Lesson 8: Lower Extremity Wounds Flashcards

(43 cards)

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
Lymphedema - causes
- Congenital - Radical surgery - Chronic venous disease - Filariasis
26
Lymphedema - Pathology
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
Lymphedema - Management
- Prevention and early treatment - Need lymphedema treatment center for advanced disease
28
Neuropathy - Definition
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
Neuropathy - Pathology
- Hyperglycenia - Ischemic damage to nerves due to microangiopathy - B12 deficiency - Spina bifida - Spinal cord injury
30
Sensory Neuropathy
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
Motor Neuropathy
Damage to nerves controlling muscles - Causes foot and toe deformities - Alters weight-bearing status Routine screening - Visual inspection - Assess for foot deformities
32
Autonomic Neuropathy
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
Neuropathic Ulcers - Pathology
- 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
Neuropathic Ulcers - Characteristics
- 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
Neuropathic Ulcers - Management
- 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
Neuropathic Ulcers - Patient Education
- 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
Vasculitis Ulcers
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
Pyoderma Gangrenosum
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
Sickle Cell Ulcers
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
Basal Cell Carcinoma
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
Squamous Cell Carcinoma
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
Calciphylaxis
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
Necrobiosis Lipoidica Diabeticorum
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