Venous thrombosis deep in the lower extremity I80.28

Sudden or gradual, partial or complete occlusion of at least one segment of the deep veins of the pelvis and/or leg (or arm) leading and muscular veins by a thrombus with a tendency to grow and the risk of embolization into the lungs.

Phlebitis is a thrombotic change in the superficial venous system.

The risk of DVT depends on age and risk factors (see also Man.) Risk of developing the disease at age < 60 years = 1:10,000 per year; at age > 60 years = 1:1,000 per year.

The proportion of TV-OUs is 4-10% of the total collective of TVs (Encke A et al. 2016)

• Slowing of blood flow, endothelial injuries (see endothelium below), changes in the vein wall, increased blood coagulation (= Virchow's triad).
• Other risk factors:
  • Age, previous thrombosis, pregnancy, pelvic vein spur, varicose veins, heart failure, overweight, ovulation inhibitors; previous or still existing superficial thrombophlebitis;
  • coagulation disorders: lack of antithrombin III, protein C, protein S; congenital resistance to activated protein C(APC resistance); factor V (Leiden) defect; elevated levels of von Willebrand factor or factor VIII; mutation in the factor II gene (polymorphism of prothrombin).
  • Acquired disorders: antiphospholipid-antibody syndrome and lupus anticoagulant, which may occur primarily or as part of an underlying disease (autoimmune disease).

Occurrence especially in middle and old age (median 60 years), intra- and postoperatively, in bedridden patients, after myocardial infarction, after trauma of the lower extremities, surgery, overexertion (thrombosis par èffort); immobilization, prolonged sitting (e.g. air travel - see below travel thrombosis), use of ovulation inhibitors (especially in combination with cigarette smoking), during pregnancy, in the puerperium.

The risk of deep vein thrombosis during general surgical/urological/gynecological procedures (>30 min.) is 10-40%, the risk of pulmonary embolism is 1-4%.

Especially deep leg and pelvic veins 90% of the cases; in 60% of the cases left leg, in 30% right leg, in 10% both legs. 4 levels: V.ilica 10%, V.femoralis 50%; V. poplitea 20%, lower leg veins 20%. >90% of pulmonary embolisms originate from the catchment area of the inferior vena cava, 60% of these from the V. femoralis.

Acute, also subacute to chronic, insidious onset.

Early symptoms: Feeling of heaviness of the legs, cramp-like pain in the sole of the foot and calf, subfebrile temperatures, tachycardia, leg edema, cyanosis when standing, pain.

Unilateral increase in muscle consistency (subfascial oedema), superficial vein dilatation = warning veins.

Possibly palpable, pressure-painful vein strand in the depth. Fever, chills, climbing pulse.

Further clinical signs are:

• n. Payr: pressure sensitivity of the medial muscles of the sole of the foot (medial plantar pain)
• n. Bisgaard: Kulisse pressure pain behind the lateral malleolus
• n. Homans: Calf pain with dorsiflexion
• n. Lowenberg: Calf pain due to blood pressure cuff (100 mm Hg)

S.a. venous pressure points

• Duplex compression sonography(method of first choice) taking into account clinical probability.
• If the results of compression sonography are uncertain or negative, phlebography or D-dimer testing.
• Diagnosis of thrombophilia: exact family history. Determination of laboratory parameters in individual cases: resistance to activated protein C (factor V Leiden mutation), deficiency of protein C, protein S, antithrombin III, presence of a lupus anticoagulant or anti-cardiolipin antibody, disorders in fibrinolysis or hyperhomocysteinemia, possible clarification of family members who may also have a tendency to thrombosis.

• Early complications (1-3 days): pulmonary embolism (3%), Phlegmasia coerulea dolens.
• Late complications: postthrombotic syndrome.

Initial anticoagulation:

• Full heparinization in therapeutic dosage (good evidence): Weight-adapted with low molecular weight heparin (NMH) e.g. nadroparin (fraxiparin) 2 times/day 0.1 ml/10 kg KG s.c.; only in exceptional cases with unfractionated heparin. S.u. Heparin, systemic.
• Oral therapy with rivaroxaban (initially 2x15mg p.o./day, after 3 weeks 20mg p.o./day) is also approved.
• For heparin allergy, see below lepirudine.
• A sufficient anticoagulant effect must be guaranteed at all times. Therefore, after initiating oral anticoagulation with Marcumar, discontinue NMH only when the INR/Quick value is within the therapeutic range or contraindications have been ruled out.

Changeover to oral anticoagulants:

• For uncomplicated lower leg thrombosis: 3-6 months.
• For pulmonary embolism: 6-12 months.
• In case of the first recurrent thrombosis: at least 12 months.
• In case of repeated recurrent thrombosis, AT III deficiency, protein C and S deficiency or other thrombophilia factors: 1 year to lifetime.
• Preparations (see below coumarins, systemic): e.g. phenprocoumon (e.g. marcoumar): HWZ 5 -7 days or warfarin (e.g. coumadin): HWZ 40 days.

• Remember! Control by the prothrombin time, which is given in INR units. The target therapeutic INR range is between 2.0 and 3.0. However, DOACs are also increasingly used in maintenance therapy, with the advantage of reducing major bleeding. Furthermore in the renunciation of INR controls. The duration of maintenance therapy is 3-6 months, depending on the cause.

Alternative: For the initial therapy of DVT-UE (deep vein thrombosis of the lower extremity), the direct oral anticoagulants (DOAC) such as rivaroxaban (initial 2x15mg p.o./day, after 3 weeks 1x20mg p.o./day) and apixaban (initial 2x10mg p.o./day, after 7 days maintenance dose 2x5mg p.o./day). They can also be used in DVT-OE (deep vein thrombosis of the upper extremity) in this dosage.

Alternative: Regional hyperthermic fibrinolytic perfusion: New procedure derived from hyperthermic perfusion of the extremities in malignant melanoma. Advantages: No AI, no age limits, no systemic NW.

Alternative: Regional hyperthermic fibrinolytic perfusion: New method derived from hyperthermic perfusion of the extremities in malignant melanoma. Advantages: No AI, no age limitations, no systemic NW. Also recanalization of the lower leg floor is possible. Perioperative heparinization, followed by oral anticoagulation (1-1.5 years) and compression therapy (see above)

Further accompanying measures:

• Sufficient compression therapy!
  • Compression therapy: Apply short-stretch bandages at least up to the height of the thrombus, better up to the groin and until the edema has completely receded. Subsequently prescription of a compression stocking class II-III for 6 months. If the thrombi do not dissolve completely and defects of the venous wall or valve function occur, lifelong compression therapy is indicated as a prophylaxis against postthrombotic syndrome.
• Mobilisation (good evidence):
  • Immediate mobilization of the patient with isolated lower leg thrombosis is generally advocated today to prevent further growth of the thrombus. In numerous observations, the generally accepted assumption that early mobilization favors the development of a pulmonary embolism could not be confirmed.

• Possibly weight-adapted heparinization with low-molecular-weight heparin in therapeutic dosage.
• Compression bandage up to the groin.
• Short-term inducement of a duplex sonography.
• Bed rest is not required for mobile patients.

• Thrombolysis: Only in exceptional cases possibly indicated in young people with extensive initial thrombosis, short medical history, thrombi washed around, acute threat to the extremity and exclusion of thrombophilia. Contraindications must be observed extremely strictly! Treatment by thrombolysis or thrombectomy should be reserved for specialised centres with sufficient experience. Preparations: Streptokinase, Urokinase, Alteplase (rtPA, recombinant tissue-type plasminogen activator), Tenecteplase (TNK-t-PA).
• Thrombolysis methods: systemic lysis therapy (very high rate of side effects), locoregional lysis therapy.

• Mostly spontaneous recanalization, valvular insufficiency. In the case of pelvic vein thrombosis, persistent venous occlusion is more frequent than in the other veins.

• Cave! The higher the location of the thrombosis, the greater the risk of pulmonary embolism.

• A high percentage of phlebothromboses are clinically silent or without the known - typical - clinical symptoms. The risk of pulmonary embolism is highest during the first 3 days of thrombosis development.
• Untreated leg vein thrombosis has a lethality rate of 10% (pulmonary embolism), 80% of patients develop a post-thrombotic syndrome.

Duration of coumarin therapy

1. Avila ML et al (2016) Pediatric post-thrombotic syndrome in children: Toward the development of a new diagnostic and evaluative measurement tool. Thromb Res 144:184-191.
2. Encke A et al. (2016) The prophylaxis of venous thromboembolism. Atsch Arztebl. Int 113: 532-538
3. EINSTEIN Investigators (2011) Oral rivaroxaban for symptomatic venous thromboembolism. N Engl J Med 363: 2499-2510
4. Ginsberg J et al (1996) Management of venous thromboembolism. N Engl J Med 335: 1816-1828
5. Lensing AW et al (1999) Deep-vein thrombosis. Lancet 353: 479-485
6. Lewis BE et al (2007) Direct thrombin inhibition during percutaneous coronary intervention in patients with heparin-induced thrombocytopenia. Expert Rev Cardiovasc Ther 5: 57-68
7. Pietrzyk WS (2016) Air travel-related symptomatic deep venous thrombosis in cruise ship passengers. Int Marit Health 67:66-71.
8. Qi X et al (2016) Splenectomy Causes 10-Fold Increased Risk of Portal Venous System Thrombosis in Liver Cirrhosis Patients. Med Sci Monit 22:2528-2550.
9. Ridker PM et al (2003) Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thromboembolism. N Engl J Med 348: 1425-1434
10. Scurr JH et al (2001) Frequency and prevention of symptomless deep-vein thrombosis in long-haul flights: a randomised trial. Lancet. 357: 1485-1489
11. Turpie AG et al (2002) Venous thromboembolism: pathophysiology, clinical features, and prevention. BMJ 325: 887-890
12. Wells PS et al (1998) Use of a clinical model for safe management of patients with suspected pulmonary embolism. Ann Internal Med 129: 997-1005
13. Wells PS et al (1995) Accuracy of clinical assessment of deep-vein thrombosis. Lancet 345: 1326-1330