Venous dysfunction Notes

NOTES NOTES VENOUS DYSFUNCTION GENERALLY, WHAT IS IT? PATHOLOGY & CAUSES ▪ Venous system defects affecting blood flow from lower extremities ▪ Localized hyperpigmentation/skin discoloration ▪ Hard, cord-like veins/prominent dilated tortuous veins DIAGNOSIS CAUSES ▪ Blood clot partially/completely blocking way/venous valves failing to pump blood against gravity Virchow’s triad ▪ Hypercoagulability, increased clot formation ▫ Factor V Leiden thrombophilia ▫ Protein C and protein C deficiencies ▪ Venous stasis from prolonged immobilization (e.g. bed rest) ▪ Damage to endothelial lining RISK FACTORS ▪ Prolonged immobility, hereditary clotting dysfunctions, high estrogen levels, obesity ▪ One venous dysfunction can lead to another MNEMONIC: PHD Virchow's Triad Prolonged immobilization (stasis) Hypercoagulability Damage to endothelium SIGNS & SYMPTOMS ▪ Localized pain, usually lower extremities ▪ Edema ▪ Pruritus 176 OSMOSIS.ORG DIAGNOSTIC IMAGING Doppler ultrasound ▪ Assess vein diameter, thrombi, valve status, blood flow (anterograde vs. retrograde) Venography ▪ X-ray, contrast medium injected into vein ▪ Assess status of vein network, detect thrombi LAB RESULTS ▪ D-Dimer: High sensitivity (~100%) and negative predictive value (~100%) for detection of venous thromboembolism TREATMENT MEDICATIONS ▪ Acute manifestation: unfractionated heparin/low-molecular-weight heparins ▪ Long-term management: oral anticoagulants (e.g. warfarin) ▪ Prior DVT ▫ Long term anticoagulation therapy, antiplatelet treatment, parenteral anticoagulants SURGERY ▪ Vein transplant/repair/removal

Chapter 26 Venous Dysfunction OTHER INTERVENTIONS ▪ Preventative: calf exercises, compression stockings/devices, raise affected areas to decrease swelling CHRONIC VENOUS INSUFFICIENCY (CVI) osms.it/chronic-venous-insufficiency PATHOLOGY & CAUSES ▪ Veins cannot push blood back to heart, resulting in blood pooling in leg CAUSES ▪ Develops from varicosities, DVT, phlebitis ▫ Varicose veins affect superficial veins, but blood sometimes rerouted to collateral veins deep in leg, preventing blood stagnation ▪ When deep veins carry more blood than normal ▫ Deep veins stretch over time, blood pools ▫ Blood flow stagnation in lower extremities causes inflammatory reaction in vessels, tissue, causing fibrosis, venous stasis ulcers RISK FACTORS ▪ Biological females, inactive standing/sitting for long periods, aging, family history, ligamentous laxity, obesity, smoking, lowextremity trauma, prior venous thrombosis, arteriovenous shunt, pregnancy SIGNS & SYMPTOMS ▪ Calf/ankle pain (most common symptom) ▪ Worse with prolonged standing/sitting, improves with leg elevation, movement ▪ Brown hyperpigmentation of skin (hemosiderin deposits) ▪ Pruritus, stasis dermatitis ▪ Painless, wet ulcers, particularly on medial malleolus ▪ Edema ▪ Atrophie blanche: hypopigmented atrophic areas with telangiectasia (clusters of red/ purple capillaries), red dots DIAGNOSIS DIAGNOSTIC IMAGING Doppler ultrasound imaging ▪ Most common diagnostic ▪ Modified vein diameter (increased = acute thrombus, decreased = chronic thrombus) ▪ Absent color flow: vein completely occluded ▪ Increased flow in surrounding superficial veins Venography ▪ Most effective, but invasive and costprohibitive TREATMENT SURGERY ▪ Vein transplant/repair/removal OTHER INTERVENTIONS ▪ Preventative: calf exercises, compression stockings/devices, raise affected areas to decrease swelling OSMOSIS.ORG 177

Figure 26.1 The clinical appearance of mild CVI. Hemosiderin deposition is clearly visible. Figure 26.2 Illustration of varicose veins that have developed into a case of CVI. 178 OSMOSIS.ORG

Chapter 26 Venous Dysfunction DEEP VEIN THROMBOSIS (DVT) osms.it/deep-vein-thrombosis PATHOLOGY & CAUSES SIGNS & SYMPTOMS ▪ Blood clotting in deep leg veins (iliofemoral, popliteal, femoral veins) ▪ Arterial clots usually due to artery wall damage; venous clots don’t require vein damage ▪ Valves inside veins can lower blood oxygen levels → venous stasis-associated hypoxemia can activate reactive oxygen species, other hypoxia-inducible factors → tissue factor released into blood ▫ Tissue factor activation → prothrombin turns into thrombin → fibrin fibers form net → traps red blood cells, white blood cells, platelets → venous thrombus ▪ 50% asymptomatic due to venous collateral channels ▪ Localized inflammation around clot ▪ High venous pressure engorges visible superficial veins ▪ If PE occurs: sudden dyspnea, chest pain ▫ Fatal if enough lung tissue affected CAUSES ▪ Virchow’s triad ▪ Antiphospholipid syndrome ▪ Prolonged immobilization (bed rest, orthopedic casts, long-distance air travel) ▪ Genetic ▫ Antithrombin, protein C, S deficiencies RISK FACTORS ▪ Pregnancy, oral contraceptives, old age, major surgery (e.g.orthopedic surgery), malignancy, obesity, trauma, heart failure COMPLICATIONS ▪ Pulmonary embolism (PE) most common ▫ Can cause pulmonary infarction, death ▪ Post-thrombotic syndrome ▫ Develops in 50% of individuals with DVT ▪ Extreme cases: phlegmasia cerulea dolens (blue, painful, swollen leg, possible venous gangrene) DIAGNOSIS DIAGNOSTIC IMAGING Doppler ultrasound imaging ▪ Most common diagnostic ▪ Modified vein diameter ▫ Increased: acute thrombus ▫ Decreased: chronic thrombus ▪ Absent colour flow: vein completely occluded ▪ Increased flow in surrounding superficial veins Venography ▪ Most effective, but invasive/cost-prohibitive LAB RESULTS ▪ D-dimers → rule out DVT ▫ Increased level: plasmin dissolves thrombus OTHER DIAGNOSTICS Wells’ score ▪ Higher score indicates increased chance of DVT (Scale of -2 to 9 points) ▫ High score = high chance: > 2 points ▫ Moderate score = moderate chance: 1–2 points ▫ Low score = low chance: < 1 point OSMOSIS.ORG 179

TREATMENT MEDICATIONS ▪ Acute manifestation: unfractionated heparin/low-molecular-weight heparins ▪ Long-term management: oral anticoagulants (e.g. warfarin) ▪ Prior DVT: long term anticoagulation therapy, antiplatelet treatment, parenteral anticoagulants OTHER INTERVENTIONS ▪ Preventative: calf exercises, compression stockings/devices, raise affected areas to decrease swelling Figure 26.3 An IVC filter, used to prevent embolization of the deep vein thrombus into the pulmonary vasculature. 180 OSMOSIS.ORG Figure 26.4 Clinical appearance of a deep vein thrombosis of the right leg. The lower leg is erythematous and swollen.

Chapter 26 Venous Dysfunction THROMBOPHLEBITIS osms.it/thrombophlebitis PATHOLOGY & CAUSES ▪ Vein inflammation caused by clot in deep leg veins ▪ Increased coagulability (Virchow’s triad) ▪ Potential locations ▫ Upper limbs (usually at site of IV cannula) ▫ Lower limbs (coupled with varicose veins) ▫ Periprostatic venous plexus in biological males ▫ Pelvic venous plexus in biological females ▫ Large veins of cranium, dural sinuses ▫ Portal vein TYPES Migrating thrombophlebitis ▪ Occurs in several different locations, usually in pancreatic carcinomas due to proclotting factors secreted by tumoral cells Superficial thrombophlebitis ▪ Thrombus develops in vein near skin’s surface ▫ Mondor’s syndrome: thrombophlebitis of subcutaneous veins of breast/arm / penis; presents as lump Suppurative (septic) thrombophlebitis ▪ Infection from IV cannula; possible purulence CAUSES ▪ Most commonly: needle/catheter ▪ Prolonged immobilization: bed rest, orthopedic casts, long-distance air travel ▪ High estrogen: pregnancy, estrogen replacement therapy, oral contraceptives ▪ Hereditary clotting disorders: protein D/C deficiencies/factor V Leiden mutations ▪ Vasculitis, Behcet’s disease COMPLICATIONS ▪ DVT, superficial thrombophlebitis, pulmonary embolism SIGNS & SYMPTOMS ▪ Pain, inflammation/swelling, hard, cord-like veins ▪ Sometimes asymptomatic, can be revealed by applying pressure ▫ Hoffman’s sign (forced dorsiflexion on foot creates soreness behind knee); not 100% accurate DIAGNOSIS DIAGNOSITC IMAGING Venous duplex ultrasound ▪ Thrombosed veins thickened, poorly compressible ▪ Completely occluded vein = hypoechoic (low level echoes) ▪ No internal flow present distal to clot Imaging studies ▪ Thrombus detection (e.g. CT venography (CTV) with contrast, magnetic resonance (MR) venography) ▪ Blood coagulation tests (e.g. elevated D-dimers) LAB RESULTS Blood coagulation tests ▪ Elevated D-dimers OTHER DIAGNOSTICS ▪ Inspection of affected area ▫ Pulse (weak/absent) ▫ Blood pressure (high) ▫ Temperature (high) OSMOSIS.ORG 181

TREATMENT MEDICATIONS ▪ Acute manifestation: unfractionated heparin/low-molecular-weight heparins ▪ Long-term management: oral anticoagulants OTHER INTERVENTIONS ▪ Preventative: calf exercises, compression stockings/devices, raise affected areas to decrease swelling Figure 26.5 Illustration showing blood clots discovered via imaging studies. Figure 26.6 Illustration showing a surgically-implanted filter in the inferior vena cava preventing a pulmonary embolism. 182 OSMOSIS.ORG

Chapter 26 Venous Dysfunction VARICOSE VEINS osms.it/varicose-veins PATHOLOGY & CAUSES ▪ Enlarged, twisted superficial veins (most commonly in leg) ▪ Downward gravitational pull causes walls of veins to stretch over time, blood leaks backwards → extra blood volume twists veins → veins become varicose ▪ Blood sometimes rerouted to collateral veins deep in leg TYPES Varicocele ▪ Abnormal enlargement of pampiniform venous plexus in scrotum ▪ Mechanism same as varicose veins ▪ Most common in left testicle ▫ Left testicular vein brings blood to left renal vein at 90º angle → difficult → blood backs up → vein becomes varicose → loops back and forth on itself ▫ “Bag of worms” appearance CAUSES ▪ Obesity, pregnancy, standing for long periods of time, menopause ▫ Pelvic vein reflux (PVR): ovarian vein reflux, internal iliac vein reflux ▪ Hyperhomocysteinemia destroying structural proteins in vessels ▪ Chronic alcohol use COMPLICATIONS ▪ Chronic venous insufficiency ▪ Venous ulcers ▫ Can develop into carcinomas, sarcomas over time (rare) ▪ Superficial thrombophlebitis SIGNS & SYMPTOMS ▪ Twisted superficial veins ▪ Edema, pain (usually in evening) ▪ Pruritus in affected area/stasis dermatitis because of undrained waste in leg ▪ Prolonged bleeding, slowed healing in injuries to adjacent areas ▪ Restless legs syndrome DIAGNOSIS DIAGNOSTIC IMAGING Doppler ultrasound ▪ Used to discover subcutaneous varicosities, assess saphenofemoral junction ▪ If blood reflux spotted during Valsalva manoeuvre → valve incompetence ▪ Reflux > 1s → surgical intervention OTHER DIAGNOSTICS Trendelenburg test ▪ Person laid back on flat surface, leg raised above heart, blood will flow towards heart → compress upper thigh with tourniquet (not too tightly) → lower leg onto flat surface → person stands, refilling times assessed ▫ Normal: superficial saphenous vein fills < 30–35s ▫ Faster filling → valvular incompetence below compressed area → deep/ communicating veins ▫ Slower filling → tourniquet released → if filling sudden → incompetent superficial veins OSMOSIS.ORG 183

TREATMENT SURGERY ▪ Radiofrequency/laser ablation ▪ Sclerotherapy ▪ Ambulatory phlebectomy: removal of surface vein through slits in skin OTHER INTERVENTIONS ▪ Preventative: compression stockings/ devices, avoid prolonged standing Figure 26.7 An X-ray image demonstrating varicose veins of the left leg. Figure 26.8 Illustration of a varicocele in the left testicle. 184 OSMOSIS.ORG