Wounds/Burns Flashcards

1
Q

Phases of Wound Healing

A

Hemostasis, Phase 1: inflammatory, phase 2: proliferative, phase 3: maturation; all overlap and should follow a standard timeline

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2
Q

Hemostasis

A

Vasoconstriction following skin injury to stop bleeding, platelet aggregation, growth factors are stimulated to begin healing

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3
Q

Inflammatory Phase

A

Occurs within 24hrs and continues for several days, fluid flows from capillaries, caused by enzymes and other cells, vasodilation caused by histamine and leukotrienes, phase involves neutrophils and macrophages

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4
Q

Proliferation phase

A

Fibroblasts begin to move into area to regenerate tissue, neovascularization and granulation tissue formed, re-epithelialization occurs as the keratinocytes migrate to cover the wound

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5
Q

Maturation

A

After wound is healed, protein degradation and collagen rearrangement, redness swelling ichy, lasts 6 mo to 2 years

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6
Q

Acute Vs Chronic

A

Acute wounds are uncomplicated, orderly, and rapidly healing; chronic wounds have prolonged healing and deviate from expected sequence of repair

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7
Q

Why arent they healing normal?

A

Look for infection, too much or too little moisture, deabris or necrotic tissue, too much heat or cold, another reason (comorbities)

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8
Q

Comorbities

A

Age, mechanical stress (walking on wound), behavioral problems (smoking), circulation problems, sensation problems, lack of nutrition, medications impeding healing

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9
Q

Aging

A

Cellular turnover decreased, decreased dermal vasculature thus thinner skin, impaired collagen and protein synthesis, decreased calories = decreased collagen, decreased sweat glands and oil glands causing dry skin, pain perception decreased, other comorbidities from old age

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10
Q

Behavior

A

Alcohol abuse - usually malnutrition, less likely to seek medical attentionl; Smoking - vasoconstriction, increased clot, decreased O2; Noncompliance with meds or controlling blood sugar

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11
Q

Circulatory Disease

A

Arterial insufficiency: decreased blood flow to area, ischemia, tissue death, usually distal; Venous sufficiency: decreased ability to pump blood out of extremities, edema resulting in wounds from leaking fluid, usually medial extremities bc less blood flow medial than lateral

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12
Q

Decreased Sensation

A

Diabetes: elevated glucose leads to neuropathy, decreases all phases of wound healing, common on bottom of foot; Spinal cord injuries: nerve injury causing loss of sensation

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13
Q

Big no no for weight bearing

A

Should not bear weight on a wound, should not perform non weight bearing on unaffcted foot of a diabetic this could lead to problems with skin breakdown and breakdown of foot biomechanics. May need to think of ways to safely off load the wounded foot but keep the patient mobile

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14
Q

Burn injury

A

Healed skin is only 80% as strong as original, deeper the burn the more scarring, scarring is based on genetics and outside forcee, age when burned impacts healing (younger burn victims may require more surgery bc scars do not grow with skin)

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15
Q

Burn Injury Types

A

Thermal, Chemical, Friction, Electrical, Radiation

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16
Q

Pathophysiology of thermal burn injury

A

30% have systemic inflammatory response: results in dehydration and hypovolemia which affects oxygen transport and can arrest blood flow, decreased pulmonary function, decreased bacteiral killing function, BMR increases, burn shock can occur

17
Q

Metabolic Rate and Burns

A

Resting metabolic rate reaches astronomical levels depending on the size of the burn, burns exceeding 40% TBSA increases RMR 2 fold, negative effects at the cellular and systemic level, not just wound but the heart liver muscles and immune system negatively impacted

18
Q

what gets secreted

A

ceatecholamine, cortisol, glucagon, dopamine which trigger a series of events that lead to hypermetabolic response

19
Q

Donald Jackson 3 zones

A

zone of coagulation: irreversible damage of tissues, zone of stasis: adjacent to above zone, moderate degree of damage with vascular leakage, zone of hyperemia: increased blood supply with healthy tissue

20
Q

Electrical burn

A

body converts electricity to heat, blood nerves and vessels have low resistance making electricity easier to travel inside the body causing major damage. Rhabdo form major muscle damage, electricity can cause defib and arrhythmias

21
Q

Chemical burns

A

PH immediately checked to determine if alkali or acid; Alcohol - causes least injury with de-epithelialization; acid - usually dcauses tissue coagulation and shrinking of collagen fibers, coagulation prevents acid from penetrating further; alkalis: cause changes in the fat (liqueficatoin necrosis) along with shrinking of collagen tissue fibers allowing further penetration and alkali into deeper tissues (worst because the damage is ongoing, more rapid and deeper advancement)

22
Q

Treatment (autograft, homograft, allograft)

A

Autografting: taking skin from your own body and putting it on the burned area, permanent (split skin thickness skin graft, sheet graft, cultured skin); Homografting: cadaver skin, temporary cover, for large burns, allows donor sites to heal for more harvesting; Allografting: fish skin, pig skin, temporary cover, for large burns, fish skin shown to enhance wound healing

23
Q

Hypertrophic Scarring

A

raised and rigid, hyper pigmented, can limit ROM, darker skin types more likely to scar

24
Q

Keloid Scarring

A

Excessive growth of scar tissue, hard benign growth, darker skins more likely to scar

25
Q

Standard of care for burn treatments

A

begin positioning in anatomical position as soon as possible, boots and splints, begin ROM quickly, immobilization due to grafting (typically 4-6 days after autografting, strength training quickly due to high metabolism and loss of muscle, know where tendons are and take care to minimize forces during ROM, older you are the lower life expectancy (closer to 140, higher likelihood of death), get patients to walk and up

26
Q

Contraindications to exercise or ambulation when you have a wound

A

Wound on foot, NWB should be tried; special shoes to off load area of wound; wound on achilles tendon and it is exposed, no forceful ROM as this could tear tendon; heterotrophic ossification: no passive motion, pain is the guid (mostly in burn patients)

27
Q

Goal and plan for wound care

A

Debridement: remove the obstacles; cleaning, modalities to improve circulation, topicals to prevent and treat infections, protection: various dressing to protect infection and facilitate healing

28
Q

Pulsed Lavage

A

Delivery of a liquid agent such as saline under about 5-15psi which breaks up bacteria to the wound bed. Applies a negative pressure during the suction aspect

29
Q

Electical Stimulation

A

Improves blood flow, transfers energy to the wound, treat infected wounds

30
Q

Mist Therapy

A

Uses sterile saline claims to disrupt and remove bacteria

31
Q

Oxygen therapy

A

increases O2. Studies show tha tmost non-healing of wounds is secondary to tissue hypoxia (increased edema, increased ischemia, increased infection)

32
Q

Negative pressure wound therapy

A

Suction that removes excess fluid allowing for enhanced circulation and disposal of cellualr waste

33
Q

Debridement

A

removal of dead tissue to decrease potential infection and allow healing (scalpel, forceps, scissors, curette, maggots)

34
Q

Maggot therapy

A

larvae ingect necrotic tissue, throught to be antimicrobial bc the larvae secrete ammonia which raises wound PH, larvae also ingest bacteria

35
Q

Arterial wounds

A

Decreased blood flow
ischemia and tissue death (necrosis)
Amputation

36
Q

Venous wounds

A

Edema resulting in wound from leaking fluid

Decreased ability to pump blood

usually medial extremities bc less blood flow medial than lateral

37
Q

Areas of risk for pressure injury

A

Elbow, back of head and ears, inner knee, greater trochanter, shoulder, lower back and glutes, hip, heel