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Venous Thromboembolism (VE)- Deep Vein Thrombosis (DVT) and Pulmonary Embolus (PE) Victoria E. Judd M.D.

Venous Thromboembolism (VE)- Deep Vein Thrombosis (DVT) and Pulmonary Embolus (PE) Victoria E. Judd M.D

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  • Venous Thromboembolism (VE)- Deep Vein Thrombosis (DVT) and Pulmonary Embolus (PE) Victoria E. Judd M.D.
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  • Objectives Discuss common presentation of Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) Describe evidence-based diagnostic and therapeutic strategies for DVT/PE Identify when to screen for a hypercoaguable state
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  • Causes of Thromboembolism Inherited Acquired
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  • Inherited VE Inherited thrombophilia Factor V Leiden mutation Prothrombin gene mutation Protein S deficiency Protein C deficiency Antithrombin (AT) deficiency Rare disorders Dysfibrinogenemia
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  • Other Plasma Factors In a single, large, population- based case control study performed in the Netherlands, a two to threefold increased risk for a first episode of venous thrombosis was found for elevated levels of a number of plasma components, coagulant factors, and inflammatory chemokines.
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  • Other Plasma Factors Plasma factor IX antigen Plasma factor XI antigen Thrombin activatable fibrinolysis inhibitor (TAFI) Interleukin 8 Fibrinogen Low levels of tissue factor pathway inhibitor Low plasma fibrinolytic activity Elevated plasma fibronectin levels
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  • Acquired VE Malignancy Presence of a central venous catheter Surgery, especially orthopedic Trauma Pregnancy Oral contraceptives Hormone replacement therapy
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  • Categories of risk for venous thromboembolism in surgical patients Low risk: Minor surgery in patients
  • Categories of risk for venous thromboembolism in surgical patients 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
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  • Categories of risk for venous thromboembolism in surgical patients 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
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  • Categories of risk for venous thromboembolism in surgical patients * Additional risk factors include one or more of the following: advanced age, cancer, prior venous thromboembolism, obesity, heart failure, paralysis, or presence of a molecular hypercoagulable state (e.g., protein C deficiency, factor V Leiden). Data from Geerts, WH, et al. Chest 2004; 126:3385.
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  • 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.
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  • Acquired VE Tamoxifen, Bevacizumab, Thalidomide, Lenalidomide Immobilization Congestive failure Antiphospholipid antibody syndrome Myeloproliferative disorders Polycythemia vera Essential thrombocythemia Paroxysmal nocturnal hemoglobinuria
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  • Acquired VE Inflammatory bowel disease Nephrotic syndrome Hyperviscosity Waldenstrom's macroglobulinemia Multiple myeloma Marked leukocytosis in acute leukemia Sickle cell anemia HIV/AIDS
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  • Causes of Thromboembolism Fifty percent of thrombotic events in patients with inherited thrombophilia are associated with the additional presence of an acquired risk factor (e.g., surgery, prolonged bed rest, pregnancy, oral contraceptives).
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  • Causes of Thromboembolism Some patients have more than one form of inherited thrombophilia or more than one form of acquired thrombophilia and appear to be at even greater risk for thrombosis.
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  • Causes of Thromboembolism In a population-based study of the incidence of venous thromboembolism (VTE), 56 percent of the patients had three or more of the following six risk factors present at the time of VTE:
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  • Causes of Thromboembolism >48 hours of immobility in the preceding month Hospital admission Surgery Malignancy Infection in the past three months Current hospitalization
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  • Incidence of pulmonary embolism according to distance traveled by air
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  • This figure indicates the incidence of pumonary embolism per million passenger arrivals, arranged according to flight distance in kilometers. Error bars indicate 95 percent confidence limits. To convert kilometers to miles, multiply by 0.62. Data from Lapastolle, F, et al. N Engl J Med 2001; 345:779.
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  • Seasonal variation in venous thromboembolism
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  • Depicted are the monthly percentage variations in French hospital admissions for deep vein thrombosis and pulmonary embolism. Hospital admissions for venous thromboembolism were most frequent in the winter and least frequent in the summer. Reproduced with permission from: Boulay, F, Berthier, F, Schoukroun, G, et al. Seasonal variations in hospital admission for deep venous thrombosis and pulmonary embolism: analysis of discharge data. BMJ 2001; 323:601. Copyright 2001, BMJ.
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  • Risks Factors for DVT The risk of thrombosis is increased in all forms of major injury. In one study of 716 patients admitted to a regional trauma unit, DVT in the lower extremities was found in 58 percent of patients with adequate venographic studies; 18 percent had proximal vein thrombosis.
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  • 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.
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  • Risk Factors for DVT Minor injuries A large population- based study investigated the VTE risk following a minor injury (i.e., 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.
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  • Risks Factors for DVT 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.
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  • Risk Factors for DVT 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.
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  • 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)
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  • Deep Vein Thrombosis (DVT) The thrombotic risk associated with the inherited thrombophilias has been assessed in two ways: evaluation of patients with deep vein thrombosis, and evaluation of families with thrombophilia.
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  • DVT In a Spanish study of 2132 consecutive unselected patients with venous thromboembolism, for example, 12.9 percent had an anticoagulant protein deficiency (7.3 percent with protein S, 3.2 percent with protein C, and 0.5 percent with antithrombin). An additional 4.1 percent had antiphospholipid antibodies (aPL).
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  • Risks and incidence of a first episode of venous thrombosis Adult subjects only. Data from the Leiden Thrombophilia Study.
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  • Condition/risk factor(s)Relative risk Incidence, percent per year Normal 10.008 Hyperhomocysteinemia (MTHFR 677T mutation) 2.50.02 Prothrombin gene mutation 2.80.02 Oral contraceptives 40.03 Factor V Leiden (heterozygous) 70.06 Oral contraceptives plus heterozygous factor V Leiden 350.29 Factor V Leiden (homozygous) 800.5-1.0
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  • DVT Similar findings were noted in a series of 277 Dutch outpatients with deep vein thrombosis: 8.3 percent had an isolated deficiency of antithrombin, protein C, protein S, or plasminogen compared to 2.2 percent of controls. The incidence of a protein deficiency was only modestly greater in "high risk" patients with recurrent, familial, or juvenile onset deep vein thrombosis (9, 16, and 12 percent respectively).
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  • DVT The overall 8 to 13 percent incidence of an isolated anticoagulant protein deficiency in patients with deep vein thrombosis does not include the contribution of factor V Leiden or the prothrombin gene mutation, now considered to be the most common causes of inherited thrombophilia.
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  • DVT The Physicians' Health Study and the Leiden Thrombophilia Study found a 12 to 19 percent incidence of heterozygosity for the factor V Leiden mutation in patients with a first DVT (or pulmonary embolism in the Physicians' Health Study) compared to 3 to 6 percent in controls.
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  • DVT The incidence reached 26 percent in the Physicians' Health Study in 31 men over the age of 60 with no identifiable precipitating factors. The incidence of the prothrombin gene mutation is approximately 6 to 8 percent in patients with deep vein thrombosis compared to 2 to 2.5 percent in controls.
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  • DVT The total incidence of an inherited thrombophilia in subjects with a deep vein thrombosis ranges from 24 to 37 percent overall compared to about 10 percent in controls. Another 25 percent of patients appear to have elevated factor VIII levels, although it has not been proven that this is an inherited characteristic.
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  • DVT There are a number of questions that arise when a patient is suspected of having deep vein thrombosis (DVT) of the lower extremity.
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  • DVT What is the differential diagnosis and what are the possible risk factors for DVT? What is the best way to diagnose or exclude DVT?
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  • DVT What is the appropriate initial therapy for DVT; when is hospitalization not required? What is the recommended long- term treatment for DVT (e.g., agents to use, monitoring the degree of anticoagulation, length of time treatment is needed)?
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  • DVT When should one screen for the presence of a hypercoagulable state, not only in the patient, but also in family members?
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  • DVT INITIAL APPROACH When approaching the patient with suspected DVT of the lower extremity, it is important to appreciate that only a minority of patients actually have the disease and will require anticoagulation.
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  • DVT This illustrates the importance of using validated algorithms to evaluate patients with suspected DVT, along with objective testing to establish the diagnosis. Given the potential risks associated with proximal lower extremity DVT that is not treated (e.g., fatal pulmonary emboli) and the potential risk of anticoagulating a patient who does not have a DVT (e.g., fatal bleeding), accurate diagnosis is essential.
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  • DVT History Classic symptoms of DVT include swelling, pain, and discoloration in the involved extremity. There is not necessarily a correlation between the location of symptoms and the site of thrombosis.
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  • DVT History Symptoms in the calf alone are often the presenting manifestation of significant proximal vein involvement, while some patients with whole leg symptoms are found to have isolated calf vein DVT.
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  • DVT History A complete thrombosis history includes the age of onset, location of prior thromboses, and results of objective diagnostic studies documenting thrombotic episodes in the patient, as well as in any family members. A positive family history is particularly important, since a well documented history of venous thrombosis in one or more first-degree relatives strongly suggests the presence of a hereditary defect.
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  • DVT History Recent potential precipitating conditions Underlying conditions: i.e. cancer, collagen-vascular disorders Medications
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  • DVT Physical Exam Special attention should be directed to: The vascular system Extremities (e.g., looking for signs of superficial or deep vein thrombosis) Chest Heart Abdominal organs Skin (e.g., skin necrosis, livedo reticularis).
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  • DVT Physical Exam There may be pain and tenderness in the thigh along the course of the major veins ("painful deep vein syndrome"). Tenderness on deep palpation of the calf muscles is suggestive, but not diagnostic. Homan's sign is unreliable.
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  • DVT Physical Exam A 2005 meta-analysis of diagnostic cohort studies of patients with suspected DVT concluded the following concerning these physical findings: Only a difference in calf diameters (likelihood ratio, LR 1.8; 95% CI 1.5- 2.2) was of potential value for ruling in DVT.
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  • DVT Physical Exam Only absence of calf swelling (LR 0.67; 95% CI 0.58-0.78) and absence of a difference in calf diameters (LR 0.57; 95% CI 0.44-0.72) were of potential value for ruling out DVT Individual clinical features are poorly predictive of DVT when not combined in a formal prediction rule (e.g., Wells score, see below).
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  • DVT Physical Exam Many patients are asymptomatic; however, the history may include the following: 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).
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  • DVT Physical Exam Homans 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 Homans sign is found in more than 50% of patients without DVT and, therefore, is nonspecific.
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  • 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
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  • DVT Physical Exam oSuperficial thrombophlebitis is characterized by the finding of a palpable, indurated, cordlike, tender, subcutaneous venous segment. oForty 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.
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  • DVT Differential Diagnosis In one study of 160 consecutive patients with suspected DVT who had negative venograms, the following causes of leg pain were identified: Muscle strain, tear, or twisting injury to the leg 40 percent Leg swelling in a paralyzed limb 9 percent
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  • DVT Differential Diagnosis Lymphangitis or lymph obstruction 7 percent Venous insufficiency (reflux) 7 percent Baker's cyst 5 percent Cellulitis 3 percent Knee abnormality 2 percent Unknown 26 percent
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  • DVT Diagnosis The clinical assessment of patients with suspected DVT is often difficult because of the interplay between risk factors and the nonspecific nature of the physical findings. Clinicians have observed that a discordance is often present between the clinical assessment and the results of objective testing.
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  • DVT Diagnosis One report of 593 patients with suspected DVT validated a measure of pretest probability in conjunction with an algorithm designed to minimize the use of venography or repeat ultrasonography. The measure of pretest probability is referred to as the Wells score or Wells criteria for DVT probability:
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  • 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.
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  • DVT Diagnosis For example, patients deemed to be at high risk for DVT may have a negative finding on duplex ultrasonographic study. In this case, the probability of DVT is still greater than 20% when the known sensitivity, specificity, and negative likelihood ratio of duplex ultrasonography are considered. Having an objective method to determine pretest probability simplifies clinical management.
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  • 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)
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  • 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)
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  • 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)
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  • Clinical Parameter ScoreScore 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 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>3 Moderate probability1 or 2 Low probability95 percent) and specific (>95 percent) for proximal vein thrombosis.">
  • Compression Ultrasonography Prospective studies have demonstrated that lack of compressibility of a vein with the ultrasound probe is highly sensitive (>95 percent) and specific (>95 percent) for proximal vein thrombosis.
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  • 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.
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  • 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.
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  • Compression Ultrasonography In comparison, the presence of an echogenic band, although sensitive for DVT, has a specificity of only about 50 percent. The variation of venous size with the Valsalva maneuver has a low sensitivity and specificity for the presence of DVT and is not performed in many centers.
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  • Compression Ultrasonography Serial studies need to be performed when the initial test is negative; approximately 2 percent of patients with an initially negative ultrasound develop a positive study when retested seven days later. A single repeat study that is negative five to seven days after an initial negative study predicts a less than 1 percent likelihood of venous thromboembolism over months of follow-up.
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  • Compression Ultrasonography oDuplex ultrasonography is also helpful to differentiate venous thrombosis from hematoma, Baker cyst, abscess, and other causes of leg pain and edema. oDiagnostic accuracy varies depending on local expertise.
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  • MRI oMRI is the diagnostic test of choice for suspected iliac vein or inferior vena caval thrombosis when CT venography is contraindicated or technically inadequate. oIn the second and third trimester of pregnancy, MRI is more accurate than duplex ultrasonography because the gravid uterus alters Doppler venous flow characteristics. oExpense, lack of general availability, and technical issues limit its use.
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  • Screening For A Hypercoaguable State A biologic risk factor for venous thrombosis can be identified in over 60 percent of Caucasian patients with idiopathic DVT. In addition, there is often more than one factor at play in a given patient. As an example, 50 percent of thrombotic events in patients with inherited thrombophilia are associated with an accompanying acquired risk factor (e.g., surgery, pregnancy, use of oral contraceptives).
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  • Screening For A Hypercoaguable State There is currently no consensus regarding whom to test for inherited thrombophilia. The likelihood of identifying an inherited thrombophilia is increased several-fold by screening only patients with one or more of the following:
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  • Screening For A Hypercoaguable State Initial thrombosis occurring prior to age 50 without an immediately identified risk factor (i.e., idiopathic or unprovoked venous thrombosis) A family history of venous thromboembolism
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  • Screening For A Hypercoaguable State Recurrent venous thrombosis Thrombosis occurring in unusual vascular beds such as portal, hepatic, mesenteric, or cerebral veins A history of warfarin-induced skin necrosis, which suggests protein C deficiency
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  • Screening For A Hypercoaguable State Patients at increased risk for inherited thrombophilia can be identified. There is no clear clinical value to screening for the following reasons: Even if a hypercoagulable workup uncovers abnormalities predisposing to VTE, the strongest risk factor for VTE recurrence is the prior VTE event itself, particularly if idiopathic.
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  • Screening For A Hypercoaguable State Patients with idiopathic VTE, whether or not they have an identifiable inherited thrombophilia, are at high risk for recurrence (as high as 7 to 8 percent per year in some studies) after warfarin is discontinued, at least for the first few years after the event. Thus, the presence or absence of an inherited thrombophilia will usually not change the decision regarding length of warfarin therapy.
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  • Screening For A Hypercoaguable State Screening information can be used to identify family members with an inherited thrombophilia, but anticoagulant prophylaxis is rarely recommended in asymptomatic affected family members outside of high risk situations.
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  • 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.
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  • Screening For A Hypercoaguable State Confounding Factors Acute thrombosis Heparin therapy Coumadin therapy
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  • Treatment of DVT The primary objectives of treatment of DVT are to prevent and/or treat the following complications: Prevent further clot extension Prevention of acute pulmonary embolism
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  • Treatment of DVT 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.
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  • Treatment of DVT Anticoagulant therapy is indicated for patients with symptomatic proximal DVT, since pulmonary embolism will occur in approximately 50 percent of untreated individuals, most often within days or weeks of the event.
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  • Treatment of DVT The use of thrombolytic agents, surgical thrombectomy, or percutaneous mechanical thrombectomy in the treatment of venous thromboembolism must be individualized. 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.
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  • Treatment of DVT Inferior vena caval filter placement is recommended when there is a contraindication to, or a failure of, anticoagulant therapy in an individual with, or at high risk for, proximal vein thrombosis or PE.
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  • Treatment of DVT It is also recommended in patients with recurrent thromboembolism despite adequate anticoagulation, for chronic recurrent embolism with pulmonary hypertension, and with the concurrent performance of surgical pulmonary embolectomy or pulmonary thromboendarterectomy.
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  • 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, long- term therapy can be undertaken with either adjusted-dose unfractionated heparin, low molecular weight heparin, or fondaparinux.
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  • Treatment of DVT The general medical management of the acute episode of DVT is individualized. Once anticoagulation has been started and the patient's symptoms (i.e., pain, swelling) are under control, early ambulation is advised.
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  • 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.
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  • PE classification Acute vs. chronic Massive vs. submassive
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  • 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.
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  • PE Epidemiology In a study of more than 42 million deaths that occurred over a 20-year duration, almost 600,000 patients (approximately 1.5 percent) were diagnosed with PE. PE was the presumed cause of death in approximately 200,000. This study certainly underestimates the true incidence and prevalence of PE, since more than half of all PE are probably undiagnosed.
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  • PE Prognosis PE is associated with a mortality rate of approximately 30 percent without treatment, primarily due to recurrent embolism. However, accurate diagnosis followed by effective anticoagulant therapy decreases the mortality rate to 2 to 8 percent.
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  • PE Prognosis Poor Prognosis: Elevated Brain Natriuretic Peptide (BNP) Right Ventricular dysfunction Hypotension RV thrombus Elevated Troponin I
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  • PE Pathophysiology Most PE arise from thrombi in the deep venous system of the lower extremities. However, they may also originate in the right heart or the pelvic, renal, or upper extremity veins.
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  • PE Pathophysiology Iliofemoral veins are the source of most clinically recognized PE. It is estimated that 50 to 80 percent of iliac, femoral, and popliteal vein thrombi (proximal vein thrombi) originate below the popliteal vein (calf vein thrombi) and propagate proximally. The remainder arise within the proximal veins. Fortunately, most calf vein thrombi resolve spontaneously and only 20 to 30 percent extend into the proximal veins if untreated.
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  • PE Pathophysiology After traveling to the lung, large thrombi may lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Smaller thrombi continue traveling distally and are more likely to produce pleuritic chest pain, presumably by initiating an inflammatory response adjacent to the parietal pleura.
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  • PE Pathophysiology Only about 10 percent of emboli cause pulmonary infarction, usually in patients with preexisting cardiopulmonary disease. Most pulmonary emboli are multiple, with the lower lobes being involved in the majority of cases.
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  • PE Pathophysiology Impaired gas exchange due to PE cannot be explained solely on the basis of mechanical obstruction of the vascular bed and alterations in the ventilation to perfusion ratio. Gas exchange abnormalities are also related to the release of inflammatory mediators, resulting in surfactant dysfunction, atelectasis, and functional intrapulmonary shunting.
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  • 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.
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  • PE Additional Risks Factors in Women Obesity (BMI 29 kg/m2) Heavy cigarette smoking (>25 cigarettes per day) Hypertension
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  • PE Symptoms Specific symptoms and signs are not helpful diagnostically because their frequency is similar among patients with and without PE. 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:
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  • 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)
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  • 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)
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  • 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.
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  • PIOPED II Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Stein PD; Beemath A; Matta F; Weg JG; Yusen RD; Hales CA; Hull RD; Leeper KV Jr; Sostman HD; Tapson VF; Buckley JD; Gottschalk A; Goodman LR; Wakefied TW; Woodard PK. Am J Med. 2007 Oct;120(10):871-9.
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  • PE Labs Routine laboratory findings are nonspecific. Leukocytosis An increased erythrocyte sedimentation rate (ESR) Elevated serum LDH or AST (SGOT) Normal serum bilirubin.
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  • PE Arterial Blood Gases (ABGs) Arterial blood gas (ABG) measurements and pulse oximetry have a limited role in diagnosing PE. ABG s usually reveal hypoxemia, hypocapnia, and respiratory alkalosis.
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  • PE ABGs Patients with room air pulse oximetry readings