Pulmonary Embolism in A Patient with Superficial Thrombophlebitis ...

Case Report
Acta Cardiol Sin 2004;20:2414
Pulmonary Embolism in A Patient with Superficial
Thrombophlebitis ReportofACase
Wei-Shin Liu 1 and Bing-Hsiean Tzeng 2
A 62-year-old woman presented with mild swelling, pain, and exercise intolerance in the right lower limb for nearly
a week; chest pain, dyspnea, and palpitation also subsequently bothered her, and then she suffered 2 attacks of
syncope, which prompted hospital admission. Acute coronary syndrome was our impression at first, but emergent
coronary angiography did not support this diagnosis. An acute pulmonary embolism was then diagnosed based on
the clinical presentation, laboratory data, and imaging findings. Duplex scan of the right lower limb revealed diffuse
thrombosis of the great saphenous vein from the saphenous-femoral junction to the level of the knee; the thrombosis
was incompressible. However, there was no evidence of deep-vein thrombosis. We supposed that superficial
thrombophlebitis might have been the possible etiology of her pulmonary embolism, and suggest that pulmonary
embolism may be concurrent in patients with varicose veins and superficial thrombophlebitis.
Key Words:
Varicose veins Superficial thrombophlebitis Pulmonary embolism Acute coronary
syndrome
INTRODUCTION
A diagnosis of pulmonary embolism (PE) is often
delayed, especially in patients with no significant predisposing
factors. Pulmonary embolism rarely originates
from superficial thrombophlebitis (STP). 1 This is because
venous wall inflammation causes adherence of the
thrombus. Furthermore, diameters of the superficial
veins are smaller than those of the deep veins, thus even
though PE takes place, it usually does not induce significant
clinical symptoms. We report on a patient with an
acute pulmonary embolism, who was misdiagnosed as having
acute coronary syndrome; STP was the likely etiology.
Received: December 26, 2003 Accepted: March 24, 2004
1 Division of Cardiology, Buddhist Tsu-Chi General Hospital, Hualien,
2 Division of Cardiology, Tri-Service General Hospital, Taipei, Taiwan.
Address correspondence and reprint requests to: Dr. Bing-Hsiean
Tzeng, Division of Cardiology, Tri-Service General Hospital, 325,
Sec. 2, Cheng-Kung Road, Nei-Hu, Taipei 114, Taiwan.
Tel: 886-2-8792-7160; Fax: 886-2-8792-7161;
E-mail: bhtzeng@gcn.net.tw
CASE REPORT
A 62-year-old woman visited our medical emergency
room with the chief complaint of syncope twice in a day.
By tracing back her history, she had suffered from mild
swelling, pain, and exercise intolerance in her right lower
limb for nearly 1 week. Symptoms persisted, and chest
pain, palpitation, and dyspnea were noted in the following
days. She suffered 2 attacks of syncope thereafter, and she
was sent to our medical emergency room. Physical exams
revealed tachypnea (25/min), tachycardia (109 bpm), and
clear bilateral breathing sounds, and a grade II/VI
holosystolic murmur was audible over the lower left sternal
border. There were obvious varicose veins over the
bilateral calves. Hard indurations along a varicose vein of
the right lower limb with tenderness were also found. Surface
electrocardiogram (ECG) revealed sinus tachycardia,
with an S wave in lead I, a Q wave in lead III, an inverted
T wave in V1-4, and ST depression in V2-6 (Figure 1).
Acute coronary syndrome (ACS) was our impression at
first. Oral aspirin and intravenous heparin and nitrite were
administered. However, coronary angiography revealed
241 Acta Cardiol Sin 2004;20:2414

Wei-Shin Liu et al.
Figure 1. Surface ECG at ER revealed sinus tachycardia, S wave in lead I, Q wave in lead III, inverted T wave in V1-4, ST depression in V2-6.
insignificant stenosis of around 50% at the first diagonal
branch of the left anterior descending artery. The chest
pain, palpitation, and dyspnea persisted. The arterial
blood gas showed a PaO 2 of 79 mmHg (under 40% FiO 2
supplementation). Chest film revealed no specific findings.
Echocardiography revealed dilatation of the right
ventricle, moderate tricuspid regurgitation, with an estimated
pulmonary arterial pressure of 40 mmHg, and no
regional wall motion abnormality of the left ventricle.
Perfusion and ventilation lung scans revealed multiple
segmental and subsegmental perfusion defects in both
lung fields (Figure 2A). The D-Dimer level was > 0.2
ug/mL. A pulmonary embolism was impressed.
The patient had no history of recent trauma or immobilization.
Protein C was 119% (60%~120% as normal),
protein S was 107% (60%~120% as normal), antinuclear
antibody was negative, anti-cardiolipin was 2.2 GPL U/mL
(< 15 GPL U/mL as normal), and lupus anticoagulant was
1.12 (with < 1.5 indicating a weak presence as normal). A
compressive duplex scan of the right lower limb (Figure 3)
revealed a diffuse thrombosis of the right great saphenous
vein from the saphenous-femoral junction to the level of
the knee joint; the thrombosis was incompressible. The
femoral vein was completely compressible with flow velocity
of 24.5 cm/s (Figure 4). STP was the most likely
etiology of the patient’s PE, although iliac vein thrombosis
could not be demostrated. A venogram was not performed
because of her hypoxic condition.
Intravenous heparin infusion with target activated
prothrombin time of 46~70 seconds was initiated. High li-
Figure 2. (A) Initial lung perfusion scan revealed multiple segmental
and subsegmental perfusion defects in both lung fields. (B) Lung
perfusion scans 6 months later revealed normal findings.
Acta Cardiol Sin 2004;20:2414 242

Pulmonary Embolism and Superficial Thrombophlebitis
Figure 3. Duplex scan of right thigh revealed a thrombus (arrow) in
the great saphenous vein, which was incompressible.
patients. 3,5-7 In our patient, ACS was our impression at
first, but it was not confirmed by coronary angiography.
An echocardiogram is helpful in differentiating PE from
ACS. In ACS, a regional wall motion abnormality can
usually be found, while in PE, however, high pulmonary
pressure and right ventricle dilatation with
dysfunction is found. Another concern was the etiology
of our patient’s PE. Only varicose veins with superficial
thrombophlebitis were found by duplex scan. A
normal popliteal vein and femoral vein were documented
by compressed duplex scan. The femoral vein was completely
compressible. Deep-vein thrombosis was unlikely
although iliac vein thrombosis could not be identified.
However, the patient’s condition improved after medication
and high ligation at the saphenous-femoral junction.
All presenting evidence suggested that superficial
thrombophlebitis was the most likely etiology of her pulmonary
embolism. The possible pathophysiology of her
acute PE was dislodged thrombi from the STP of the
great saphenous vein. Her STP may have extended to the
deep-vein system via the saphenous-femoral junction or
incompetent perforating veins and thus induced PE. 1,5
Our experience suggests that STP might not always be
benign and self-limiting as previously described. The
possibility that it can induce a pulmonary embolism cannot
be ignored.
Figure 4. Duplex scan of femoral vein revealed completely compressible,
and the flow velocity was 24.5 cm/sec.
gation of the right great saphenous vein at the saphenousfemoral
junction was performed the following day. The
patient was discharged asymptomatic 3 weeks later and
was put on oral warfarin. Follow-up lung scans 6 months
later revealed no evidence of PE (Figure 2B).
DISCUSSION
Verlato et al. reported an unexpectedly high rate
33.3% (7 of 21 cases) of PE in patients with STP of the
thigh, although clinical symptoms were present in only 1
patient. 2 Whether STP alone produces PE is still controversial,
3,4 however, previous research revealed that STP
may extend to the deep venous system in 8.6% to 40% of
REFERENCES
1. Belcaro G, Nicolaides AN, Stansby G. The Venous Clinic. London:
Imperial College Press, 1998:52-7.
2. Verlato F, Zucchetta P, Prandoni P, et al. An unexpectedly high rate of
pulmonary embolism in patient with superficial thrombophlebitis of
the thigh. J Vasc Surg 1999;30:1113-5.
3. Ascer E, Loresen E, Pollina RM, et al. Preliminary results of a
non-operative approach to saphena femoral junction thrombophlebitis.
J Vasc Surg 1995;22:616-21.
4. Blumemberg RM, Barton E, Gelfand ML, et al. Occult deep vein
thrombosis complicating superficial thrombophlebitis. JVasc
Surg 1998;27:338-43.
5. Bounameaux H, Reber-Wasem MA. Superficial thrombophlebitis
and deep vein thrombosis. Arch Intern Med 1997;157:1822-4.
6. Kesteven P. Superficial thrombophlebitis followed by pulmonary
embolism. J R Soc Med 2001;94:186-7.
7. Jorgensen JO, Hamel KC, Morgan AM, et al. The incidence of deep
venous thrombosis in patients with superficial thrombophlebitis of
the lower limbs. J Vasc Surg 1993;18:70-3.
243 Acta Cardiol Sin 2004;20:2414

Case Report
Acta Cardiol Sin 2004;20:241−4
表 淺 靜 脈 栓 塞 性 靜 脈 炎 患 者 之 肺 栓 塞 ⎯ 一 病 例 報 告
劉 維 新 曾 炳 憲 *
花 蓮 市 慈 濟 醫 院 心 臟 內 科
台 北 市 三 軍 總 醫 院 心 臟 內 科 *
一 位 六 十 二 歲 女 性 從 一 週 前 右 腿 開 始 有 輕 微 腫 痛 及 無 法 久 站 或 走 遠 的 現 象 , 其 後 數 日 又 有
胸 痛 、 呼 吸 困 難 及 心 悸 。 之 後 因 昏 厥 送 入 本 院 急 診 。 最 初 診 斷 為 急 性 冠 心 症 但 心 導 管 排 除
之 。 由 臨 床 症 狀 , 實 驗 室 及 影 像 學 檢 查 診 斷 肺 栓 塞 。 右 下 肢 的 都 普 勒 超 音 波 掃 瞄 顯 示 並 無
深 部 靜 脈 栓 塞 , 然 而 卻 發 現 在 大 隱 靜 脈 從 膝 關 節 附 近 到 股 靜 脈 交 界 處 有 栓 塞 性 靜 脈 炎 。 經
大 隱 靜 脈 結 紮 及 抗 凝 劑 治 療 後 , 其 症 狀 改 善 。 六 個 月 後 之 肺 部 掃 瞄 顯 示 正 常 。 我 們 認 為 其
肺 栓 塞 最 可 能 的 原 因 是 由 表 淺 靜 脈 栓 塞 性 靜 脈 炎 所 引 起 , 並 建 議 靜 脈 曲 張 合 併 表 淺 靜 脈 炎
之 病 患 須 考 慮 併 發 肺 栓 塞 之 可 能 性 。
關 鍵 詞 : 靜 脈 曲 張 、 表 淺 靜 脈 栓 塞 性 靜 脈 炎 、 肺 栓 塞 、 深 部 靜 脈 栓 塞 。
244