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Wound 2.2 > Lesson 8: Lower Extremity Wounds > Flashcards

Lesson 8: Lower Extremity Wounds Flashcards

1
Q

LEAD Risk Factors

A
  • Smoking
  • DM
  • hyperlipidemia
  • hypertension
  • Age >66
  • obesity
  • family HX of CVD
  • autoimmune/inflammatory states
  • elevated homocysteine levels
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2
Q

LEAD Clinical presentation

A
  • Intermittent claudication: pain with activity relived with 10 minutes of rest
  • Progresses to nocturnal pain and rest pain
  • Progressive disease = progressive pain
  • Reported as heaviness or difficulty walking
  • Neuropathic pain: reduced by activity or walking
  • Ischemic pain: worse with activity/elevation, better with 10 minutes of rest or dependency
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3
Q

Signs of Chronic Tissue Ischemia

A
  • Diminished hair growth
  • Thin, ridged nails
  • Thin, shiny skin
  • Elevational pallor/dependent rubor
  • Coolness to touch
  • Prolonged venous filling time >20 seconds
  • Diminished DP and PT pulses
  • Abnormal ABI
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4
Q

LEAD Diagnostics

A
  • ABI
  • Toe brachial index
  • Transcutaneous oxygen levels
  • Capillary refill time
  • Auscultation of larger arteries for bruit
  • Sensory assessment
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5
Q

ABI Calculation + Values

A

Lower extremity SBP / highest brachial SBP

  • 0.9 - 1.3 = normal
  • 0.8 - 0.9 = mild LEAD, blood flow sufficient for standard compression
  • 0.5 - 0.8 = moderately severe disease with borderline perfusion; vascular consult
  • <0.5 = severe ischemia; urgent vascular consult
  • <0.4 = critical ischemia with potential limb loss
  • > 1.3 = elevate due to calcification
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6
Q

Arterial Ulcer Characteristics

A
  • Located to distal toes and feet with nonhealing injuries
  • Heel ulcers usually due to pressure injury
  • Wound bed = pale or necrotic
  • Wound edges = “punched out” appearance
  • Minimal exudate
  • Infection possible but will present muted
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7
Q

Arterial Ulcer Management

A

Improve perfusion!

RX
- Cilostazol
- Statins
- Aspirin
- Clopidogrel

Progressive walking program
- Only AFTER wound is healed

Lifestyle modification
- Smoking cessation
- Hydration status
- Tight glucose control
- Diet modification

Secondary = prevent further injury
- Aggressive patient education
- Protective footwear
- Professional nail care
- Daily visual inspection
- Prompt attention of any injuries

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8
Q

Arterial Ulcer Topical Therapy

A

Use of hyperbaric oxygen therapy +/- Dynamic compression therapy

Dry eschar with no infection
- Maintenance until adequate perfusion established
- Paint with iodine

Necrotic wound with active infection
- Debride with chemical or enzymatic
- Need to also be on IV antibiotics

Open wound with adequate perfusion
- Principles of moist wound healing

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9
Q

Venous Insufficiency

A
  • Reflex of blood from deep system to superficial system
  • Venous congestion causes back pressure on capillaries
    — Edema
    — Hemosiderosis (iron leaking into skin causing staining)
    — Inflammation
    — Fibrosis
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10
Q

Venous Insufficiency Risk Factors

A

Increases venous resistance
- Multiple pregnancies
- Obesity

Damage valves
- DVTs
- Phlebitis

Thrombophilic conditions
- Protein S deficiency
- Protein C deficiency
- Factor V mutation

Inflammatory conditions
- Lupus

Prolonged standing with sedentary lifestyle

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11
Q

CEAP Classification for Chronic Venous Insufficiency

A

C: clinical manifestations
- C1: telangiectasis, reticular veins, ankle flare
- C2: varicosities
- C3: edema but no skin changes
- C4: skin changes
- C5: skin changes + healed ulcer
- C6: skin changes + open ulcer

E: etiological factors

A: anatomical factors

P: pathological factors

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12
Q

Venous Ulcers

A

Ulceration due to hypertension and impact of extravasated molecules

Creates inflammatory and fibrotic changes

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13
Q

Venous Ulcer Characteristics

A
  • Edema
  • Telangiectasias (spider veins)
  • Hemosiderosis
  • Aching pain relived by elevation
  • Venous dermatitis
  • Ankle flare
  • Atrophic blanche
  • Lipodermatosclerosis
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14
Q

Venous Ulcer Presentation

A
  • Located between ankle and knees
  • Wound bed is dark red/ruddy or covered with thin yellow eschar
  • Irregular wound edges
  • Moderate to large amounts of exudate
  • Feet are warm with palpable pulses
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15
Q

Venous Ulcer Diagnostics

A
  • venous Doppler ultrasound
  • ABI
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16
Q

Venous Ulcer Management

A

Priority = improve venous return

Pentoxifylline
- For management of refractory venous ulcers

  • Surgical intervention to reduce hypertension
  • Leg elevation
  • Compression therapy
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17
Q

Venous Ulcer Topical Therapy

A

Goal = control exudate, reduce bacterial burden, protect periwound skin

Options
- Liquid skin barrier
- Alginates or foams
- AMD dressing for wounds with surface infection

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18
Q

Venous Ulcer - Patient Education

A
  • Pathology of LEVD
  • Smoking cessation
  • Weight management
  • Trauma avoidance
  • Leg elevation + daily walking
  • Consistent compression
19
Q

Compression Therapy

A

Partially collapses distended veins = improved valve function

Supports calf muscle pump = improves venous return

Increases interstitial pressure = reduces/eliminates edema

20
Q

Compression Therapy - Contraindications

A

Uncompensated + symptomatic heart failure

Advanced LEAD

Active DVT

Active cellulitis

21
Q

Static Compression - 4-Layer System

A

Layers 1+2 = padding and absorption
Layer 3 + 4 = 50% stretch and 50% overlap

22
Q

Static Compression - 3-Layer System

A

For both active and sedentary patients
- Layer 1 = padding and absorption
- Layer 2 = active stretch
- Layer 3 = 50% stretch and 50% overlap

23
Q

Static Compression - 2-Layer System

A

Layer 1 = padding and protection
Layer 2 = 100% stretch and 50% overlap

24
Q

Static Compression - Unna’s Boot

A

The gold standard in compression therapy

Gelatin-zinc oxide gauze layer + Coban outer layer

For actively ambulating patients

25
Q

Lymphedema - causes

A
  • Congenital
  • Radical surgery
  • Chronic venous disease
  • Filariasis
26
Q

Lymphedema - Pathology

A

Stage 1: reversible
- Fluid accumulation responds to elevation and compression

Stage 2: spontaneously irreversible
non-pitting edema, papillomatosis
- Elevation is ineffective

Stage 3: lymphostatic elephantiasis
- Severe papillomatosis
- Severe edema
- Ulceration
- Requires complex decongestive therapy

27
Q

Lymphedema - Management

A
  • Prevention and early treatment
  • Need lymphedema treatment center for advanced disease
28
Q

Neuropathy - Definition

A

Damage to sensory, motor, and autonomic nerves

Results in
- Compromised sensation
- Neuropathic pain
- Altered foot contours/deformity
- Osteopenia/fractures/Charcot’s foot
- Reduced sweating

29
Q

Neuropathy - Pathology

A
  • Hyperglycenia
  • Ischemic damage to nerves due to microangiopathy
  • B12 deficiency
  • Spina bifida
  • Spinal cord injury
30
Q

Sensory Neuropathy

A

Damage to nerve controlling sensory input
- Paresthesia: burning/tingling pain that occurs spontaneously
- Progressive anesthesia: loss of protective sensation + increases risk of painless trauma

Routine screening
- Monofilament testing
- Vibratory sense testing
- Proprioceptive testing

Clinical presentation
- Loss of vibratory sense
- Loss of protective sensation
- Less of proprioceptive sense

31
Q

Motor Neuropathy

A

Damage to nerves controlling muscles
- Causes foot and toe deformities
- Alters weight-bearing status

Routine screening
- Visual inspection
- Assess for foot deformities

32
Q

Autonomic Neuropathy

A

Damage to nerves controlling sweat glands and blood vessels
- Reduced sweating
- Persistent vasodilation
- Demineralization of bones
- Increased risk of fractures

Screening
- Skin hydration status
- Assess foot contours and weight bearing pattern
- Skin temperature checks

33
Q

Neuropathic Ulcers - Pathology

A
  • Painless repetitive trauma
  • Usually focused on sites in contact with footwear
  • Heels, toe tips, or plantar surface
  • Breakdown between toes due to excess moisture
  • Corn and calluses indicate future ulcer
34
Q

Neuropathic Ulcers - Characteristics

A
  • Located on tips/tops of toes and sides of feet
  • Well defined edges
  • Wound base red
  • Moderate exudate
  • Callus formation is common

Wagner Classification System
- 0: pre-ulcerative lesions, healed lesions, presence of bony deformity
- 1: partial thickness ulcer
- 2: ulcer involving subcutaneous tissue
- 3: osteitis, abscess or osteomyelitis
- 4: gangrene of digit
- 5: amputation +/- joint disarticulation

35
Q

Neuropathic Ulcers - Management

A
  • Appropriate footwear
  • Daily foot inspection
  • Prevent pressure injuries in bed-bound patients
  • Avoid dry, cracked feet
  • Reduce/eliminate repetitive trauma
  • Pressure relief for heel ulcers
  • Deep + wide toe box for toe ulcers
  • Offloading
  • Tight glucose control
36
Q

Neuropathic Ulcers - Patient Education

A
  • Offloading
  • Glucose control
  • Wound management
  • Preventative care
    — daily foot inspection

If wound fails to progress
- Active wound therapy
- Hyperbaric oxygen therapy
- Refer to pedorthist +/- orthotist
- Gradually increase walking time

37
Q

Vasculitis Ulcers

A

Caused by inflammation and necrosis of blood vessels
Usually associated with autoimmune disorders

Pathology
- Antigen-antibody complex deposits on vessel wall and becomes inflamed and occluded

Clinical presentation
- Depends on vessel involved and severity of inflammation
- Usually full thickness, extremely painful
- Wound bed is pale or necrotic with minimal exudate
- Petechial or purpuric rash may precede ulcer

Diagnosis
- Systemic symptoms
- Signs of vessel damage
- Lab indicators
— Sedimentation rate
— ANA
- Biopsy

Management
- Address underlying disorder
- Anti-inflammatory drugs
- Plasmapheresis
- Pain management and moist wound healing

38
Q

Pyoderma Gangrenosum

A

Inflammatory ulcers of the skin

Clinical presentation
- Ulcers or pustular lesions with purple borders
- Acutely painful
- Exudative and causes dermal destruction
- 4 P’s
— Purulent drainage
— Painful
— Pathergy
— Purple edges

Diagnosis
- Diagnosis of exclusion
- Biopsy confirms inflammation but nonspecific

Treatment
- Topical and systemic anti-inflammatory agents
- Pain management
- Moist wound management to manage exudate
- Assure atraumatic removal

39
Q

Sickle Cell Ulcers

A

Sickle-shaped cells obstruct vessels and cause ulcer formation
- Edema common due to loss of normal vasoconstrictive response

Clinical presentation
- Usually distal 1/3 of leg
- Sharply demarcated edges
- Scant exudate
- Pale wound bed
- Acutely painful
- Ulcers are slow to heal and prone to reoccurrence

Diagnosis
- Relevant patient history of sickle cell disease

Management
- Systemic support
— Hydration
— Infection management
— Nutritional support
— Hydroxyurea
- Pain management
- Topical therapy +/- compression if edema

40
Q

Basal Cell Carcinoma

A

Pathology
- Malignancy of basal cell layer of epidermis
- May be primary lesion or develop into chronic wound

Clinical presentation
- Hypergranulation tissue with doesn’t respond to cauterization
- Red/pink nodules
- Ulcerative lesions with rolled borders

Diagnosis
- Biopsy

Treatment
- Surgery or radiation

41
Q

Squamous Cell Carcinoma

A

Pathology
- Malignancy involving keratinocytes
- Usually associated with prolonged sun exposure

Clinical presentation
- Indurated papule, plaque, or nodule
- Possible crusted areas
- Shallow lesion with raised and indurated border

Diagnosis
- Biopsy

Treatment
- Surgery or radiation

42
Q

Calciphylaxis

A

Pathology
- Rare but potentially fatal condition
- Involves calcification of arterioles and soft tissue
- Unknown true cause

Clinical presentation
- Painful, mottled lesions that progress to necrotic nodules
- Common on fatty tissue areas
- Mortality rate 50 – 80%

Diagnosis
- History and physical presentation
- Lab values for calcium, phosphorus, and parathormone
- Bone scan

Treatment
- Systemic measures to normalize extended lytes
- Sodium thiosulfate infusion
- Pain management
- Topical therapy
— Leave lesions open to air until systemic issues are corrected
— Chemical or autolytic debridement
— Possible NPWT vs grafting
**all dependent on goals of care

43
Q

Necrobiosis Lipoidica Diabeticorum

A

Pathology
- Rare condition usually associated with glucose intolerance
- Etiology and pathology is unknown

Clinical presentation
- Well-demarcated “waxy” lesions on anterior and lateral surfaces of lower extremities
- Lesions may be red, yellow, or brown
- May be painful

Diagnosis
- Medical history
- Clinical presentation

Treatment
- Systemic or intralesional steroids
- Principles of moist wound healing

Wound 2.2 (9 decks)

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