Hurie: Lower Extremity Vessel Disorders

Front 1

Leg venous anatomy

Back 1

Deep system
-Contained within muscle and fascia
Superficial system
-Drains into deep system
Perforators
-Branches that connect the systems, penetrating through holes in the fascia

Front 2

Venous drainage

Back 2

Postcapillary blood collects in venules which drain into progressively larger veins.

Superficial system drains into the deep system both by direct connections (saphenofemoral junction, saphenopopliteal junction) and by perforators.

Front 3

Venous valves

Back 3

Allow flow towards larger outflow veins, prevent backward flow towards the capillary bed

Often found at junctions, perforators

Reduce column height blood

Valves only mechanism preventing transmission of entire pressure head to lower extremity venous circulation

Front 4

Muscle pump

Back 4

Calf muscles surround deep veins and the muscles are covered by fascial linings

Muscle contraction increases the compartment pressure and forces blood out of the deep veins. Valves prevent back flow to the superficial system and net result is to propel blood to proximal deep veins

Front 5

Causes of increased hydrostatic pressure

Back 5

Valve failure
-Increased column height increases static pressure
-Allows muscle pump to drive blood from deep veins back into superficial veins

Obstruction
-Distal distention, induced valve failure

Front 6

Effects of high venous pressure

Back 6

Additional valve failure as walls are farther apart and valve leaflets no longer approximate

Capillary bed influence with edema, extravasation of proteins, subsequent inflammation

Over time vein wall and valve undergo structural changes, surrounding tissue change with activation of inflammatory cascades

Front 7

Varicose veins overview

Back 7

Dilated subcutaneous and superficial veins

Genetic component – thought autosomal dominant with variable penetrance

Valve Incompetence at:
-Saphenofemoral junction
-Saphenopopliteal junction
-Perforators

Front 8

Varicose veins: clinical symptoms, treatments

Back 8

Pain, aching sensation, worse as day proceeds, better in the morning

Treatment:
-Compression stockings
-Elevation
-Intervention focuses on elimination of source of reflux, may need to remove varicosities as well

Front 9

Telangiectasias

Back 9

Same process as varicose veins on a smaller scale

Symptoms– cosmetic, sometimes pain at the site

Treatment – exclude larger vein reflux, injection sclerotherapy, laser

Front 10

Skin changes with venous stasis

Back 10

Lipodermatosclerosis
Pigmentation – hemosiderin deposition
Eczema
Ulceration – often at site of perforating vein

Front 11

"Gaiter area"

Back 11

Retrograde flow (reflux) from deep veins to superficial leads to ulceration at the site of perforating veins

Most common area for ulceration and sever skin changes

Front 12

Management of venous stasis ulceration

Back 12

Aggressive Compression (mainstay of treatment)
Elevation
Antibiotics and debridement when infected or necrotic
Skin grafts

Front 13

Deep vein thrombosis overview

Back 13

Major consideration in hospitalized patients
Difficult to diagnosis without imaging
Two main sequelae – local effects on the leg and embolization
Major cause of avoidable morbidity and mortality

Front 14

DVT causes

Back 14

Stasis-
-“pump failure” – immobile patients don’t contract their calf muscles, auto or plane trips
-Valvular dysfunction or venous obstruction
-Pregnancy- pelvic vein compression

Vessel Wall Injury
-Iatrogenic
--Catheters, punctures, indwelling lines
-Traumatic
--Fractures, traction injuries, etc.

Hypercoagulability
-Inherited thrombophilia
--Factor V Leiden/Activated protein C resistance
--Protein C/S deficiency
--Antithrombin III deficiency
--Many others
-Malignancy
-Pregnancy
-Surgery
-Trauma

Other risk factors:
age, surgery, obesity, IBD

Front 15

Surgery and DVT risk

Back 15

Risk varies with type and length of operation
Highest with hip/knee/pelvic procedures (~50-60%)
Intermediate for neurosurgical and oncologic procedures
May be due in part to increased procoagulant activity
Over 50% develop in the OR

Front 16

Malignancy and DVT risk

Back 16

Release tissue factor and cancer procoagulant
Recognized in 5-20% of patients with idiopathic DVT
Up to 10% more will develop CA within 2 years
High incidence of complication (~15%)

Front 17

DVT diagnosis: History and physical

Back 17

History
Warmth/redness
Homan’s sign (calf pain with dorsiflexion of the foot)
In general, the sensitivity and specificity of H&P are poor

Front 18

DVT diagnosis: Laboratory and imaging

Back 18

D-Dimer – elevation associated with clot formation and subsequent degredation
Currently used to supplement probability estimation of DVT coupled with H&P.

Venous Duplex in the vascular lab
-High sensitivity/specificity

Front 19

DVT local consequences

Back 19

Swelling distal to the obstruction
Long term potential for vein dysfunction from chronic obstruction or valve dysfunction

Postphlebitic syndrome in up to 28% of patients after DVT

Front 20

DVT and PE

Back 20

Over 90% Pulmonary emboli thought to originate in the legs
Risk thought lower for calf vein DVT compared to more proximal DVT
Possible to embolize to the arterial system in the setting of patent foramen ovale (i.e. stroke)

Front 21

DVT prevention

Back 21

Mechanical – compression stockings, intermittent compression devices, mobilization
Pharmacologic – low dose anticoagulants
New initiatives tie reimbursement to DVT preventative measures

Front 22

Trauma and DVT risk

Back 22

Very high risk
Increased even more with LE or pelvic fractures, spinal cord injuries, and major venous injuries
Frequently bilateral/ multifocal
-Possibly due to depletion of coagulation inhibitors or upregulation of fibrinopeptides

Front 23

DVT treatment

Back 23

Anticoagulation
-Some controversy over optimal treatment of isolated calf vein DVT, and discussion as to duration of therapy)
Thrombolysis of clot in rare cases
Graduated compression stockings
-Long term therapy to minimize sequelae of post-thrombotic syndrome

Front 24

Phlegmasia cerulea dolens

Back 24

Limb threatening extensive venous thrombosis
Often associated with cancer (20-40% of cases)
Surgical/interventional emergency

Front 25

Normal lymphatic anatomy/physiology

Back 25

Excess interstial fluid enters lymphatic capillaries
Drainage parallels arterial/venous
Drainage dependent on compressive forces
One way valves similar to veins
Over 80 % of lymphatics drain into venous system in chest – predominately the left internal jugular vein
Some lymphatics do have smooth muscle contractions
Variations in intrathoracic and intraabdominal pressures drive the lymphatic fluid as well

Front 26

Lymphedema

Edema

Back 26

Lymphedema = protein-rich interstitial volume overload, secondary to lymph drainage failure in the face of normal capillary filtration
-primary: inherent defect within lymph carrying conduits
-secondary: acquired damage

Edema = increase interstitial fluid volume that is enough to produce clinical, palpable swelling (more generic term)

Front 27

Primary lymphedema

Back 27

Congenital (<1 year)
-Familial type = Milroy’s Disease
--VEGFR-3 mutation

Lymphedema praecox (age 1-35)
-Most common
-Usually unilateral, adolescent women
-Hypoplastic lymphatics

Lymphedema tarda (age >35)
-Congenitally “weakened” lymphatics, event triggers onset

Front 28

Secondary lymphedema

Back 28

Obstruction versus interruption
Developing world>Wuscheria bancrofti (filariasis) – most common worldwide cause
Industrialized world>malignancy and associated treatments

Front 29

Lymphedema signs and symptoms

Back 29

Painless swelling initially dorsum of foot
Eventual proximal involvement
Subcutaneous fibrosis
Skin becomes hyperkeratotic, papillomatous or verucous
Recurrent infections

Front 30

Lymphedema management

Back 30

No cure
Elevation has little effect
Exercise
-Increases muscle pump, increased variations in thoracic pressure inducing lymph flow
Compression garments/devices
Manual lymph drainage
Skin care practices
Surgery in rare cases