those with thick skin (palms, soles, and scrotum) tend to be grafted with full-thickness grafts. This is because split-thickness can be meshed at different ratios and therefore covers larger wound areas. However, STSG tends to result in worse contractures and “mesh-pattern scarring” when compared to FTSG.

Figure 12. Teaching points: The surgical methods of debridement include tangential or fascial excision. The choice is often based on surgeon presence but the size and location of the injury do play a role. Tangential excision is performed in a step-wise fashion. The eschar is removed layer by layer with a Weck or Goulian blade or with newer technologies such as hydrostatic debridement instruments until diffuse punctate bleeding is reached. The presence of bleeding represents healthy, uninjured tissue that will support a graft. The advantage of this method is that minimal to no healthy tissue is removed. Fascial debridement, on the other hand, involves debridement of all tissue to the level of the muscle fascia. Invariably, this involves removal of some healthy tissue and creates a large defect affecting cosmesis. Fascial debridement is often performed with bovie electrocautery and thus hemostasis is maintained throughout the procedure.

Figure 14. Teaching points: Contractures over the eyelids, extremities and especially the joints can lead to disfigurement and disability. Those over the eyelid can lead to ulcers and potential blindness, while contractures of the hand can prevent the individual from opening and/or closing their hand which affects grasping and/or lifting objects. The inability to use one's hand affects everyday activity and can have significant effects on one's health and occupation. Therefore, the treatment of a function limiting contracture is a surgical release. A release involves removing (excising) the hypertrophic scar or placing incisions through the scar in effort to release the tension of the underlying tissues. Often, this returns anatomic structures back into their normal location. Once the release has been completed the defect is covered with either a split-thickness of full-thickness graft. For larger defects, a tissue flap can be considered.

Figure 15. Teaching points: Significant contracture frequently requires more than a local flap such as a Z-plasty to fully correct (as seen in this figure). The surgical approach to these types of contractures can be difficult and the standard contracture release would result in a defect that is difficult to be closed. When faced with this scenario, free or distant pedicled flaps can be used.