wound care (M 1-9: measurements, tissue types and staging, exam, diabetes, arterial, venous) Flashcards

1
Q

integument – skin is

A
  • the body’s largest organ
  • 15-2-% of body weight
  • surface area between 1.5-2 m^2 (~22ft^2) in the average adult
  • thickness of 0.5-4 mm (average 1-2 mm)
  • thinnest on eyelids, thickest on heels
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2
Q

functions of the skin

A
  • protection/immunity: protects against pathogens, decreases water loss
  • temperature regulation: provides insulation, related to dilation and constriction of blood vessels within the layers of the skin, allows for sweating
  • sensation: contains various nerve endings, including for pain, light touch, etc
  • assists in vitamin D synthesis, and indicator of vitamin B levels
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3
Q

anatomy of the skin - layers of the epidermis

A
  • stratum corneum
  • stratum lucidum
  • stratum granulosum
  • stratum spinosum
  • stratum basale
  • basement membrane
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4
Q

stratum corneum

A
  • most superficial - acts as the primary barrier
  • composed of soft keratin-containing, dead squamous cells, constantly sloughing or shedding
  • 15-20 layers od ead cells
  • can also indicate hydration - ashy skin means dehydration
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5
Q

stratum lucidum

A
  • thin, clear layer od dead skin cells
  • typically only seen in regions like the palms of the hands and soles of the feet
  • areas of increased stress to the tissues
  • function to reduce sheer/friction to epidermis
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6
Q

stratum granulosum

A
  • layer that contains transition zone for the development of keratin
  • becoming more active cells again
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7
Q

stratum spinosum

A
  • layer contains “spiky/spiny” projections
  • gives integrity, holds things together
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8
Q

stratum basale

A
  • deepest and most continuous layers of epidermis
  • typically 1-3 cell layers thick
  • regenerates the epidermis: growing new cells, go up, slough off eventually
  • contianing a variety of other cells, including:
  • merkel cells - touch receptors
  • langerhands cells - immune cells
  • melanocytes - pigment production
  • keratinocytes - produces keratin (fibrous proteins), antibodies and enzymes
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9
Q

basement membrane

A
  • the layer that separates the epidermis and dermis
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10
Q

dermis

A
  • the thickest layer
  • primary functions
  • thermoregulation
  • storage of water/maintaining hydration
  • provides nutrients and waste removal for itself and the epidermis
  • also contains: blood vessels, lymphatic vessels, glands - sebacious, sweat, nerve endings, hair follicles, collagen
  • papillary region
  • bumpy surface that interdigitates with dermis, strengthening the connection
  • influences the contours of the skin’s surface - finger prints
  • reticular region
  • contains collagen, elastic, and reticular fibers - provides strength, extensibility, and elasticity
  • contains the roots of the hair, sebaceous glands, sweat glands, receptors, nails, and blood vessels
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11
Q

hypodermis

A
  • subcutaneous tissue
  • attaches skin to underlying bone and muscle
  • contains loose connective tissue, adipose tissue, and elastin
  • contains 50% of body fat
  • provides insulation and shock absorption
  • contains Pacinian cells and free nerve endings - cold and pressure
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12
Q

risk factors for wound healing

A
  • comorbidities: CV, diabetes, SCI
  • nutrition: malnutrition
  • obesity
  • smoking, alcohol/drug use
  • sedentary or limited mobility
  • impaired sensation
  • risk-prone behavior - high-risk activities, exposure
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13
Q

extrinsic factors of wound healing

A
  • shoes - condition and fit
  • orthotics, prosthetics
  • seating - cushions and positioning
  • hairstyles
  • vital signs and sensory testing
  • other exam items: MMT, goniometry
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14
Q

how many people per year in teh US develop pressure injuries, associated with pain, risk for infection, increased health care utilization

A

more then 2.5 million people per year

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15
Q

diabetic foot ulcers have a mortality rate of []% and as high as []% after BKA

A
  • 43-55%
  • 74%
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16
Q

venous leg ulcers have a 6-month healing rate of []% and a [] recurrence within 5 years

A
  • 45-70%
  • 25-70%
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17
Q

patients > 45 YO have a prevalence of PAD (peripheral arterial disease) of []%

A
  • 14.9%
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18
Q

primary intention

wound closure managment choices

A
  • clean, straight line, edges well approximated with sutures
  • rapid healing, usually best cosmetic outcome
  • usually after surgeries
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19
Q

secondary intentions

wound closure managment choices

A
  • larger wounds with tissue loss, edges not approximated, heals from inside out
  • granulation tissue fills in wound, longer healing time, larger scars
  • edges do not come together
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20
Q

tertiary intention (delayed primary)

wound closure managment choices

A
  • delay is typically 3-5 days before injury is sutured
  • used to manage infected or unhealth wounds, larger scar
  • secondary with surgery to close: may be surgeon preference, may be due to other factors
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21
Q

wound healing: inflammatory phase

A
  • start immediately with hemostasis and includes the innate immune system (inflammation)
  • exposed collagen activates clotting cascade
  • cytokines/chemokines and growth factors are released by resident cells and cells that migrate to area of wound
  • neutrophils, monocytes, and macrophages are essential:
  • pathogen control: production reactive oxygen species (ROS)
  • pathogen and debris removal: phagocytosis
  • angiogenesis: PDGE, TGF alpha and beta, TNF alpha
  • fibroplasia: interleukins, EGF, TNF alpha
  • what you notice: local erythema, edema, tenderness
  • main function is to remove debris, start healing cascade, and prepare wound for regeneration
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22
Q

wound healing: proliferative phase

A
  • day 4 through several weeks
  • fibroblasts are most important cell type: produces collagen to fill wound and provide support
  • angiogenesis (neovascularization): capillaries “bud” from nearby vessels and grow into wound
  • epitheliazation: epithelial cells from wound margins migrate across wound surface
  • wound contraction: pulling of edges toward center making wounds smaller
  • myofibroblast: contractile properties and collagen synthesis
  • growth of blood vessels, deposition of collagen, formation of granulation tissue, epithelialization, wound contraction
  • granulation tissue: new connective tissues into a space, red/pink, “beefy” looking
  • epithelializing tissue: thin shiny over red, good
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23
Q

epithelialization

A
  • epithelial cells migrate across the new tissue to form a barrier between the wound and the environment
  • basal epithelial cells at the wound margin: multiply (mitosis) in horizontal direction, flatten (mobilize) and migrate into open wound
  • basal cells behind margin undergo vertical growth (differentiation)
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24
Q

wound healing: remodeling phase

A
  • up to 2 years
  • collagen Type III replaced by Type I
  • disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines (Langer’s lines - natural orientation of collagen fibers in dermis)
  • wound may increase in strength for up to 2 yearss after injury (return to about 80% of natural strength, at day 14 have about 30-50% tensile strength)
  • apoptosis – works to prevent keloids
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25
Q

wound healing: system factors

A
  • nutrition/hydration
  • diabetes
  • peripheral vascular disease (PVD)
  • GERD
  • collagen disease
  • end stage renal disease (ESRD)
  • immunosuppression
  • aging
  • medications
  • social/health habits
  • functional status and activity level
  • infection
  • paresthesia
  • perfusion
  • incontinence
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26
Q

wound healing: local factors

A
  • psychological function - stress, memory, anxiety
  • hypergranulation
  • tobacco use
  • high bacterial burden
  • biofilms
  • edema
  • pressure/friction/shear
  • maceration/motion
  • hyperkeratosis
  • cellulitis
  • nonviable tissue
  • lack of growth factors
  • cytokines
  • matrixmetalloproteases (MMPs)
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27
Q

blanchable vs non-blanchable

A
  • blanchable: reddened area that turns pale under applied light pressure
  • non-blanchable: an area of redness that does not blanch under applied light pressure – more concerning for pressure injuries
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28
Q

abnormal: blue skin colors

A

cyanosis

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29
Q

abnormal: purple skin color

A
  • deep tissue injury
  • may be darker or gray in darker skin
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30
Q

abnormal: red color

A
  • infection or inflammation
  • could be cellulitis or dermatitis - raised
  • erythemia - flat, shiny
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31
Q

erythema

A
  • abnormal red color
  • may indicate underlying infection
  • indicative of Stage 1 pressure injuries if over bony prominence
  • may be a 1st degree burn
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32
Q

abnormal: red skin with covid

A
  • pediatric multisystem inflammatory syndrome (PMIS) – purplish lesions on toes and feet, rash
  • Covid toes
  • Coronavirus rash
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33
Q

abnormal: red skin colors indicative of other issue

A
  • bulls-eye rash: Lyme disease
  • rashes - drugs
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34
Q

other abnormal skin colors

A
  • white: reynaud’s, dully ashy/gray in darker skin
  • black: necrosis, gangrene
  • yellow: jaundice, visible in eyes (liver disease, hemolytic disease
  • hemosiderin staining: mostly in LEs, red/rusty brown or brownish purple, usually in gaiter area (socks), common in chronic venous insufficiency (starts distal and moves proximally
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35
Q

petechiae, purpura, and ecchymoses differences

A
  • petechia: small (1-2 mm; < 3 mm), red or purple spot on the skin
  • purpura: > 3 mm
  • ecchymosis: > 1 cm, commonly called a bruise
  • all do not blanch with pressure
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36
Q

edema

A
  • excess fluid in interstitial tissue
  • can be multi-factorial in cause
  • impedes healing regardless of etiology
  • extent and type of edema helps identify wound etiology
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37
Q

localized edema

A
  • sign of infection
  • result of inflammatory response in the immediate wound area
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38
Q

unilateral edema

A
  • can be indicative of venous insufficiency, DVT, lymphatic blockage
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39
Q

bilateral edema

A
  • probably more central body cause – heart failure
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40
Q

pitting edema

A
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41
Q

edema - induration

A
  • orange-peel texture
  • more chronic edema
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42
Q

signs of acute inflammation

A
  • rubor - redness
  • fumor - swelling
  • calsor - heat
  • dolor - pain
  • loss of function
  • odor, pain, palpation, systemic changes, wound cultures
43
Q

chronic wounds

A

wounds that fail to progress through a normal, orderly, and timely sequence of repair or wounds that pass through the repair process without restoring anatomic and functional results

44
Q

diagnosing wounds

A
  • by tissue involvement – to determine local care: superficial/erosion, partial thickness, full thickness
  • by etiology – to determine systemic care: arterial, venous insufficiency, neuropathic, pressure, atypical
45
Q

questions to ask in exam about wounds

A
  • when did the wound begin
  • how did the wound begin – trauma, falls, bites
  • other s/s – fever, itching, pain
  • treatments already tried
  • allergies relevant – latex, sulfa, adhesives
  • tobacco, alcohol, drugs
46
Q

wound examination – objective measures

A
  • dimension/extensions
  • tissue type
  • staging
  • wound bed color
  • drainage
  • wound edges
47
Q

dimensions

size

A
  • methods
  • perpendicular: widest points x widest points
  • clock: 12 at head
  • volumetric: how much saline can you put in
  • tracing
  • photography
  • typically documented as: length (cm) x width (cm) x depth (cm)
48
Q

subcutaneous extensions

A
  • tunneling/sinus tract: narrow passage of tissue destruction within the wound
  • undermining: destruction of the conenctive tissue between teh dermis and subcutaneous tissue – extends under the intact skin along the periphery of a wound
  • fistula: tunneling that connects with a body cavity
49
Q

abrasion

A
  • skin is rubbed/scraped
  • usually not much bleeding
  • heals fairly quickly
  • ex: road rash
50
Q

avulsion

A
  • partial or complete tearing away of skin/tissue
  • bleeds heavily and rapidly
  • ex: violent accidents, crush accidents, explosions, gunshots
51
Q

puncture

A
  • small hole caused by pointy object
  • may not bleed much, can damage organs
  • ex: nail, bullet, needle
52
Q

laceration

A
  • deep cut or tearing of skin
  • bleeding can be rapid and extensive
  • ex: knives, tools, machinery
53
Q

granulation tissue

A
  • red, “beefy” looking
  • result of angiogenesis – formation of new blood vessels
  • composed of new capillaries and ECM
  • varies in color from anemic (pale pink) to bright red
  • necessary for closure by secondary intention or for split thickness skin grafts
  • carefully protected in good wound management
54
Q

slough

A
  • softer, lighter necrotic debris
  • normal by-product of autolysis
  • usually seen beneath eschar (black)
  • more common in the inflammatory phase of healing
  • differs from adhered connective tissue in that it is soft and mushy, sometimes hard to grasp with forceps
  • yellowish
55
Q

eschar tissue

A
  • composed of dead cells and fibrin
  • may be dry and hard or soft and rubbery, leathery
  • may be dry gangrene or wet gangrene – wet is infections
  • can be burn, fungal infectoin, bug bites
  • can let it be until infected
  • gangrene generally in hands and feet
56
Q

muscle tissue

A
  • striated
  • reddish when healthy – brownish-gray when devitalized
  • sensate when healthy – painful when exposed
  • may see movement if you ask pt to move
57
Q

tendons

A
  • shiny and stringy when healthy – becomes dull and dry when devitalized/necrotic
  • covered with a fibrous sheath of connective tissue containing synovial fluid or fatty fluid (paratenon)
  • may see movement if you ask patient to move
58
Q

bone

A
  • tan in color – dark brown when necrotic, can soften (osteomyolitis)
  • hard to palpation with metal instrument
  • covered with periosteum when healthy – has to be debrided if necrotic
59
Q

adipose

A
  • shiny, yellow-white globules when healthy – shriveled and dry when devitalized
  • poorly vascularized – challenging to heal
  • frequent sources of abscess formation
60
Q

skin loss/wounding

A
  • erosion: loss of epidermis only (abrasion)
  • partial thickness: loss of epidermis and part of dermis
  • full thickness: loss of all epidermis, dermis, and into subcutaneous tissue

NOT pressure injuries – classification of skin loss

60
Q

skin loss/wounding

A
  • erosion: loss of epidermis only (abrasion)
  • partial thickness: loss of epidermis and part of dermis
  • full thickness: loss of all epidermis, dermis, and into subcutaneous tissue

NOT pressure injuries – classification of skin loss

61
Q

pressure injury stages

A
  • stage 1: warm to touch, no breaks or tears in skin
  • stage 2: no slough, can look like blister, partial thickness
  • stage 3: full thickness but no muscle, tendon, or bone; can see tunneling and fat
  • stage 4: full thickness with muscle, bone, tendon; do see tunneling and undermining, can see eschar and slough
  • unstageable: cannot see full depth of wound due to eschar or slough in the way
62
Q

deep tissue injury

DTI

A
  • looks like bad bruise
  • mushy, boggy, non-blanchable
  • may be intact or not
  • from high presure, prolonged pressure, sheer forces
  • often open as stage 3 or 4 pressure injuries
  • common over greater trochanter, sacrum, heels – but can be over any bony prominence
  • ex: elderly patient who fell and was down for a long time until found
63
Q

necrotic wounds are dry and [color]

A

black – eschar

64
Q

wounds with slough are [color]

A

yellow

65
Q

granulating wounds are

A

red

66
Q

epithelising wounds are shiny and [color]

A

pink

67
Q

infection in tissue is [color]

A

green

68
Q

drainage/exudate

A
  1. sanguineous: thin, bright red
  2. serosanguinous: thin, watery, pale red to pink
  3. serous: thin, watery, clear
  4. purulent: thick or thin, opaque tan to yellow
  5. foul purulent: thick opaque yellow to green with offensive odor
69
Q

how much drainage

A
  • none: wound tissues dry
  • scant: wound tissues moist, no measurable drainage
  • small: wound tissues very moist, drainage <25% dressing
  • moderate: wound tissues wet, drainage involves 25-75% dressing
  • large: wound tissues fill with fluid, involves >75% dressing
70
Q

wound edges can tell you

A
  • type of wound or healing process occurring within a wound bed
71
Q

even wound edges are typical of

A

arterial wounds

72
Q

irregular wound edges are typical of

A
  • venous wounds
  • may occur as wound epithelializes
73
Q

rolling wound edges are

A
  • sign of halted healing process
  • cells are termed senescent, meaning they are unable to reproduce
  • rolled edge is termed epibole
74
Q

hyperkeratosis wound edges are

A
  • overdevelopment of the horny layer of the skin
  • appears as thickened skin around the edge of a wound or as a callus
75
Q

maceration wound edges are result of

A
  • too much moisture on skin for too long
  • can slow healing process
  • creates high risk for infection and/or wound becoming larger
76
Q

dehisced wound

A
  • wound edges come apart
  • may be superficial layers only
  • or can open full depth
77
Q

pain

A
  • deep pain: cramping, indicative of ischemia or hypoxia, more comfortable in dependent position
  • throbbing, localized pain: indicative of infection, deep pain that increases with pressure may be indicative of osteomyelitis
  • superficial tenderness: exposed nerve endings, may be accompanied by sharp shooting pains
  • pain with stimulation of red tissue: living muscle
78
Q

vascular testing - arterial

A
  • pulses: use grading scale, compare side to side/above and below
  • doppler: for pulses that are not palpable
  • ABI: ankle brachial index
79
Q

indications for a wound culture

A
  • local signs of infection: pus, change in color or character of exudates, redness, induration, changes in wound odor
  • systemic signs of infection: fever, leukocytosis
  • suddenly elevated glucose
  • pain in neuropathic extremity
  • lack of healing after 2 seeks in a clean wound despite optimal care
80
Q

DIMES

A
  • debridement
  • infection/inflammation
  • moisture balance
  • edges
  • support services
81
Q

diabetes mellitus

A
  • 25.8 million children and adults in US (8.3% of population)
  • up to 14.5% in ethnic groups
  • 15% of people with DM will have wounds: 14-24% of those with diabetic ulcers will ultimately have an amputation
  • mortality following amputationincreases with level of amputation and range from 50-68% at 5 years
  • hyperglycemia can lead to stiffer blood vessels: leads to reduced tissue oxygenation, more difficult healing, more likely to get a wound
82
Q

clinical manifestations of DM

A
  • neuropathy: diabetic peipheral neuropathy
  • type I: after 20 years of disease duration, at least 20% of people have DPN
  • type II: after 10 years of disease duration, 50% of people have DPN (more likely)
  • sensory: decreased sensation, vibration, proprioception, loss of reflexes (distal to proximal) – impacts longer nerve fibers
  • experience neuropathic pain: gabapentin
  • motor: progressive weakness and atrophy
  • autonomic: decreases sweat and oil production: leads to dry, inelastic skin
  • heart and vasculature: orthostasis and silent MI
  • GI tract: gastroparesis, diarrhea
  • neuropathy/DPN: most common complication of DM type I and II
  • testing should involve neuromuscular assessment
83
Q

monofilament sensory exam

A
  • for protective sensation
84
Q

vibration sensory exam

A
  • more sensitive than monofilament testing
  • 128 Hz tuning fork
  • clanging tuning fork test
  • 4s - 100% sensitive for sensory loss: monofilament testing 76% sensitive
85
Q

DM clinical manifestations – osteopathy

A
  • Charcot’s disease: neuropathic arthropathy – progressive degeneration of weight-bearing joints, increase risk of skin breakdown
  • due to abnormal pressure distribution
  • combined with DPN – increased wound risk
86
Q

complications of vascular and neuropathic changes

A
  • ulceration (often painless): can lead to amputation
  • neuropathic edema
  • charcot arthropathy
  • callus formation: wound can develop under callus
87
Q

skin and nail changes with diabetes

A
  • nearly 1/3 of patients with DM have some type of dermatologic manifestation
  • up to 50% of patients with type 2 DM are at an increased risk of developing skin infections
  • related to: poor glucose control, abnormal carbohydrate metabolism, artherosclerosis (4x more likely in pts with DM), microangiopathic changes, neuro degneration, pharmacological therapy for DM (use of insulin)
  • diabetic thick skin: loss of elasticity, commonly with shiny appearance, can lead to limited joint mobility and contractures, more common in hands and fingers, usually dorsum, overall thickening
  • diabetic yellow skin: yellow nails and skin discoloration, usually on palms of hands or soles of feet
87
Q

skin and nail changes with diabetes

A
  • nearly 1/3 of patients with DM have some type of dermatologic manifestation
  • up to 50% of patients with type 2 DM are at an increased risk of developing skin infections
  • related to: poor glucose control, abnormal carbohydrate metabolism, artherosclerosis (4x more likely in pts with DM), microangiopathic changes, neuro degneration, pharmacological therapy for DM (use of insulin)
  • diabetic thick skin: loss of elasticity, commonly with shiny appearance, can lead to limited joint mobility and contractures, more common in hands and fingers, usually dorsum, overall thickening
88
Q

changes in skin and nails with diabetes

A
  • diabetic yellow skin: yellow nails and skin discoloration, usually on palms of hands or soles of feet
  • diabetic dermopathy: most common cutaneous change, present in 30-60% of patients with DM, usually seen in men > 50 YO
  • presents as round/oval atrophic, hyperpigmented raised lesions, usually on pretibial area of LEs
  • xerosis: 75-82% had dryness of the skin with fissures/cracks, most common on heels and feet, increased risk of infection
  • acanthosis nigricans: development of dark, thick, velvety skin in body folds and creases, can indicate benign and malignant conditions, common in axilla, groin, posterior neck
  • acquired perforating dermatosis: large papules with central keratin plugs, usually on LEs
  • vitiligo: progressive, 1-7% of pts with DM
  • nail changes: thickening, yellowing, red/borwn/black discoloration, green, whitening of entire nail or transverse white bands, toenail deformities
89
Q

cutaneous reactions to insulin

A
  • lipoatrophy: occurs within 6-24 months of starting treatment, most common in children and women
  • lipohypertrophy: resemble lipoma
  • both though to be related to repeat injection sites
90
Q

chronic wounds

A
  • present for at least 6 weeks
  • characteristics: necrotic tissue, bioburden, chornic inflammation, impaired hemodynamics, senescent fibroblasts and keratinocytes, chronic wound fluid with growth inhibiting proteases, overgrowth of epithelium with lack of underlying connective tissue (epibole)
91
Q

90% of chronic wounds belong to 4 categories

A
  • arterial: ischemia, micro or macro vascular disease, smoking
  • venous insufficiency: DVT, recent surgery, ankle fusion, prolonged standing, pregnancy, congestive heart failure
  • neuropathic/diabetic: diabetes, PVD, Hansen’s disease
  • pressure: pressure or shear, immobility, moisture, decreased sensation, poor nutrition
92
Q

neuropathic wounds

A
  • occur on the foot, usually on plantar surface or toes
  • caused by mechanical forces or minor trauma
  • occur in patients wit hdiabetes or PVD, Hansen’s disease, spina bifida, lupus, toxic syndromes, Chacot-Marie-Tooth
  • patients typically have sensory, autonomic, and motor neuropathies
93
Q

arterial wounds

A
  • caused by ischemia
  • usually located at the peripheral extremities
  • caused by macro- or microvascular disease
  • macro: obstruction of the larger named arteries by PAOD, emobolus, thrombus, trauma
  • micro: disease of the small unnamed arterioles and capillaries, usually associated with diabetes or small emobli
94
Q

peripheral vascular disease (peripheral arterial occlusive disease [PAOD])

A

critical phases
1. collateral circulation insufficient for metabolic needs: shunting of blood to muscles where there is less resistance, delayed healing of traumatic wounds
2. claudication: pain with activity: can be effectively treated with exercise (thigh and buttock claudication - aortoiliac or iliac involvement, calf claudication - femoral or popliteal involvement
3. rest pain: requires revascularization surgery, may be accompanied by signs of ischemia at distal digits

95
Q

arterial screening and wounds

A
  • ABI: diminished
  • pulses: diminished
  • capillary refill time: > 3s
  • buergers test: elevation and rubor of dependency
  • skin appearance: shiny, thin, pale, no hair growth
  • conditoin of nails and hair
  • location: distal toes or fingers
  • wound edges: even, punched out appearance
  • wound tissue: dry, necrotic, little or no granulation
96
Q

venous wounds

A
  • relate to 70% of LE wounds
  • 500,000-1,000,000 in UE
  • 40% occur before age of 50
  • recurrence rate is as high as 72%
  • estimated cost of care is $40k/case
  • superficial veins: great saphenous, small saphenous, perforator veins, lymphatic system
  • deep veins: femoral, popliteal
97
Q

chronic venous insufficiency

A

causes
* reflux as a result of incompetent valves in the perforator, superficial, or deep veins
* obstruction: e.g. chronic deep vein thrombosis
* lack of venous pump activation during gait cycle

  • results in venous hypertension and excessive moisture in the interstitial tissue
  • prevents adequate oxygen and nutrients from reaching the skin
98
Q

chronic venous insufficiency - pathophysiological changes

A
  • vessel dilation and elongation
  • increased collagen deposition in both vein walls and skin
  • plasma protein leaks into interstitial space with resulting fibrin cuff around arterioles
  • increased inflammatory cells resulting in tissue remodeling and dermal fibrosis
99
Q

chronic venous insufficiency - risk factors

A
  • history of DVT (37%)
  • history of hip/knee/calf surgery
  • ankle hypomobility/fusion
  • employment involving prolonged standing
  • morbid obesity
  • pregnancy
  • heart failure
  • progression: heavy, aching feeling in legs, telegentsia or reticular veins, varicose veins, edema without ulceration, skin changes without ulceration, skin changes with ulceration
100
Q

chronic venous insufficiency - common skin changes

A
  • hyperpigmentation (hemosiderin)
  • lipodermatosclerosis
  • dilated long saphenous vein
  • atrophie blanche
  • unilateral or bilateral edema
  • dermatitis
  • thickened skin
  • cellulitis
  • located in gaiter area
101
Q

mixed venous and arterial wounds (MAVLU)

A
  • presenation isn’t clean for one or the other
  • ABI is gold standard test to determine
  • ABI 0.6-0.8 is “mixed ulcer
  • accounts for approximately 10% of LE ulcers
  • origin primarily due to chronic venous insufficiency with poor healing, with coexisting arterial insufficiency
  • pathophysiology: typically a combination of venous HTN, primary or post-thrombotic venous reflux and/or obstruction, and reduction in blood inflow due to PAOD