ClinMed 2 Cards 4: Peripheral Venous Disorders PDF

CLINMED 2 Jennifer Rayburn, M.D. MTSU Physician CARDS 4 Assistant Studies  1. Compare and contrast the various forms of peripheral venous disorders OBJECTIVES 2. Question the causes and treatment for various...

CLINMED 2 Jennifer Rayburn, M.D. MTSU Physician CARDS 4 Assistant Studies  1. Compare and contrast the various forms of peripheral venous disorders OBJECTIVES 2. Question the causes and treatment for various lymphatic disorders including lymphadenopathy and lymphedema  PERIPHERAL VENOUS SYSTEM Veins are high-capacitance vessels that contain more than 70% of the total blood volume In contrast to the muscular structure of the arteries, the subendothelial layer of veins is thin, and the tunica media comprises fewer, smaller bundles of smooth muscle cells intermixed with elastic and reticular fibers While veins of extremities possess intrinsic vasomotor activity, transport of blood back to the heart relies greatly on external compression by the surrounding skeletal muscles and on a series of one-way endothelial valves (skeletal muscle pump) Veins of the extremities are characterized as either superficial or deep. The deep veins generally course along the arteries, whereas the superficial veins are located subcutaneously The superficial veins drain into deeper veins through a series of connectors, ultimately returning blood to the heart.  DEEP VEIN ANATOMY HTTPS://WWW.YOUTUBE.COM/WATCH?V=FKJR5UQPV5S (VENOUS RETURN)  VARICOSE VEINS Dilated, tortuous superficial veins that often develop in the lower extremities due to failure of the venous valves in the saphenous veins leading to retrograde flow, venous stasis & pooling of blood Affect women two to three times more than men; 50% have a FH of varicose veins Most commonly seen in the saphenous veins May also see them in the anorectal area (hemorrhoids), lower esophageal veins (esophageal varices), and spermatic cord (varicocele) Pathophysiology: Intrinsic weakness in the vessel wall from increased intraluminal pressure, or from congenital defects in the structure and function of venous valves. Risk factors: Female gender, aging, pregnancy, prolonged standing, obesity, FH of varicose veins, chronic venous insufficiency, increased estrogen (OCP use) Symptoms: Most are Asymptomatic (cosmetic); Symptoms can include: dull ache, heaviness or pressure sensation of legs during prolonged standing relieved with elevation Physical exam: Visibly dilated tortuous veins, telangiectasias, swelling, discoloration, venous stasis ulcers, mild ankle edema Conservative Treatment: elevate legs when supine, avoid prolonged standing, external graduated compression stockings that counterbalance increased venous hydrostatic pressure Symptomatic treatment: sclerotherapy, endovenous thermal ablation or direct ligation and removal  CHRONIC VENOUS INSUFFICIENCY Characterized by elevated venous pressure with extravasation of edema into the tissues of the lower extremities due to venous valvular incompetence and/or skeletal muscle pump dysfunction Most commonly occurs after superficial thrombophlebitis, after DVT, or trauma to the affected leg. Twice as prevalent as CAD in the United States Risk factors: history of DVT, advancing age, FH of venous disease, ligamentous laxity, prolonged standing, increased BMI, smoking, LE trauma, some hereditary conditions, high estrogen states, pregnancy  CHRONIC VENOUS INSUFFICIENCY Symptoms: pain or achiness in legs particularly when standing for prolonged periods & relieved with ambulation and leg elevation, chronic lower extremity edema, hyperpigmentation, dry, flaky skin PE: Stasis Dermatitis: pruritic, eczematous rash, excoriations, weeping erosions, & brownish or dark purple hyperpigmentation of the skin (hemosiderin deposition) Venous stasis ulcers (medial malleolus) Dependent pitting leg edema (swelling, varicosities & erythema with normal pulse and temp) Atrophie blanche (atrophic, hypopigmented areas with telangiectasias & punctate red dots) Diagnosis: Presence of typical symptoms, PE findings, Venous Duplex Ultrasound demonstrating venous reflux (>500 msec for superficial or perforator veins and >1000 msec for deep veins)  CHRONIC VENOUS INSUFFICIENCY TREATMENT Asymptomatic Symptomatic Usually considered to be cosmetic & Non-operative: skin care, leg not covered by insurance elevation, exercise, and compression therapy (cornerstone of treatment), Telangiectasias and reticular veins weight management (spider veins) can be treated with If refractory symptoms, then need to sclerotherapy and surface laser undergo comprehensive lower extremity therapy duplex exam to confirm diagnosis and extent of venous reflux These treatments do not prevent the Superficial venous ablation or endovenous future development of venous reflux interventions for symptoms and venous and occurrence of chronic venous reflux not responsive to nonoperative disease therapy CHRONIC VENOUS STASIS ULCERS Affect up to 5% of the population over 65 years. Caused by chronic venous disease produced by venous hypertension, which typically results from valvular incompetence within the deep venous system or obstruction of venous outflow. Treatment: 1. Compression Therapy: Compression >30 mmHg is typically needed for treatment of VLUs with 30 to 40 mmHg and 40 to 50 mmHg as the most common levels. 2. Wound debridement and dressings/surrounding tissue therapy 3. Topical agents are used selectively (eg, hydrogel with or without silver, collagenase [enzyme], honey, topical antibiotics ) to manage bioburden or residual necrotic tissue; however, some topical agents are irritating and can cause contact sensitization, or are cytotoxic (eg, silver sulfadiazine, antiseptics), resulting in delayed healing 4. Venous Intervention – Surgical treatment of CVI 5. Aspirin can accelerate healing  DEEP VENOUS THROMBOSIS (DVT) DVT can be seen in the lower or upper extremities. Most commonly in the deep veins of the lower extremities. Reminder of the anatomy  DEEP VENOUS THROMBOSIS Wells Criteria DVT DVT Venous thrombosis in a deep vein (mostly of calves but can be in proximal vein such as popliteal, femoral, and Iliac vessels) Remember Virchow’s Triad (pathogenesis of DVT): 1. Venous stasis: immobilization or prolonged sitting > 4 hours, surgery, stroke with immobility 2. Vascular endothelial injury: trauma, infection, inflammation triggers the clotting cascade. 3. Hypercoagulable state: inherited disorders, OCP use, malignancy, pregnancy, cigarette smoking Typically, can find a risk factor in over 80% of patients Risk Factors: inherited thrombophilia, >48 hours of immobility, hospital admission within past three months, surgery within past three months (orthopedic, major vascular, neurosurgery and cancer surgery), malignancy within past three months, infection within past three months, current hospitalization, major trauma, IV drug use, pregnancy, OCPs, HRT, testosterone, tamoxifen, prolonged sitting, extended travel, smoking, etc. Wells Criteria for DVT (far right pic)  CONDITIONS THAT PREDISPOSE TO DVT VIRCHOW’S TRIAD Stasis of blood flow Antithrombin deficiency Prolonged inactivity (following surgery, Deficiency of protein C or protein S prolonged travel) Immobilized extremity (following bone Antiphospholipid antibodies/lupus fracture) anticoagulant Heart failure (with systemic venous Neoplastic disease (eg, pancreatic, lung, congestion) stomach, or breast cancers) Hyperviscosity syndromes (eg, Pregnancy and oral contraceptive use polycythemia vera) Hypercoagulable states Myeloproliferative diseases Inherited disorders of coagulation Smoking Resistance to activated protein C (factor Vascular damage V Leiden) Instrumentation (eg, intravenous catheters) Prothrombin gene mutation (PT G20210A) Trauma  D-DIMER ASSAY WHEN TO ORDER??? Fibrin D-dimer is one of the major fibrin degradation products released upon cleavage of crosslinked fibrin by plasma Normal plasma levels are 500 ng/mL for fibrin equivalent units and 250 ng/mL for D-dimer units Elevated concentrations of plasma D-dimer units indicate recent or ongoing intravascular coagulation and fibrinolysis A FEW CAUSES OF ELEVATED D-DIMER LEVELS  DEEP VENOUS THROMBOSIS DVT Symptoms: Swelling or edema Pain Warmth Usually unilateral but can be bilateral Calf or whole leg PE: dilated superficial veins, unilateral edema or swelling with difference in calf or thigh diameters, pain and tenderness along course of major veins Calf diameter can be the most useful finding (>3cm difference) Labs: CBC, BMP (at least; for med treatment); hypercoagulable panel if warranted; +/-D- dimer Diagnosis: First line: Venous Duplex Ultrasound of Lower extremities (Most DVT’s originate in the calf) Compresion ultrasonography with Doppler is the diagnostic test of choice in patient’s suspected of DVT. Non-compressibility of the vein=DVT. D-Dimer: Highly sensitive but NOT specific. See notes for two main uses for this test. Contrast venography: Gold standard but is invasive and difficult to perform and rarely used.  MANAGEMENT OF DEEP VENOUS THROMBOSIS Treatment: Anti-coagulation is the mainstay of treatment for all patients with proximal DVT (popliteal, femoral and iliac vein) and select cases of distal DVT (calf vein such as posterior tibial and peroneal)) (weigh risk and benefits). Over 90% of acute PE arise from the proximal veins Anti-coagulation is to prevent further thrombosis and early and late complications of DVT Early complications: further clot extension, acute pulmonary embolism (PE), major bleeding from anticoagulation and death Late complications: recurrent clot, post-thrombotic syndrome, chronic thromboembolic pulmonary hypertension  DEEP VEIN THROMBOSIS DVT TREATMENT 1. Immediate anti-coagulation Options: 1. Low molecular weight heparin plus Warfarin, 2. LMWH plus either Dabigatran or Edoxaban, or 3. Monotherapy with either Rivaroxaban or Apixaban Can be treated as an outpatient in most cases (hemodynamically stable, low bleeding risk, no renal insufficiency, good home support) A minimum of three months of oral therapy has been suggested after a first episode of DVT (provoking events, risk factors for recurrence and bleeding, patient preferences, etc.) Early ambulation is safe and encouraged as soon as feasible Typically, avoid use of compression stockings (if started, must be after anti-coagulation is started) 2. Thrombolytics and thrombectomy: Usually reserved for those with phlegmasia cerulean dolens or massive iliofemoral DVT or patients who fail anti-coagulation therapy 3. IVC Filter: not routinely used; but, if used 1. patients with proximal DVT and PE with absolute contraindications to anticoagulant therapy 2. recurrent embolism despite adequate anti-coagulant therapy (as adjunct) 3. embolic event would be poorly tolerated (RV dysfunction with enlarged RV on ECHO)  Anticoagulant Options for DVT Treatment What To Know: 1. First event with reversible cause: treat for at least three months 2. First event of Idiopathic DVT ( no malignancy): Long term anticoagulation or three months if severely symptomatic distal DVT 3. Pregnancy: use LMWH 4. Malignancy: LMWH preferred; warfarin or DOACS as alternatives 5. Antiphospholipid syndrome: Warfarin preferred in nonpregnant patients. 6. DOACS are preferred over warfarin therapy in the management of DVT in non- cancer patients Copyrights apply  PHLEGMASIA CERULEAN DOLENS Uncommon; typically seen in patients with massive iliofemoral DVT that causes obstruction of the venous drainage May need more aggressive management and consideration of thrombolytics or thrombectomy (only accepted indication for this treatment in DVT) Present with sudden, severe pain, swelling, cyanosis, edema, venous gangrene, compartment syndrome that together may impair the arterial supply Delay in treatment may result in death or loss of the patient’s limb  SUPERFICIAL VENOUS THROMBOSIS (SVT) Less severe disorder than DVT Generally benign and self-limited However, if the axial veins are involved (great saphenous, accessory saphenous, small saphenous), thrombus propagation into the deep venous system can occur. Risk Factors: varicose veins, vein excision or ablation, pregnancy and estrogen therapy, prior vein thrombosis, malignancy and hypercoagulable states, IV catheter use (much more common in upper extremity veins), etc. Symptoms: tenderness, induration, pain, erythema along the course of a superficial vein, palpable/nodular cord Diagnosis: Venous duplex ultrasound: especially if lower extremity involvement to rule out co-existent DVT and determine the exact location and extent of thrombosis. May see vein wall thickening and perivenous subcutaneous edema. Noncompressibility of the vein if thrombosis present.  TYPES OF SUPERFICIAL VENOUS THROMBOSES Superficial phlebitis: presence of pain and inflammation involving a vein in the absence of thrombus. More of a clinical diagnosis. Great saphenous vein (60- 80%) and small/short saphenous vein (10-20%). Superficial Thrombophlebitis: Due to inflammation which may is accompanied by thrombosis of the vein. If thrombus is apparent as a thickened cord or identified on imaging, then the terms superficial thrombophlebitis or superficial vein thrombosis are preferred. Suppurative thrombophlebitis: high fever, fluctuance, and/or purulent drainage along a superficial vein. Erythema extends significantly beyond the margin of the vein. Trousseau syndrome: migratory thrombophlebitis associated with malignancy (Pancreatic cancer) or other vasculitis disorders. Do malignancy workup!! MANAGEMENT OF SUPERFICIAL VENOUS THROMBOSIS (SVT) Low Risk for VTE: Supportive care is the mainstay; NSAIDS for pain and inflammation, extremity elevation, warm or cool compresses, compression stocking therapy as tolerated if not contraindicated (PAD) Intermediate Risk for VTE: Prophylactic anticoagulation with uncomplicated axial vein thrombosis (SVT in proximity 3-5 cm of deep vein, etc.) High Risk for Thromboembolism: Supportive care plus therapeutic anticoagulation  Diagnosis of Superficial phlebitis and thrombophlebiti s Don’t have to know this algorithm for test, just FYI Copyrights apply  SUPERIOR VENA CAVA (SVC) SYNDROME Obstruction of blood flow through the superior vena cava because of intraluminal thrombus, invasion, or SVC Syndrome external compression Can be due to processes involving the lung, regional lymph nodes, or other mediastinal structures (neoplastic, infectious, foreign bodies like central lines or pacemaker leads) Most cases due to malignancy (Small cell bronchogenic carcinoma most common; NHL), SVC stenosis Symptoms: Dyspnea is the most common presenting symptom. Facial, neck, or upper extremity edema; facial plethora; chest pain, respiratory symptoms, or neurologic manifestations. PE: edema and cyanosis of face, neck, arms; dilated veins covering anterior chest wall and neck, tongue swelling Diagnosis: high clinical suspicion, CT Chest with contrast gives better imaging and assesses the degree of obstruction, venography (gold standard) Treatment: Treat underlying etiology; thrombolysis, stent placement and anticoagulation if catheter induced or life-threatening symptoms  LYMPHATIC SYSTEM Functions of the Lymphatic System 1. Drains excess interstitial fluid (from tissue spaces and returns it to the heart) 2. Returns filtered plasma proteins back to the blood 3. Carry out immune responses 4. Transport dietary lipids  LYMPHEDEMA The abnormal accumulation of interstitial fluid Primary lymphedema: lymphedema without an and fibroadipose tissues resulting from injury, inciting factor. Generally due to a congenital or infection or congenital abnormalities of the inherited condition lymphatic system Often occurs in childhood Occurs when the lymphatic load exceeds the transport capacity of the lymphatic system, Congenital: swelling at birth up to 2 years which causes filtered fluid to accumulate in the Lymphedema praecox: puberty or pregnancy up interstitium to 35 years Persistent accumulation of lymphatic fluid promotes proliferation of adipocytes and Lymphedema tarda: occurs after age 35 years deposition of collagen fibers in the extracellular Involves mostly lower limbs and increased matrix and around capillary and collecting incidence in females lymphatics Lymphedema is a low-output failure of the Secondary lymphedema: occurs as a result of lymphovascular system. The capillary other conditions or treatments (cancer and cancer filtration is normal in patients with treatment, infection, inflammatory disorders, lymphedema. obesity and lymphatic overload)  LYMPHEDEMA Worldwide most common cause is Symptoms: Insidious onset; aching pain in filariasis (infection by a affected limb, feeling of heaviness, tightness or discomfort in the limb with swelling nematode Wuchereria bancrofti) PE: two-thirds are unilateral In the developed world, the Soft and pitting swelling in early stages, majority of cases are secondary dermal thickening, skin dry and firm with and due to malignancy or its progressive fibrosis (cutaneous and treatment subcutaneous thickening) Risk Factors: Cancer and cancer Non-pitting edema in later stages treatment, infection, inflammatory Diagnosis: Clinical disorders (arthritis, dermatitis, Treatment: Conservative management (skin sarcoidosis, inflammatory joint care, physiotherapy and compressive disease), obesity, hereditary therapy/UNNA boots); surgical treatment syndromes (lymphovenous anastomosis or vascularized lymph node transfer) LYMPHEDEMA VS. OTHER CAUSES OF LE EDEMA Lymphedema Edema due to CHF  LYMPHADENOPATHY (LAD) Swollen lymph nodes Evaluation: H&P, labs, imaging, Many potential causes (diseases lymph node biopsy and drugs) Normal lymph nodes are typically 1cm typically abnormal) Consistency of the LN: Hard nodes are found in cancers that induce fibrosis and when previous inflammation has left fibrosis. Fixation of the LN: Normal LN are freely movable in the subcutaneous space; abnormal LN can become fixed to adjacent tissues by invading cancers or inflammation in the tissues surrounding the nodes or fixed to each other Tenderness: suggests recent, rapid enlargement (inflammatory process, immunologic stimulation, and malignancy) Complete physical for signs or symptoms of systemic disease  WORK UP LYMPHADENOPATHY Labs based on history and physical examination clues Imaging: helpful if it is not clear after PE that there is LAD and/or to evaluate surrounding structures for abnormalities. Imaging by CT, US, Doppler, or MRI can help distinguish enlarged LN from other structures and define pathologic process Biopsy Options: Open biopsy, FNA for cytology, Core needle biopsy QUESTIONS??????