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Medicine 1 > Venous Disease > Flashcards

Venous Disease Flashcards

1
Q

Prevalence of venous disease

A
  • Estimated 25 million people in the United States are affected by venous insufficiency
  • Estimates suggest prevalence is 5 times more than arterial insufficiency
  • VLU’s comprise 80-90% of all ulcers
  • Estimated 1.5 million new cases per year
  • Newer data suggests up to 50% of the population to varying degrees with venous disease (telangectasias, varicose veins, chronic venous insufficiency)
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2
Q

Prevalence and etiology of venouse insufficiency

A
  • Of the estimated 25 million people with symptomatic superficial venous reflux1 :
    • Only 1.7 million seek treatment annually2
    • Over 23 million go untreated
  • Statistics show that of the 25 million people in the U.S. who suffer from symptomatic reflux, less than 10% seek treatment annually2
  • When left untreated, venous reflux can lead to significant clinical issues, like pain, swelling, varicose veins, skin changes, and ulcers
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3
Q

Risk factors

A
  • Prior ulcers – if you’ve already had one, the likelihood of having another is very high
  • DVT’s
  • Smoking
  • Trauma/prior venous thrombosis
  • Oral contraceptives/estrogen replacement
  • Prolonged standing/sedentary lifestyle – more pressure from gravity and standing = more pressure on veins
  • Genetics
  • Pregnancy – have much more pressure in lower extremities
  • Obesity
  • Advancing age
  • Ligamentous laxity (flat feet, hernias)
  • Prior DVT/trauma associated with only less than 1/3 of severe chronic venous disease-5. Some studies show strong familial component-5. Others have shown strong correlation with obesity-7, multiple pregnancies-6
  • age 5
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4
Q

Vein abnormalities

A
  • Reticular veins (spider veins) and telangiectasias
    • Subdermal and intradermal
    • Up to 50% of population W>M
  • Varicose veins
    • 3mm or greater in diameter
    • Up to 30% of population
  • Chronic venous insufficiency
    • Edema and ulceration
    • Up to 7 million affected
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5
Q

CEAP classification - chronic venous disease

A
  • Clinical
    • 0 no signs of disease
    • 1 telangiectasias or reticular veins
    • 2 varicose veins
    • 3 edema
    • 4 pigmentation or eczema
    • 5 healed venous ulcer
    • 6 active venous ulcer
  • Etiology
    • c congenital (eg, Klippel Trenaunay syndrome)
    • p primary (valve degeneration)
    • s secondary (post-thrombotic/trauma
  • Anatomy
    • s superficial veins
    • p perforator veins
    • d deep veins
  • Pathophysiology
    • r reflux
    • o obstruction
    • r, o reflux and obstruction
  • CEAP
    • C2EcAsPr
    • Varicose veins
    • Congenital
    • Superficial veins
    • reflux
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6
Q

Anatomy of veins

A
  • Superficial veins are superficial to the deep muscular fascia
  • Deep veins are deep to the muscular fascia and are either within the muscle or between them.
  • The perforating veins communicate between the superficial and the deep venous systems
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7
Q

Superfician venous system - lower extremity

A
  • GSV great saphenous vein and small saphenous vein
  • GSV sometimes is duplicated in the thigh or calf
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8
Q

deep veins of lower extremity

A
  • Posterior tibial
  • Peroneal
  • Anterior tibial
  • Popliteal vein becomes the femoral vein in the adductor canal
  • Profunda femoris vein drains lateral thigh muscles and joins with the femoral vein to become the common femoral vein in the groin
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9
Q

Perforating veins

A
  • They connect the superficial with the deep veins (direct perforators)
  • Or superficial with the venous sinuses (indirect perforators)
  • Venous sinuses are thin-walled and valveless
  • Located in the calf musculature
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10
Q

normal physiology

A
  • Normal standing pressures are 90-100mmHg
  • Calf pump reduces venous pressures by over 70% within 10 steps
  • Recovery refill after exercises is about 20-70s
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11
Q

Calf-muscle pump

A
  • Contraction produces upwards of 200mmHg pressure which propels the blood towards the heart
  • Normal displacement >60% of venous blood within the leg to the popliteal vein with each contraction
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12
Q

venous disease and ulcer development

A
  • Venous hypertension caused either by reflux or obstruction
  • Prolonged hypertension=“leaky capillaries”
    • RBC’s and macromolecules leak, causing inflammatory response into interstitial space
    • Matrix metalloproteinases (MMP’s) and cytokines released which cause tissue fibrosis which impair healing
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13
Q

venous valves reflux

A
  • Bicuspid, one way flow towards the heart
  • present in both the superficial and deep veins
  • Greater number of valves in the lower extremity below the knee
  • Decreasing in number until the inguinal ligament
  • common iliac, vena cava, and portal venous system do not have valves
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14
Q

superficieal and deep venous insufficiency

A
  • Patients with superficial venous insufficiency may only be able to reduce pressure by 30-40%
  • Deep venous insufficiency reduction <20% with very fast calf refill
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15
Q

deep venous obstruction

A
  • Pressures may not decrease and may actually increase
  • This can lead to ambulatory venous hypertension and venous claudication
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16
Q

Diagnosing venous disease - patient history

A
  • Typical symptoms
    • Heaviness, fatigue, pain, itching
    • Chronic iliofemoral obstruction can result in venous claudication—thigh pain and feeling of tightness with exercise
    • Leg symptoms are more common in chronic obstruction than in those who have recanalized and have incompetent valves
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17
Q

clinical presentation of venous disease

A
  • The obvious bulges may or may not be present
  • Symptoms may not correlate well with the amount of defect
  • Abrasions can lead to impressive bleeding
  • Superficial thrombophlebitis relatively common. Can be quite painful. Rarely leads to PE
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18
Q

signs of venous insufficiency

A
  • Edema
  • Lipodermatosclerosis
  • Hyperpigmentation (hemosiderin staining)
  • Absence of hair (also seen in PVD)
  • Thickened nails
  • Varicosities
  • Blistering/bullae
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19
Q

Manifestations of venous insufficiency

A
  • Superficial venous reflux is progressive and if left untreated, may worsen over time
  • Although often underestimated as a cosmetic problem, venous insufficiency can produce significant clinical problems for the patient
  • An estimated 25 million people in the United States have varicose veins, 2 to 6 million have more advanced forms of chronic venous insufficiency (swelling, skin changes), and nearly 500,000 have painful venous ulcers8
  • Overall, as the severity of the disease progresses, quality of life may decrease
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20
Q

Lipodermatosclerosis

A
  • Hypoxia of subcutaneous fat lobules lead to inflammatory response
  • Hard “woody” induration à their skin is really hard
  • Starts at ankles and progresses proximally
  • Inverted champagne bottle or bowling pin appearance
  • Avoid biopsy—poor healing
  • Stanozol-anabolic steroid with fibrinolytic properties helps with pain, inflammation and pigmentation
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21
Q

Hemosiderin staining

A
  • Valves fail->regurgitated blood (and venous hypertension) force RBC’s to leak from capillaries
  • RBC’s degrade and release iron which is stored in the skin tissues as hemosiderin
  • Often irreversible and can be confused as cellulitis
  • Hemosiderin does not extend, no calor (not hot), and doesn’t respond to antibiotics
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22
Q

Identifying VLUs

A
  • Well defined borders surrounded by erythematous or hyperpigmented indurated skin (yellow-white exudate is common)
  • Located on lower 1/3 of leg above the ankle “gaiter distribution” most commonly at medial malleolus
  • Never found above the knee and rarely on the foot
  • Varicose veins and ankle edema are common
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23
Q

Physical exam

A
  • Check pedal pulses
  • Get an ABI (ankle brachial index) (<0.70 consult vascular)
  • Rule out other causes
    • Untreated CHF
    • Lymphedema
    • Arterial disease
    • Cellulitis
    • DVT
    • Squamous cell carcinoma – a lot of people do have skin cancers and they will often present on lower extremities
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24
Q

Ultrasound and other tests

A
  • CT and MR Venography -invasive, expensive. Useful for evaluating central veins which are hard to assess w/US. Anatomic abnormalities, no use in physiologic evaluation. Usually reserved for those needing reconstruction
  • Duplex ultrasound –non-invasive, inexpensive and very reliable. confirms reflux > 0.5s
  • Who needs? Those who you are considering surgical intervention, atypical cases (age <40), questionable disease
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25
Q

Normal ultrasound?

A
  • Differential diagnosis
    • Lymphedema
    • Rheumatoid ulcer
    • Arterial disease
    • Sickle Cell ulcer
    • Marjolin’s ulcer
      • Squamous cell carcinoma
  • Biopsy if you need to, refer if you need to
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26
Q

Treatment

A
  • Compression to reduce venous hypertension-mainstay therapy
  • Elevate
  • Walk! Improve the pump
  • Lose weight
  • Avoid prolonged standing or sitting
  • Maintain skin integrity
  • Consider adding 40mg Simvastatin-Grade B
27
Q

Treatment - if there is an ulcer

A
  • Control exudate
  • Debride/eliminate bacterial burden
  • VNUS (RF ablation) may be an option
  • Consider pentoxifylline (400mg TID up to 6 months) to improve ulcer healing rates (this is an unlicensed indication—Grade A evidence
  • Prevent recurrence
28
Q

To culture or not to culture

A
  • Culturing wound is not indicated unless infection is suspected
  • Iodosorb, Silvadene and medi-honey have not been proven to be effective
  • Hyperbaric treatment has not been shown to be effective
  • Pneumatic compression, electromagnetic therapy also not helpful
  • Washing with soap and water is encouraged
29
Q

Compression therapy contraindications

A
  • Contraindications
    • Arterial disease
      • Check pedal pulses/obtain ABI
    • CHF
      • Treat before compression
    • Neuropathy
      • Consider alternate treatments (Circaids)
    • Active cellulitis
      • Treat first
30
Q

Expected outcomes

A
  • Ulcers that heal by more than 40% at 4 weeks have high incidence of closure at 12 weeks
  • Those that don’t respond well in 4 weeks are unlikely to heal with another 8 weeks of compression—time to rethink or refer!
  • 60%-70% of ulcers closed after 3-6 months of treatment
  • Recurrence rate of 25% within 1 year
31
Q

Expected outcomes

A
  • Reassure your patients that venous ulcerations are neither life or limb threatening
    • Unlike arterial, there is not a lack of blood flow
    • Caution if infected/sepsis
32
Q

Not responding to compression?

A
  • Alternative etiologies
  • Issue__Treatment
  • arterial insufficiency doppler/ABI
  • vasculitis wound biopsy
  • Marjolin’s ulcer wound biopsy
  • Enough compression? Compliance?
33
Q

Types of compression

A
  • Compression stocking
  • Multilayer (Profore)
  • Unna’s boot
  • Circaids
  • ACE wraps should NEVER be used for compression!
34
Q

Compression stockings

A
  • Hard to put on especially for elderly and mobility impaired. Thus reduced compliance
  • Butler, gloves available to help with donning
35
Q

How to measure for compression stockings

A
  • Thickest part of calf, or thigh if ordering thigh-high stockings
  • Ankle
  • From popliteal fossa of the knee to floor
  • 20-30mmHg compression just as effective and have increased compliance
36
Q

Compression stockings do’s and don’ts

A
  • Donning
  • Hand washing/gentle wash
  • Line dry
  • Replace every 3-6 months
37
Q

Profore (multilayer)

A
  • WCL (wound contact layer)
  • 1st layer cotton wrap for comfort (may substitute kerlix) à she usually just uses a kurlex
  • 2nd layer conformable bandage
  • 3rd layer light compression bandage
  • 4th layer flexible cohesive bandage (coban)
  • Graduated compression
  • Weekly dressing changes unless exudate dictates more frequent changes
38
Q

Unna’s boot

A
  • Dermatologist Paul Gerson Unna
  • Short stretch your patient must be mobile
  • With or without calamine/zinc oxide
  • Spiral wrap, must start at base of toes and work proximally to tibial tuberosity
  • No wrinkles, no tension
  • Cover with coban dressing, 50% tension
  • Cover with stockinette if possible
39
Q

Circaids

A
  • Circaids - what are they? – DO NOT USE ACE WRAP FOR COMPRESSION THERAPY!!! Great for sprained ankle, NOT FOR VENOUS INSUFFICIENCY
    • Inelastic compression garments which have a velcro strapping system to provide compression
    • Use once your VLU is healed for continued compression
    • There are several different types
      • Several different pieces
    • Can be used for lower leg, upper and lower leg, foot, arms and hands
    • Option which may be best for those who cannot reach feet
    • Neuropathic patients
    • Lymphedema
40
Q

How to measure for circaids

A
  • Standard legging Circaids
    • Popliteal fossa to floor (length: short/long)
    • Widest part of calf
    • Ankle around malleoli
    • Arch of foot
    • Patients MUST be instructed on donning appropriately after receiving them
    • You can become a Circaid certified fitter
41
Q

care for circaids

A
  • Most can be machine washed (in garment bag) on gentle cycle and either drip dried or machine dried on low setting
  • Usage varies 6m-18m depending on type
42
Q

Once edema has been treated and wound has healed

A
  • Long term compression to reduce ulcer recurrence
  • Compression stockings
    • 20-30mmHg equally effective as 30-40mmHg
  • Circaids
  • Venous ablation
    • >50% are candidates for surgical/endovascular correction
43
Q

Additional treatment options

A
  • Consider radiofrequency venous ablation
    • Covered by most insurances w/dx of reflux
  • Laser ablation
  • RFA “Venefit” (formerly known as “VNUS”)
    • Similar efficacy ~ 93% closure at 3 years
  • Vascular surgery or plastics referral
    • Order duplex ultrasound to be completed prior to appointment—looking specifically for saphenous femoral junction reflux, check to ensure no deep system thrombosis
44
Q

Differences between RFA and laser

A
  • RFA uses radiofrequency at 20 second intervals which destroys the collagen within the wall of the vein. This causes collapse and shrinkage of the vein thus occlusion
  • Laser uses heat at variable frequencies also targeted at the vein wall. Can puncture the wall. Causes clot formation within the vessel
45
Q

Radiofrequency Ablation Therapy (RFA)

A
  • The RFA procedure is a minimally invasive treatment alternative for patients with symptomatic superficial venous reflux and varicose veins
  • Using a catheter-based approach, the RFA generator delivers radiofrequency (RF) energy to the venous ablation catheter
  • The catheter heats the vein wall and contracts the vein wall collagen, thereby occluding the vein8
  • Collagen Contraction
    • The application of heat to human tendon tissue causes collagen tissue to be shortened (Vangsness CT Jr, Et al: “Collagen Shortening: An Experimental Approach with Heat,” Clin Orthop Relat Res. 1997 Apr (337):267-71)
  • Effects of controlled heating of the vein wall
    • Thermal energy is transferred from the ClosureFAST™ catheter’s heating element to the vein wall through conduction. Heating of the vein wall tissue causes endothelial destruction and collagen contraction that result in vein occlusion. Thermal energy causes collagen to undergo the following changes:
      • Heat sensitive bonds break at 60ºC
      • Crystalline extended structure begins to uncoil, causing the collagen fibrils to shorten and thicken. As the molecule contracts, its diameter increases, causing a reduction in vein lumen diameter
  • Histological Effects of RF heating
    • Controlled thermal injury to the vessel wall causes the following changes in the histology of the vessel resulting in vein contraction.
    • When the vein wall is exposed to sufficient thermal energy it causes: endothelial denudation, collagen denaturation, smooth muscle necrosis, vein wall shrinkage and thickening, and vessel lumen reduction.
    • Following these immediate effects, the treated vessel undergoes an inflammatory response, fibroblast infiltration, new collagen deposition, and eventual fibrosis.
  • The procedure can be performed under general and/or local anesthesia
  • Using ultrasound, the ClosureFAST catheter is positioned into the diseased vein through a small opening in the skin
  • The catheter powered by radiofrequency (RF) energy delivers heat to the vein wall.
  • As the thermal energy is delivered, the vein wall shrinks and the vein is sealed closed.
  • Once the diseased vein is closed, blood is re-routed to other healthy veins.
46
Q

Recovery trial

A
  • Radiofrequency Endovenous Ablation versus 980nm Laser Ablation for the Treatment of Great Saphenous Reflux
    • A comparison of the patient experience between those treated with the RFA Catheter vs. 980nm Endovenous Laser
      • Six center, single-blinded randomized trial
      • 69 patients; 87 limbs treated (46 CLF; 41 EVL)
      • Patient follow up at 2, 7, 14, and 30 days after treatment
    • From March 23, 2007 to December 14, 2007 a six-center single-blinded randomized trial was conducted evaluating the patient recovery experience of patients treated with the VNUS ClosureFAST™ RF Catheter and the 980nm endovenous laser.
    • The study was sponsored by VNUS Medical Technologies.
    • The data presented here has been independently reviewed for completeness and accuracy. Data is on file.
  • RECOVERY Trial: Conclusion
    • Compared to 980 nm laser ablation, at 14 days, treatment with RFA Ablation produced significantly:
      • Less pain p < 0.0001
      • Less bruising p < 0.0001
      • Less tenderness p = 0.005
      • Greater improvement in VCSS scores p = 0.0035
      • Better quality of life p = 0.045
47
Q

surgical treatment options

A
  • Sclerotherapy
    • in office 3% hypertonic solution
  • Vein stripping
    • saphenous vein greater potential of nerve injury if stripping down to ankle
  • Stab phlebectomies
    • Often used in conjunction with stripping and RFA
48
Q

Obstructive causes of venous disease

A
  • Phlebitis
    • Inflammation of the vein
  • Thrombosis
    • Indicates presence of a clot
  • Thrombophlebitis
    • Term used to describe venous inflammation even when it is unclear whether thrombosis of the vein has occurred.
49
Q

Obstruction

A
  • Post thrombotic/trauma
  • May-Thurner syndrome
    • Compression of L CIV by the R CIA
    • Often asymptomatic, as many as 20% of population affected, but only a small fraction have symptoms of edema, leg asymmetry or thrombosis
    • Treat with angioplasty/stent
50
Q

Epidemiology - phlebitis

A
  • Lower extremity superficial phlebitis is rather common.
  • Estimated that 3-11% of population affected
  • More common in varicose veins
  • Patients w/o varicose veins also affected 5-10%
  • The estimated annual incidence of venous thromboembolism (defined as both DVT and PE) is 117 cases per 100,000 persons. The incidence rises markedly in persons 60 years and older and may be as high as 900 cases per 100,000 by the age of 85 years10
  • Estimated 3,000 deaths per year, only 7% detected and treated.
51
Q

Risk factors for thrombosis

A
  • Virchow’s triad
    • Stasis
    • Hypercoaguable state
    • Vein injury
  • Surgery
  • Malignancy
  • Estrogen
  • And many others….
52
Q

Phlebitis

A
  • Signs and symptoms
  • Pain, warmth, redness, may feel a cord
    • Feels like a piece of cord that you can follow up the arm
    • Can resemble cellulitis, lymphangitis
    • Confirm w/US and or D-Dimer
      • Low clinical suspicion and normal D-Dimer has negative predictive value of greater than 99% so US not warranted
53
Q

treatment of phlebitis

A
  • Mostly supportive as superficial phlebitis is not life threatening and will resolve on it’s own in a few weeks.
  • Schedule a follow up appointment in 7-10 days to reassess your patient
  • Warm or cool compress
  • Anti-inflammatories
  • Compression
  • elevation
  • Topical diclofenac may be helpful for pain. Piroxicam and topical heparin have not been shown to be effective in pain relief of resolution of symptoms.
54
Q

Thrombosis

A
  • Clot formation following inflammation
  • Deep vs superficial
  • Signs and symptoms similar to phlebitis
  • Homan’s sign 56% sensitivity 39% specific
  • Get an ultrasound to determine location and extent (highly sensitive 90-100% in fem-pop, less so in calf 60-90%)
  • Get a D dimer
55
Q

Treatment of superficial thrombosis

A
  • Mainly supportive
  • However, those at higher risk for DVT, and those whose thrombosis is >5cm or <5cm from the deep system should be considered for anticoagulation therapy (warfarin) for at least 4 weeks.
  • High risk of recurrence, consider surgical intervention
56
Q

Deep vein thrombosis

A
  • History-Virchow’s triad
  • Exam-not very specific
  • Labs/testing-US/D-dimer
  • Well’s score
  • Treatment and for how long
  • Phlegmasia alba dolens
  • Phlegmasia cerulea dolens
  • Massive leg swelling
  • alba-white discoloration
  • Cerulea-blue discoloration
  • Surgical thrombectomy is indicated
  • Postphlebitic syndrome is found in all patients 1-2 years after a DVT. Leg discomfort and edema
  • 80% of those patients who have had a DVT will develop venous insufficiency signs after 5-10 years.
57
Q

Anticoagulation

A
  • Involves the collateral veins
  • Increased congestion
  • Affects arterial flow
  • Risk of gangrene
  • Goal is to prevent the propagation of thrombus or embolism to the pulmonary circulation. It does not dissolve the present clot but allows the fibrinolytic system to eliminate it over time
  • There are many thoughts about this…
  • If you patient has a distal DVT (in the lower leg) and is stable, no renal issues, low risk of bleeding and able to safely administer LMWH at home..
  • Start with 5mg warfarin PO QD, and LMWH injections BID until INR 2-3
58
Q

Phlegmasia alba dolens

A
  • Spares the collateral veins
  • Less venous congestion
  • No ischemia
  • Higher incidence in 3rd trimester and post-partum
59
Q
A
60
Q

ADMIT

A
  • Iliofemoral DVT
  • PE (of course!)
  • Co-morbidities warrant it
  • High risk of bleeding (anticoagulation contraindicated)
61
Q

Absolute contraindications to anticoagulation

A
  • Active bleeding
  • Severe bleeding diathesis
  • Platelet count <50,000/microL
  • Recent, planned, or emergent surgery/procedure
  • Major trauma
  • History of intracranial hemorrhage
  • History of heparin-induced thrombocytopenia
62
Q

Relative contraindications to anticoagulation

A
  • Recurrent bleeding from multiple gastrointestinal telangiectasias
  • Intracranial or spinal tumors
  • Platelet count <150,000/microL
  • Large abdominal aortic aneurysm with concurrent severe hypertension
  • Stable aortic dissection
63
Q

Anticoagulation therapy duration

A
  • Minimal 3 months if first DVT and unprovoked-this can and often is extended
  • If 1st DVT by provoked reversible event (ie surgery) or patient at high risk for bleeding then 3 month treatment is usually NOT extended
  • Recurrent 6-12 months
  • High risk for recurrent DVT indefinite

Medicine 1 (8 decks)

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