Patho Exam 1 (Burns)

normal capillary exchange

-not all capillaries in a bed are always open

—changes depending on what cells need to take in or get rid of

—inflammation increases permeability

-movement of fluid is based on net HP in arterial end and net OP in venous end

inflammation

-vasodilation, blood flow increases to injured area → warmth

-increased capillary permeability → fluid leaves vessels and enters tissue → swelling

-RBCs become more concentrated b/c fluid is leaving vessels → redness

-WBCs: adhere to vessel lining and then migrate out of blood into tissue

-S/S: redness, warmth, swelling, pain, loss of function

steps of inflammation

-injury

-bradykinin released from injured cells

—activates pain receptors

-mast cells & basophils release histamine

-bradykinin & histamine dilate capillaries

—increased blood flow to injured area

-bacteria enter tissue

-neutrophils and monocytes come to injury site and enter tissue from blood

-WBCs phagocytize bacteria

-macrophages leave blood and enter tissue to phagocytize

causes of burns

-thermal

—heat: contact with hot air

—flame: contact with fire

—scald: contact with hot liquid

—contact: touching a hot object

-non-thermal

—chemical:

• contact: touching a strong chemical (often extreme pH)

• inhaled: breathing in chemical fumes (or smoke)

• ingested: eating a dangerous chemical

-electricity: contact with an electric current (e.g. lightning)

-radioactive: exposure to radiation

1st degree burns*

-superficial (only burns epidermis)

-S/S: pain, redness, maybe blisters (after 24 hr), blanches

-may lead to chills, HA, edema, N/V

-most common example is sunburn

-dangerous in young or old pt

2nd degree burns*

-superficial partial thickness (all of epidermis and part of dermis)

—blisters and vesicles that may rupture → more pain

—most painful type

—3-4 weeks to heal (w/o complications)

—tx: nutrition

—scarring is rare

-deep partial thickness (entire dermis)

—waxy and white appearance (similar to full thickness)

—may take weeks to heal

—tx: surgical excision of dead tissue, skin graft

—may lead to hypertrophic scar

3rd degree burns*

-full thickness (all of epidermis and dermis, into SQ)

-appearance: white, dry, leathery

-edema, no elasticity, decreased circulation distal to site (d/t pressure from edema)

—edema also compresses nerves

-no pain (nerves destroyed)

*4th degree: all of SQ and into muscle or deeper

compartment syndrome*

-nerves and blood vessels are compressed by swelling from injury, burn, etc

-leads to hypoxia, ischemia, necrosis

-S/S distal to injury site: pallor, weak pulses, numbness or tingling

escharotomy*

procedure to create an incision into scar tissue

-full thickness circumferential burns lead to eschar (nonviable)

—may lead to compartment syndrome, which leads to tissue death

-need surgery to divide eschar and give underlying tissue room to expand

-prevents necrosis that could necessitate amputation

how to assess burns

-use rule of 9s (for adults) to know % of TBSA burned

—20% of TBSA = major

—use Lund and Browder scale for peds

-burns are OFTEN combined with other injures

—e.g. smoke inhalation → ARDS is usually the cause of death in fire victims

criteria to go to burn unit

-partial thickness burns >10% TBSA

-burns on face, hands, feet, genitalia, or joints

-3rd degree

-electric or chemical burns

-inhalation injury (e.g. smoke)

-preexisting problem

-burn + other major trauma

-young or old pt

-socioemotional or long term rehab needed

burn shock*

-burns → inflammation → increased capillary permeability → fluid leaves bloodstream and enters tissue

—low blood volume

-decreased cardiac output and contractility from release of myocardial depressant factors

-EPI and NE released because of SNS activation

—blood is shunted away from visceral organs

• → oliguria b/c kidneys are not getting blood

• toxins and bacteria leak from gut → endotoxemia → sepsis

-low BV and low CO → hypovolemic shock

—S/S: tachycardia, weak thready pulse, hTN

burn shock and pH*

—hypovolemia → low O2 to tissues → anaerobic glycolysis and protein breakdown for ATP → lactic acid byproduct → metabolic acidosis

how does shock end?*

-end point of shock = capillary seal (after 24 hr)

—b/c increased permeability stops

—so giving IVF actually will work now to increase BV (and BP)

body’s response to burns*

-impaired Na+-K+ pump

-metabolism

—increased catecholamines

—increased cortisol, glucagon, and insulin

—increased oxygen use

—increased clot factors from liver → hypercoagulable state

-decreased immune response (risk for sepsis)

—d/t decreased phagocytosis and loss of skin barrier

-risk of pulmonary edema (b/c inflammatory mediators are going to lungs)

—may → ARDS

phases of burn response

-emergent

—72 hr

—fluids move to interstitial d/t increased permeability

• causes protein loss from blood to decrease OP and cause more fluid shifts to the interstitial

• causes edema and shock, and hemolysis

—increased Hct b/c of fluid loss

—Na+ and K+ shifts

—coagulation causes necrosis

—decreased immunity (because of loss of skin barrier)

—may lead to AKI

-acute

—fluid balance begins to restore → diuresis

—may cause electrolyte problems

-rehab

—wounds mostly healed (by 2 wk to 8 mo)

other types of burns

electric

-often skin does not appear severely burned, damage is far more extensive internally than on surface

chemical

-d/t contact with acid, base, or vesicant

-FIRST priority is getting the chemical off the skin via flushing

—do NOT get the chemical on yourself!

frostbite

-can happen from cold air or contact with cold object

-ice crystals form in cells → anoxia and impaired metabolism

-categorized same as burns