Burns

Question 1

What are functions of the skin?

Answer 1

Protective barrier: infection, pathogens, underlying tissues from trauma. Thermoregulation. Fluid loss: skin sweats to get rid of heat as needed. Sensation: temp changes, pain, pressure, touch. Absorbs sunlight to make inactive vitamin D which is made active in the kidneys.

Question 2

What are the effects of burns?

Answer 2

Loss of skin function which depends on the extent of destruction: causative agent (source of burn), intensity of heat, duration of exposure, thickness of skin.
Plasma loss, in which worry about fluid balance, protein loss, electrolyte imbalance.
Some of the most traumatic injuries sustained, initial injury can worsen/evolve over time.

Question 3

> = 20% TBSA (total burn surface area). Causes?

Answer 3

Major burns. Larger burns are associated with morbidity and mortality disproportionate to their initial appearance
Fluid imbalances: systemic inflammatory response, capillary permeability throughout the entire body, fluid loss, edema throughout.
Hemodynamic changes: CO decrease, SNS response, hypermetabolism

Question 4

Thermal, chemical, radiation burns?

Answer 4

Thermal is most common. Dry thermal: contacting flame. Wet is scalding liquids, steam. Frostbite is included in thermal because effects are similar.
Chemical from fumes (carbon monoxide, fire accelerant), ingestion, injection, touching. Concentration of chemical and volume.
Radiation: most common is sunburn. Thermal effect, resulting in cutaneous burn injuries. Also can damage DNA, which may be localized or affect whole body.

Question 5

Electrical burns?

Answer 5

High (over 1,000 volts)/low voltage. Entry point, exit point has more explosive tissue damage. Current moves from the path of least resistance to the path of most resistance.
SA node can reset, Brain damage. Renal concerns. rhabdomyolysis causes issues

Question 6

Burn injuries that involve only the outermost layer of skin, the epidermis. Erythematous but skin is intact. Sunburn or superficial scald. Not included in calculations of TBSA.

Answer 6

1st degree, superficial thickness.
If rubbed the burned tissue does not separate from underlying dermis (Nikolsky’s sign). Blanches with pressure. Takes a few days to heal. Painful.

Question 7

2nd degree burns?
Usually painful, involving blisters and edema. moist. Some tissue still alive but not necrotic. Hair follicles/skin appendages remain intact.

Answer 7

Superficial partial: Burns that involve epidermis and halfway into the dermis. Doesn’t require grafting.
Deep partial: epidermis and entire dermis. Generally does need grafting, ruined the dermis which now needs help recovering with new tissue.
Healing time depends on depth, 2-3 wks.

Question 8

Burns causing total destruction of the epidermis, dermis, and in some cases subcutaneous layer/underlying tissue. Needs grafting. Edema is present. Leathery, dry, dead tissue.

Answer 8

3rd degree. Burn color in 3rd degree ranges from pale white to red, brown, charred. Lacks sensation, nerve fibers damaged. Hair follicles, sweat glands destroyed.

Question 9

Burn injuries that extend into deep tissue, muscle, or bone. High voltage electrical burns.

Answer 9

4th degree. May need amputation, too much tissue loss to graft over.

Question 10

What factors impair recovery time in major burns?

Answer 10

TBSA, type of burn, depth, zones, body parts (worry about airway/edema in the face area, hands, feet, major joints), age, presence of inhalation injury, past medical history (alcohol/substance abuse, HF, DM, already have fluid in the lungs to start with)

Question 11

Part of burn with characteristic coagulation necrosis.

Answer 11

Zone of coagulation. Center of the wound. Dead tissue that’s not recoverable and needs debridement.

Question 12

Result of a chemical injury or heat transfer from one site to another, causing tissue destruction through coagulation, protein denaturation, and ionization of cellular contents. How is depth determined?

Answer 12

Burn injury. Burn depth is classified according to how the injury occurred, causative agent, temp, duration of contact with cause, thickness of skin. Tissue necrosis occurs at the center of the injury with regions of viability toward the periphery.

Question 13

An area of injured cells in a burn wound that may remain viable but with persistent decreased blood flow from edema will undergo necrosis within 24-48hrs. Needs fluids within 48 hours. Compromised blood supply, inflammation, tissue injury.

Answer 13

Zone of stasis. Surrounds zone of coagulation. May recover with some debridement. Plan may change depending on edema, which determines whether the tissues dies or not. Causes pressure constricting blood flow in the tissues, causing further issues and death instead of recovery.

Question 14

Outermost zone of a burn injury that sustained minimal injury and may fully recover over time.

Answer 14

Zone of hyperemia (referencing blood vessel supply to the tissue). Sustained the least damage of all the zones.

Question 15

Burns that are more than 20% of TBSA.

Answer 15

Major burns are characterized by burn wound edema, generalized edema in noninjured tissues, altered cardiovascular function, impaired organ perfusion.

Question 16

What is the initial systemic event after a burn injury?

Answer 16

Hemodynamic instability. Results from loss of capillary integrity leading to shift of Na, fluid, protein from intravascular space into interstitial, hypovolemic shock.

Question 17

Explain cardio alterations in emergent phase of burns (remember fluid loss!)?

Answer 17

Immediate decrease in CO that precedes the loss of plasma volume. Inflammation causes release of free O2 radicals that lead to vascular premeability, peripheral edema. Fluid loss leads to SNS response (catecholamines), increasing HR, vasoconstriction to compensate (increasing workload of heart).

Question 18

The body is divided into anatomic regions each representing about 9% of the TBSA. Done by EMS as a quick guide. Most commonly used.

Answer 18

Rule of nines. 1st degree isn’t included, 2nd and 3rd are counted as the same.
18%: per leg, anterior torso, posterior torso
95: per arm, anterior head, posterior head.
1%: perineum/groin, each palm of hands

Question 19

Palmar method for determine TBSA?

Answer 19

Size of the pt’s hand, including fingers, is about 1% of the TBSA. Use this rule when there’s a small area burned, like a splash instead of like the whole leg, or scattered burns

Question 20

More precise TBSA measurement tool that recognizes the percentage of surface area of various body parts as it relates to the age of the pt.

Answer 20

Lund and Browder.

Question 21

The first phase of burn care, which lasts from the onset of injury until the completion of fluid resuscitation, about 24-48hrs with 24hrs to regain capillary integrity? Priorities?

Answer 21

Emergent/resuscitative phase. Primary survey: ABCDE (airway/breathing, circulation, determine disability (pain control), expose/examine (temp regulation). Prevention of shock, respiratory distress. Find/treat other injuries/traumas (inhalation?). Wound assessment, initial care. Place foley. Hydrotherapy to clean wounds. Probably intubated, no PO meds.
Create sufficient CO to hemodynamically stabilize, complete the parkland formula.

Question 22

The second phase of burn care, from the start of diuresis to near completion of wound closure. Priorities?

Answer 22

Acute/intermediate phase. Wound care/closure, prevention/treatment of complications like infection, nutritional support, maintain healing.

Question 23

Third phase of burn care, from major wound closure to return to pt.’s optimal physical and psychosocial adjustment (can take years). Priorities?

Answer 23

Rehabilitation phase. Prevention/treatment of scars, contractures (mobility). Physical, occupational, vocational rehab. Functional/cosmetic reconstruction. Psychosocial counseling.

Question 24

Treatments for compartment syndrome (as related to burns)?

Answer 24

Decompression via escharotomy. Surgical incision into eschar down to the superficial fat to allow edema to escape. May be done bedside. If fluid is let out perfusion should reestablish.
Allows expansion of skin to accommodate edema & permit blood flow.
Fasciotomy: surgical opening of the full length of fascial compartments, extending through the fascia (covering muscle). Risk cutting major vessels so done in the OR, needs to be sterile.

Question 25

Inhalation of thermal (hot smoke, more oral cavity and upper tissues)/chemical irritants (toxic chemicals the can burn all the way down into the lung tissue itself) are inhalation injuries. Because the cooling effect of rapid vaporization in pulmonary tract, direct heat injury does not usually occur below the level of the glottis. Two types?

Answer 25

Upper airway (above glottis): Direct thermal injury or face/neck burns, which cause obstruction of the upper airway in early hrs post burn. More from direct heat in the oral cavity as inhaled. 
Lower airway burns, below vocal cords (below glottis): From inhaling the products of incomplete combustion or noxious gases. Can be from soot and particles going down lower even if the heat from gas is less up above. Often the source of death at scene, carbon monoxide

Question 26

S/s of smoke inhalation, inhalation injury?

Answer 26

Indications of inhalation injury include: injury occurring in an enclosed space, burns of the face or neck, singed facial/nasal hair, hoarseness, high-pitched voice change, stridor (laryngeal edema), dyspnea/tachypnea or other signs of hypoxemia, erythema/blistering of oral/pharyngeal mucosa, altered mental status (agitation, restlessness, anxiety). Expectoration of carbon particles in sputum is the cardinal sign.

Question 27

Further explain smoke inhalation?

Answer 27

Mechanisms of injury are thermal damage, asphyxiation, irritation of the pulmonary tissues. These injuries cause loss of ciliary action, trigger inflammatory response causing hypersecretion, produces severe mucosal edema, bronchospasm. Alveolar surfactant is reduced, resulting in atelectasis.

Question 28

Tasteless, odorless, gas present from incomplete combustion of carbon-containing fuels. W/ poisoning, it combines with hemoglobin to form carboxyhemoglobin, for which it has an affinity 200x greater than O2, binds to O2 receptors. Affects brain, cardiovascular system especially. Most frequent cause of death at scene r/t smoke.

Answer 28

Carbon monoxide. Decreases O2 carrying capacity. Metabolic acidosis from anaerobic metabolism. Doesn’t burn the airway but is toxic to the body. Affects the cardiac muscle since it binds with myoglobin. Normal carboxyhemoglobin level <10% in a normal person, 1-3% in normal person, higher in smokers. >60% coma, death in late stages

Question 29

Treatment for carbon monoxide poisoning? S/s?

Answer 29

Main treatment is to give oxygen, 100%. Prevent acidosis if possible so give as soon as possible. Get the pt. out of the environment.
Over 10% level in body: headache, flushing, vision changes. >60% requires intubation most likely. Intubation depends on how much exposure the pt. had.

Question 30

Smoke inhalation interventions?

Answer 30

High suspicion of it, then intubate. Baseline CXR (may worsen in a few days). Main treatment is 100% O2 via tight fitting mask, but ideally a non-breather. Elevate HOB. Baseline VS, keep assessing. ABGs and carboxyhemoglobin level. Bronchodilators. Remove pt. from the environment!

Question 31

Inhalation injuries and intubation?

Answer 31

Assess exactly how their injury was caused, inhalation means they’re more likely to be intubated because airway is more likely to become edematous. Fluid can shift into lungs because they still have fluid shifting overall, permeable capillaries for about 48 hours.
Edema can still get worse for next 2 days after the burn. Becomes harder to intubate if it keeps getting worse. High risk for pneumonia, ARDS w/ edema.

Question 32

Late pulmonary complications secondary to inhalation injuries?

Answer 32

Mucosal sloughing of airway, which can lead to obstruction, increased secretions, inflammation, atelectasis, airway ulceration, pulmonary edema, tissue hypoxia.

Question 33

In the emergent phase of inhalation injury/burns edema occurs, leading to what?

Answer 33

Acute airway obstruction. Cells die, lysis causes a further inflammatory response and worsening edema in both upper and lower airway. There’s already edema from the SIRS, plus this true inhalation injury edema which doubles it and makes it worse in the airway.

Question 34

Upon injury, there is an immediate decrease in CO that precedes loss of plasma volume. Fluid moves into the interstitial space w/in 30min of burn injury (peak 6-8hrs post), capillaries leak for 48hrs throughout the entire emergent phase. Results in what cardiovascular effects in emergent phase?

Answer 34

Burn shock potential, distributive. ↓ CO from fluid loss (hypovolemia) leads to vasoconstriction. Tachycardia to compensate, workload of heart increases, cardiac dysrhythmias from elevated K+ in this phase.
If CO isn’t under control and urine OP starts to significantly decline (can already be oliguric here because the kidneys are holding onto fluid) if there’s significant oliguria you can have organ dysfunction which moves into severe sepsis/MODS.

Question 35

GI system in the emergent phase of burns?

Answer 35

Decreased perfusion to gut leads to decreased peristalsis. R/f translocation of intestinal bacteria r/t permeability in first 48hrs. Bacteria that’s normally helpful can shift out and into bloodstream, lymph, causing sepsis. Risk of severe sepsis w/GI permeability.

Question 36

Why the NG in the emergent phase of burns? Bowel care?

Answer 36

NG tube because you want to take the acid out (decompress). Monitor bowel sounds because although you can’t feed right way, give nutrition as soon as possible, ideally after 24 hours if they have bowel sounds, which they will have if they have enough perfusion

Question 37

Renal system in the emergent phase of burns? Tubules are blocked in kidney, causing ischemia how?

Answer 37

Decreased kidney perfusion triggers RAAS, leading to oliguria. Destruction of RBCs at injury site leads to free hgb in urine. If muscle damage occurs, myoglobin is released by muscle cells and secreted by kidneys. Rhabdomyolysis has dark brown urine color. If there’s inadequate blood flow through kidneys, hgb and myglobin occlude the tubules, resulting in necrosis. Ideally adequate urine OP by the 2nd phase, with good CO after parkland formula is through

Question 38

Further explain burn shock?

Answer 38

As fluid loss continues and vascular volume decreases, CO continues to decrease and the BP drops. This is the onset of burn shock. Results from combo of direct cutaneous injury, intravascular volume loss, and systemic inflammatory mediators affecting the body systems. Increasing vascular permeability, peripheral edema. Vasoconstriction, increase HR

Question 39

Serum K+, Na, glucose labs on admission in a major burn during the emergent phase, before fluid resuscitation?

Answer 39

↑ K+, hyperkalemia. Leaves the cell and goes into the bloodstream from K-Na pump failure. Also massive cell destruction.
↓ Na, hyponatremia. Na goes into the cell, leaves the bloodstream moving opposite K+. Also lost through burns themselves, plasma loss.
↑ Glucose, SNS response, liver dumps glucose

Question 40

Blood labs on admission in a major burn during the emergent phase, before fluid resuscitation?

Answer 40

↑ HGB/HCT due to plasma loss, causing hemo concentration.
Coagulation: decreased platelets (thrombocytopenia), prolonged clotting/prothrombin times. Fluid loss means no perfusion which means metabolic acidosis (possible). At time of burn injury, some RBCs may be destroyed/damaged, resulting in anemia.

Question 41

Used to estimate amount of replacement fluid required for first 24hrs in burn pt to ensure they remain hemodynamically stable. Only area covered by 2nd degree or greater, as 1st don’t cause bad fluid shift.

Answer 41

Parkland/Baxter formula. Four times the product of the body weight and the burn area percentage. Successful fluid resuscitation is based on urine output [30-50 ml/hr for most burns, except electrical burns at 75-100 ml/hr]. Excessive fluid admin increases edema in both burned and non-burned tissue

Question 42

Calculating Parkland formula, used for burns greater than or equal to 20% TBSA?

Answer 42

IV LR: 2mL x %TBSA x pt. weight in kg. 4mL with electrical instead of 2, needs more fluid to prevent rhabdomyolysis.
Calculate from time of injury, not admission. First half of fluid is given within 8hrs of burn, remaining over the next 16hrs.

Question 43

What are indications of adequate fluid resuscitation?

Answer 43

Clear sensorium. HR <120bpm. Systolic BP >100mmHg. MAP >=65mmHg. Urinary OP >=30-50mL/hr (non-electrical). Blood pH within normal range.

Question 44

Acute/intermediate phase goals, form the start of diuresis (good urine, around 48hrs) to near wound closure?

Answer 44

Continue ABC assessment. Maintain GI & renal function. Address hypermetabolism and nutritional needs. Wound care & infection control. Continue pain management. Positioning & mobility

Question 45

Pulmonary system in the intermediate phase?

Answer 45

Increased r/f pulmonary edema r/t fluid resuscitation if this hasn’t already occurred. Lead to increased r/f bronchial pneumonia or ARDS. Potential for infection w/ intubation, VAP.
Prevent fluid in lungs: TCDB, turning, ambulating, incentive spirometry, HOB up

Question 46

What’s involved in a secondary survey of the burn pt.?

Answer 46

Focuses on obtaining a history, the completion of total body system assessment, initial fluid resuscitation, and provision of psychosocial support of the pt.

Question 47

Cardiovascular in intermediate phase in which the pt. is starting to have resolution of capillary leakage, moved past the 48hrs. Should have good urine OP and CO. Goal is to have diuresis w/ fluid required to maintain hydration

Answer 47

K+ is better but can be hypokalemic. Can re-enter the cell as the K-Na pump is re-established, may occur later w/ fluid shifts, inadequate K+ replacement. Na is low during first week of phase because of dilution from fluids, water shifting from interstitial and returning to vascular space. H/h can be lower because of fluid dilution instead of hemoconcentration.

Question 48

Renal in the intermediate/acute phase?

Answer 48

Potential for AKI w/out good urine OP. This is mostly electrical burn pts because they have rhabdomyolysis which affects the kidneys.
Strict I/O, make sure they keep up good urine OP. Might take out foley, maybe day 3 from original injury which is the start of this phase or later depending.

Question 49

GI in intermediate aka acute phase of burns?

Answer 49

Still r/f stress ulcer, continue to watch. Give h2 antagonists or antacids. 3 of the most common GI alterations are paralytic ileus, Curling’s ulcer, translocation of bacteria. Decompression needed if there’s gastric distention

Question 50

Nutrition in intermediate phase of burns?

Answer 50

Increase calories/protein. Protein is 2-4xnormal amount, 3500-5000 calories. Burn shakes for supplementation.
Hypermetabolism: 100-200% above basal rate. Stress due to fluid loss, inflammatory mediators, wounds (heat loss). r/f muscle atrophy, if not managed. Daily weights. Consider vitamins: B1, zinc, absorbic acid for wound healing

Question 51

Pain control and mobility in intermediate phase?

Answer 51

Analgesics, anxiolytics, non-pharmacological. Consider pre-existing tolerance. Pre-medicate before dressing changes: morphine, Ativan most commonly used PO about 30min before IV morphine during change. Monitor RR, pulse ox, airway with narcotic admin. Encourage early ambulation in most pts: prevents ileus, helps with lung fluids, prevents contractures.
Specialty beds, e.g. air mattress decreases r/f skin breakdown. Specific positioning to prevent edema.

Question 52

Immune system in intermediate phase of burns?

Answer 52

Goal is timely wound closure w/ minimal complications. Early surgical debridement ideally within the first few days to remove bacteria building on wound. Immune system dysfunction (suppression)
Primary bacteria source is hair, so clip it around burn. Cultures per MD, checking for new/different growth. Barrier techniques with every dressing change. No fresh fruit, flowers, plants, they carry spores and can potentiate infections

Question 53

Pre-graft wound care? 2 types of contamination?

Answer 53

Wear PPE, remove dressings. Gentle cleaning debriding nonviable tissue w/ dial soap, water, washcloth. Keep wound moist to encourage granulation tissue to grow. Maintain comfort (room temp, pain control, communication). Monitor level of sedation, airway, VS.