Varicose Veins PDF

Varicose veins Prof Ahmed Hussein Varicose vein Dilated elongated turtous veins engorged with blood. Membrane adhesion Molecule expression (ICAM-1, E-selectin,…) Venous valve Venous wall remodeling Pressure and shear stress induced gene expression (TNF, IL-1, …) Causes/ complications: 1- Oedem...

Varicose veins Prof Ahmed Hussein Varicose vein Dilated elongated turtous veins engorged with blood. Membrane adhesion Molecule expression (ICAM-1, E-selectin,…) Venous valve Venous wall remodeling Pressure and shear stress induced gene expression (TNF, IL-1, …) Causes/ complications: 1- Oedema (1) Oedema (2) Oedema (3) 2- Phlebitis Inflammation of the inner layer Healthy vein Vein with phlebitis 3- Venous thrombosis (1) Venous thrombosis (2) Surgical Anatomy of the Lower Limb Veins I. Superficial Veins Long & Short saphenous veins & their tributaries Communicating Veins II.Deep Veins Tibial venae comitantes, popliteal & femoral veins Surgical Anatomy of the Lower Limb Veins Superficial Veins 1. Long & short saphenous veins and their tributaries. 2. Lie in the subcutaneous tissue superficial to the muscle fascia. 3. They have their own, welldeveloped muscle coat. The Long Saphenous Vein The longest vein in the body Surface Anatomy •1 cm anterior to the medial malleolus •One hand breadth posterior to the medial aspect of the patella •Ends on the anteromedial side of the femoral vein 3.5 cm below & lateral to the pubic tubercle It receives the following tributaries near its termination: •Superficial & deep external pudendal vv. •Superficial circumflex iliac v. •Superficial inferior epigastric v. The Short Saphenous Vein Anatomy •Behind the lateral malleolus •Pierces the deep fascia before it enters the popliteal vein •Invariably terminates above the popliteal fossa into the superficial femoral vein •Communicates with the long saphenous vein by several channels Surgical Anatomy of the Lower Limb Veins Deep Veins 1.Accompany axial arteries. 2.Run within the muscles deep to the muscle fascia. Surgical Anatomy of the Lower Limb Veins Comunicating Veins “Perforators” Perforate the fascia connecting the superficial & deep veins at certain points. Perforators Main sites of superficial to deep venous communication Sapheno-femoral junction Dodd perforator Thigh perforators connect to the long saphenous main trunk Mid thigh perforator (Hunter’s canal) Medial calf perforators Boyd gastrocnemius perforators The lower perforators are joined to form the Posterior arch vein Cockett lower leg perforators(3) May or Kuster ankle perforators Just below the knee 10 cm above Just above Just below Medial malleolus Surgical Anatomy of the Lower Limb Veins All lower limb veins have valves to direct venous return in one direction only From below upwards, and from superficial to deep. Venous return With dependency The heart pump Gravity maintaining a pressure gradient across the veins Pooling in dependent limbs may reduce cardiac output by 2 L/min & may cause fainting Venomotor tone Under control of sympathetic system This is counter acted by: [Upright position -- dependant pooling – dec. cardiac output -- inc. sympathetic discharge -- inc. venous tone -- inc. venous return.] Calf muscle contraction Blood is pushed upwards and prevented from retrograde flow by competent venous valves With calf muscle contraction in walking Competent Veno-muscular Pump is composed of: 1. Superficial & deep veins with competent valves. 2. Competent perforating veins communicating the deep & superficial systems 3. Powerful lower limb muscles. Definition The ankle venous pressure during walking is called the “ambulatory venous pressure” A competent venomuscular pump will push the blood towards the heart, thus lowering the ambulatory venous pressure. Varicose veins: Pathological Condition Dilated tortious veins and filled with blood presented with blow outs Types: A- Primary no cause appear B- Secondary: after a previous or current problem as DVT, Pregnancy or obesity CEAP Varicose Veins Classification System Varicose veins are classified according to CEAP classification, which denotes their severity. The classification offers clinicians a choice of 8 stages of varicose vein: •C0 – no visible or palpable signs of venous disease •C1 – telangectasia or reticular veins – dilated blue veins beneath the skin surface •C2 – varicose veins – sub-divided into • C2A = Varicose veins with no symptoms • C2S = Varicose veins with symptoms •C3 – edema – swelling or swollen varicose veins •C4a – varicose veins with associated skin conditions e.g. pigmentation, eczema •C4b – varicose veins with more severe associated skin conditions e.g. lipodermatosclerosis, atrophie blanche •C5 – varicose veins with healed ulcers •C6 – varicose veins with active ulcers, which can be very painful CEAP Varicose Veins Classification System The CEAP system was created in order to standardise the reporting of varicose veins. This comprehensive classification system means that diagnosis and treatment is more uniform. The system was created in 1994 by a committee of the American Venous Forum and is now accepted as the standard scheme by which chronic venous disorders can be classified. CVI Definition CVI collectively describes the manifestations of impaired venous return due to abnormal venous system function. In the majority of cases, it is caused by valve incompetence, and less commonly by venous obstruction. Patho-physiology of CVI chronic venous insufficiency The main defect (problem) in the lower limb venous system may be in the superficial, deep or perforating veins. This problem is usually in the valves (reflux), but sometimes it is in the form of obstruction. (or a combination of both reflux & obstruction) Patho-physiology of CVI The defect may be: Primary defect: related to structural weakness of valves or venous wall, as in 1ry varicose veins Secondary defect: for example due to previous deep venous thrombosis, as in post-phlebitic syndrome Patho-physiology of CVI Whatever the cause of CVI, it will eventually cause venous hypertension of the microcirculation, giving the same symptoms & signs. The severity of symptoms & signs depend on the degree & duration of venous hypertension. When veins fail, the microcirculation suffers. Symptoms & Signs of “CVI” Early 1. Posture related discomfort 2. Lower limb oedema 3. Muscle cramps Persistent & Sever 4. Ankle brown pigmentation 5. Venous eczema 6. Lipodermatosclerosis 7. Venous ulcer Clinical Examination Look for: The patient should be standing The extent and distribution of VV Long saphenous VV Antro-lat. tributary of LSV Short saphenous VV Communicating vein varicosity Clinical Examination Look for: Scars of previous op. Lipodermatosclerosis Some ulcers may potentially bleed Eczema Pigmentation Ulcer Clinical Examination Palpate for: Feel for saphena varix (1cm medial to the femoral a.) & a transmitted cough impulse Dilated short saph v. suggestive of saph-pop incompetence Indurated tender veins suggestive of thrombophlebitis Test for incompetence Brodie –Trendelenburg test Empty the veins & apply a mid thigh tourniquet Let the patient stand If the veins remain empty, but fill after removal of tourniquet, the incompetence must be above the tourniquet If the veins fill before removal of tourniquet, the incompetence must be below the tourniquet Perthes’ walking test Place a tourniquet around the thigh while the patient is standing (note that the vv are full) Let the patient walk in place If the veins empty with walking, then the tourniquet is preventing superficial reflux from an incompetent valve above, while deep veins are patent with intact valves. Investigations of Venous Disease Investigations have two aims: 1. Identify the existence, site & degree of venous reflux. 2. Confirm deep venous patency. Identification of venous reflux: 1. Doppler Ultrasound: portable bedside examination It is accurate in detecting sapheno-femoral reflux in the groin. •Hold the Doppler probe on the groin and detect the venous signal •Squeeze the calf. This will augment the signal •If the SFJ is incompetent, you will hear a biphasic signal due to retrograde flow Identification of venous reflux: 2. Coloured Duplex Ultrasonography: 1. Visually demonstrates venous reflux into the superficial and deep veins. 2. The degree of venous reflux can be assessed. (Dynamic Study) 3. Can detect incompetent perforators. Coloured Duplex Ultrasonography The colour reflects the direction of blood flow Coloured Duplex Ultrasonography With straining: Normal direction of venous return Reflux into the GSV with arrest of flow in the femoral vein (competent deep system) Identification of venous reflux: 3. Photoplethysmography: Gives a global idea about the existence & degree of reflux as a whole 4. Descending venography: Mainly used to detect reflux into the deep veins. It is a static study, and is now replaced by colour duplex. Confirming Deep Venous Patency: As in patients with suspected post-phlebitic syndrome (chronic complication of maltreated DVT) 1. Duplex Ultrasound 2. Ascending Venography Normal Ascending Venography A.P. Lat. Management of 1ry VV Minor VV Support stocking Trunk VV (long or short saphenous) with incompetence Sapheno-femoral / sapheno-popliteal ligation with stripping of the long or short saphenous vein. (no need to strip the long saph. In the leg) Injection compression sclerotherapy Branch Varicosities Avulsion/ligation via multiple stabs Incompetent perforators (detected by Duplex) Individual ligation Sapheno-femoral incompetence: A. Can be assessed by the Brodie – Trendelenburg test B. Can be treated by sapheno-popliteal ligation C. Can be treated by sclerotherapy D. Can be treated by Trendelenburge procedure E. May transmit a cough impulse to the long saphenous vv Recurrent varicose veins A. Are more common if the long saphenous vein is not tied flush in the first procedure B. Are more common if incompetent perforators are not identified at the first procedure C. Should be investigated by duplex ultrasound D. Can be treated with sclerotherapy Surgery for VV affecting the long saphenous system A. The skin incision is placed lateral to the femoral artery B. A vertical incision is used routinely C. The sapheno-femoral junction is usually 3-4 cm inferolateral to the pubic tubercle D. There are usually 4 named tributaries E. The long saphenous vein must be stripped from ankle to groin to avoid damage to the saphenous nerve A. Varicose vein surgery B. IV heparin C. Elevation and NSAIDs D. Compression and warfarin For each of the patients described below, select the most likely intervention from the list of options above Each option may be used once, more than once, or not at all. 1. A 54-year-old man with varicose veins and bleeding varicose ulcer 2. A 30-year-old woman with varicose veins and an acute episode of thrombophlebitis 3. A 45-year-old woman with varicose veins and a swollen leg. Duplex confirms DVT. Venous Ulcers Is a complication of varicose veins Site: Starts at Medial Maleeolus Siz1e” Can attain any size Venous Ulcers Pathophysiology Venous Ulcers Venous Ulcers Venous Ulcers Pathology High velocity of blood stream from in-out during muscle contraction Injury to the long saphenous and skin Venous Ulcers Complications” 1- Increase in size 2- Chronicity 3= Malignant change (Marjolin Ulcer) 4- Infections and disability Venous Ulcers History of DVT Physical Examination” 1- in majority of cases “ only ulceration 2- Combination with Varicose veins is not common 3-Site” in front of the medial malleolus can extend above over the medial side of the ;eg 4- Extensive oozing from the ulcer always wet Venous Ulcers Investigations: A- Lab 1- D-Dimers 2- PT and APTT B- Imaging 1- Doppler 2- Diplex C- Invasive 1- Angiography 2- Biopsy Venous Ulcers Treatment 1- devascularization by removal of the long saphenous vein below the knee 2- SSG Venous Ulcers Pathology High velocity of blood stream from in-out during muscle contraction Injury to the long saphenous and skin Venous Ulcers Complications” 1- Increase in size 2- Chronicity 3= Malignant cjange 4- Infections and disability Phlegmasia Alba Dolin's Phlegmasia cerulea dolens Phlegmasia cerulea dolens CHRONIC VENOUS ULCERS 2008- ESPRS AHMED RAHOMA CHRONIC VENOUS ULCERS 2008- ESPRS AHMED RAHOMA CHRONIC VENOUS ULCERS Introduction: Varicose veins without ulcer 2008- ESPRS AHMED RAHOMA DEEP VEIN THROMBOSIS Causes 1- Slow venous stream 2- More viscosity of blood 3- Endothelial injuries • Example Post partum • After long surgeries Pathophysiology 1-Platelet plug 2- Blood clot 3- Mild infection Destruction of valve systems Clinical Features Pain, low grade fever Tachycardia Risks factors for DVT • • • • Thrombi were detected in: 54 percent of patients with major head injuries 61 percent of patients with pelvic fracture 77 percent of patients with tibial fracture 80 percent of those with femoral fracture. Risk Factors for DVT • Minor injuries — one not requiring surgery, a plaster cast, hospitalization, or extended bed rest at home for at least four days). • A minor injury occurring in the preceding 3 to 4 weeks was associated with a 3- to 5-fold increase in DVT risk. • In carriers of factor V Leiden, this risk was increased 50-fold. • Intravenous drug use — Direct trauma, irritation, and infection may be responsible for the high incidence of DVT noted in young drug users who inject these agents directly into their femoral veins. • Pregnancy — Pregnancy is associated with an increased risk of thrombosis that may be due in part to obstruction of venous return by the enlarged uterus, as well as the hypercoagulable state associated with pregnancy. • Estimates of the age-adjusted incidence of VTE range from 5 to 50 times higher in pregnant versus non-pregnant women. Pathophysiology • VIRCHOW'S TRIAD — A major theory delineating the pathogenesis of venous thromboembolism (VTE), often called Virchow's triad, proposes that VTE occurs as a result of: • Alterations in blood flow (i.e., stasis) • Vascular endothelial injury • Alterations in the constituents of the blood (i.e., inherited or acquired hypercoagulable state) • Classic symptoms of DVT include swelling, pain, and discoloration in the involved extremity. • Personal or Family history • Cancer DVT Physical Exam General : • Tachycardia • Low grade fever • Pain in affected lower limb • Swelling Signs: • Edema, principally unilateral, is the most specific symptom. Massive edema with cyanosis and ischemia (phlegmasia cerulea dolens) is rare. • Leg pain occurs in 50% of patients, but this is entirely nonspecific. Pain can occur on dorsiflexion of the foot (Homans sign). DVT Physical Exam Homan’s sign • Discomfort in the calf muscles on forced dorsiflexion of the foot with the knee straight has been a time-honored sign of DVT. However, this sign is present in less than one third of patients with confirmed DVT. • The Homan’s sign is found in more than 50% of patients without DVT and, therefore, is nonspecific. DVT Physical Exam -Tenderness occurs in 75% of patients but is also found in 50% of patients without objectively confirmed DVT. -Clinical signs and symptoms of PE as the primary manifestation occur in 10-50% of patients with confirmed DVT. -The pain and tenderness associated with DVT does not usually correlate with the size, location, or extent of the thrombus. -Warmth or erythema of skin can be present over the area of thrombosis DVT Physical Exam o Superficial thrombophlebitis is characterized by the finding of a palpable, indurated, cordlike, tender, subcutaneous venous segment. o Forty percent of patients with superficial thrombophlebitis without coexisting varicose veins and with no other obvious etiology (e.g., intravenous catheters, intravenous drug abuse, soft tissue injury) have an associated DVT. DVT Diagnosis • The Wells clinical prediction guide quantifies the pretest probability of DVT. • The model enables providers to reliably stratify their patients into high-, moderate-, or low-risk categories. • Combining this with the results of objective testing greatly simplifies the clinical workup of patients with suspected DVT. • The Wells clinical prediction guide incorporates risk factors, clinical signs, and the presence or absence of alternative diagnoses. Wells Score • Paralysis, paresis, or recent orthopedic casting of a lower extremity (1 point) • Recently bedridden for longer than three days or major surgery within the past four weeks (1 point) • Localized tenderness in the deep vein system (1 point) • Swelling of an entire leg (1 point) Wells Score • Calf swelling 3 cm greater that the other leg, measured 10 cm below the tibial tuberosity (1 point) • Pitting edema greater in the symptomatic leg (1 point) • Collateral non-varicose superficial veins (1 point) Wells Score • Active cancer or cancer treated within six months (1 point) • Alternative diagnosis more likely than DVT (e.g., Baker's cyst, cellulitis, muscle damage, post phlebitic syndrome, inguinal lymphadenopathy, external venous compression (-2 points) Clinical Parameter Score Score Active cancer (treatment ongoing, or within 6 mo or palliative) +1 Paralysis or recent plaster immobilization of the lower extremities +1 Recently bedridden for >3 d or major surgery <4 wk +1 Localized tenderness along the distribution of the deep venous system +1 Entire leg swelling +1 Calf swelling >3 cm compared with the asymptomatic leg +1 Pitting edema (greater in the symptomatic leg) +1 Previous DVT documented +1 Collateral superficial veins (nonvaricose) +1 Alternative diagnosis (as likely or greater than that of DVT) -2 Total of Above Score High probability >3 Moderate probability 1 or 2 Low probability <0 Reference for Modified Wells Score • Adapted from JAMA. 1998 Apr 8;279(14):1094-9. • Value of assessment of pretest probability of deep-vein thrombosis in clinical management. Wells PS; Anderson DR; Bormanis J; Guy F; Mitchell M; Gray L; Clement C; Robinson KS; Lewandowski B. Lancet 1997 Dec 20-27;350(9094):1795-8. DVT Diagnosis • DVT was documented in 3, 17, and 75 percent of patients with low, moderate, and high pretest probabilities, respectively. • Serial ultrasonography was required in 28 percent and venography in 6 percent of patients; venous thromboembolism was diagnosed during a three month follow-up period in only 0.6 percent of patients thought not to have a DVT by this algorithm. DVT D-dimer • Recent interest has focused on the use of D-dimer in the diagnostic approach to DVT. • D-dimer fibrin fragments are present in fresh fibrin clot and in fibrin degradation products of cross-linked fibrin. • Monoclonal antibodies specific for the D-dimer fragment are used to differentiate fibrin-specific clot from non–cross-linked fibrin and from fibrinogen. • These specific attributes of the D-dimer antibodies account for their high sensitivity for venous thromboembolism. DVT D-dimer • D-dimer level may be elevated in any medical condition where clots form. • D-dimer level is elevated in trauma, recent surgery, hemorrhage, cancer, and sepsis. • Many of these conditions are associated with higher risk for DVT. • The D-dimer assays have low specificity for DVT; therefore, they should only be used to rule out DVT, not to confirm the diagnosis of DVT. Medical Conditions Associated With an Elevated D-dimer Arterial thromboembolic disease • Myocardial infarction • Stroke • Acute limb ischemia • Atrial fibrillation • Intracardiac thrombus Medical Conditions Associated With an Elevated D-dimer • • • • Venous thromboembolic disease Deep vein thrombosis Pulmonary embolism Disseminated intravascular coagulation Preeclampsia and eclampsia Abnormal fibrinolysis; use of thrombolytic agents Medical Conditions Associated With an Elevated D-dimer Systemic inflammatory response syndrome Vasoocclusive episode of sickle cell disease Severe liver disease (decreased clearance) Malignancy Medical Conditions Associated With an Elevated D-dimer Renal disease • Nephrotic syndrome (e.g., renal vein thrombosis) • Acute renal failure • Chronic renal failure and underlying cardiovascular disease Normal pregnancy Venous malformations DVT D-dimer • D-dimer levels remain elevated in DVT for about 7 days. • Patients presenting late in the course, after clot organization and adherence have occurred, may have low levels of D-dimer. • Similarly, patients with isolated calf vein DVT may have a small clot burden and low levels of D-dimer that are below the analytic cut-off value of the assay. • This accounts for the reduced sensitivity of the D-dimer assay in the setting of confirmed DVT. DVT D-dimer • Many different D-dimer assays are available, with varying sensitivities and specificities. • The assays are not standardized. • They incorporate different monoclonal antibodies to the D-dimer fragment. • Results may be reported quantitatively or qualitatively. • Different units may be used. • Some assay results are reported as fibrinogen equivalent units (FEU) and others in nanograms per milliliter (ng/mL). • The results of one assay cannot be extrapolated to another. DVT D-dimer • Most studies have confirmed the clinical utility of D-dimer testing, and most clinical algorithms incorporate their use. • Providers should know their lab's D-dimer assay DVT D-dimer D-dimer results should be used as follows: o A negative D-dimer assay result rules out DVT in patients with low-tomoderate risk and a Wells DVT score less than 2. o All patients with a positive D-dimer assay result and all patients with a moderate-to-high risk of DVT (Wells DVT score >2) require a diagnostic study (duplex ultrasonography). DVT D-dimer • A D-dimer level less than 200 to 500 ng/mL by ELISA or a negative SimpliRED assay in conjunction with a low clinical probability of DVT appears to be useful and cost- effective in excluding DVT without the need for an ultrasound examination. DVT D-dimer • This has been shown to hold in populations at high risk of having DVT, such as those with malignancy, as well as in populations in which the Wells score and the D-dimer may have reduced specificity, such as in the elderly. Diagnosis of DVT • In most circumstances, compression ultrasonography is the noninvasive approach of choice for the diagnosis of patients with suspected DVT. • If unavailable, impedance plethysmography with serial studies is an acceptable alternative. • One exception noted above is that impedance plethysmography is preferred for possible recurrent DVT since it normalizes more quickly after a previous episode than compression ultrasonography. Compression Ultrasonography The diagnosis of venous thrombosis using compression ultrasonography is made by the findings such as: • Abnormal compressibility of the vein • Abnormal Doppler color flow • The presence of an echogenic band • Abnormal change in diameter during the Valsalva maneuver Compression Ultrasonography • Color flow imaging, in addition to duplex Doppler ultrasound, is a less demanding study and is also highly accurate for the diagnosis of above the knee DVT. Duplex-Doppler ultrasound image of an acute superficial femoral vein thrombosis (labeled "V") Blue color indicates venous blood flow and red indicates arterial blood flow (labeled "A"). Echogenic white speckles are seen in the vein which was non-compressible with the ultrasound probe. Compression Ultrasonography o Duplex ultrasonography is also helpful to differentiate venous thrombosis from hematoma, Baker cyst, abscess, and other causes of leg pain and edema. o Diagnostic accuracy varies depending on local expertise. MRI o MRI is the diagnostic test of choice for suspected iliac vein or inferior vena caval thrombosis when CT venography is contraindicated or technically inadequate. o In the second and third trimester of pregnancy, MRI is more accurate than duplex ultrasonography because the gravid uterus alters Doppler venous flow characteristics. o Expense, lack of general availability, and technical issues limit its use. Screening For A Hypercoaguable State Screening test interference — • A number of factors can interfere with screening tests for thrombophilia. • Therefore, it is generally best not to undertake testing at the time of presentation with VTE. Screening For A Hypercoaguable State Confounding Factors • Acute thrombosis • Heparin therapy • Coumadin therapy Complications 1- Recurrence 2- Pulmonary embolism 3- Varicose veins 4- Venous ulcer 5- Post phlebetic Syndrome 6- Deep venous insufficiency Complications 1- Recurrence Patient should be on anticoagulants for life as recurrence may occur any time. 2-Thromboembolism • Inherited • Acquired Inherited VE Inherited thrombophilia • Factor V Leiden mutation • Prothrombin gene mutation • Protein S deficiency • Protein C deficiency • Antithrombin (AT) deficiency • Rare disorders • Dysfibrinogenemia Acquired VE • Malignancy • Presence of a central venous catheter • Surgery, especially orthopedic • Trauma • Pregnancy • Oral contraceptives • Hormone replacement therapy Categories of risk for venous Thromboembolism in surgical patients A- Low risk: Minor surgery in patients <40 years of age with no additional risk factors present* • Risk of calf DVT: 2 percent • Risk of proximal DVT: 0.4 percent • Risk of clinical PE: 0.2 percent • Risk of fatal PE: <0.01 percent Categories of risk for venous thromboembolism in surgical patients • • • • B- Moderate risk: Minor surgery in patients with additional risk factor present*, or Surgery in patients aged 40-60 with no additional risk factor Risk of calf DVT: 10-20 percent Risk of proximal DVT: 2-4 percent Risk of clinical PE: 1-2 percent Risk of fatal PE: 0.1-0.4 percent Categories of risk for venous thromboembolism in surgical patients • • • • C- High risk: Surgery in patients >60, or Surgery in patients aged 40-60 with additional risk factor* Risk of calf DVT: 20-40 percent Risk of proximal DVT: 4-8 percent Risk of clinical PE: 2-4 percent Risk of fatal PE: 0.4-1.0 percent Categories of risk for venous thromboembolism in surgical patients D- Highest risk: Surgery in patients >40 with multiple risk factors*, or Hip or knee arthroplasty, hip fracture surgery, or Major trauma, spinal cord injury • Risk of calf DVT: 40-80 percent • Risk of proximal DVT: 10-20 percent • Risk of clinical PE: 4-10 percent • Risk of fatal PE: 0.2-5 percent Acquired VE • Oral contraceptive pills that contain third-generation progestins are the most important cause of thrombosis in young women. • The risk of thrombosis increases within four months of the initiation of therapy and is unaffected by duration of use. • The risk decreases to previous levels within three months of cessation. • An increased risk for VTE has also been found in women using contraceptive transdermal patches and ring. Acquired VE • • • • • • • • Tamoxifen, Bevacizumab, Thalidomide, Lenalidomide Immobilization Congestive failure Antiphospholipid antibody syndrome Myeloproliferative disorders Polycythemia vera Essential thrombocythemia Paroxysmal nocturnal hemoglobinuria Acquired VE • • • • • • • • Inflammatory bowel disease Nephrotic syndrome Hyperviscosity Waldenstrom's macroglobulinemia Multiple myeloma Marked leukocytosis in acute leukemia Sickle cell anemia HIV/AIDS Causes of Thromboembolism • Inherited causes • >48 hours of immobility in the preceding month • Hospital admission • Surgery • Malignancy • Infection in the past three months • Current hospitalization Other complications • Venous ulcer Other complications • Varicose veins Other complications • Post phlebitis Syndrome Other complications Post phlebitis Syndrome Other complications Treatment of DVTObjectives • Prevention of acute pulmonary embolism • Reducing the risk of recurrent thrombosis • Treatment of massive iliofemoral thrombosis with acute lower limb ischemia and/or venous gangrene (i.e., phlegmasia cerulea dolens) • Limiting the development of late complications, such as the postphlebitic syndrome, chronic venous insufficiency, and chronic thromboembolic pulmonary hypertension. Treatment of DVT • Anticoagulant therapy Treatment of DVT • The use of thrombolytic agents, (Kinases) • Patients with hemodynamically unstable PE or massive iliofemoral thrombosis (i.e., phlegmasia cerulea dolens), and who are also at low risk to bleed, are the most appropriate candidates for such treatment. Treatment of DVT • Inferior vena caval filter Treatment of DVT • Oral anticoagulation with warfarin should prolong the INR to a target of 2.5 (range: 2.0 to 3.0). • If oral anticoagulants are contraindicated or inconvenient, longterm therapy can be undertaken with either adjusted-dose unfractionated heparin, low molecular weight heparin, or fondaparinux. Treatment of DVT • During initial ambulation, and for the first two years following an episode of VTE, use of an elastic compression stocking has been recommended to prevent the postphlebitic syndrome. PE classification • Acute vs. chronic • Massive vs. submassive PE Classification • A saddle PE is a PE that lodges at the bifurcation of the main pulmonary artery into the right and left pulmonary arteries. • Most saddle PE are submassive. • In a retrospective study of 546 consecutive patients with PE, 14 (2.6 percent) had a saddle PE. • Only two of the patients with saddle PE had hypotension. • 1- Pulmonary Hypertension • 2- Pulmonary Infarction • 3- Central Shock PE Risk Factors • PE is a common complication of deep vein thrombosis (DVT), occurring in more than 50 percent of cases with phlebographically confirmed DVT. • This suggests that factors that promote the development of DVT also increase the risk for PE. PE Additional Risks Factors in Women • Obesity (BMI ≥29 kg/m2) • Heavy cigarette smoking (>25 cigarettes per day) • Hypertension PE Symptoms • In the Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II), the following frequencies of symptoms and signs were noted among patients with PE who did not have preexisting cardiopulmonary disease: PE Symptoms • Dyspnea at rest or with exertion (73 percent). The onset of dyspnea was usually within seconds (46 percent) or minutes (26 percent). • Pleuritic pain (44 percent) • Cough (34 percent) • >2-pillow orthopnea (28 percent) • Calf or thigh pain (44 percent) • Calf or thigh swelling (41 percent), • Wheezing (21 percent) PE Signs The most common signs were • Tachypnea (54 percent) • Tachycardia (24 percent) • Rales (18 percent) • Decreased breath sounds (17 percent) • An accentuated pulmonic component of the second heart sound (15 percent), • Jugular venous distension (14 percent) PE DVT Symptoms • Symptoms or signs of lower extremity deep venous thrombosis (DVT) were common (47 percent). • They included edema, erythema, tenderness, or a palpable cord in the calf or thigh. PE Labs Routine laboratory findings are nonspecific. • Leukocytosis • An increased erythrocyte sedimentation rate (ESR) • Elevated serum LDH or AST (SGOT) • Normal serum bilirubin. PE Arterial Blood Gases (ABG’s) • Arterial blood gas (ABG) measurements and pulse oximetry have a limited role in diagnosing PE. • ABG’s usually reveal hypoxemia, hypocapnia, and respiratory alkalosis. PE ABG’s • Patients with room air pulse oximetry readings <95 percent at the time of diagnosis are at increased risk of inhospital complications, including respiratory failure, cardiogenic shock, and death. PE Chest X-Ray • Radiographic abnormalities are common in patients with PE; however, they are not helpful diagnostically because they are similarly common in patients without PE. PE Ventilation/Perfusion V/Q Scan • Unfortunately, the combinations of clinical and lung scan probability that was found in most patients had a diagnostic accuracy of only 15 to 86 percent, which is insufficient to either confirm or exclude the diagnosis of PE. • Additional testing is required in this situation. PE Venous Ultrasound However, there are flaws to this approach: • False positive venous ultrasound studies (3 percent in one report) will result in the anticoagulation of some patients who do not have DVT or PE, thus subjecting them to unnecessary risk. • Many patients with PE are likely to be missed. • In one report, only 29 percent of patients with PE (determined by V/Q scan or pulmonary angiogram) had venous thrombosis detected by compression ultrasound. PE D-dimer Sensitivity • D-dimer levels are abnormal in approximately 95 percent of all patients with PE when measured by ELISA, quantitative rapid ELISA, or semi-quantitative rapid ELISA. PE D-dimer Specificity • D-dimer levels are normal in only 40 to 68 percent of patients without PE, regardless of the assay used. • This is a consequence of abnormal D-dimer levels being common among hospitalized patients, especially those with malignancy or recent surgery. • The specificity may decrease further with increasing patient age. PE Spiral CT • Due to its widespread availability, spiral (helical) CT scanning with intravenous contrast (i.e., CT pulmonary angiography or CTPA) is being used increasingly as a diagnostic modality for patients with suspected PE. • One of the most commonly cited benefits of CT-PA is the ability to detect alternative pulmonary abnormalities that may explain the patient's clinical presentation. PE Echocardiography • Only 30 to 40 percent of patients with PE have echocardiographic abnormalities suggestive of acute PE.