Superficial (1st degree): erythema, blanching on pressure, pain and mild swelling, no vesicles or blisters [structures: superficial epidermal damage with hyperemia, tactile and pain sensation intact]
-Deep (2nd degree): Fluid filled vesicles that are red, shiny, wet (if vesicles ruptured); severe pain caused by nerve injury; mild to mod edema [structures: epidermis and dermis involved]
Full-Thickness Skin Destruction
Third & Fourth degree: dry-waxy white-leathery or hard skin; visible thrombosed vessels; insensitivity to pain bc of nerve destruction; possible involvement of muscles/tendons/bones [structures: ALL skin elements and local nerve endings destroyed]
Fluid and Electrolyte Shifts: what to watch for
-Hypovolemic shock (caused by massive fluid shifts out of blood vessels as a result of increased capillary permeability and can begin early..like 20 min after)
Synopsis of electrolyte shifts:
-As capillary walls become more permeable, water-sodium-and later plasma proteins (albumin) moves into intersitial space and surrounding tissue
-Even more fluid shifts out of vascular space into interstitial spaces (second spacing) bc colloidal osmotic pressure decreases with progressive loss of protein from vascular space
Net result of fluid shift:
Intravascular volume depletion.
S+S: decreased BP, increased pulse rate, manifestations of hypovolemic shock
-Also...insensible loss by evaporation from large denuded body surfaces
Impaired circulatory status bc of _____?
HEMOLYSIS of RBCs
-This happens by a circulating factor released at time of burn. Elevated hct is caused by hemoconcentration resulting from fluid loss.
-Na rapidly shifts to interstitial spaces and remains there until edema ceases. K shift initially develops bc injured cells and hemolyzed RBCs release K into circulation
Pathophysiology of burn injuries:
-Loss of skin integrity
-Complication of circumferential injuries
Inflammation & Healing:
Coagulation necrosis--tissue and vessels damaged/destroyed
Neutrophils and monocytes accumulate at the site of injury. Fibroblasts and newly formed collagen fibrils appear and begin wound repair within first 6-12 hrs after injury
Skin barrier destroyed, resulting in bone marrow depression and decreasing circulating levels of immunoglobulins
Inflammatory cytokine cascade triggered by tissue damage impairs function of lymphocytes, monocytes, & neutrophils-which put pt at greater risk for INFECTION!
Complications of Circumferential Burns
-Infection, circulatory compromise distal to burn with subsequent neuro impairment of affected extremity
-compartment syndrome: increase pressure in compartment which compromises nerve function of tissue
Complications during acute phase of burn injury: INFECTION
Pathogens invade through destroyed skin layer. May progress to transient bacteremia as a result of burn wound manipulation (debridement)