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Spontaneous superficial venous thrombophlebitis: Does it increase risk for thromboembolism?

The Journal of Family Practice. 2006 January;55(1):52-57
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A historic follow-up study in primary care.

OUTCOMESVTP (N=185)NO SVTP (N=370)
Deep venous thrombosis5 (2.7%)1 (0.2%)
Pulmonary embolism1 (0.5%)2 (0.5%)
Stroke2 (0.5%)2 (0.2%)
Myocardial infarction1 (0.5%)1 (0.2%)

TABLE 2
Association between SVTP and cumulative 6-mo occurrence of major thromboembolic events

OUTCOMEOR (95% CI)ADJUSTED OR* (95% CI)
Deep venous thrombosis10.3 (2.0–51.6)7.1 (0.9–65.6)
Pulmonary embolism1.0 (0.07–15.0)NE
Stroke0.7 (0.04–10.3)NE
Acute myocardial infarction2.0 (0.1–45.0)NE
OR, odds ratio; CI, confidence interval; NE, not estimable.
*ORs were adjusted for age and sex (matched design). The adjusted OR is adjusted for a history of the particular outcome event at issue.
Within practice clustering was accounted for by using robust variance estimation commands in Stata (version 8.2).

TABLE 3
Treatment of thrombophlebitis

TREATMENTN (%)
NSAIDs15 (8)
Compression stockings7 (4)
Heparinoid cream4 (2)
Acenocoumarol2 (1)
NSAIDs and compression stockings3 (2)
No treatment registered154 (83)
NSAIDs, nonsteroidal anti-inflammatory drugs.

Discussion

This study reveals that in the absence of prior DVT, primary care patients with spontaneous SVTP of the leg have a 10-fold increased risk of developing DVT during the subsequent 6 months when compared with an age- and sex-matched group without SVTP. The absolute risk of DVT, however, is just 2.7%. The associations between SVTP and other primary outcomes (coronary syndromes, stroke, and PE) were not statistically significant.

Strengths of this study

The strengths of this study are that, as far as we know, this is the first study in general practice on arterial and venous events after a SVTP. With our search strategy within our patient registry, the identification of cases (patients with SVTP) is quite complete. The incidence of DVT in our patients is comparable with the incidence observed in previous studies in a referred population.8 We were able to identify an almost perfectly matching control group.

Limitations

Weaknesses are that we identified SVTP retrospectively, so no objective assessment of the diagnosis was undertaken. Family physicians diagnose this condition clinically.

It is possible that we had some misclassifications, but we scrutinized the files for alternative diagnoses. It cannot be excluded, however, that family physicians changed their diagnosis when it proved wrong without writing that down. In that case, misclassification would lead to underestimation of the associations found.

A small proportion (13%) of the patients received an active pharmacological treatment. As NSAIDs could prevent DVT following SVTP, the finding of a 7- to 10-fold increased risk probably is a slight underestimation of the risk without active treatment.

Our study was not meant to detect concomitant DVT. Although DVT occurs simultaneously with SVTP quite frequently, patients with a concomitant DVT were excluded as they all will be referred for objective testing and consecutive treatment.12

Factors known to predict complications in patients with SVTP are severe venous insufficiency, varicose veins, male gender, older age, hypercoagulable state, and a history of DVT.10,13 We controlled for age and gender and adjusted for a history of DVT, but were not able to identify the other predictive factors because of the retrospective identification of cases in our study. Especially venous insufficiency and varicose veins will not be recorded by family physicians, unless it causes medical problems. Inclusion of these risk factors would probably have led to information bias, as general practitioners would be inclined to register these conditions when SVTP or DVT occurs.

Treatment of SVTP

Treatment with low-molecular-weight heparin or NSAIDs during the 10 days following SVTP decreases the risk of developing a DVT with about 15% and 9% respectively.9 To prevent 1 case of DVT in this group of patients, a family physician would have to treat 247 patients with low-molecular-weight heparin (absolute risk=2.7%) or 412 patients with an NSAID.

Although low-molecular-weight heparin therapy does have a low risk of major bleeding complications, treatment with NSAIDs has clear risks. The frequency of both gastrointestinal bleeding as well as renal failure increases by about 30% with the use of NSAIDs.14-16 Moreover, this strategy appears not to be cost effective in preventing DVT. At this time, watchful waiting is probably the best strategy. Swelling of a leg following SVTP must raise the suspicion of a DVT and needs prompt further investigation.

CORRESPONDENCE
Dr. H. van Weert, Department of General Practice, Academic Medical Centre/University of Amsterdam, PO Box 22660, 1100 DD Amsterdam, The Netherlands. E-mail: h.c.vanweert@amc.uva.nl