This looks like a scald Regarding the degree, i will directly quote Sabiston ( for those who may wish to revise ) Burn Depth Burn depth is classified into degree of injury in the epidermis, dermis, subcutaneous fat, and underlying structures (Fig. 21-2). First-degree burnsare, by definition, injuries confined to the epidermis. → First-degree burns are painful, erythematous, and blanch to the touch, with an intact epidermal barrier. →Examples include→ sunburn or a minor scald from a kitchen accident. → These burns do not result in scarring, and treatment is aimed at comfort with the use of topical soothing salves, with or without aloe, and oral nonsteroidal anti-inflammatory drugs (NSAIDs). Second-degree burnsare divided into two types, superficial and deep. All second-degree burns have some degree of dermal damage, by definition, and the division is based on the depth of injury into the dermis. Superficial dermal burns are erythematous, painful, blanch to touch, and often blister. →Examples include scald injuries from overheated bathtub water and flash flame burns. These wounds spontaneously reepithelialize from retained epidermal structures in the rete ridges, hair follicles, and sweat glands in 1 to 2 weeks. After healing, these burns may have some slight skin discoloration over the long term. Deep dermal burnsinto the reticular dermis appear more pale and mottled, do not blanch to touch, but remain painful to pinprick. These burns heal in 2 to 5 weeks by reepithelialization from hair follicles and sweat gland keratinocytes, often with severe scarring as a result of the loss of dermis. Third-degree burnsare full-thickness burns through the epidermis and dermis and are characterized by a hard, leathery eschar that is painless and black, white, or cherry red. → No epidermal or dermal appendages remain; thus, these wounds must heal by reepithelialization from the wound edges. → Deep dermal and full-thickness burns require excision with skin grafting from the patient to heal the wounds in a timely fashion. Fourth-degree burns involve other organs beneath the skin such as muscle, bone, and brain. Currently, burn depth is most accurately assessed by the judgment of experienced physicians. Accurate depth determination is critical to wound healing because wounds that will heal with local treatment are treated differently than those requiring operative intervention. Examination of the entire wound by the physicians ultimately responsible for their management is the gold standard used to guide further treatment decisions. Newer technologies, such as the multisensor laser Doppler flowmeter, hold promise for determining burn depth quantitatively. Several studies have claimed superiority of this method over clinical judgment in the determination of wounds requiring skin grafting for timely healing, which may lead to a change in the standard of care in the future. - Ref Sabiston 19[SUP]th[/SUP] ed So i guess this is a scald of 2nd degree with areas of superficial and deep dermal injury. Now there is another confusion term called zones of injury ( and this term applies to more superficial burns ). I will again quote Sabiston The area of cutaneous or superficial injury has been divided into three zones— zone of coagulation, zone of stasis, and zone of hyperemia. → The necrotic area of burn where cells have been disrupted is termed the zone of coagulation. This tissue is irreversibly damaged at the time of injury. → The area immediately surrounding the necrotic zone has a moderate degree of insult, with decreased tissue perfusion.This is termed the zone of stasis and, depending on the wound environment, can survive or go on to coagulative necrosis. The zone of stasis is associated with vascular damage and vessel leakage. Thromboxane A2, a potent vasoconstrictor, is present in high concentrations in burn wounds, and the local application of inhibitors improves blood flow and decreases the zone of stasis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressures also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Treatment directed at the control of local inflammation immediately after injury may spare the zone of stasis, indicated by studies demonstrating the blockage of leukocyte adherence with anti-CD18 or anti-intercellular adhesion molecules; monoclonal antibodies improve tissue perfusion and tissue survival in animal models. → The last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. This region contains the clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis. Related self Assessment Questions from Sabiston (Y)
