Clinical Slide Set. Venous Leg Ulcers
Download
Report
Transcript Clinical Slide Set. Venous Leg Ulcers
In the Clinic
Venous Leg
Ulcers
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
Why do patients with chronic venous
insufficiency develop VLU?
CVI most common cause of VLU
VLU patients have venous hypertension, or abnormally
sustained elevation of venous pressure on walking
Caused by vein valve reflux, outflow problems or both
Venous outflow issues
Venous obstruction
Poor function of calf muscle pump impairs venous
system's ability to return venous blood to heart
Ankle movement limitations contribute to calf muscle
pump failure
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What are the risk factors for VLU?
Age older than 55 years
Family history of CVI
Ulcer history, parental history of ankle ulcers
Higher body mass index
History of pulmonary embolism
Venous reflux in deep veins, history of superficial/DVT
Lower extremities skeletal or joint disease
Number of pregnancies
Physical inactivity
Severe lipodermatosclerosis
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
Are there measures that can prevent VLU
or their recurrence?
Aggressive management of reversible risk factors
Control of relevant comorbid conditions (CHF, PVD)
Healthy diet, appropriate exercise, weight control
Management of a hypercoagulable state
Stockings that achieve at least 20-30 mm Hg pressure
Patients should use highest level of compression tolerable
Surgical venous ablation
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
CLINICAL BOTTOM LINE: Prevention...
CVI is the leading cause of VLU
Venous hypertension with calf muscle pump dysfunction
Manage comorbid risk factors
CVI, obesity, hypercoagulable states
Skeletal and joint disease of the lower extremities
Compression stockings
For primary and secondary prevention
Venous intervention
For secondary prevention
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What symptoms and physical findings are
suggestive of CVI?
Swelling and aching of legs, worse at end of day and
improved by leg elevation
History of ulcer recurrence, particularly at same location
Dependent edema, telangiectasias, varicose veins,
reddish-brown pigmentation and purpura, and
subsequent hemosiderin deposition
Eczematous changes with redness, scaling, pruritus
Smooth, ivory-white, stellate atrophic plaques of
sclerosis with telangiectases (atrophie blanche)
Chronic lipodermatosclerosis (LDS) and acute LDS
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
Chronic venous insufficiency
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
Atrophie blanche
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What symptoms and physical findings
suggest that VLU are due to CVI?
VLU may be painful—dull, aching, or burning pain
Location over medial lower third of the legs
Usually 1 ulcer w/ irregular, flat, or only slightly steep borders
Ulcer bed shallow, with granulation tissue or fibrinous material
Wound surface rarely shows necrosis, exposed tendons, bone
Venous dermatitis, LDS, or atrophie blanche around ankle
Assessment: Test for neuropathy
Severity of CVI correlates with decreased range of motion at ankle
and is associated with peripheral neuropathy
VLU pain neuropathic in origin in some patient
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
Venous leg ulcer
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What other conditions should be
considered during evaluation of a patient
with possible VLU?
Common causes of lower extremity ulcers
CVI
Arterial insufficiency
Diabetic neuropathy
Prolonged pressure
Less common causes
Trauma
Inflammatory or metabolic conditions
Cancer
Infections
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of laboratory testing?
No single laboratory test is diagnostic
Testing may be indicated depending on specific patient
history, comorbidities, and family history
In patients with history of recurrent ulceration or
thrombosis, evaluate for hypercoagulable states
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of noninvasive tests, such
as ankle-brachial index and duplex
ultrasonography?
Ankle-brachial index should be performed
For PAD screening: concomitant arterial disease in ~20%
Compression therapy could worsen an arterial ulcer
Color duplex ultrasonography
For accurate diagnosis and to provide prognostic info
Photo and air plethysmography
Whole-limb venous hemodynamics at rest and after exercise
CT exam
Intractable edema associated with pain despite compression
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of routine testing for
infection?
Swab culture testing unwarranted w/o signs of infection
If atypical infection suspected: send tissue from wound
biopsy for microscopic examination and culture
Use antibiotic therapy only for clinically infected ulcers
Evidence supports topical cadexomer iodine for healing
No evidence supports use of systemic antibiotics
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
When should clinicians consider obtaining a
biopsy or referring the patient to a surgical
or nonsurgical specialist for diagnosis?
To rule out other causes of VLU, especially cancer
When ulcers are atypical-appearing ulcers
When ulcers have not healed after 4 weeks of active
treatment
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
CLINICAL BOTTOM LINE: Diagnosis...
Typically based on clinical history and physical examination
Presence of CVI
Single, painful ulcer with irregular, flat borders and
granulating or fibrinous bed on medial lower third of legs
Color duplex ultrasonography to characterize venous disease
in all patients
Ankle-brachial index to exclude concurrent PAD
If VLU do not improve within 4 weeks of active therapy:
consider referral to specialist or biopsy
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the overall approach to treatment?
Treatment goals
Reduce edema and pain
Heal ulcers
Prevent recurrence
Systematic approach needed
Assess frequently and escalate treatment if unresponsive
Simplest treatment: bed rest with leg elevation
Elevate legs above heart 30 minutes, 3 to 4x/d + at night
Reduces swelling, improves venous microcirculation
Most patients struggle to follow this recommendation
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of compression therapy?
Cornerstone of therapy
Because sustained leg elevation often difficult to achieve
Gold standard: multiple elastic layers for graduated
compression
Increases interstitial hydrostatic pressure
Improves venous return
Reduces venous hypertension and edema
Improves ulcer healing rates
Use cautiously with CHF and with arterial insufficiency
Don’t use with severe arterial insufficiency
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
How long should clinicians prescribe
compression therapy?
Continue until the ulcer heals
Continue indefinitely after healing to prevent recurrence
To enhance adherence, instruct how to put on stockings
Ensure proper measurement and fit
Assistive devices may help arthritic, obese, elderly patients
Replace at least every 6 months
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of medication?
To improve healing in combination with compression
Aspirin (300 mg daily)
Pentoxifylline (400-800 mg 3x/d)
To reduce LDS inflammation, pain, induration
Stanozolol
Oxandrolone
Horse chestnut seed extract (active ingredient: aescin)
To reduce pain (based on neuropathic origin)
Amitriptyline, gabapentin, pregabalin
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of growth factors?
Granulocyte macrophage colony-stimulating factor
Topical and perilesional injection increases ulcer healing
Promotes wound healing through many mechanisms
(homeostasis, inflammation, proliferation, maturation)
Increases vascularization
FDA-approved for neutropenia but not wound healing
Phase 3 trials stopped due to bone pain associated with
perilesional injections
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of physical therapy or
exercise?
Aim: to improve range of ankle movement and calf
muscle pump function
Might enhance ulcer healing
But evidence conflicting and RCTs lacking
RCT underway: comparing compression therapy with
compression therapy + 12 weeks of supervised exercise
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of hyperbaric oxygen
therapy?
Adjunct to standard wound care
Controversial because evidence for treating VLU extremely
limited
100% oxygen at 2-2.5 atmosphere absolute for 60- to 120minute periods over 15-30 sessions
Goal: increase partial pressure of oxygen at the wound
Role in pathogenesis and treatment unclear
Fibrin cuff theory: fibrin cuffs formed around precapillary
vessels may result in wound hypoxia, so increased oxygen
might aid healing
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of surgical debridement or
skin grafting?
Debridement
Removes nonviable tissue to achieve an appropriate
wound bed with granulation tissue
Standard care despite lack of controlled data on healing
Skin grafting
Enhances healing for large or slow-healing ulcers
May rapidly decrease pain and aid functional status
Pinch grafts, split-thickness skin grafts, and micro-skin
grafts used successfully but RCTs lacking
Skin equivalents (cellular, acellular) may aid healing
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
What is the role of venous surgery in
treatment and prevention?
Venous surgery
Doesn’t improve healing but reduces recurrence
Open surgery has significant potential morbidity
Cochrane review found no evidence for benefit or harm
Subfascial endoscopic perforator surgery
Safer, possible improved healing, decreased recurrence
Minimally invasive procedures
Treat CVI and recurrence
Endovenous thermal ablation (laser, radiofrequency, steam)
US-guided foam sclerotherapy; cyanoacrylate embolization
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
When should clinicians consider referring
the patient to a surgical or nonsurgical
specialist for treatment?
Prognostic factors associated with slower healing
Larger wound area (>5 cm2) and long duration (>6 months)
LDS and ulcer history, BMI >33 kg/m, physical inactivity
Prolonged venous filling time, deep venous insufficiency
Ulcer depth >2 cm, atypical ulcer location (posterior calf)
Refer to wound specialist when wounds fail to decrease
in size during first month of treatment
Expertise may be found in a variety of specialties
Vascular medicine and surgery, podiatry, dermatology
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
How should clinicians educate patients?
Encourage patients to adhere to compression therapy
Provide educational materials on pathophysiology,
management, and prevention
Consider video-based educational interventions to teach
patients about the disease
Consider patient support groups for education on selfmanagement
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.
CLINICAL BOTTOM LINE: Treatment...
Goals: reduce edema, improve pain and LDS, heal ulcer,
prevent recurrence
Maintenance:
Moist wound bed and regular sharp debridement
Infection control
Compression with elastic multilayer bandages
If no improvement in 4 weeks: consider referral to wound
expert and adjuvant therapies
Prevent recurrence: indefinite use of compression stockings
and vascular intervention
© Copyright Annals of Internal Medicine, 2016
Ann Int Med. 165 (2): ITC2-1.