Do we need a consensus on diagnostic and treatment of superficial thrombophlebitis? Viera Stvrtinova II.nd Clinic of Internal Medicine II.nd Clinic of Internal Medicine Medical Faculty Comenius University BRATISLAVA, Slovak republic 18th Congress of the European Chapter ot the IUA, PALERMO, October 2009

INTRODUCTION Traditionally ST has been considered a relatively benign and limited disease or sign of chronic venous insufficiency In recent years it seems that ST is not such a banal condition Some physicians consider ST an integral part of venous thromboembolism, together with DVT and PE

ST and VTE Association between ST and DVT vary in the literature from 6 to 53% and pulmonary embolism up to 33% The relationship between ST and DVT is supported also by the same risk factors that triggers ST as well as DVT.

in ST a DVT – always other part of Virchow´s triad is more important Rudolf VIRCHOW ( )

RISK FACTORS for ST Slowing of the blood flowSlowing of the blood flow Varicose veinsVaricose veins Prolonged bed rest (immobilization) for several reasons (operation, trauma, serious infection, heart failure, pulmonary emphysema, etc.)Prolonged bed rest (immobilization) for several reasons (operation, trauma, serious infection, heart failure, pulmonary emphysema, etc.)

RISK FACTORS for ST Coagulation disordersCoagulation disorders Thrombophilia – Factor V Leiden mutation, protein C deficiency, protein S deficiency, AT III deficiency, prothrombin G20210A mutation, etcThrombophilia – Factor V Leiden mutation, protein C deficiency, protein S deficiency, AT III deficiency, prothrombin G20210A mutation, etc CancerCancer PregnancyPregnancy Oral contraceptivesOral contraceptives Anti-phospholipid syAnti-phospholipid sy

RISK FACTORS for ST Damage of the venous wallDamage of the venous wall Intravenous injectionsIntravenous injections Intravenous cathetersIntravenous catheters Injury, traumaInjury, trauma Varicose veins and chronic venous insufficiencyVaricose veins and chronic venous insufficiency

RISK FACTORS for ST Other risk factors and diseasesOther risk factors and diseases Winiwarter-Buerger´s diseaseWiniwarter-Buerger´s disease Behcet´s diseaseBehcet´s disease Other chronic inflammatory autoimmune diseasesOther chronic inflammatory autoimmune diseases ObesityObesity Age (over 60 yrs)Age (over 60 yrs)

ST - incidence ST is a frequent disease, but its exact incidence is not known. The incidence of ST could be around 400 cases in person – years according to UK estimates It is depending on the age of the population, on the used investigation method (clinical dg. or DUS), and the fact, that ST is mostly managed on GPs level

ST - Classification According the etiology: 1.PRIMARY ST (inflammation affects only the venous wall and surrounding peri-venous tissue) 2.SECONDARY ST (inflammation of the venous wall is associated with other inflammatory process or systemic disease in the body

Primary ST 1. varicophlebitis 2. septic catheter´s ST (e.g. non sterile i.v. injections in drug abusers, i.v.catheters in patients with immunodeficiency ) 3. “sterile” ST due to intravenous drug administration (scleroterapy) 4. Mondor thrombophlebitis

Secondary ST 1. Winiwarter – Buerger´s disease 2. Behcet´s disease 3. other vasculitic or chronic rheumatic syndromes with autoimmune etiology (e.g.anti-phospolipid syndrome) 4. malignant tumors

FORMS of ST 1.varicophlebitis – ST of a varicose vein (VST) 2. ST on a healthy, non-varicose superficial vein – non-varicose ST (NVST) 88% of ST are VST

Endothelial injury in NVST Circulatory stasis in Circulatory stasis in varicophlebitis always other part of Virchow´s triad is more important

Varicophlebitis and DVT In a retrospective study of 114 patients with ST the incidence of a concomitant DVT was 15.6% when ST affected the vena saphena magna or vena saphena parva, but only 5.2% when side branches were involved. In a retrospective study of 114 patients with ST the incidence of a concomitant DVT was 15.6% when ST affected the vena saphena magna or vena saphena parva, but only 5.2% when side branches were involved. With varicose veins as a single risk factor, the frequency of a concomitant DVT was 6%, varicose veins combined with further risk factors showed a DVT frequency of 15.4% (Noppeney et al, 2006). With varicose veins as a single risk factor, the frequency of a concomitant DVT was 6%, varicose veins combined with further risk factors showed a DVT frequency of 15.4% (Noppeney et al, 2006).

NVST (“non-varicose” superficial thrombophlebitis) is a miscellaneous group of disorders, where inflammation is a dominating feature in some conditions, while thrombosis dominates in other cases. Among 2319 patients diagnosed with Behcet´s disease ST was present in 53.3% and DVT in 29,8% of cases

ST in Winiwarter´s – Buerger´s dis. ST in Buerger´s disease belongs to the diagnostic criteria Thrombophlebitis migrans (inflammation of the venous wall goes up or down – proximally or distally on a superficial vein) or thrombophlebitis saltans (inflammation “jumps” from one vein to another vein) are specific forms of ST often seen in patients with Winiwarter- Buerger´s disease.

NVST In a prospective analysis of 42 patients with non varicose ST investigation for risk factors revealed a neoplasm in 2 patients (4.8%), a non neoplasic systemic disease in 4 (9.5%) a thrombophilic condition in 20 patients (48%). The most frequent thrombophilia was the heterozygous mutation of coagulation factor V Leiden – (Gillet et al, 2004).

ST diagnosis In many cases ST is a banal condition, which resolves spontaneously, but in recent years due to systematic ultrasound investigation of the venous system a large number of deep venous thromboses concomitant with ST has been revealed.

Thrombophlebitis Thrombophlebitis DUS

ST treatment On contrary to the treatment of deep venous thrombosis, only little is known about the most appropriate management of ST. ST is etiologically a heterogeneous group of disorders with a different degree of inflammation and thrombosis the main etiological factor and contribution of different risk factors always should be considered before treatment decision.

ST th. – compression, mobilization The main therapeutic procedure in all types of ST is compression and mobilization. There have been no randomized studies demonstrating the effectiveness of compression, although this approach is considered by all experts to be essential. In all cases of ST immediate mobilization with elastic compression is necessary.

All patients with ST should be treated with compression therapy. Regular walking supports the effectiveness of the compression bandage on the LL. The patient must walk regularly throughout the day and avoid prolonged periods of being seated or standing. Confinement to bed would favor progression of the thrombus in both the superficial and the deep venous system

ST treatment - DRUGS Anticoagulants Non-steroidal anti-inflammatory drugs (NSAIDs) Topical local anti-inflammatory treatment (gel, cream, spray) Topical local anti-inflammatory treatment (gel, cream, spray) Venoactive drugs – in patients with varicose ST Venoactive drugs – in patients with varicose ST Antibiotics – in patients with septic ST Antibiotics – in patients with septic ST Corticosteroids – in patients with vasculitic and autoimmune syndromes Corticosteroids – in patients with vasculitic and autoimmune syndromes

ST treatment - anticoagulants Especially in cases of extensive ST anticoagulant therapy is a good choice. LWMH, UFH as well as oral anticoagulants are used in prophylactic as well as therapeutic doses. Not only the doses, but the duration of the treatment is different in individual hospitals and medical care centers.

LMWH and ST ? ? ? ? ? ? ? Dosage – prophylactic or therapeutic Duration – 10, 20, 30 days ????????

Proposal for ST management from CEVF Recommendation n.1: In every patient with NVST and in every patient with recurrent VST look carefully for risk factors for superficial thrombophlebitis, especially for thrombophilia and cancer 18th Congress of the European Chapter ot the IUA, PALERMO, October 2009

Recommendation n.2: Clinical investigation may the real extent of superficial thrombophlebitis underestimate, and does not give enough information on the status of deep venous system, therefore after clinical investigation it is important to perform duplex ultrasound investigation of the superficial and deep venous system, too. 18th Congress of the European Chapter ot the IUA, PALERMO, October 2009

Recommendation n.3: Duplex ultrasound investigation should be done bilaterally - on both lower limbs, not only on the limb affected with ST. 18th Congress of the European Chapter ot the IUA, PALERMO, October 2009

It is necessary (mandatory) to perform duplex ultrasound investigation immediately after clinical diagnosis of ST in the case of ST localized on the trunk of the great saphenous vein 10 cm and less from the sapheno-femoral junction or on the trunk of small saphenous vein 10 cm or less from the sapheno-popliteal junction. Recommendation n.4: 18th Congress of the European Chapter ot the IUA, PALERMO, October 2009

Recommendation n.5: All patients with superficial thrombophlebitis should be treated with compression therapy. Recommendation n.6: In all cases of ST immediate mobilization with elastic compression is necessary (mandatory). Patients should not be confined to bed. Proposal for ST management from CEVF 18th Congress of the European Chapter ot the IUA, PALERMO, October 2009

Patients with ST, with an inflamed and thrombosed superficial vein longer than 5 cm in duplex ultrasound investigation should have anticoagulant treatment with LMWH for 4 weeks. The dosage and duration of anticoagulation depends on the concomitant diseases and other risk factors for VTE. Patients with ST, with an inflamed and thrombosed superficial vein longer than 5 cm in duplex ultrasound investigation should have anticoagulant treatment with LMWH for 4 weeks. The dosage and duration of anticoagulation depends on the concomitant diseases and other risk factors for VTE. Recommendation n.7: 18th Congress of the European Chapter ot the IUA, PALERMO, October 2009

In conclusion Do we need a consensus on diagnostic and treatment of superficial thrombophlebitis?