Deep Venous Thrombosis ROSENS EM MAJIDI ALIREZA RESIDENT OF EM SBMU PEZESHMAJIDY@YAHOO.COM

Pathophysiology of Thrombosis VTE represents the end product of imbalanced clot formation versus clot breakdown. Factors that enhance fibrin formation include systemic inflammation (which includes almost all so-called acquired states of hypercoagulability sluggish blood flow in large veins permits the process of fibrin deposition.

Hypercoagulable states: Three generic factors promote clotting Hypercoagulable states: Cancer Nephrotic syndrome Sepsis Inflammatory conditions: Ulcerative colitis Increased estrogen: Pregnancy Oral contraceptives Antiphospholipid syndrome Protein S, C, and antithrombin III deficiencies, Factor V Leiden, prothrombin gene mutations, others Stasis: Prolonged bed rest Immobility (such as from a cast) Long plane, car or train ride Neurologic disorders with paralysis Congestive heart failure Obesity Vascular damage: Trauma Surgery Central lines: Especially with upper extremity DVT Multifactorial issues: Advancing age: Prior DVT or PE

Pathophysiology of Thrombosis Virchow, triad of venous injury, slow blood flow, and hypercoagulability as the cardinal factors that the clinician should use to classify a patient as at risk for excessive fibrin deposition relative to fibrin removaL'

Pathophysiology of Thrombosis DVT represents a disease spectrum ranging from a minimally symptomatic isolated calf vein thrombosis to a limb-threatening iliofemoral venous obstruction.

Anatomy calf veins deep venous system includes the anterior The venous anatomy of the lower extremity can be divided into the deep and superficial systems deep venous system includes the anterior tibial, posterior tibial, and peroneal veins, calf veins Proximal DVT refers to clot in the popliteal vein or higher, whereas distal clot refers to an isolated calf vein thrombosis

Clinical Presentation The initial symptoms of DVTcan be as subtle and nonspecific as a mild cramping sensation or sense of fullness in the calf, without objective swelling, and may be difficult to differentiate clinically

Clinical Presentation 6 mo recent ;,3 days tenderness 3 cm larger Pitting edema Alternative

Diagnosis Estimation of the pretest probability of DVT is the initial step in the diagnostic strategy. Contrast venography has been considered the gold standard in the evaluation of DVT and has the advantage of being able to differentiate between acute and chronic thrombus

Diagnostic Tests for DVT tintinali

Diagnosis hours. Venous duplex ultrasonography has a sensitivity and specificity of approximately 95% for proximal DVT and is the diagnostic test of choice in most centers plasma concentration indicates the presence of clot formed somewhere in the body within the past 72 hours.

Diagnosis D-Dimer concentration is elevated with any condition fibrin deposition, including malignancy, pregnancy, advanced age, prolonged bed rest, recent surgery, infection, inflammation, new indwelling catheters, stroke, and myocardial infarction

Diagnosis a negative D-dimer result excludes the diagnosis ofDVT only in patients with a low pretest probability of disease.

Diagnosis Magnetic resonance imaging (MRI) can image the pelvic vasculature and vena cava, Impedance plethysmography and strain-gauge plethysmography measure changes in venous outflow from the extremities to diagnose DVT.

Differential Diagnosis

Treatment When the diagnosis of DVT has been established, anticoagulation should be initiated, unless contraindicated un fractionated heparin (80 U/kg intravenous bolus followed by 18 U/kg/h infusion) enoxaparin, 1 mg/kg subcutaneously every 12 hours) Treatment requires anticoagulation with warfarin for at least 3 months. 6- or 8-hour delay

Treatment starting with a dose of 10 mg of warfarin sodium in most adults achieves a therapeutic effect faster and without increase in bleeding complications."

Superficial Thrombophlebitis many patients with clinically suspected superficial thrombophlebitis have a synchronous DVT Patients with clot in the greater saphenous vein thatextends above the knee are at risk for progression to DVT via the saphenous-femoral junction and should be considered for anticoagulation.

Superficial Thrombophlebitis superficial thrombophlebitis should be treated symptomatically with nonsteroidal antinflammatory drugs, heat, and graded compression stockings (fitted to exert 30 to 40 mm Hg of pressure on the extremity). Increased ambulation and elevation of the extremity above the level of the heart while at rest help to decrease venous stasis. Routine anticoagulation is not indicated for superficial thrombophlebitis

Isolated Calf or Saphenous Vein Thrombosis saphenous, tibial or peroneal veins remains controversial. Longitudinal studies subsequently found that approximately 25% of isolated calf vein thromboses propagate proximally, prompting many experts to recommend treatment with anticoagulation as for DVT. healthy, ambulatory patient with an isolated calf thrombus and no other indication for anticoagulation is to prescribe anti platelet therapy with aspirin (325 mg/day

Phlegmasia Cerulea Dolens (Painful Blue Leg) Massive iliofemoral occlusion results in swelling of the entire leg with extensive vascular congestion and associated venous ischemia producing a painful, cyanotic extremity. arterial spasm resulting in phlegmasia alba dolens (painful white leg or milk leg), which may mimic an acute arterial occlusion.

Upper Extremity Venous Thromboses associated most often with central venous catheters, pacemakers, and malignancies Upper extremity DVT can cause PE, and all patients with upper extremity DVT require definitive treatment.B.' Anticoagulation usually is indicated, and thrombolysis should be considered to treat apparent phlegmasia cerulea dolens of the arm.

Complications fatal PE chronic venous varicose veins insufficiency, resulting in disabling pain and swelling varicose veins skin changes nonhealing ulcers

Pathophysiology of Thrombosis Aging leads to venous valvular incompetence, which impairs venous return, and causes blood stasis; aging also increases the probability of an acquired hypercoagulability, such as malignancy. Older patients have more cumulative effects of inflammatory damage to venous endothelium and are more likely to be exposed to the independent risk factor of surgery. Older patients may be predisposed to dehydration, which probably accelerates clot deposition. Older patients are more likely to have heart and lung disease,

Discharge Criteria 5-minute Outpatient treatment with a LMWH: No serious concomitant disease that requires hospitalization Patient has means of communication and transportation to return to the hospital if needed. Patient (or family member) is willing and able to inject the medication. Patient needs hematocrit, platelet count, and international normalized ratio (INR) checked in two to three days. aPTT does not need to be checked. Heparin-induced thrombocytopenia is less common with the LMWH but still occurs. INR needs to be checked at about day three. Patients with superficial or distal thrombophlebitis can be discharged with close follow-up.