Week 8; Trauma Cont. Flashcards
(142 cards)
Burns impact bodily functions in three ways:
Physiologic, metabolic, and psychological
Patho of burn injury
Tissue destruction caused by a burn injury
leads to local and systemic problems that
affect fluid and electrolyte imbalance leading
to protein losses, sepsis, changes in metabolic, endocrine, respiratory, cardiac, hematologic, and
immune functioning.
Types of burns
Heat/thermal, electrical, cold, chemical, radiation, and friction
Heat/Thermal Burn
Caused by fire, liquid, steam, grease, tar,
hot objects. Inhalation injury may occur
Electrical Burn
From electrical current, damages
skin and other structures under skin. Iceberg effect (worse underneath), causes heart muscle and dysrhythmias, muscle damage, and release myoglobin into blood and lead to kidney
damage (acute tubular necrosis).
Cold Burn
Frostbite
Chemical Burn–
Caused by powders, gases, or food (hot
pepper). Acid or base (alkali), watch for inhalation injuries
Radiation Burn–
D/t sun, cancer treatment
Friction Burn –
Abrasions, road rash
Extent of burn injury depends on
Age, general health (diabetes, compromised
circulation, heart failure where heart muscle is
weak), depth and extent of injury, specific body area injured – face/head/neck can
cause respiratory issues, torso can restrict
breathing, perineum can be related to infection, as well as inhalation injury.
Physical skin changes r/t burns
Epidermis can grow back after a burn, sweat
and oil glands and hair follicles extend into the
dermal tissue and regrow to heal partial
thickness wounds. Skin can regrow as long as parts of dermis are left. When entire dermal layer is burned, skin can no longer restore itself.
Functional changes of skin r/t burns
Skin maintains fluid and electrolyte balance. Massive fluid loss occurs through excessive evaporation proportionate to the total body surface area. Full thickness burns destroy sweat glands reducing this ability.
First degree burn
Superficial thickness, least damage; epidermis is only part of skin that is injured. Red, pink and painful, but all nerve endings still there. Warm to touch. Desquamation (peeling of dead skin) occurs
2 to 3 days after burn.
Desquamation
Peeling of dead skin
Second degree burn
Partial Thickness; superficial partial thickness or deep partial thickness. Involves entire epidermis and dermis (varying depths). Shiny and moist, red and pink, blisters, scars can result, very painful.
Third degree burn
Full Thickness; black, yellow, brown, white, or red. Severe and extends into hypodermis, no blisters. Eschar present – hard, leathery. Grafts required. Not as painful, nerve layers destroyed. Destruction of entire epidermis and dermis; skin does NOT regrow.
Fourth degree burn
Deep Full Thickness; worst of all – bone, muscle, ligaments. Black and charred with eschar, pain and sensation is absent, no blisters, grafts required.
Vasular changes r/t burns
Fluid shift after initial vasoconstriction. Blood vessels near the burn dilate and leak fluids into interstitial space. Also called “third spacing” or capillary leak syndrome. Profound imbalance of fluid, electrolyte, acid-base; hyperkalemia and hyponatremia. Fluid remobilization after 24 hour, diuretic stage begins 48 to 72 hour after injury, hyponatremia and hypokalemia occur as potassium moves back into cells.
Cardiac changes r/t burns
Hypovolemic shock—Common cause of
death in early phase in patients with serious
injuries and cardiac rhythm, especially in cases of
electrical burn injuries.
Respiratory changes r/t burns
Occurs even when lung tissues have not
been damaged directly; Burns on nose and mouth
Torso burns – restrictive to chest, impeding
respirations
Histamine, other inflammatory mediators
cause capillaries to leak fluid into pulmonary
tissue space
GI changes r/t burns
Decreased blood flow and sympathetic
stimulation during early phase cause reduced
GI motility, paralytic ileus
GI bleeding – gross and occult
Curling’s ulcer – acute gastroduodenal ulcer
from stress injury, not as common because of
use of H2 histamine blockers and proton
pump inhibitors
Metabolic changes r/t burns
Increased secretions of catecholamines,
antidiuretic hormone, aldosterone, cortisol. Increased core body temperature as
response to temperature regulation by
hypothalamus.
Compensatory responses r/t burns
Inflammatory compensation – triggers healing
bur is also responsible for the fluid shift and
edema and hypovolemic shock.
Sympathetic nervous system compensation –
increased heart rate, increased BP, widen
bronchial passages, slow intestines.
Emergent management of burns
Assess airway (A)
Administer Oxygen (B) Breathing
Maintain Circulation (C) – loosen clothing
Disability (D) - All patients should be assessed for
responsiveness with the Glasgow coma scale; they may be confused because of hypoxia or hypovolemia.
Exposure (E) Cover with linens, blanket – maintain
warm, prevent nerve endings from air currents, security and calm.
Make NPO, start IVs, head to toe