Lesson 3: Venous Insufficiency Flashcards
Prevalence of chronic venous insufficiency:
9.4%
70–90% of leg ulcers are due to VI
Who is at risk for VI:
Women have 3x greater risk
Risk of VI ulcer is 7.5x greater after age 65
Recurrence rate of VI:
13–81%
Recurrence correlated with nonadherence
According to research, who is most likely to develop VI?
Patients > 60 years old, with history of blindness, cataracts, renal insufficiency, or a history of pressure ulcers
How much blood does the venous system store?
70-80% of total blood volume
Anatomy of Leg Veins
Deep system
Superficial System
Perforators
Deep Vein Function
Lay beneath the muscle fascia
Responsible for 80- 90% of the venous return
Drain the lower extremity musculature
Typically paired with an artery (femoral, popliteal, tibial)
Superficial Vein Function
Lay above the deep fascia
Drain the cutaneous microcirculation
Great and small saphenous veins lay between the muscle fascia and the saphenous fascia
Reticular veins lay between the saphenous fascia and the dermis
What do superficial veins assist with?
temperature regulation
Carry about 10% of the venous return
Perforators Vein Function
Penetrate the deep fascia
Connect the Superficial and deep systems
An average of 64 perforators between the ankle and the groin
1 to 3 valves to direct flow from superficial to deep
What does the intimal layer excrete?
antithrombogenics
What does the medial layer contain?
3 thin layers of smooth muscle adrenergically innervated muscle weaker than that in arteries
Adventitial layer-
thick outer wall rendering veins stiffer than arteries aiding in calf pump
Proximal flow of venous blood relies on
Respiratory pump
Calf muscle pump
Valves
Calf Pump
Most efficient of the venous pumps (foot, calf, and thigh)
What does calf pump use?
crural fascia and extensive valves to generate 65% ejection fraction.
Pressure in venous system:
As blood is pushed from deep veins, venous pressure decreases allowing veins to refill from the superficial system through the perforators
Vein Bicuspid Valves
Formed from folds of vein endothelium
More numerous distally, lessen toward the hip
Insure flow from superficial to deep and from caudal to cephalad
Close when pressure gradient is reversed, <0.5 second reflux/delay is normal
Common causes of venous insufficiency
Vein dysfunction
Calf muscle pump failure
Ulceration Pathophysiology
Venous hypertension causes leakage into interstitial space of fluid and white blood cells
Edema and blood products cause inflammation
Inflammation leads to skin failure
Risk factors contributing to VI ulcers
Vein dysfunction Calf muscle pump failure Trauma Previous VI ulcer Advanced Age Diabetes
Vein Dysfunction
Venous hypertension Valve damage Degeneration Scarring Inflammation Clot sequelae Varicosity
Calf muscle pump function:
Calf weakness/paralysis
Decreased dorsiflexion
Prolonged standing
Incompetent valves
Trauma
Benign trauma to venous-insufficient leg may result in ulceration due to edema-induced local tissue hypoxia
Previous VI Ulcer:
Recurrence rate as high as 81%
Local tissue hypoxia and malnutrition
Scar tissue from prior ulcer increases risk of skin breakdown
Precipitating factors/wound etiology not successfully addressed
Advanced Age:
Anatomical and functional changes that occur
with aging
Valve degeneration
Diabetes:
Increased microvascular disease
Impaired immune response
Impairs all 3 phases of wound healing
PT Tests and Measures for VI
Clinical Assessment for DVT
Ankle-Brachial Index
Trendelenburg Test
Venous Filling Time
What is the gold standard for DVT:
venogram
Trendelenburg Test
Supine, leg in 45° elevation for 1 minute
Note venous distension
Tourniquet to distal thigh
Stand upright
Note time for superficial venous distention
Release tourniquet
Trendelenburg Test indications:
To differentiate deep or perforating vein incompetence from superficial vein incompetence
Brodie-Trendelenburg Test
Differentiates between perforator and GSV incompetence
Legs elevated to 45 degrees and tourniquet placed at groin
Patient stands and tourniquet is removed
Vein re-filling determines level of incompetence
Tendelenburg test time to venous distention greater than 20 seconds, tourniquet on:
deep or perforator vein incompentence
Tendelenburg test time to venous distention greater than 10 seconds, tourniquet off
superificial vein incompetence
Perthes Test
Tourniquet placed below knee and 10 heel raises performed
If varicose veins empty, site of reflux is cranial to the tourniquet in the SFJ, SPJ, or thigh perforators
If varicose veins remain distended, site of reflux caudal to the tourniquet in calf perforators
Pain with heel raising indicates possible of deep venous obstruction
Indications of venous filling time:
Unable to tolerate ABI
ABI > 1.1
History of diabetes or vessel calcification
Suspected concomitant arterial insufficiency
Venous Filling Time
Predictor for arterial insufficiency
Patient supine, note superficial veins on dorsal foot
Elevate the limb 60° for 1 minute or until veins are drained by gravity
Lower limb to dependent position, note time for veins to refill
Doppler Ultrasound
Gold standard for venous system More subjective than arterial Doppler Resting test Augmentation test Reflux test
Indications for Doppler Ultrasound:
Gold standard for venous system More subjective than arterial Doppler Resting test Augmentation test Reflux test
CO
asymptomatic
CI
telangiactasias or spider veins <3mm
C2
varicose veins>/= 3mm
C3
leg edema
C4
skin and subcutaneou tissue change
C4A:
hemosideran deposition
C4B:
lipodermatosclerosis
C5
healed venous ulcer
C6
current venous ulcer
Telangiectasis and Reticular Veins
Treated for cosmesis
Indicate early stages of chronic venous insufficiency
Dilation of surface veins causes vein prominence
Telangiectaisis/spider veins-
0.5 to 1 mm diameter
Reticular veins-
bluish discoloration- 1-3 mm diameter
Varicosities
Present in 10-15% of men and 20-25% women in Western population
Dilated >4mm in diameter
Mainly occur in great and short saphenous veins
Hemosiderin Staining
Venous dilatation allows passage of red blood cells through the endothelium into the interstitium
Breakdown converts hemoglobin to hemosiderin
Brown pigment stain usually occurs on the lower medial third of the leg
Darkens over time
Lipodermatosclerosis
Inflammation of the layer of fat under the skin
Lipodermatosclerosis results in:
Pain Hardening of skin Redness Swelling Tapering of the legs above the ankles (champagne bottle deformity)
VI etiology:
Impaired venous return > increased hydrostatic pressure> Stasis hypertension > dermal ulceration
Venous signs:
Eschar or slough, wet, yellow fibrous
Moderate to heavy exudate
Tortuous veins
Edematous leg
Wound edges in VI:
Shallow wounds
Irregular wound edges
Location of VI insufficiency:
Superior to Malleoli, usually medial
Surrounding skin dry and scaly
Pulses with VI:
present
Pain with VI ulcers:
Pain in dependent position, decreased with elevation, usually minimal dull ache or heaviness
What is pain in VI ulcers caused by?
Caused by valvular incompetence, obstruction of deep venous system, or congenital absence or malformation of venous valves
Foot warm, ABI >.8
Periwound and Structural Changes
Venous ulcer:
Edema
Cellulitis, dermatitis
Hemosideran deposition
Lipodermatosclerosis
Temperature in VI:
normal to mild warth
Healing time for full-thickness venous ulcers with appropriate interventions
Average eight weeks
Smaller ulcers 5–7 weeks
Larger ulcers 10–16 weeks
VI ulcers with good healing:
Small size Decrease in size in first 2–3 wks of treatment No deep vein involvement Adherence with compression
VI ulcers with poor healing:
Large size Increase in size over 4 wks of treatment Concomitant PAD Older age, higher BMI
Not Predictive of CVI Healing
Gender
Race
Skin condition
Presence of infection
Patient/Client-Related Instruction
Educate about etiology
Explain link between disease process and interventions for wound healing
Inform of risk factors for re-ulceration
Identify patient and caregivers’ beliefs about treatment to maximize adherence and outcomes
Provide guidelines
Control swelling Protect your feet and legs Live healthy Know when to call clinician Inform patients of proper positioning and exercises to enhance venous return
Request for Further Medical Testing
Patients scoring 3 or more on DVT clinical prediction guidelines
Wounds that fail to progress
Wound culture and sensitivity if suspect infection
Bone scan/X-rays if exposed capsule or bone
Wounds that do not present with typical VI ulcer characteristics
Keys to Local Wound Care
Protect surrounding skin
Address wound bed
Enhance venous return
Educate patient/caregiver
Protect Surrounding Skin
Moisturize dry, scaling skin
Use topical steroids to decrease inflammation or weeping
Use topical agents prudently to avoid sensitization
Intervention Goals
Non adherent dressings to protect delicate skin
Gentle debridement- enzymatic or autolytic due to severe tenderness
Compression to promote venous return- 4-layer wraps, short stretch wraps, compression stockings
Elevation
Exercise to promote venous return
Effects of Compression
enhances calf muscle pump improves venous return decreases peripheral edema reduces venous distention increases tissue oxygenation softens lipdodermtosclerosis protects limb from trauma limits need for prolonged elevation/bed rest
Compression Parameters
30–40 mm Hg at ankle
10 mm Hg at infrapatellar notch
If severe VI, can increase to 40–50 mm Hg
If mild AI, can decrease to 20–30 mm Hg
Contraindications to Compression
ABI < 0.7 Acute infection Pulmonary edema Uncontrolled or severe congestive heart failure Active DVT Claustrophobia (relative)
Therapeutic Exercise
Range of motion exercise
Aerobic exercise
Gait and mobility training
Focus on Calf pump!!!!
Stripping and Ligation of the Great Saphenous Vein
A Saphenectomy strips the vein from the SFJ to the popliteal fossa
Stripping into the calf can be complicated by Saphenous nerve injury
Skeletonization or ligating and disconnection of each saphenous tributary in the groin contributes
Varicose Vein Ligation
In the 70’s-80’s segmental ligation of visible varicosities utilizing multiple incisions was performed but missed affected veins not visible
Research shows venous insufficiency must be addressed at its point of highest reflux
Microphlebectomy
May be performed alone or in combination with other vein procedures
Hooks are used to pick up the vein and bring it through the incision where it is transected
Used to remove visible varicose saphenous tributaries or clusters are associated with incompetent perforating veins
Endovenous Vein Obliteration
Radiofrequency (RF) or laser thermal energy used to destroy the vein endovascularly
Mostly used to treat great and small saphenous veins
Preoperative vein mapping with duplex ultrasound to determine location to be treated
Need to perform at least 2 cm distal from the SFJ to prevent femoral vein DVT
Sclerotherapy
Non-surgical option for ablation
Injection of a special chemical (sclerosant) damages and scars the inside lining of the vein causing the vein to close.
May cause staining visible through the skin
Liton’s Procedure
1950s technique
Surgical ligation of subfascial perforators through three long calf incisions
Abandoned because of wound complications
Later modified using smaller incisions and skin grafts but complications still common
Phlebotome Device
Introduced through a small incision just below the knee and is advanced subfascially toward the medial malleolus
Disrupts the perforators blindly as it is advanced
SEPS
Subfascial Endoscopic Perforator Surgery
Instruments are introduced into the subfascial space through two small incisions
Each perforator is identified and clipped
Often combined with saphenous vein ablation
Valvuloplasty
most frequent procedure used for primary deep reflux
Good result in 70% of cases in freedom of ulcer recurrence and the reduction of pain, valve competence and hemodynamic improvement 5 years post
External transmural valvuloplasty not as reliable as internal valvuloplasty in providing long-term valve competence or ulcer free-survival
