Venous Insufficient Ulcers Flashcards
Recurrences rates in venous ulcers
26-69% high
Venous system
- Low-pressure system
- Carries blood from tissue capillaries back to the heart
- High in CO2 and metabolic wastes
- 15 mmHg (capillaries on venous side)
- 0 mmHg up one reaching right atrium via vena cava (5 mmHg)
Anatomy of venous system
- Three layers, innermost produces enzymes which help reduce clot formation
- Layers are thin and there is less smooth muscle
- Veins more extensible than arteries and able to accommodate greater volumes of blood
Total blood volume stored in veins
70%
Intact valves
Reflux of blood is prevented during calf muscle relaxation
Damaged valves
Reflux of blood can occur during calf muscle relaxation and may cause venous hypertension (get retro-grade flow)
Perforating veins
Pierce the fascia connecting the deep and superficial vein systems throughout the lower leg
- Contain bicuspid valves that only allow unidirectional flow towards the heart preventing retrograde venous flow
Deep veins
Located within muscles and roughly run parallel to the arteries, contain one-way valves
- Greater pressure than superficial
Superficial veins
Contain same type of valves as deep but not surrounded by muscle (no muscle pump)
- Assist with temperature regulation
Calf muscle pump
Helps to return venous blood back to body, applies pressure on deep veins and valves pushing blood towards heart
Respiratory pump
Helps to get venous blood back to body via negative pressure pulling blood from LE
Venous hypertension
All pathophysiology of venous insufficiency starts here
Causes of venous hypertension
- Vein dysfunction (failure of one-way valves)
- Calf muscle pump failure
- Combination
- All leads to pooling of venous blood in LE
Fibrin cuff theory
Fibrinogen leaked out from capillaries creating barrier to diffusion of oxygen and nutrients
- Fibrinogen -> insoluble layer of fibrin -> fibrosis of capillaries themselves -> no gas exchange or waste elimination
Inflammatory trap theory
WBC adhere to vessel walls, activate inflammatory process -> releasing proteolytic cells -> endothelial damage
Cytokine dysregulation
Trapping of growth factors making them unavailable for repair of damaged tissue -> tissue in chronic inflammatory phase
Varicosity
- Primary venous distention may be caused by inherent weakness within the vein itself
- Dilated veins with increased length and tortuosity
- May be present for years prior to ulceration
- Peripheral edema from CHF, pregnancy, obesity, limited mobility cause secondary venous distention by decreasing VR (venous return?)
Calf muscle pump failure
- Calf weakness, paralysis, OA, or decreased mobility decreases muscle pump
- Occupations requiring prolonged standing without movement are at an increased risk of developing VI and ulcers
Trauma and VI
Minor injury may initiate wound formation (brush against thorn bush, itching dry skin) to already at risk tissue
Previous venous ulcer
- High recurrence rate
- Repeat ulcer happen for same reason first one began
- Less tensile strength and elasticity of scar tissue
- Precipitation factors not addressed
Advancing age and VI
- Decreases inflammatory and immune responses
- Decreased collagen synthesis & tensile strength
- Increase skin atrophy
- Increased number of co-morbidities
Diabetes
- Microvascular disease and impaired immunoreactivity
- Impaired all three phases of wound healing
- Poor glucose control -> hyperglycemia
- Greater the hyperglycemia the greater the adverse affect on wound healing and greater risk of infection
Homan’s sign
- Identification of deep veins thrombosis
- Ankle passively dorsiflexed with knee extended
+ result: pain with test movement, tenderness with deep palpation of gastroc - Not very sensitive or specific
- Positive test can be found with superficial phlebitis or MSK injuries ie. Achilles tendinitis
- If + request further medical assessment especially if they have a history of reduced activity or long periods of sitting
Co-existing arterial and venous insufficiency occurs in … of all LE ulcers
15%, called mixed wounds
- Until proven otherwise, arterial insufficiency should be suspected in all chronic LE ulcerations
ABI <0.7
Contraindication to compression as management of venous wounds
Trendelenburg test
- Identifies vein incompetence
- Pt supine with leg elevated 45 deg x 1min -> severe tourniquet lightly around distal thigh to occlude SUPERFICIAL veins -> pt stands up -> release tourniquet and watch for vein distention up to 1 minute
- If veins fully distend < 5 sec before tourniquet released = incompetence in perforator veins
- Time to venous distention < 10 seconds = superficial vein incompetence
Rubor of dependency test
- Assess foot in sitting -> pt placed in supine with limb elevated to 60 deg x 1 minute or until veins drained by gravity (leg becomes pale = arterial insufficiency) -> place limb in dependent position and record superficial vein refill time
- Refill < 5 seconds =venous insufficiency
- Refill > 20 seconds =arterial insufficiency
- Leg becomes hyperemic (bright red) = arterial insufficiency
1+ edema
Barely perceptible depression
2+ edema
Easily identified depression <15 sec to resolve
3+ edema
Depression takes between 15-30 sec to resolve
4+ edema
Depression lasts > 30 sec
Cardinal signs of venous stasis
- Firm (indurated)
- Brawny edema
- Hemosiderin staining
- Ankle flare
- Atrophie Blanche
- Eczema - dermatitis
- Lipodermatosclerosis 0 fat in dermis that is sclerotic
- Palpable pulses
- Irregular borders
- Shallow
- Weepy, lots of fluid
- Medial malleolus
- Heavily contaminated
- Usually painless - not getting hypoxic pain
Hemosiderin staining
- Seen with chronic venous insufficiency
- From a by-product of the breakdown of RBC’s forced into the interstitium by venous HTN
- RBC contains hemoglobin which breaks down into Hemosiderin
- Skin becomes stained a dark pigment (dark purple/brown) due to hemosiderin/iron deposition
Ankle flare
- Inverted champagne bottle appearance
- Piano leg
- From extensive lipodermatosclerosis - fat pushed into dermis that becomes fibrotic -> firmness pushes fluid into calf
Varicose eczema/dermatitis
- Itchy, erythematous, weeping and scale areas of skin
Contact dermatitis
- Local allergic reaction to preservatives, emulsifiers and/or dressing components are common
- Over 50% venous ulcer pts have allergy to lanolin and some topical antimicrobials
- Erythema and pruritis, increasing discomfort and perpetuating inflammatory process, ends where contact ends
- Higher cotton content in clothes less offending than synthetic fibers
Gold standard of treatment for patients with venous insufficiency ulcers
COMPRESSION
- Enhances calf muscle pump
- Improved venous return
- Decreases peripheral edema
- Reduces venous distention
- Increases tissue oxygenation
- Softens lipodermatosclerosis and fibrosis
- Protects limb from further trauma
- Limits need for bed rest or prolonged elevation
Nonelastic compression
- Resist deformation and thus maintain a fixed volume compartment around leg
- When calf contracts, it meets resistance of bandage and deep veins are compressed forcing blood proximally
- Graduated compression** most compression applied distally and less proximally
Elastic compression
- Elastic bandages not appropriate for management of venous ulcers
- Expands every time calf muscle moving and loses effect of calf muscle pump
- Difficult to get consistent pressure
Contraindication to compression therapy for patients with venous insufficiency
- Arterial insufficiency with ABI <0.7
- Acute infection
- Pulmonary edema
- Uncontrolled or severe congestive heart failure
- Active DVT
- Claustrophobia
Compression stockings
- Graduated compression must exceed venous intralumenal pressure
Class II (30-40 mmHg) mimics compression that would be gotten from multi-layer compression - Regular use reduces edema and ulcer recurrence
- Measure for garments after edema has been reduced as much as possible
- Measure after pt gets OOB or after elevating legs above heart for about 1-2 min
Vasopneumatic compression devices
- Decrease venous HTN
- 60 min 5x/wk
- 90 sec on/30 sec off
- 40 - 45 mmHg
- Rapid inflation better than slow
- Contraindications: DVT, active CHF
Therapeutic exercise
- Ankle pumps when sedentary and throughout the day to increase venous return
- Light aerobic exercise will improve:
- Respiratory pump -> increasing venous return
- Calf muscle pump
- Weight loss
- Control blood sugar
Toe brachial pressure index
Used when calcification occurs at the ankle
- Medical testing method
Vascular duplex ultrasound scanning
- Painless exam using US to image blood movement
- Allows for identification of location of impaired blood flow
- Refer to vascular surgeon when ABI <0.5
- Medical testing method
Sclerotherapy
Foam/liquid solution injected into spider or varicose vein -> collapses veins that are incompetent
- Nonsurgical medical tx for VI
Endovenous thermal ablation
Laser or high-frequency radio waves to heat large veins -> collapses incompetent veins
- Nonsurgical medical treatment for VI
Surgical treatment for VI
- Ligation and stripping (through two small incisions)
- Phlebectomy (microincision) for surface varicose veins
- Subfascial endoscopic perforator surgery - clips placed to block incompetent perforation veins
- Vein bypass - one vein to another one
