PERIPHERAL VASCULAR DISEASE (PVD) AND VARICOSE VEINS PTA PATHOLGY CONCEPTS ALYSSA TAUBEL & NADINE KARI

LEARNING OBJECTIVES By the end of this presentation you should: Be aware of the incidence, etiology, risk factors and prognosis for PVD and varicose veins Have an understanding of the pathophysiology of PVD and varicose veins Be informed of the clinical manifestations of PVD and varicose veins Be aware of the medical management, prevention and treatment of PVD and varicose veins Have an understanding of the implications for Physical Therapy Practice regarding PVD and varicose veins

Peripheral Vascular Disease (PVD) DEFINITION & FACTS: PVD is an umbrella term encompassing pathological disorders of both arterial and venous blood vessels which supply blood to the extremities and major abdominal organs. PVD affects the legs more than the arms. PVD is most often evident in the intestines and kidneys PVD affects about 8 million Americans over age 60; 20% of which are over age 70 Atherosclerosis is the most common cause for arterial occlusive forms of PVD The classic symptom of PAD (peripheral artery disease) is intermittent claudication Specific symptoms of the different types of PVD vary The focus of this presentation will be on venous diseases, specifically venous thrombosis, pulmonary embolus and varicose veins (Goodman, 2017) Materials Needed: None PVD includes pathological disorders of venous and arterial veins as well as major abdominal organs, affecting over 8 million Americans annually. It is seen most commonly in the LE, intestines and kidneys. Most common symptom of PAD is intermittent claudication.

Venous Thrombosis & Pulmonary Embolus OVERVIEW A Venous Thrombus is an intervascular clot consisting of platelets, erythrocytes, leukocytes and fibrin. A Venous Thrombus involves partial or complete occlusion of a vein by a clot with a subsequent secondary inflammatory reaction in the wall of the vein. It can cause significant injury and death. Venous Thrombi can be deep (DVT) or superficial and are most often found in lower extremities as a result of varicose veins. Proximal DVT’s are likely to become pulmonary emboli (PE). (Goodman, 2017) Some patients with a DVT report leg pain, swelling, tenderness and redness of the affected area. However, some have no symptoms, which can delay a life-saving diagnosis (Varaki, 2018) Materials Needed: None DVTs are clots made up of platelets, erythrocytes, leukocytes and fibrin. They can partially or fully occlude a vein, causing serious injury or death. Some people experience symptoms of pain, swelling, tenderness and redness while others are asymptomatic.

Incidence, Etiology, Risk & Risk Factors DVT is the 3rd most common cardiovascular disease DVT affects 2 million Americans each year (Goodman, 2017) About one-third of patients with DVT develop a pulmonary embolism. About 20% of those patients die before diagnosis or on the 1st day of diagnosis (Varaki, 2108) (See chart for Common Independent Risk Factors for DVT & PE) (Heit, 2016) Thrombus formation requires at least 2 out of 3 of the following conditions: Venous stasis Hypercoagulability Injury to venous wall Other risk factors may be present (Goodman, 2017) Baseline characteristic Odds ratio 95 % CI Body mass index (kg/m2) 1.08 1.05, 1.11 Major surgery 18.95 9.22, 38.97 Hospitalization for acute medical illness 5.07 3.12, 8.23 Nursing home confinement 4.63 2.77, 7.74 Trauma/fracture 4.56 2.46, 8.46 Active cancer 14.64 7.73, 27.73 Neurologic disease with leg paresis 6.10 1.97, 18.89 Pregnancy or postpartum 4.2 1.30, 13.84 Oral contraceptives 4.03 1.83, 8.89 Estrogen alone 1.81 1.06, 3.09 Non-contraceptive estrogen plus progestin 2.53 1.38, 4.63 Materials Needed: None DVT is a common and serious condition. There are several risk factors for developing a DVT. Two of three conditions must be present for a DVT to form: venous stasis, hypercoagulability, injury to venous walls or other factors in table.

Pathogenesis Damage to endothelial lining exposes subendothelial tissues to platelets in the blood which begins the growth of a thrombus (clot) The thrombus is completed when fibrin, leukocytes & erythrocytes adhere to the platelets Inflammation is caused by the adherent thrombus Thrombus may eventually be attacked and dissolved by fibroblasts, leaving scar tissue Blood flow is restored but valves may remain damaged Thrombus may detach and become an embolism Thrombi in major veins cause increased distal venous pressure & volume Thrombi in small veins cause the development of collateral circulation (Goodman, 2017) Materials Needed: None A thrombus forms after trauma to the endothelial lining of a blood vessel. It’s adherence to the wall of the vessel causes inflammation. It can be dissolved, but leaves scar tissue and the valve can be damaged. It can also detach and become a free floating embolism.

Medical Management DIAGNOSIS & PREVENTION Well’s Clinical Decision Rule for DVT has proven to be a dependable tool for clinical assessment in prediction of risk for DVT in the lower extremities, especially with orthopedic patients. Early mobilization is the best prevention for low risk patients while prophylactic anti- coagulants are used for moderate to high risk Knee elastic stockings, ankle pumping and pneumatic pressure devices are used in most hospitals for both prevention and treatment (Goodman, 2017) Four popular invasive methods used for diagnosis are angiography, venography, ambulatory venous pressure (see photo), and intravascular ultrasound. They are very accurate but expensive, painful and risky Three main validated non-invasive methods are plethysmography, Doppler ultrasound and blood pressure methods Emerging technologies include wearable sensors, which show a high potential to address the need for simple, cost-effective, accurate and timely diagnosis of PVDs (Varaki, 2018) Materials Needed: elastic stockings, ankle pumping devices There are both invasive and non-invasive techniques available for diagnosis of DVT. Research is being done to find methods that are simple, cost-effective, painless and accurate.

Medical Management (continued) TREATMENT Goals for management of DVT include: preventing advancement to PE, controlling enlargement of the clot, limiting damage to the vein and preventing additional clot formation Low molecular weight heparin followed by long term oral anti-coagulants (warfarin) is the current treatment for DVT Ambulation is allowed in all cases, but care must be taken that aggressive ambulation isn’t begun before adequate anticoagulation has been provided Whenever a person is upwardly mobile they must wear elastic stockings Patients are generally Injected with heparin before discharge. They are sent home with doses to self inject over the next week, along with anticoagulants. Thrombolysis, thrombectomy and embolectomy are being used where massive DVTs are present. (Goodman, 2017) Materials Needed: elastic stockings Early ambulation, use of anti-coagulants and blood thinners and wearing elastic stockings are most common forms of treatment. Surgery is sometimes needed with a massive DVT.

Prognosis With appropriate intervention and no complications, patients with a calf DVT can return to normal function within1-3 weeks, 6 weeks for a pelvic DVT Prognosis depends on: size of vessel, presence of collateral circulation and underlying cause of the thrombosis Survival after VTE (venous thromboembolism) is worse than expected, and survival after PE is much worse than after DVT alone (See chart for Survival % After DVT vs. PE) The risk of early death is 18 times higher for PE patients compared with patients with DVT alone For nearly one-quarter of PE patients, the initial clinical presentation is sudden death. Some predictors of reduced early survival after VTE are: advancing age, male sex, lower body mass index, being confined to a hospital or nursing home when VTE occurs, congestive heart failure, chronic lung disease, serious neurologic disease, and active cancer Survival times may be improving for PE patients who live long enough to be diagnosed and treated (Heit, 2016) Time Deep vein thrombosis alone Pulmonary embolism 0 days 97.0 76.5 7 days 96.2 71.1 14 days 95.7 68.7 30 days 94.5 66.8 90 days 91.9 62.8 1 year 85.4 57.4 2 years 81.4 53.6 5 years 72.6 47.4 8 years 65.2 41.5 Materials Needed: None When a patient is properly diagnosed and there are no complications, recovery from DVT is possible. Survival rates after PE are much worse.

Implications for Physical Therapy Practice Post-op, postpartum and immobilized clients are at risk for developing DVT and should be monitored closely. Utilize risk factor assessment scales. Upon removal of a lower extremity cast, patient should be monitored carefully. Normal calf size without atrophy could indicate swelling related to DVT. Patients with thrombophlebitis should be checked for signs of PE like: chest pain, hemoptysis, cough, diaphoresis, dyspnea and uneasiness. These should be reported. Must be monitored for life as reoccurrence is common. Recent studies have shown that men are 2-4 times more likely to have a recurrent venous thrombosis than women (Reibero, 2012) Things to monitor and report immediately when patient is on blood thinners: blood in urine, stool, along gums or teeth; subcutaneous bruising; back, pelvic or flank pain. Encourage patients to discuss use of herbs, medications and supplements with their doctor as they can interfere/negatively interact with warfarin. Encourage patients limit alcohol use as it can increase the potency of warfarin. Use caution with soft tissue mobilization, manual therapy and weight training as bleeding under the skin and bruising can easily occur with slight trauma. Some ways to prevent DVT or a DVT becoming a PE include: active and passive ROM exercise, avoid prolonged sitting, early ambulation, frequent position changes but keep legs elevated slightly above heart, coughing, deep breathing and proper positioning, use of elastic support hose for 6-8 weeks for calf DVT to prevent movement of thrombus inside blood vessel. (Goodman, 2017) Materials needed: risk factor assessment scales, elastic support stockings It is imperative for the PT and PTA to monitor their patients for signs of DVT or PE because these conditions can be life-threatening. Prevention is huge when dealing with these patients. Having open communication about their use of alcohol, supplements and medications can also be very important because of how these things can interact with warfarin.

Varicose Veins An abnormal dilation of veins, usually the saphenous veins in the LE, leading to tortuosity, incompetence of the valves and a propensity to thrombosis. The enlarged veins are the most visible sign, with the twisted appearance most easily seen in standing As Goodman describes, the clinical manifestations do not indicate the severity of the disease; extensive varicose veins may have no symptoms and minimal may have several: cramping, dull aching, heaviness, restless legs, or fatigued feeling after periods of standing (Goodman 2017) Often viewed as a cosmetic issue, but can indicate serious underlying problems. If left untreated, it becomes hard and the impaired circulation can lead to ulcer formation A progressive disease with no cure but effective treatment focusing on lifestyle changes or sometimes surgery with intentions of minimizing symptoms and preventing complications Accounts for an estimated 2% of all USA healthcare costs (Deatrick, Kristopher, Wakefield, Thomas & Henke, 2010) Materials needed: none Varicose veins are dilated, twisted veins, typically in the lower extremities. This condition is common and they are seen usually as a cosmetic issue but serious health problems can develop, especially if left untreated. There is no cure but there is effective treatments.

Incidence, Etiology & Risk Factors The American Venous Forum estimates 23% of US adults have varicose veins; 5% of these have venous edema, skin changes, and venous ulcerations (Zhang & Melander, 2014) Research indicates that the following play a role in varicose veins: Genetics can predispose some to having valvular incompetence, venous hypertension, weak veins walls and reflux from deep to superficial venous system Damage to valves and vein walls due to wear and tear/trauma Hormones, such as increased production of estrogen during pregnancy (Deatrick, Kristopher, Wakefield, Thomas & Henke, 2010) Risk Factors: Increased age ○ Female Gender & Pregnancy ○ Tight Clothing ○ Obesity Smoking ○ Hypertension ○ Injury ○ Work involving prolonged standing/sitting Immobility especially with legs crossed (Li, Xiao-Yan, Ge, Wang, Guo-Jun, Xu & Yi-Han (2014) Materials needed: none Causes of VV are mainly genetics, damage to the veins and vein walls and hormone changes. Risk factors are age, gender/pregnancy, injury and lifestyle

Pathogenesis To return blood to the heart from the LE’s, it needs to travel against gravity. This is accomplished mainly by the calf muscle pump contracting and putting pressure on the deep veins to push the blood upwards. One-way valves prevent backflow. There are two main theories accepted that mainly debate over what fails first; the valves or the wall. Valve Failure: when the one-way valves are not functioning properly, the calf pumps make the blood flow in both directions and the lower part of the veins are unable to fully empty. This stress causes the elasticity of the distal vein walls to weaken from too much pressure. This then weakens more valves and creates a cycle. Wall Failure: when the vein wall is weakened, it is stretched out and enlarged, causing the valves to be unable to close completely. This creates more blood pooling and further enlarging it. Because of these patterns, this makes the disease progressively worse overtime, but it can be slowed with specific interventions, however, the disease itself cannot be cured. (Allen, 2013) Materials Needed: Be able to click the link to go to an external site. The exact process is not fully understood, but there is agreement that the vein walls and valves are incompetent and cause the other to be damaged, leading to a cycle of failure to function properly. The link in the slide leads to more information of the pathophysiology that includes images and flow charts. https://www.slideshare.net/BharathiPriya5/pathophysiology-of-varicose-veins

Medical Management DIAGNOSIS & PREVENTION To diagnose, the area should be inspected for ankle venous flair (pictured), telangiectasias/spider veins (dilated small vessels <1 mm), reticular veins (non-palpable 1- 3mm), varicose veins (over 3mm), edema, skin changes (pigmentation, venous ulcer formation). A duplex ultrasound will find reflux of the veins and is most commonly used method but additional tests like a venogram may be needed in some cases. Use the duplex to record the competency of the segments, junctions and locations of both the deep and superficial venous system in the LE’s as well as the diameter of the veins. CEAP is use to classify. (Wright & Fitridge, 2013) Varicose veins cannot be prevented, but the process can be slowed for the ones present and there are ways to minimize risk for developing VV. The Heart, Lung, and Blood Institute recommends taking breaks from standing/sitting long periods of time and do not cross legs while sitting. Elevating legs above the heart while sleeping or sitting will make gravity aid the veins in returning blood to the heart. Having a physically active lifestyle will increase muscle strength and the calf pump will perform better as well as promote circulation. Being in a healthy weight range will take pressure off the legs and veins. Avoiding clothing that constricts the waist and legs will keep blood flowing easier. Compression stockings should be recommended by a doctor and will aid the calf pump in pushing the blood upwards and lower reflux. Materials needed: CEAP classification chart, duplex to demonstrate The physician often uses a duplex to see the blood flow and use the CEAP to classify the VV. Although VV cannot be fully prevented, wearing loose clothing, elevating legs, using compression stockings, being a healthy weight and physically active can lower risk and progression speed. Avoiding static standing/sitting will also aid in minimizing.

Medical Management Treatment Conservative management includes using lifestyle changes, like the previously mentioned, prevention techniques and education on venous insufficiency and varicose veins. Procedures can be done to improve the appearance of the veins and may be necessary for more serious cases such as those with skin changes, pain or blood clot formation. Sclerotherapy is a chemical solution/foam injected into the affected vein to cause scarring and close it off. This can take a varying number of treatments, depending on the size. It is a permanent fix for that specific affected vein, but depending on the issue that caused it to become a varicose vein, more VVs may develop elsewhere. Endovenous ablation therapy uses lasers to create heat to close off a varicose vein by making a small incision and inserting a tube. The tube end heats up to seal the vein. With severe varicose veins, endoscopic vein surgery may be used. A small cut is made in the affected area and a small tube is inserted to close off the vein. Vein stripping and ligation is for severe cases only as well. The veins are tied shut and are taken out through incisions. (Wright & Fitridge, 2013) Materials needed: none Mild cases are given conservative management consisting of lifestyle changes, but some with cosmetic concerns may have small procedures. Serious conditions that involve ulcers, blood clots, etc. will likely require surgery.

Prognosis When untreated, the disease will continue to progress and complications, such as ulcers, can develop Long-term studies indicate13.5% of varicose vein surgeries have recurrence. 90-98% success with radiofrequency ablation after two years  The success for endovenous laser treatment after two years was 93.4%  Foam sclerotherapy clinical recurrence of significant symptoms after 5 years was 4% (Knott, 2016) Surgery may improve appearance, but may not reduce the physical symptoms, suggesting that the lower limb symptoms form from a nonvenous cause (Goodman, 2017) Overall, prognosis is positive, especially with early intervention.

Implications for Physical Therapy Practice PTA can be instrumental in developing prescriptive exercise and preventative measure for those at risk or diagnosed with varicose veins Avoiding static postures and taking breaks while practicing deep breathing Utilizing special compressive hose that do not constrict behind the knee, upper leg, waist or groin and worn as much as possible during the day At the end of the day, legs should be elevated above the heart for 10-15 minutes Encourage good breathing, aerobics, strength training and resistive exercises but avoid high-impact activities; good alternatives are brisk walking, biking and swimming (Goodman, 2017) Materials needed: fitted compressive hose, pillows to elevate legs, exercise and education handouts The PTA is instrumental in preventing or minimizing varicose vein risks and symptoms. Education is key in treatment.

Summary Materials needed: none PVD: general term for diseases affecting the arterial and/or venous blood vessels, affecting 8 million Americans over 60. Atherosclerosis is most common to cause arterial occlusive forms of PVD. Symptoms can vary with different types of PVD but the classic for peripheral artery disease is intermittent claudication. (Goodman, 2017) A Venous Thrombus is an intervascular clot made up of platelets, RBCs, WBCs and fibrin. Involves partial/complete occlusion of a vein, causing a secondary inflammatory response in the vein wall; this can cause injury or death. Venous Thrombi often are a result of varicose veins in the lower extremities and proximal ones can become a pulmonary embolism Although many suffer leg pain, swelling, redness, and tenderness in the affected area, some are asymptomatic. About one-third of patients with DVT develop a pulmonary embolism. About 20% of those patients die before diagnosis or on the 1st day of diagnosis . DVT is the 3rd most common cardiovascular disease, affecting 2 million Americans each year (Varaki, 2018) Thrombus formation requires at least 2 out of 3 of the following conditions: venous stasis, hypercoagulability, injury to venous wall and other risk factors may be present. Varicose Veins: An abnormal dilation of veins, usually the saphenous veins in the LE, leading to tortuosity, incompetence of the valves and a propensity to thrombosis. The enlarged veins are the most visible sign, with the twisted appearance most easily seen in standing and some may have no symptoms while others feel dull aches, cramping and fatigued after periods of standing. No cure but effective treatments. 23% of US adults have VV, and 5% of these have severe conditions. (Zhang & Melander, 2014) Research finds that valve and vein wall incompetence likely are a role in VV formation; either by genetics or trauma (Deatrick, Kristopher, Wakefield, Thomas & Henke, 2010) Major risk factors: age, gender, weight, pregnancy, and prolonged sitting/standing Materials needed: none PVDs in general are serious conditions and very common. The symptoms for the specific diseases vary, and sometimes they are asymptomatic. The best way to treat all of these is to minimize risk/take preventative measures

BIBLIOGRAPHY Abihu, A., (Dec 20, 2013) How Deep Vein Thrombosis Develops, Medical Course. https://www.youtube.com/watch?v=EeNcS9RgZ94 Allen, L. (2009). Assessment and management of patients with varicose veins. Nursing Standard (through 2013), 23(23), 49-57; quiz 58. Retrieved from http://ezproxy.nwtc.edu:2048/login?url=https://ezproxy.nwtc.edu:2206/docview/219881575?accountid=4328 Deatrick, K. B., M.D., Wakefield, T. W., M.D., & Henke, P. K., M.D. (2010). Chronic venous insufficiency: Current management of varicose vein disease. The American Surgeon, 76(2), 125-32. Retrieved from http://ezproxy.nwtc.edu:2048/login?url=https://ezproxy.nwtc.edu:2206/docview/212838543?accountid=4328 Goodman, C.C., Fuller, K.S. (2017). Pathology for the Physical Therapist Assistant, Second Edition. St. Louis, MO: Elsevier. Heit, J. A., Spencer, F. A., & White, R. H. (2016). The Epidemiology of Venous Thromboembolism. Journal of Thrombosis and Thrombolysis, 41, 3–14. http://doi.org/10.1007/s11239-015-1311-6. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4715842/pdf/11239_2015_Article_1311.pdf Knott, L. (2016, August 31). Varicose Veins. How to remove varicose veins, information. Retrieved from https://patient.info/doctor/varicose-veins-pro Li, X., Xiao-Yan, J., Ge, J., Wang, J., Guo-Jun, C., Xu, L., . . . Yi-Han, C. (2014). Aberrantly expressed lncRNAs in primary varicose great saphenous veins.PLoS One, 9(1) doi:http://ezproxy.nwtc.edu:2087/10.1371/journal.pone.0086156 Ribeiro, D. D., Lijfering, W. M., Barreto, S. M., Rosendaal, F. R., & Rezende, S. M. (2012). Epidemiology of Recurrent Venous Thrombosis. Brazilian Journal of Medical and Biological Research, 45(1), 1–7. http://doi.org/10.1590/S0100-879X2011007500166. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3854137/pdf/0100-879X-bjmbr-45-01-001.pdf Varaki, S.E., Garguilo, G.D., Pekala, S. & Breen P.P. ((2018). Peripheral Vascular Disease Assessment in the Lower Limb: A Review of Current and Emerging Non‑Invasive Diagnostic Methods. Biomedical Engineering Online,17(1), 61 https://doi.org/10.1186/s12938‑018‑0494‑4 Retr https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5948740/pdf/12938_2018_Article_494.pdf Wright, N., & Fitridge, R. (2013). Varicose veins: Natural history, assessment and management. Australian Family Physician, 42(6), 380-4. Retrieved from http://ezproxy.nwtc.edu:2048/login?url=https://ezproxy.nwtc.edu:2206/docview/1430265967?accountid=4328 Zhang, S., & Melander, S. (2014). Varicose veins: Diagnosis, management, and treatment. The Journal for Nurse Practitioners, 10(6), 417-424. doi:http://ezproxy.nwtc.edu:2087/10.1016/j.nurpra.2014.03.004