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MED CON III > Wound Exam: Color, Drainage, Edges > Flashcards

Wound Exam: Color, Drainage, Edges Flashcards

1
Q

Types of exudate (drainage)

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

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2
Q

Amount of exudate:

A

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

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3
Q

Maceration

A

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.

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4
Q

What should you look for in the areas surrounding the wound?

A

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

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5
Q

What can excessive lipids cause the skin to look like?

A

Waxy appearance, dilated pores, acnes

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6
Q

Description of wound edges:

A

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

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7
Q

When is wound odor test most accurately done?

A

after debridement and rinsing the wound

-get slough and necrotic tissue out of the way

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8
Q

Types of wound odors:

A

ammonia-like

sickly sweet

fout, putrid, fetid

*blue/green colored wound–> bad sign

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9
Q

Types of pain and what they mean:

A

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!

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10
Q

Sensory testing can include:

A

pressure
vibration
light touch
temperature
proprioception
sharp: wartenberg wheel/pinwheel
reflexes/DTR

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11
Q

Vascular testing: arterial system

A

-pulses: use grading scale, compare BL, above and below

doppler for pulses that are not palpable

ABI

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12
Q

Why would a wound culture be indicated?

A

-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

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13
Q

CLINICAL DIAGNOSIS: DIMES- what does it stand for?

A

DEBRIDEMENT

INFECTION/INFLAMMATION

MOISTURE BALANCE

EDGES

SUPPORT SERVICES

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14
Q

Characteristics of chronic wounds:

A

-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)

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15
Q

What are the 4 types of chronic wounds? (90% of chronic wounds)

A

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

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16
Q

What are the most prevalent types of wounds?

A

MOST
surgical infection
diabetic infection
surgical wound
traumatic wound
skin disorder
venous infection
LEAST

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17
Q

Neuropathic wound characteristics:

A

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.

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18
Q

Arterial wound characteristics:

A

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

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19
Q

How many people with DM have wounds?

A

15%

-14-24% of those with diabetic ulcers end up having amputation

–> 50-68% mortality rate following amputation at 5 years

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20
Q

How does hyperglycemia affect vasculature in ppl with DM?

A

hyperglycemia can lead to stiffer blood vessels

-leads to reduced tissue oxygenation

-occluded vessel
-damaged myelinated nerve fiber

*vascular and neurological damage

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21
Q

Is it more common to have DPN with type I or type II diabetes?

A

type II

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22
Q

What is neuropathy (DPN) ?

A

-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

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23
Q

Sensory exam for DPN:

A

-increased temperature by 2.2 degrees celsius

-monofilament for protective sensation, temperature, position sense, vibration, pin, light touch

-usually vibration test is first

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24
Q

What is a common osteopathy that occurs with diabetes mellitus?

A

Charcot’s disease:
(neuropathic arthropathy)

-progressive degeneration of weight bearing joints

-increased skin breakdown risk
–> abnormal pressure distribution
–> more wound risk combined with DPN

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25
Common foot deformities for patients with DM?
clock toe deformity charcot foot bunions --> may lead to ulceration on toes
26
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
27
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
28
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)
29
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
30
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
31
What artery could be involved with thigh and buttock pain (claudication)?
aortoiliac or iliac
31
What artery could be involved with calf pain (claudication)?
femoral or popliteal
32
When is revascularization surgery required with PAOD?
pain at rest -could have signs of ischemia at distal digits
33
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
34
Stage I arterial wound
limb viable, not immediately threatened
35
Stage IIa arterial wound
limb marginally threatened, salvageable if promptly treated
36
Stage IIb arterial wound
limb immediately threatened, salvageable with immediate revascularization
37
Stage III arterial wound
limb irreversibly damaged major tissue loss or permanent nerve damage inevitable
38
What is the recurrence rate of venous wounds?
72%
39
What type of wound makes up the majority of LE wounds?
venous wounds
40
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
41
Examples of superficial veins:
great saphenous small saphenous
42
Examples of deep veins:
femoral popliteal
43
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
44
What is venous obstruction called?
chronic deep vein thrombosis
45
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
46
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
47
What is atrophie blanche?
Atrophie blanche describes the result of healed ulcers. These characteristically present as a white, atrophic stellate scar with peripheral telangiectasias.
48
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.
49
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.
50
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.
51
What is the most common location of a venous woune:
From the malleoli to just under the bulk of calf muscle
52
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
53
CEAP Classification System and Reporting Standard Revision 2020
CLINICAL MANIFESTATIONS ETIOLOGY ANATOMIC DISTRIBUTION PATHOPHYSIOLOGY
54
What does MAVLU stand for?
Mixed venous and arterial wounds
55
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
56
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
57
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
58
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
59
Once a pressure injury has been staged, _______
the stage cannot be reversed when there is healing happening
60
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
61
Are pressure injuries in hospitalized patients considered never events?
yes stage III-IV
62
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
63
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
64
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
65
What populations are skin tears common in?
-extremes of age -critically or chronically ill -10-54% prevalence in LTC
66
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!
67
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
67
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
68
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
69
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
70
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
71
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
72
RED-YELLOW-BLACK SYSTEM (RED)
WOUND BED: pale pink --> beefy red, granulation tissue TREATMENT GOALS: protect wound, maintain warm & moist environment, protect periwound
73
RED-YELLOW-BLACK SYSTEM (YELLOW)
WOUND BED: – moist & yellow slough, may vary in adherence TREATMENT: debride necrotic tissue, absorb drainage, protect periwound
74
RED-YELLOW-BLACK SYSTEM (BLACK)
Wound Bed – thick, black, adherent eschar Treatment Goals – debride necrotic tissue that may appear wet or infected
75
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
76
INDICATONS FOR DEBRIDEMENT
-necrotic tissue -foreign material -debris -residual topical agents -blisters -callus
77
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
78
Things to consider before debridement:
nutrition concomitant med conditions immunosuppression thrombocytopenia - lack of platelets use of anticoagulants -bleeding risk setting where the patient is
79
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
80
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
81
CONS OF AUTOLYTIC DEBRIDEMENT
-slow results -no occlusive dressing to be used with infection
82
CONS OF SHARP DEBRIDEMENT
-pain -can require surgery -risk of vessel, nerve, tendon damage
83
CONS OF MAGGOTS
-expensive -limited resources -reputation
84
CONS OF ENZYMATIC DEBRIDEMENT
-very expensive -slow results
85
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
86
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
87
Should you measure the wound before or after you debride it?
before AND after
88
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
89
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
90
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.
91
Types of sharp debridement tools:
scalpel, curette, scissors, forceps
92
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

MED CON III (14 decks)

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