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
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
3
Q
anatomy of the skin - layers of the epidermis
A
- stratum corneum
- stratum lucidum
- stratum granulosum
- stratum spinosum
- stratum basale
- basement membrane
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
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
6
Q
stratum granulosum
A
- layer that contains transition zone for the development of keratin
- becoming more active cells again
7
Q
stratum spinosum
A
- layer contains “spiky/spiny” projections
- gives integrity, holds things together
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
9
Q
basement membrane
A
- the layer that separates the epidermis and dermis
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
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
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
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
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
15
Q
diabetic foot ulcers have a mortality rate of []% and as high as []% after BKA
A
- 43-55%
- 74%
16
Q
venous leg ulcers have a 6-month healing rate of []% and a [] recurrence within 5 years
A
- 45-70%
- 25-70%
17
Q
patients > 45 YO have a prevalence of PAD (peripheral arterial disease) of []%
A
- 14.9%
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
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
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
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
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
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)
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
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
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)
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
28
Q
abnormal: blue skin colors
A
cyanosis
29
Q
abnormal: purple skin color
A
- deep tissue injury
- may be darker or gray in darker skin
30
Q
abnormal: red color
A
- infection or inflammation
- could be cellulitis or dermatitis - raised
- erythemia - flat, shiny
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
32
Q
abnormal: red skin with covid
A
- pediatric multisystem inflammatory syndrome (PMIS) – purplish lesions on toes and feet, rash
- Covid toes
- Coronavirus rash
33
Q
abnormal: red skin colors indicative of other issue
A
- bulls-eye rash: Lyme disease
- rashes - drugs
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
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
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
37
Q
localized edema
A
- sign of infection
- result of inflammatory response in the immediate wound area
38
Q
unilateral edema
A
- can be indicative of venous insufficiency, DVT, lymphatic blockage
39
Q
bilateral edema
A
- probably more central body cause – heart failure
40
Q
pitting edema
A
41
Q
edema - induration
A
- orange-peel texture
- more chronic edema
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
- sanguineous: thin, bright red
- serosanguinous: thin, watery, pale red to pink
- serous: thin, watery, clear
- purulent: thick or thin, opaque tan to yellow
- 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
