Stared slides Flashcards

1
Q

Dressing should be?

A

If its too wet dry it
If its too dry wet it
Drainage drives the dressing decisions

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2
Q

Exception to removing necrotic tissue on the lower extremity:

A

Dry and stable eschar heals
Arterial insufficiency (ABI<0.5)
Patient taking blood thinner medication (does not soften or remove)

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3
Q

Wound healing Myths

A

Traditional myths
Let a scab form
Let it dry out
Wounds should be open to air and sunlight
DSD = dry sterile dressing (wet to dry sterile dressings are not good)

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4
Q

What is the definition of burn?

A

Definition: thermal destruction of skin from direct contact or exposure to a source
Thermal
Chemical
Electrical
Radiation

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5
Q

how do you measure the depth?

A

Depth is function of temperature or source of energy and duration of exposure

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6
Q

Epidemiology

A

Peak incidence children 1-5 yo
Scalds bimodal
Adults and adolescents
Flammable liquids
Men ages 16-40 higher incidences
House fires 85% of deaths
Overall incidence down-prevention

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7
Q

Risk factors for burn?

A

Higher incidence for children <4 yo and adults >65yo
Lower income
Psychomotor disorders/alcohol use
Rural locations
Mobile home residence/substandard housing
Occupational
Lack of smoke detectors
Fireworks
Misuse of cigarettes

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8
Q

Severity-assessed with:

A

Risk of infection
Risk of mortality
Risk of cosmetic or functional disability

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9
Q

Factors affecting severity:

A

Burn depth
Burn size
Location
Age of patient
General health
Mechanism of injury

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10
Q

how would you measure wound size:

A

Rule of nines
Lund-Browder (pediatric population)

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11
Q

what is the determination of burn sizes

A

Rule of 9s
18% each leg
18% anterior and posterior trunk
9% each arm
9% for the head
1% perineum
Can give an over estimate of burn wound size
%TBSA
Rule of nines

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12
Q

Burn types

A

Thermal
Electrical
Chemical
Radiation
UV
Ionizing radiation

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13
Q

Burn classification

A

Superficial
Superficial partial thickness
Deep partial thickness
Full thickness

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14
Q

zone of injury

A

Zone of coagulation
Localized in the center of the burn
Area of greatest damage contains non-viable tissue (eschar)
Zone of stasis
Surrounding the zones of coagulation and constraints marginally viable tissue
Zone of hyperemia
Outermost area
Least damaged and heals rapidly

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15
Q

acute burn management

A

American Burn Association’s criteria for admission to a burn center
Partial and full-thickness burns>10% of total body surface area (TBSA) in patients under 10 and 50 years ago.
Partial and full thickness burns >20% TBSA in all other ages groups
Full-thickness burns greater than 5% TBSA in any age group.

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16
Q

Burns- Emergency treatment

A

Treatment
Emergency
Remove person from burn source
CPR
Lavage chemical agent
Local measures
Cold water
Sterile dressings

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17
Q

Escharotomy

A

Excision of the burn through the eschar to allow for edema.
Prevents compression of vital structures
Not to confused with fasciotomy
Excision through the fascia
Usually performed to address compartment syndrome

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18
Q

Burns-continued treatment

A

Debridement of necrotic tissue
Elevation of affected areas
Infection control
Sterile cleansing/dressings
Topical antibiotics
Pain management
Body temperatures maintenance
Nutrition
Skin grafting

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19
Q

Role of PT in burn management

A

Goals:
Contracture prevention
Functional recovery
Interventions:
Postioning
Splinting
ROM
Ambulation/endurance
Gait
ADL’s
Scar management
Pain control

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20
Q

What are the positions of comfort and positions of function?

A

positions of comfort are normally crossed arms and legs in a slouched position

portions of function are in portions for slowing contracture development.

place your patient in positions of function.

21
Q

what do pressure garments look like for burn patients?

A

Essential for scar management
Earlier the application the better the result
Pressure should be 25-30 mmHg
Decreased vascularity
Decreased collagen deposition
Decreased local edema
May begin pressure therapy with elasticized tubular stockinette
Progress to custom made pressure garments
Warn up to 23 hours/day for 12-18 months

22
Q

Diabetic facts for DFU

A

Greatest risk for diabetic foot ulcer (DFU) is neuropathy
15% of those with diabetes will have a DFU
Greatest risk for amputation is a DFU
Diabetic amputations >3.3/1000 according to the CDC
25-68% incidence of contralateral amputations within 3-5 years
50% Three year mortality rate
Each amputation costs $25,000-40,000

23
Q

what are the risk factors for DFU

A

Interrelated/cumulative
PVD
Neuropathy
Sensory
Motor
Autonomic
Mechanical stress
Impaired ROM
Foot deformities
Previous ulcer or amputation
Inadequate footwear
Impaired healing and immune responses
Poor vision

24
Q
A

Not nessarily
DFU are a result of
Neuropathy
Mechanical stress
+/- PVD

25
Q

neuropathy in diabetic foot ulcer patients

A

Most common complication
30-40% affected (type 2); higher with type 1
Symmetrical
Affects distal nerves first
May be caused by neural ischemia or segmental demyelination
Incidence and severity increase with age and duration of disease

26
Q

Sensory neuropathy

A

Inability to perceive trauma to the feet
Sensory loss occurs gradually and is painless
Patients may be unaware
Paresthesia’s
5.07 semmes-weinstein monofilament= 10 grams of pressure =protective sensation

27
Q

what causes motor neuropathy in diabetic foot ulcers

A

Paralysis of intrinsic muscles= muscle imbalances
Alters weight bearing patterns
Increases plantar pressures and shear forces
Excessive plantar pressure and shear forces on the metatarsals
Loss of intrinsic function-foot less stable during stance

28
Q

What is the sequential process of getting hammer toe?

A

Contractures – hammer toes- improper weight bearing- into ulcers- infections- osteomyelitis – amputation

29
Q

Autonomic neuropathies have alterations in?

A

Sweating mechanisms (hydration)
Callus formation
Blood flow (Vasomotor regulation)

30
Q

abnormal foot function and inadequate footwear

A

Impaired motion
Foot deformities
Previous ulcer or amputations
Combine with poor footwear and decreased sensations

31
Q

foot deformities with DFU

A

Plantar flexion contractures
Forefoot varus/valgus
Neuropathic fractures and dislocation= charcot foot
Combined with sensory neuropathy= increased ulceration risk

32
Q

previous ulcers or amputations cause what in patients

A

Altered skin performance
Less elastic
Decreased strength
Altered foot structure from amputation
Predisposing factors causing old injury are still present

33
Q

Neuropathic foot ulcers are associated with what?

A

Associated with:
Morbidity
Mortality
Financial burden
25x > lower extremity amputation in diabetic people
600,000 annually (80% after foot ulcers)
More than ½ get 2nd amp within 3-5 years

34
Q

what are the grades to the wagner classification of diabetic foot ulcers

A

Grade 0: no ulcer in a high risk foot
Grade 1: superficial ulcer involving the full skin thickness but not underlying tissues
Grade 2: deep ulcer, penetrating down to ligaments and muscle, but no bone involvement or abscess formation
Grade 3: deep ulcer with cellulitis or abscess formation often with osteomyelitis.
Grade 4: localized gangrene
Grade 5: Extensive gangrene involving the whole foot

35
Q

what are the layers of the skin?

A

Two distinct layers
Epidermis
Dermis

Dermal-Epidermal
Junction
Aka Basement membrane

Subcutaneous
Aka hypodermis

36
Q

check out slide 9 and explain blanch able and unbalanceable skin

A
37
Q

what are the functional components of the epidermis

A

stratum corneum
keratinocytes
melanocytes
Merkel cells
Langerhans’ cells
basal cells
eccrine unit
apocrine unit
hair folicules
nails
elations glands

38
Q

what are the cells in the dermis?

A

fibroblasts
collegen
elastin
macrophages
mast cells
lymphatic cells
blood vessels
nerve fibers

39
Q

what are the cells of the subcutaneous tissue

A

adipose

40
Q

what are the functions of the epidermis?

A

Protection:
infection, shear/friction, water loss, toxic irritants
Vitamin D synthesis
Thermoregulation
Regulation, retention, dissipation
Sensation (light touch)
Pigmentation (melanocytes)

41
Q

Dermal appendages are?

A

Hair follicles
Sebaceous glands
Sweat glands

Lined with epithelial cells
Epithelial islands

42
Q

review what are the main things that the skin provides? how can injury occur?

A

Provides thermoregulation
Sensation
Metabolism

Organ of communication and identification
Injury can result in:
Functional change
Physiologic change
Body image change
Facial skin, along with underlying muscles capable of expressions

43
Q

what are the classifications of skin loss?

A

Wounds are classified by depth of tissue injury
Erosion- loss of superficial epidermis, probably not bleed, redness, repair by local inflammatory response
Partial thickness skin loss- loss of epidermis and part of the dermis, bleed, reepithelization for repair
Full thickness skin loss- loss of epidermis, dermis extending into subcutaneous/hypodermis, secondary intention repair through scar
Full thickness with muscle, tendon, bone

44
Q

what are the skin changes with aging?

A

Decreased:
Epidermal/Dermal thickness
Decreased subcutaneous fat
Collagen and elastin
Size of Rete ridges/pegs
Sensation and metabolism
Sweat glands
Circulation
Reduced mast cells
Epidermal regeneration
Up to 4X slower healing than younger populations

45
Q

what are the characteristics of acute wounds?

A

planned/unplanned events
healing proceeds in a orderly and timely fashion
surgical
abrasions/lacerations

46
Q

what are the characteristics of chronic wounds?

A

exists two weeks or longer
does not proceed through normal healing tissue processes

examples:
pressure ulcers and diabetic neuropathic ulcers

47
Q

what are the stages of wound healing?

A

hemostasis
inflammatory phase
proliferation phase
maturation phase

48
Q

what occurs in the hemostatic phase?

A

Injury exposes blood to collagen and initates coagulation factor
Platelet aggregation causes fibrin clot formation(plug)
Platelets release growth factors which attract cells and chemical substances needed for repair

49
Q
A