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NURS 412 > Burns > Flashcards

Burns Flashcards

1
Q

What is classified as a burn?

A

A burn is a an injury to tissue caused by contact with dry heat (fire), moist heat (steam or hot liquid), corrosive chemicals, electric current, or radiation.

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2
Q

What is a burn influenced by?

A

1) temperature of burning agent
2) duration of contact time
3) type of tissue that has been injured

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3
Q

Types of burns: Thermal/contact burns

A

Flame
Scalding
Contact with hot objects

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4
Q

Types of burns: Chemical burns

A

Contact, concentration, volume and type are significant factors.
- alkalis (more difficult to manage b/c they adhere to tissue causing protein hydrolysis and liquification
- Acids (hydrochloric, oxalic)
- organic compounds (cause contact burns and systemic toxicity)

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5
Q

Types of burns: smoke and inhalation

A

3 types:

Carbon monoxide poisoning and asphyxiation
- carbon monoxide is produced by the incomplete combustion of burning materials
- Co displaces O2 on the hgb resulting in decreased arterial O2 content (Co has greater affinity – faster)
- Co decreases cellular respiration by binding with cytochrome (unable to make ATP, no muscle function – energy, unable to breath)
- O2 sats do not make the distigusher of what is bound to the hgb (not accurate representation)

Inhalation injury above the glottis:
- hot air steam or smoke; mucosal burns of oropharynx and larynx causing blistering, redness and edema and results in obstruction
- early indicators include facial burns, singed nasal haris, hoarsness of voice, painful swallowing, darkened oral and nasal mucous, carbonaceous sputum, clothing burns

Inhalation injury below the glottis: chemically (toxic fumes) getting into lower airways. Acute respiratory distress 24 hours after

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6
Q

S and S of carbon monoxide poisoning

A

headache - dizziness
nausea - dyspnea
visual disturbances - confusion
syncope - seizures and coma
cardiopulmonary dysfunction - death

skin is cherry red

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7
Q

What is the treatment for inhalation burns

A

most worried about airway obstruction
high flow 100% O2 in non-rebreather mask

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8
Q

Types of burns: Electrical burns

A

Types: lightening or contact with high voltage wire produces heat as electricity moves through the body.
Direct damage to nerves and vessels, causing tissue anorexia and death (difficult to assess affect because it is below the skin - iceberg effect)
Remember the pt may have been thrown and the cause of immediate death is cardiac failure because electrical current in heart has been compromised (AED).
- Due to this and possible falls all patients with electrical burns should be on spinal precautions
Contact with electrical currents can cause muscle contractions strong enough to fracture the long bones and vertebrae.
Current that passes through vital organs will produce more life threatening sequelae than current that passes through other tissues. (more density)
Also at risk for severe metabolic acidosis and myoglobinuria (myglobin from injured muscle and hgb from damaged RBCs are released into circulation whenever massive muscle and blood vessel damage occurs. The myoglobin travels to kidneys and blocks renal tubules (ATN) and AKI)

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9
Q

What are electrical burns influenced by

A

Duration of contact
Intensity of current (voltage)
Type of current (direct or alternating)
Pathway of current
Resistance of tissues as it passes through the body.

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10
Q

Layers of the skin

A

Epidermis- protective layer
Dermis - CT containing BV, nerves, sweat glands
SQ layer - major vascular network, nerves, heat insulator

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11
Q

Types of burns: Radiation burns

A

Source: sunburns (erythema, edema, pain)
Influenced by:
- Distance from radiation
- strength of radiation source
- Duration of exposure
- Extent of body surface area exposed
- Amount of shielding between person and source

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12
Q

Classification of burn injury

A

1) burn depth
2) extent of burn
3) location of burn
4) pt risk factors

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13
Q

Depth of burn injury: Partial thickness

A

A. Partial-thickness burns involve injury to epidermis and dermis.
1. First degree burn- superficial: epidermis; painful, appear red, with no blistering initially (after 24h, skin may blister and peel).
2. Second degree partial thickness burns: epidermis and dermis involved; appear wet or blistered and are extremely painful but can heal on their own if area small and there is no infection

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14
Q

Depth of burn: Full thickness

A

Third degree full thickness burn – damage throughout dermis into subcutaneous tissue; unless area small and no infection, grafting is necessary.
Fourth degree full thickness burn- involves skin, fat, muscle and sometimes bone.

both are dry, waxy-white, leathery, vessels seen, insens to pain d/t nerve destruction

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15
Q

Extent of burn

A

Burn size expressed as a percentage of total body surface area (TBSA) using the:
- Lund Brower Chart
- “Rule of 9’s” – TBSA (2-4 degree burns)

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16
Q

Location of burn

A

Face, neck, circumferential chest or back – mechanical obstruction from edema, leathery tissue formation (inhibit resp function)
Hands, feet, joints, eyes – inhibit self care
Ears, nose, buttocks and perineum – high risk of infection
Extremities – circulatory impairment (compartment syndrome)

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17
Q

What are the concerns of a patient with heart disease or COPD?

A

Fluid overload causing HF and pulmonary edema, pneumonia

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18
Q

Burn patho

A

amount of damage depends on length of exposure
Immediately following burn injury vasoactive substances are released from injured tissue (These substances initiate changes in capillary integrity and allow plasma to seep into surrounding tissue). This will cause shift of fluids (second or third spacing)
Direct damage to vessels from heat further compromises vascular integrity and sodium-potassium pump fails causing cellular edema.
If the tissue is not cooled but continues to heat up cell necrosis occurs.
The burn-injured client’s hemodynamic balance, metabolism and immune status is altered.

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19
Q

Phases of burn management

A

Pre-hospital care
Emergent (resuscitative)
Acute (wound healing)
Rehabilitative (restorative)

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20
Q
  1. Pre-hospital/early emergent care
A

ABCs
Stabilize the c-spine!
Provide O2 and anticipate intubation esp with inhilation injury.
Stop the burning. (cool burn with sterile water for no longer than 10 minutes and then warm pt) - no ice or full emersion in water of limb
Remove non-adherent clothing and wrap in dry dressing to prevent infection and heat loss.
Establish IV access if burn is greater than 15% to start
Insert catheter if burn is greater then 15% (measure output and end organ perfusion - kidneys)
Elevate burn above heart level to decrease edema

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21
Q
  1. Emergent phase
A

the period of time required to resolve immediate, life-threatening problems resulting from the burn injury
Lasts up to 72h from time of injury

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22
Q

What are the primary concerns of emergent phase?

A

Onset of hypovolemic shock
Formation of edema
SEPSIS

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23
Q

Emergent phase patho

A

fluid and electrolyte shifts result in hypovolemic shock
increased permeability of BV = water, sodium, plasma proteins (albumin) to move into interstitial space
- this causes colloidal osmotic pressure to decrease with the loss of proteins in the vascular space, resulting in more fluid shifting out of the vascular space into the interstitial spaces = second spacing
- third spacing = when fluid enters areas that normally have minimal to no fluid (exudate, blister formation, edema in non-burned areas)
= hypovolemic shock - intravascular volume depletion (permeability)
Red blood cells are hemolyzed and thrombosis in the capillaries cause an additional loss of RBC’s. Elevation of the hematocrit occurs due to intravascular fluid loss.
- Injured cells and hemolyzed RBC release potassium into circulation
Na+ will shift into interstitial spaces until edema ceases.

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24
Q

What are signs of shock?

A

low BP
increased RR
increased HR

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25
Q

What are signs of volume depletion?

A

Edema
↓ Blood pressure
↑ Pulse
Normal insensible fluid loss: 30-50mL/hr

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26
Q

Why is the immune response suppressed following burns?

A

1 skin barrier is distroyed
2 bone marrow suppression occurs
3 circulating levels of immunoglobulin decreases
4 function of WBC becomes defective
5 the inflammatory cascade triggered by tissue damage impairs the function of lymphocytes, monocytes and neutrophils

significant risk of infection and sepsis with extensive burns

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27
Q

Clinical manifestations of emergent phase

A

Shock from pain and hypovolemia
Blisters
Adynamic ileus (absence, decreased BS)
Shivering
Altered mental status

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28
Q

What are the 3 major organs that have complications in the emergent phase?

A

Respiratory
Cardiovascular
Genitourinary

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29
Q

Respiratory complications in emergent phase

A

A. Upper airway injury causing upper airway obstruction and edema formation (Redness, blistering and edema) - r/t inhalation
- Burn eschar on neck and chest can become tight and constricting due to edema also making it difficult to breathe.
- evidence by: Swelling can be massive and onset sudden
B. Lower Airway injury to the trachea, bronchioles, and alveoli caused by inhalation of toxic chemicals or smoke.
- pneumonia and pulmonary edema are common in pts with pre-existing respiratory problems

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30
Q

What percentage of a burn affects all body systems?

A

> 25%

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31
Q

Cardiovascular complications

A

Dysthymias and hypovolemic shock which may progress to irreversible shock.
Impaired circulation to extremities
Tissue ischemia
Necrosis
Impaired microcirculation and ↑ viscosity → sludging

escharotomy must be done to restore circulation to compromised extremities with necrosis

32
Q

Genitourinary complications

A

hypovolemia = decreased blood flow to kidneys = renal ischemia (tubular necrosis)
myoglobin (from muscle cell breakdown) and hgb (from RBC breakdown) are released into bloodstream which can occlude renal tubules

tx= fluid replacement

33
Q

Emergent phase care

A

Patient survival depends on rapid and thorough assessment and intervention.
Assessment of burn (depth and extent)
From the onset of the burn event until the patient is stabilized, there are three primary goals of therapy:
1) airway management
2) fluid therapy
3) wound care (early prevention of risk of infection)

34
Q

Airway management for emergent phase

A

Early endotracheal intubation
Escharotomies of the chest wall
Fibreoptic bronchoscopy
Humidified air and 100% oxygen

35
Q

Fluid therapy for emergent phase

A

At least two large-bore IV lines for >15% TBSA
Type of fluid replacement based on size/depth of burn, age, and individual considerations
Parkland (Baxter) formula for fluid replacement
Colloidal solutions (capillary permeability to reverse before)

36
Q

How do we know fluid replacement is adequate in emergent phase?

A

1 urinary output that is 0.5-1kg/hour
2 cardiac factors: MAP >65, systolic greater than 90, HR<120

37
Q

Wound care in emergent phase

A

Should be delayed until a patent airway, adequate circulation, and adequate fluid replacement have been established.
Cleansing
Debridement (May need to be done in the OR, loose necrotic skin is removed)
Shower
- Tap water not exceeding 40° C is acceptable.
- Once-daily shower
- Dressing change in morning and evening
Infection is the most serious threat to further tissue injury.
- source of infection is the client’s own flora.

Sterile gloves are used when applying ointments and sterile dressings.
When open wound are exposed nurses must wear PPE.
The room must be kept warm - hypothermia

38
Q

open method of wound care

A

patient’s burn is covered with a topical antimicrobial and has no dressing over the wound.

39
Q

closed method of wound care

A

sterile gauze dressings are impregnated with or laid over topical antimicrobial.

40
Q

Hypothermia care

A

warm environment, warm blankets. Shivering increases O2 consumption and caloric demand.

41
Q

Other care in emergent phase

A

hypothermia
burned hands and arms should be elevated (edema)
ears should be kept free of pressure

42
Q

Types of pain in emergent phase

A

Background pain (non-procedural related injuries, coughing, shifting positions) – slow release pain meds
Procedural pain – acute pain when changing drsgs, acute and high intensity
Hyperalgesia – sensitivity to the skin from touch
Itchiness – when burn is healing

43
Q

Analgesia should be via IV opioids (morphine) initially. No injected or oral meds. Why? (emergent phase)

A

1 IM not absorbed adequately in burn tissue so they pool.
2 onset of action is fastest for IV meds
3 GI function is slower or impaired d/t shock for paralytic ileus

44
Q

Why are systematic antibiotics not often used why

A

Little to no blood supply to the burn

44
Q

Nutritional therapy in emergent phase

A

Fluid replacement takes priority over nutritional needs.
Early and aggressive nutritional support within hours of burn injury
- decreases mortality and complications.
- optimizes wound healing.
- minimizes negative effects.
Hypermetabolic state proportional to the size of the wound.
Early enteral feeding preserves GI function and prevents complications like curlings ulcer.
Early and aggressive nutritional support within several hours of a burn injury can decrease mortality, risks and complications, and optimize healing.

44
Q

What other meds besides pain meds are needed in emergent phase?

A

Sedatives, hypnotics, antidepressants, tetanus immunization, antimicrobials, heparin

44
Q

Acute phase

A

The acute phase begins with the mobilization of extracellular fluid and subsequent diuresis.
The acute phase is concluded when the burned area is completely covered by skin grafts, or when the wounds are healed.

45
Q

Patho of acute phase

A

Diuresis from fluid mobilization occurs, and the client is less edematous.
Bowel sounds return.
Healing begins when WBCs surround the burn wound and phagocytosis occurs.
Areas that are full- or partial-thickness burns are more evident
additional psychosocial support may be necessary
Necrotic tissue begins to slough.
Granulation tissue forms.
A partial-thickness burn wound heals from the edges.
Full-thickness burns must be covered by skin grafts. (removal of necrotic tissue and then the skin graft goes over to protect underlying skin – length of hospital stay decreases when this happens)

46
Q

Acute phase manifestations

A

Partial-thickness wounds form eschar.
- Once eschar is removed, re-epithelialization (better in a moist environment) begins around margins and appears as red or pink scar tissue
Full-thickness wounds require debridement (surgical) as it takes longer for eschar to separate from wound bed

47
Q

Acute phase lab values

A

Na
- hyponatremia (excessive GI suction, diarrhea)
- water intoxication
- hypernatremia (successful fluid replacement, improper tube feedings, inappropriate fluid admin

Potassium
- hyperkalemia (renal failure, adrenocortical insufficiency, massive deep muscle injury)
- hypokalemia (long IV therapy w/out potassium, V, diarrhea, prolonged GI suction)

48
Q

S and S of hyponatremia

A

weakness, dizziness, muscle cramps, fatigue, headache, tachycardia, and confusion.

49
Q

How can we reduce the development of water intoxication?

A

client should drink fluids other than water, such as juice, soft drinks, or nutritional supplements.

50
Q

S and S of hypernatremia

A

thirst; dried, furry tongue; lethargy; confusion; and possibly seizures.

51
Q

What can hyperkalemia cause?

A

cardiac dysrhythmias and ventricular failure.
muscle weakness.
ECG changes.

52
Q

Complications in acute phase - infection

A

The body’s first line of defense, the skin, has been destroyed by burn injury. Pathogens often proliferate before phagocytosis has adequately begun. The burn wound is now colonized with organisms. If the bacterial density at junction of eschar with underlying good tissue increases, then the client has burn infection
Localized inflammation, induration, and suppuration
Partial-thickness burns can become full-thickness wounds in the presence of infection.
Invasive wound infections may be treated with systemic antibiotics based on culture results.
Over 20% burn = susceptible to sepsis.
Wound infection may progress to transient bacteremia.
Client may develop sepsis. (condition becomes critical)

53
Q

Manifestations of SEPSIS

A

hypothermia or hyperthermia, increased heart and respiratory rate, decreased BP, and decreased urine output. Mild confusion, chills, malaise, and loss of appetite, increased WBC

54
Q

Complications in acute phase - musculo-skeletal

A

Decreased ROM
Contractures

As the burns begin to heal and scar tissue forms, the skin is less supple and pliant.
The nurse should encourage the client to stretch and move the burned body parts as much as possible.

55
Q

Complications in acute phase - GI

A

Paralytic ileus (increase acid secretion when stressed)
Diarrhea (use of ET or abx)
Constipation (meds, immobility)
Curling’s ulcer (duodenum)

56
Q

What is curlings ulcer?

A

type of duodenal ulcer characterized by superficial lesions from stress response (decreased blood flow to GI tract)

Nurse: PPI

57
Q

Complications in acute phase - endocrine system

A

↑ Blood glucose levels
↑ Insulin production (with insulin insensitivity)
Hyperglycemia

58
Q

Acute phase management

A

The predominant therapeutic interventions in the acute phase are
(1) wound care
(2) excision and grafting
(3) pain management
(4) physical and occupational therapy
(5) nutritional therapy
(6) psychosocial care.

59
Q

What are the goals of wound care in the acute phase?

A

1) prevent infection by cleansing and debriding the area of necrotic tissue that would promote bacterial growth
2) promote wound re-epithelialization and/or successful skin grafting.

60
Q

Wound care - acute phase

A

Daily observation
Assessment
Cleansing (sterile water)
Debridement
- enzymatic debridement (speeds up, eats away)
Dressing reapplication
Appropriate coverage of the graft:
- Gauze next to the graft followed by middle and outer dressings
- Unmeshed sheet grafts used for facial grafts

Grafts are left open.
Complication: Blebs

61
Q

What are blebs?

A

serosanguineous exudates that form between the graft and the recipient bed.

62
Q

Excision and grafting management for acute phase

A

Eschar is removed down to the subcutaneous tissue or fascia.
Graft is placed on clean, viable tissue (when reach homeostasis)
Wound is covered with autograft. (pts own skin)
Donor skin is taken with a dermatome.
Choice of dressings varies.
Cultured epithelial autographs (CEAs)
- Grown from biopsies obtained from the client’s own skin
- Used in clients with a large body surface burn area or those with limited skin for harvesting
Artificial skin
- Life-threatening full-thickness or deep partial-thickness wounds where conventional autograft is not available or advisable

63
Q

Pain management for acute phase

A

Clients experience two kinds of pain:
- Continuous background pain (long acting)
- Treatment-induced pain (short acting for drsg change)
Several drugs in combination
Treatment-induced pain managed with potent, short-acting analgesic
Nonpharmacological strategies
- Relaxation strategies
- Visualization, guided imagery
- Hypnosis
- Biofeedback
- Music therapy

64
Q

PT and OT care - acute phase

A

Good time for exercise is during wound cleaning.
Passive and active ROM
Splints should be custom-fitted.

65
Q

Nutritional therapy for acute phase

A

Meeting daily caloric requirements is crucial.
- hypermetabolic, high catabolic state, infection increases metabolic rate
- if pt is on ventilator and unable to consume PO, small feeding tube inserted
Caloric needs should be calculated by dietitian.
High-protein, high-carbohydrate foods
Favorite foods from home
Clients should be weighed weekly.

66
Q

Psychosocial care - acute phase

A

Social worker
Nursing staff
Pastoral care

67
Q

Rehabilitation phase

A

Restorative
starts when burn wounds are healed. Pt is able to resume self care

68
Q

Goals for rehabilitation phase

A

(1) assist the client in resuming a functional role in society
(2) rehabilitate from functional and cosmetic reconstructive surgery. Rehabilitation-focused activities that have been taking place during the earlier emergent and acute phases now begin in earnest once the client’s wounds have healed.

69
Q

Patho changes in rehab phase

A

Burn wound heals either by primary intention (inside-out) or by grafting.
Layers of epithelialization begin to rebuild the tissue structure.
Collagen fibres add strength to weakened areas.
The new skin appears flat and pink.
In approximately 4–6 weeks, the area becomes raised and hyperemic (irregular healing).
Mature healing is reached in about 12 months.
Skin never completely regains its original colour.
Discoloration of scar fades with time.
- scarring has 2 components (discoloration- goes away; and contour - slightly raised)
Pressure can help keep scar flat.
Newly healed areas can be hypersensitive or hyposensitive to cold, heat, and touch.
Healed areas must be protected from direct sunlight for 3–6 months.

70
Q

Complications of rehab phase

A

Skin and joint contractures
- abnormal condition of joint by flexion and fixation
- Most common complications during rehab phase
- areas most susceptible = neck, axilla, fingers, groin, knees, ankles
- Positioning, splinting, and exercise should be used to minimize contracture.

70
Q

Emotional needs of pt and family in rehab phase

A

A common emotional response is regression.
Early psychiatric intervention
Assess psychoemotional cues.
Issue of sexuality must be met with honesty.
Family and client support groups

70
Q

Nursing management of acute phase

A

Both client and family actively learn how to care for healing wounds. (home care?)
An emollient water-based cream should be used (increases moisture for healing)
Cosmetic surgery is often needed following major burns.
Role of exercise cannot by overemphasized.
Constant encouragement and reassurance
Address spiritual and cultural needs.

NURS 412 (21 decks)

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