Wound Exam: Color, Drainage, Edges Flashcards
Types of exudate (drainage)
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
Amount of exudate:
none- wound tissues dry
scant - moist, no measurable drainage
small - very moist, drainage <25% dressing
moderate - wound tissues wet, drainage involves 25-75% dressing
large - wound tissues fill with fluid, involves >75% dressing
Maceration
overly wet area
healthy tissue breakdown
white appearance
*Maceration chronic wounds present with a high level of exudate and whitish, swollen skin. The surface of the skin is roughened and lined with a network of grooves termed as the “sulci cutis”. It is similar in appearance to the white, wrinkly skin observed after spending a long time in a bath.
What should you look for in the areas surrounding the wound?
pulse - compare side to side, above to below
skin temperature
skin characteristics:
-blisters, calluses, other lesions
-skin color
-hair and nail growth
-moisture
-texture
-general visual assessment
What can excessive lipids cause the skin to look like?
Waxy appearance, dilated pores, acnes
Description of wound edges:
EVEN
-arterial wound
IRREGULAR
-venous wound
-may occur as wound epithelializes (shiny, translucent epithelial tissue)
EPIOBLE
-sign of halted healing process
-rolled edges of wound
-cells are termed senescent, meaning they are unable to reproduce
HYPERKERATOSIS
-overdevelopment of the horny layer of the skin
-appears as thickened skin around the edge of a wound or as a callus
-helpful to get layer of skin off to prevent wound
MACERATION
-Maceration chronic wounds present with a high level of exudate and whitish, swollen skin.
DEHISCED
-wound edges come apart
-may be superficial layers only
-can open full depth
When is wound odor test most accurately done?
after debridement and rinsing the wound
-get slough and necrotic tissue out of the way
Types of wound odors:
ammonia-like
sickly sweet
fout, putrid, fetid
*blue/green colored wound–> bad sign
Types of pain and what they mean:
Deep pain (cramping- ischemia or hypoxia; more comfortable in dependent position
Throbbing, localized pain- infection; deep pain that increases with pressure may indicate osteomyelitis
Superficial tenderness- exposed nerve endings, may be accompanied by sharp, shooting pains
Pain with stimulation of red tissue - living muscle!
Sensory testing can include:
pressure
vibration
light touch
temperature
proprioception
sharp: wartenberg wheel/pinwheel
reflexes/DTR
Vascular testing: arterial system
-pulses: use grading scale, compare BL, above and below
doppler for pulses that are not palpable
ABI
Why would a wound culture be indicated?
-infection signs: pus, change in color or character of exudate, redness, induration, changes in odor
-systemic signs of infection: fever, leukocytosis (high WBC count)
-suddenly elevated glucose
-pain in neuropathic extremity
-lack of healing after 2 weeks in a clean wound despite optimal care
CLINICAL DIAGNOSIS: DIMES- what does it stand for?
DEBRIDEMENT
INFECTION/INFLAMMATION
MOISTURE BALANCE
EDGES
SUPPORT SERVICES
Characteristics of chronic wounds:
-present for at least 6 weeks
CHARACTERISTICS:
-necrotic
-bioburden- The number of microorganisms with which an object is contaminated is referred to as the bioburden
-chronic inflammation
-impaired hemodynamics
-senescent fibroblasts and keratinocytes
-chronic wound fluid with growth inhibiting proteases
-overgrowth of epithelium with lack of underlying CT (epibole)
What are the 4 types of chronic wounds? (90% of chronic wounds)
Arterial
-causes: ischemia, micro or macro vascular disease, smoking
Venous insufficiency
-causes: deep vein thrombosis (37%), recent surgery, ankle fusion, prolonged standing, pregnancy, CHF
Neuropathic/Diabetic
-causes: DM, peripheral vascular disease, Hansen’s disease (leprosy)
Pressure
-causes: pressure or shear, immobility, moisture, decreased sensation, poor nutrition
What are the most prevalent types of wounds?
MOST
surgical infection
diabetic infection
surgical wound
traumatic wound
skin disorder
venous infection
LEAST
Neuropathic wound characteristics:
LOCATION: -usually foot, plantar surface or toes
-CAUSE: mechanical forces or minor trauma
PAIN: relieved with ambulation
APPEARANCE OF FOOT: architectural changes in foot (charcot foot)
APPEARANCE OF WOUND: pink, moist, callus formation, plantar surface, skin usually warm, cellulitis
CO-MORB: diabetes, chemo, Hansen’s
** ABI normal
-patients’ diagnoses: DM, PVD, Hansen’s disease, spina bifida, lupus, toxic syndromes, Charcot-Marie Tooth disease
-patients typically have sensory, autonomic, and motor neuropathies.
Arterial wound characteristics:
LOCATION: usually peripheral extremities
CAUSE: ischemia via micro or macrovascular disease
PAIN: occurs with ambulation
APPEARANCE OF FOOT: normal
APPEARANCE OF WOUND: pale color, dry, well-defined margins, limb color pale, hairless extremity, skin cool to touch
Co-morbidities: history of PAD, circulatory problems
**ABNORMAL ABI
MACRO: larger, named artery destruction by PAOD, embolus, thrombus, or trauma
MICRO: disease of the small, unnamed arterioles and capillaries, usually associated with diabetes or small emboli
How many people with DM have wounds?
15%
-14-24% of those with diabetic ulcers end up having amputation
–> 50-68% mortality rate following amputation at 5 years
How does hyperglycemia affect vasculature in ppl with DM?
hyperglycemia can lead to stiffer blood vessels
-leads to reduced tissue oxygenation
-occluded vessel
-damaged myelinated nerve fiber
*vascular and neurological damage
Is it more common to have DPN with type I or type II diabetes?
type II
What is neuropathy (DPN) ?
-decreased sensation, vibration, proprioception, loss of reflexes (distal to proximal)
-impacts longer nerve fibers “dying back”
-neuropathic pain can be present
MOTOR EFFECTS
-progressive weakness and atrophy –> changes in foot shape
AUTONOMIC EFFECTS
*decreases sweat and oil production –> dry, in-elastic skin
*heart and vasculature
–> orthostasis
–> silent MI
*GI tract
–> gastroparesis
–> diarrhea
Sensory exam for DPN:
-increased temperature by 2.2 degrees celsius
-monofilament for protective sensation, temperature, position sense, vibration, pin, light touch
-usually vibration test is first
What is a common osteopathy that occurs with diabetes mellitus?
Charcot’s disease:
(neuropathic arthropathy)
-progressive degeneration of weight bearing joints
-increased skin breakdown risk
–> abnormal pressure distribution
–> more wound risk combined with DPN
Common foot deformities for patients with DM?
clock toe deformity
charcot foot
bunions –> may lead to ulceration on toes
Complications of vascular and neuropathic changes for patients with diabetes:
-ulceration
–> often painless because they don’t have sensation
–> amputation may be needed
-neuropathic edema
-charcot arthropathy
-callus formation
Skin and nail changes with diabetes:
-1/3 patients have dermatologic manifestation
-up to 1/2 of ppl with type 2 DM at risk of developing skin infections
why do ppl with DM have skin and nail changes?
-poor glucose control
-abnormal carb metabolism
-atherosclerosis (4x as likely)
-microangiopathic changes
-neuron degeneration
-pharmacological therapy for DM (injection site)
Diabetic foot classification with grading:
Grade 0
-intact skin
Grade 1
-superficial ulcer
Grade 2
-deep ulcer
Grade 3
-ulcer with bone involvement
Grade 4
-forefoot gangrene
Grade 5
-full-foot gangrene
WIFI classification- WOUND, ISCHEMIA, FOOT INFECTION
-wound: 0-3
-ischemia: 0-3
–> less pressure, not good
-foot infection: 0-3
Peripheral vascular disease (PAOD)
Also called “peripheral arterial occlusive disease”
CRITICAL PHASES:
-collateral circulation is insufficient for metabolic needs–> blood shunts to muscles where there is less resistance
-traumatic wounds with delayed healing
CLAUDICATION- pain with activity
–> decreases with rest
-can be effectively terated with exercise
rest pain–> need surgery
-ulcer development possible
What artery could be involved with thigh and buttock pain (claudication)?
aortoiliac or iliac
What artery could be involved with calf pain (claudication)?
femoral or popliteal
When is revascularization surgery required with PAOD?
pain at rest
-could have signs of ischemia at distal digits
Physical examination of arterial wounds: (with peripheral vascular disease)
ABI: diminished
PULSES: diminished
CAPILLARY REFILL: > 3 seconds
BUERGERS TEST: pallor with elevation and rubor of dependency
SKIN APPEARANCE: shiny, thin, pale, NO hair
CONDITION OF NAILS AND HAIR
LOCATION: wound on distal toes or fingers
EDGES: even, punched out appearance
WOUND TISSUE: dry, necrotic, little or no granulation tissue
Stage I arterial wound
limb viable, not immediately threatened
Stage IIa arterial wound
limb marginally threatened, salvageable if promptly treated
Stage IIb arterial wound
limb immediately threatened, salvageable with immediate revascularization
Stage III arterial wound
limb irreversibly damaged
major tissue loss or permanent nerve damage inevitable
What is the recurrence rate of venous wounds?
72%
What type of wound makes up the majority of LE wounds?
venous wounds
Venous wounds risk factors:
-more common in women
RISK FACTORS
-obesity
-smoking
-lack of exercise
-standing of sitting for long periods
-family hx
-pregnancy
-history of injury, surgery, or DVT of LE
-heart failure
Examples of superficial veins:
great saphenous
small saphenous
Examples of deep veins:
femoral
popliteal
Chronic venous insufficiency causes and effects
CAUSES
-reflux as a result of incompetent valves in the perforator, superficial, or deep veins
-lack of pumping activation during gait cycle
EFFECTS:
-venous hypertension
-excessive moisture in the interstitial tissue
-prevents adequate oxygen and nutrients from reaching the skin
PATHOPHYS CHANGES:
-vessel dilation and elongation
-increased collagen deposition in vein walls and skin
-plasma protein leaks into interstitial space with fibrin cuff around arterioles
-increased inflammatory cells –> tissue remodeling and dermal fibrosis
What is venous obstruction called?
chronic deep vein thrombosis
Characteristics of progression of venous disease:
-heavy, aching feeling in legs
-telangiectasia or reticular veins
-varicose veins
-edema without ulceration
-skin changes without ulceration
-skin changes with ulceration
-skin can appear wet and macerated
Skin changes characteristics of chronic venous insufficiency:
-hyperpigmentation
-lipodermatosclerosis
-dilated long saphenous vein
-atrophie blanche–> result of healed ulcers; tension in skin
-unilateral or bilateral edema
-dermatitis
-thickened skin
-cellulitis
What is atrophie blanche?
Atrophie blanche describes the result of healed ulcers. These characteristically present as a white, atrophic stellate scar with peripheral telangiectasias.
Cellulitis vs dermatitis:
Cellulitis is a common skin infection caused by bacteria. Cellulitis causes redness, swelling, and pain. Allergic contact dermatitis is an itchy skin rash caused by contact with something that irritates the skin.
What is lipodermatosclerosis:
Lipodermatosclerosis, a chronic inflammatory disorder of the lower extremities, is characterized by subcutaneous fibrosis and skin induration. Lipodermatosclerosis is primarily associated with chronic venous insufficiency and venous hypertension and typically affects middle-aged and older adults.
What is hemosiderin staining?
Hemosiderin staining occurs when the smallest blood vessels, known as capillaries, begin to leak. This can be due to a wound, a broken bone, a surgical incision or other types of trauma. It is also associated with certain illnesses that affect circulation. The most common of these is chronic venous insufficiency.
What is the most common location of a venous woune:
From the malleoli to just under the bulk of calf muscle
Components of a venous wound exam:
Girth at arch, malleolus, calf
Type and amount of drainage
Edges: uneven
Location: gaiter, above the ankle
Pain level: usually severe with venous wound
Healing time: failure to heal with standard care
Pulse exam/ABI in case of absent pulses
Ultrasound can be used to determine valve competency/regurgitation can be detected
CEAP Classification System and Reporting Standard Revision 2020
CLINICAL MANIFESTATIONS
ETIOLOGY
ANATOMIC DISTRIBUTION
PATHOPHYSIOLOGY
What does MAVLU stand for?
Mixed venous and arterial wounds
Mixed venous and arterial wound characteristics:
ETIOLOGY: chronic venous insufficiency with poor healing, coexisting arterial insufficiency
PATHOPHYS: venous hypertension, primary or post-thrombotic venous reflux and/or obstruction, reduction in blood inflow due to PAOD
example: irregular wound borders (venous), full thickness, minimal exudate (arterial), cool pale LE (arterial)
ABI: 0.6-0.8 can indicate a mixed ulcer
<0.6- the first mode of treatment is to re-vascularize for healing, prevent recurrence
–> no compression
> 0.6: no consensus on treatment; less likely need revascularization
Arterial vs venous ulcers:
ARTERIAL
-LOCATION:distal to ankle, usually foot, toes, lateral mall.
-EDGES: punched out, well defined
-WOUND BED: pale or rubor of dependence, skin shiny and thin, hair loss and nail changes common
-PERIWOUND: thin and shiny, hair loss and nail changes
-POSSIBLE PMH: diabetes, hypertension, smoking, previous vascular disease
-OTHER: typically dry, cold skin, absent/weak pulses
-MANAGEMENT: keep dry and reduce bioburden
VENOUS
-LOCATION: lower leg or above ankle, near medial mall., feet unlikely
-EDGES: irregularly shaped
-WOUND BED: often granulating, with cellular debris/crust, usually shallow
-PERIWOUND: scaly, dry, hemosiderin staining
-POSSIBLE PMH: varicose veins, obesity, pregnancy, previous DVT
-OTHER: wet, warm skin, edema, pruritis (itchy)
-MANAGEMENT: manage moisture
Pressure vs Neuropathic wounds
PRESSURE
-LOCATION: bony prominences, especially sacrum, ischial tub, greater troch, heels
-EDGES: circular or teardrop, well-defined
-WOUND BED: can be pale, granulating, necrotic or eschar
-PERIWOUND: healthy or red/purple due to pressure
-POSSIBLE PMH: immobility, SCI, dementia, progressive neurologic disorder, dependent w/ mobility, bed or W/C bound
-MANAGEMENT: offloading, nutrition, consider stool/urine contamination, debridement
NEUROPATHIC
-LOCATION: plantar surface of foot, toes, heels, metatarsal heads
-EDGES: callused, well-defined
-WOUND BED: deep and often granulating
-PERIWOUND: thick, dry, callused
-POSSIBLE PMH: diabetes, neuropathy/loss of protective sensation, possible charcot foot
OTHER: decreased sensation, decreased reflexes
-MANAGEMENT: promote granulation and reduce infection
STAGES OF PRESSURE INJURIES
STAGE 1
-reddened
-non-blanchable
-no skin breadown
STAGE 2
-partial thickness wound
STAGE 3
-full thickness
-not seeing ms., tendon, or bone
-into subcutaneous layer
STAGE 4
-slough, eschar common
-got to ms. tendon or bone
Once a pressure injury has been staged, _______
the stage cannot be reversed when there is healing happening
Why does a pressure injury occur?
-ischemia and anoxia to tissue
-shear forces, friction forces, pressure forces, moisture
-Tissues are compressed, blood vessels are compressed and blood flow is
diverted by continual pressure on the skin and underlying structures
-cellular respiration impaired and cells die
Are pressure injuries in hospitalized patients considered never events?
yes
stage III-IV
Pressure forces- relationship between intensity versus duration
pressure injuries can be caused by:
-prolonged exposure to mild to moderate force
-short exposure to moderate severe forces
Friction vs shear:
FRICTION
-is a mechanical force exerted when two surfaces move (i.e.: ‘rub’) against another
SHEAR:
-Shear is a stress resulting from applied forces which cause two objects to deform in the transverse plane
-involves friction and gravity
-body layers are laterally shifted in relation to each other
-skeleton moves but skin stays in same place
What is a risk that can occur when you raise the HOB?
-increased load on sacrum and heels in more upright position
-good HOB height: 30 degrees
What populations are skin tears common in?
-extremes of age
-critically or chronically ill
-10-54% prevalence in LTC
Skin tears: cause and characteristics
Caused by shear, friction, and/or blunt force trauma
- Forces separation of skin layers
- Can be partial- or full-thickness
- Slow to heal
- Susceptible to secondary infection
-acute wound
high propensity
to develop into chronic wounds.
**IT IS GOOD TO PRESERVE THE FLAP!
How can documentation on dressing be modified to keep skin flap in mind?
ex: remove in this direction with arrow (the skin flap is oriented in this direction)
date and initials of therapist
What is the Braden Scale?
-objective scale to determine risk of person developing a pressure ulcer
-SNF, IRF, etc
Population: Most commonly used for patients who are bed- or chair-bound, as well as those with an impaired ability to reposition.
CATEGORIES:
-sensory perception - response to pressure-related discomfort (completely limited, very limited, slightly limited, no impairment)
-moisture (constantly moist, very moist, occ. moist, rarely)
-activity (bedfast, chairfast, walks occ., walks frequently)
-mobility
–> ability to change and control body position
–> (completely immobile, very limited, slightly limited, no limitation)
-nutrition (very poor, probably inadequate, adequate, excellent)
-friction and shear (problem, potential problem, no apparent problem)
** 1-3 or 1-4 scale
** LOWER SCORES–> GREATER RISK OF DEVELOPING PRESSURE INJURY
Acute wound vs chronic wound:
ACUTE
-TIME: 4-6 weeks
-EXAMPLE: surgical, bites, burns, abrasions, traumatic
-TREATMENT:
–> expected healing within predictable timeframe
–> minimal interventions for minor wound and clean source
–> surgical debridement, antimicrobial therapy, wound lavage for severe wound and dirty source
CHRONIC
-TIME: >6 weeks
–> caused by endogenous mechanisms related to a predisposing condition or risk factors (diabetes, AIDS, chemo)
-EXAMPLE: leg/foot ulcers, pressure injury, foot wound from vascular insufficiency or neuropathy
-TREATMENT:
1.) dressing
2.) antimicrobial agents
3.) physical therapy
4.) education
5.) treat co-morbidities
6.) supportive ints: pressure relief, compression, footwear, ADs
What should you know about wounds as a generalist PT?
-infection
-arterial
-venous
-diabetic/neuropathic ulcer
-pressure injury
-lymphedema
** on the job training is required
Components of a basic wound assessment:
full or partial thickness
wound type
location
stage
measurements
wound bed
wound edges
drainage
periwound
- start from inside and work your way outward
DIMES
-debridement
-infection/inflammation
-moisture balance
-edges - if wound edges are not migrating after wound bed prep and healing is stalled, then advanced therapies should be considered
-support services
RED-YELLOW-BLACK SYSTEM (RED)
WOUND BED: pale pink –> beefy red, granulation tissue
TREATMENT GOALS: protect wound, maintain warm & moist environment, protect periwound
RED-YELLOW-BLACK SYSTEM (YELLOW)
WOUND BED: – moist & yellow slough, may vary in adherence
TREATMENT: debride necrotic tissue, absorb drainage, protect periwound
RED-YELLOW-BLACK SYSTEM (BLACK)
Wound Bed – thick, black, adherent eschar
Treatment Goals – debride necrotic tissue that may appear wet or infected
Purpose and goal of debridement (DIMES)
PURPOSE:
-remove necrotic tissue
-remove bacteria –> prevent infection
-shorten the inflammatory phase of wound healing
-decrease energy required by body for wound healing
-increase ability to assess wound bed
GOAL: 100% granulation tissue
INDICATONS FOR DEBRIDEMENT
-necrotic tissue
-foreign material
-debris
-residual topical agents
-blisters
-callus
CONTRAS FOR DEBRIDEMENT
-granular tissue
-viable tissue
-** stable, hard, dry eschar in ischemic limbs
-urgent need for surgical debridement (gangrene, osteomyelitis)
-electrical burns
-deeper tissue: muscle, tendon, ligament, fascia, capsule, bone, nerves, blood vessels
Things to consider before debridement:
nutrition
concomitant med conditions
immunosuppression
thrombocytopenia - lack of platelets
use of anticoagulants -bleeding risk
setting where the patient is
What are the 4 types of non-selective/mechanical debridement?
-wet to dry: “waxing a wound” - with fully necrotised tissue; standard 30-40 years ago
-irrigation: saline
-hydrotherapy: whirlpool (breakdown of necrotic tissue) –> not efficient
-abraded technique: rubbing on tissue; non-selective; not good for granulation tissue
4 types of selective debridement:
AUTOLYTIC - assist body’s enzymatic cells in digesting necrotic tissue; often used with wound dressings
*occlusive- hydrocolloid- non infected wounds, days to work
*transparent- non-occlusive, not good for deep wounds or infected wounds
*hydrogel- add moisture and nutrients to area
*med honey- high in osmolarity; low pH (acidic nature helps to neutralize the naturally alkaline wound area) ** manuka honey
BIOSURGICAL
-maggots: they eat bacteria; control exudate; aren’t affected by antibiotics; can bag them or have them be free range
ENZYMATIC
-breaks down proteins necrotic tissue
-good for infected wound with topical antimicrobial
-cannot be used with silver based products
-**promotes angiogenesis
*EXPENSIVE!
EX: collagenase santyl
SHARP/SURGICAL
-conservative: can be done by PT
–> must have physician’s order, goal of 100% granulation tissue
-surgical: only by MD under anesthesia
–> large wound, lots of necrosis, heavily infected,
–> ascending cellulitis, osteomyelitis, extensive necrosis, extensive undermining
CONS OF AUTOLYTIC DEBRIDEMENT
-slow results
-no occlusive dressing to be used with infection
CONS OF SHARP DEBRIDEMENT
-pain
-can require surgery
-risk of vessel, nerve, tendon damage
CONS OF MAGGOTS
-expensive
-limited resources
-reputation
CONS OF ENZYMATIC DEBRIDEMENT
-very expensive
-slow results
CONTRAS FOR SHARP DEBRIDEMENT
-stable heel eschar
-gangrene (NEED SURGICAL DEBRIDEMENT)
-unidentified structures–> nerve, tendon, ligament, muscles, vessel, fungating wound
-terminally ill
-ABI < 0.8
-coagulopathy: INR, PT/PTT, platelets, hemoglobin
MUST HAVES before sharp debridement
-Phys. order
-chart review
-check labs
-gather tools
-pre-medicate
-comfortable positioning
-adequate lighting
-cleanse before you debride with saline! (angiocatheter, skin/wound cleanser, bulb syringe)
-measure!!- paper tape measure, cotton tip applicator
Should you measure the wound before or after you debride it?
before AND after
Techniques for selective debridement:
- Hold scalpel like a pencil
- Cut parallel to skin, not perpendicular
- Work in layers
- Use forceps or tweezers to grasp onto layers
What is the cross hatching technique of selective debridement used for?
Increases surface area for enzymatic debridement
** can help to improve healing of areas with epibole –> increase wound edge closure
-can do this with a curette
-silver nitrate can be used in epibole management as well
Function of silver nitrate:
The silver nitrate stick is considered an antimicrobial and is used in enhancing anti-inflammatory healing. A silver nitrate stick uses a chemical cautery agent made up of 75% silver nitrate and 25% potassium nitrate. When the tip of the applicator stick is moistened by wound fluid, a chemical reaction occurs: killing bacteria, removing necrotic tissue, reducing hypergranulation, reducing fibroblast proliferation, and coagulating tissue.
Types of sharp debridement tools:
scalpel, curette, scissors, forceps
Consideration of temperature regulation:
PT’S CORE BODY TEMP (necessary for wound healing): 91.4-107.6 for wound healing
-moisture loss= cooling
-degree change of 2 degrees affects healing
–> increase infection risk, inhibit platelet activation, reduction in wound strength due to decline in collagen deposition
