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<strong>Management</strong> <strong>of</strong> <strong>patients</strong> <strong>with</strong><br />

<strong>superficial</strong> thrombophlebitis<br />

Mateja Kaja Jezovnik, M.D., PhD.<br />

Pr<strong>of</strong>. Pavel Poredos, M.D., PhD.<br />

University Medical Centre Ljubljana<br />

Department <strong>of</strong> Vascular Disease<br />

Definition<br />

• Superficial thrombophlebitis (ST) is an inflammation <strong>of</strong><br />

the venous wall <strong>with</strong> subsequent secondary clot<br />

formation<br />

• Most frequently affects <strong>superficial</strong> veins <strong>of</strong> lower limbs<br />

• Thrombophlebitis<br />

• Superficial vein thrombosis<br />

1


Clinical presentation<br />

REDNESS<br />

PAIN<br />

EDEMA<br />

WA<strong>RM</strong> SKIN<br />

Epidemiology<br />

• Incidence in the general population: 3-11%<br />

May be underestimated t d (pts <strong>with</strong> minor symptoms,<br />

not present for medical attention)<br />

• Female/male ratio: 6 to 4<br />

• Mean age <strong>of</strong> presentation: 60 yrs<br />

• Often two or more factors have to be present<br />

• Age - the older the patient, the higher the prevalence<br />

DeWeese, 1991; Nordstrom 1992, Ramelet 2008<br />

2


Etiology<br />

• Hypercoagulability<br />

• Cancer<br />

• Pregnancy, puerperium, oral contraceptives, hormone<br />

replacement therapy<br />

• Antiphospholipid syndrome<br />

• Thrombophilia<br />

• Reduced blood flow<br />

• Varicosities – injury <strong>of</strong> the venous valves<br />

• immobility<br />

• Damage <strong>of</strong> the vessel wall<br />

• Surgical procedures, trauma, i.v. catheters<br />

t<br />

• Other<br />

• AGE > 60 years<br />

• OBESITAS<br />

• History <strong>of</strong> VTE or SF<br />

Virchow<br />

triad<br />

Leon LR Jr et al. Perspect Vasc Surg Endvasc Ther, 2005<br />

Primary Superficial<br />

Thrombophlebitis<br />

• Pathogenesis es s is not known, however e there e are<br />

some supposed pathogenetic mechanisms:<br />

• Damage - inflammation<br />

• Varicose veins - VARICOPHLEBITIS (4 - 59%, bilateral 5<br />

– 10%)<br />

• Hypercoagulable states<br />

• Prevalence <strong>of</strong> hypercoagulable state t in ST is high<br />

h<br />

(up to 72% in <strong>patients</strong> <strong>with</strong>out varicose veins)<br />

• Factor V Leiden Mutation, Factor II G20210A<br />

mutation, antithrombin, protein C and S<br />

deficiency<br />

3


Secondary Superficial<br />

Thrombophlebitis<br />

• accompanied by systemic (inflammatory)<br />

disease and is related to the damage <strong>of</strong> the<br />

vascular wall<br />

• Mb. Bürger<br />

• Behçet’s et’s disease<br />

• Vasculitis and rheumatic syndromes (APLS)<br />

• Malignant tumours<br />

• “SEPTIC” TF ASSOCIATED WITH VENOUS CATHETERS (i.v.<br />

application in drug users, i.v. catheters in immunocompromised<br />

<strong>patients</strong>)<br />

• “STERILE” TF<br />

• i.v. drug application<br />

The Clinical Importance <strong>of</strong> ST<br />

• traditionally ST has been considered a<br />

relatively l benign and self - limited it disease<br />

• systemic diagnostic investigation (US) <strong>of</strong><br />

<strong>patients</strong> <strong>with</strong> ST revealed interrelationship<br />

between ST and VTE, therefore it was<br />

recently accepted as an integral part <strong>of</strong><br />

venous thromboembolic syndrome<br />

4


The Incidence <strong>of</strong> VTE in<br />

Patients <strong>with</strong> ST<br />

Incidence:<br />

• association between ST in DVT was found in 2% to<br />

33%<br />

Factors related to increased risk:<br />

• protrusion <strong>of</strong> thrombus from <strong>superficial</strong> to deep venous<br />

system<br />

• the strongest association in <strong>patients</strong> <strong>with</strong>:<br />

• thrombus in <strong>superficial</strong> veins near sapheno – femoral or<br />

sapheno – popliteal junction (


US diagnostic<br />

Thrombosis extension to SFJ<br />

6


Is There Preferential Treatment<br />

<strong>of</strong> ST ?<br />

• lack <strong>of</strong> evidence<br />

– based data<br />

a. Lack <strong>of</strong> consistency in the end points<br />

b. Inadequate F-Up<br />

c. Small number <strong>of</strong> <strong>patients</strong><br />

d. Limited evaluation to rule out VTE<br />

e. Most <strong>of</strong> retrospective nature<br />

• choice <strong>of</strong> therapy is influenced by:<br />

- symptoms and progression <strong>of</strong> the disease<br />

- <strong>patients</strong> preference<br />

- available medical resources<br />

Actual treatment <strong>of</strong> ST<br />

• Compression<br />

• Bandages<br />

• Stockings<br />

• Normal physical activity<br />

• Walking <strong>with</strong> elastic compression, not bed rest<br />

• Drugs<br />

• Anticoagulants – low molecular weight heparins (LMWH),<br />

UFH, oral anticoagulants<br />

• The role <strong>of</strong> non-steroidal anti-inflammatoryinflammatory drugs (NSAIDs)<br />

and topical local anti-inflammatory inflammatory treatment (gel, cream,<br />

spray) is not well defined, they alleviate the symptoms<br />

• No place for antibiotics (except in <strong>patients</strong> <strong>with</strong> septic ST)<br />

7


The efficacy <strong>of</strong> LMWH and Nonsteroidal<br />

anti-inflammatory inflammatory drugs<br />

• LMWH better than NSAID in regard to thrombus extension<br />

• a nonsignificant reduction in the incidence <strong>of</strong> VT and PE in the<br />

LMWH group<br />

Stenox study, Arch Intern Med 2003<br />

Efficacy <strong>of</strong> LMWH<br />

in<br />

Treatment <strong>of</strong> ST<br />

• both: preventive and therapeutic ti doses <strong>of</strong><br />

LMWH prevent extension and recurrence<br />

<strong>of</strong> ST (QUENET et all J Vasc. Surg. 2003)<br />

• there is a trend <strong>of</strong> lowering incidence <strong>of</strong><br />

thromboembolic events, however no<br />

relevant study confirmed significant<br />

reduction <strong>of</strong> VTE in <strong>patients</strong> <strong>with</strong> ST<br />

treated <strong>with</strong> LMWH (Prandoni et al, J Thromb Haemost 2005)<br />

8


TREATMENT OF ST OF THE LEG<br />

(THE COHRANE COLLABORATION)<br />

• 2469 <strong>patients</strong> <strong>with</strong> ST<br />

• treatment modalities: NSAIDs, topical treatment, surgery,<br />

LMWH<br />

• 70% reduction <strong>of</strong> extension or recurrences <strong>of</strong> the disease<br />

in pts. treated <strong>with</strong> NSAID and LMWH in comparison to<br />

placebo<br />

• Any anticoagulant treatment over “any yp<br />

period <strong>of</strong> time”<br />

appear as the current best therapeutic option for ST <strong>of</strong> the<br />

legs<br />

• in spite <strong>of</strong> nonsignificant effect <strong>of</strong> LMWH on VTE<br />

complications, they concluded that an intermediate LMWH<br />

for at least 1 month might be advised<br />

Cohrane Review 2007<br />

Fondaparinux for the Treatment <strong>of</strong><br />

Superficial-Vein Thrombosis in the Legs<br />

• randomized,<br />

double-blind blind trial:<br />

CALISTO<br />

• 3002 <strong>patients</strong><br />

• Fondaparinux 2.5<br />

mg s.c. once daily<br />

vs placebo for 45 d<br />

• Follow Up- 77 days<br />

Fondaparinux significantly reduced progression <strong>of</strong><br />

the disease and thrombotic complications<br />

NEJM 2010<br />

9


Guidelines <strong>of</strong> the American College<br />

<strong>of</strong> Chest Physicians ACCP<br />

• <strong>patients</strong> <strong>with</strong> spontaneous ST<br />

- prophylactic hl or intermediate doses <strong>of</strong><br />

LMWH for at least 4 weeks (Grade 2B)<br />

- as an alternative UFH, warfarin (target INR<br />

2.0 to 3.0) (Grade 2C)<br />

- medical treatment <strong>with</strong> anticoagulants over<br />

surgical treatment is recommended (Grade<br />

1B)<br />

-oral<br />

nonsteroidal anti - inflammatory drugs<br />

should not be used <strong>with</strong> anticoagulants<br />

(Hirsch et al. CHEST 2008)<br />

CONCLUSIONS<br />

• ST is frequent and not benign<br />

disease<br />

• its ethiopathogenesis is based on<br />

similar risk factors as DVT<br />

• ST is related to DVT and is<br />

accepted as a part <strong>of</strong> thrombotic<br />

syndrome.<br />

10


CONCLUSIONS<br />

• LMWH reduces progression and recurrence<br />

<strong>of</strong> ST<br />

• prevention <strong>of</strong> VTE complications was<br />

confirmed only in one study, where pts were<br />

treated <strong>with</strong> fondaparinux (CALISTO)<br />

• therapeutic or intermediate doses <strong>of</strong> LMWH<br />

for 4-6 weeks are recommended for<br />

treatment <strong>of</strong> ST (actual guidelines)<br />

www.eurochap2011.si<br />

WELCOME TO SLOVENIA<br />

11

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