A Case of Symptomatic Deep Vein Thrombosis Mimicking Occlusive Peripheral Arterial Disease

ABSTRACT: Peripheral arterial disease (PAD) and acute deep vein thrombosis (DVT) can both result in similar calf pain presentation. Treatment modalities depend on the etiology of the pain. We present the case of a 63-year-old female with left lower extremity pain and describe our eventual diagnosis of DVT as the cause of her symptoms.

J INVASIVE CARDIOL 2013;25(1):E17-E19

Key words: peripheral arterial disease, arterial insufficiency

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In patients with peripheral arterial disease (PAD), there can be a substantial decrease in peripheral tissue perfusion. This, in turn, can cause tissue ischemia leading to various symptomatic presentations including claudication and limb pain in 50%-85% of patients.¹ The cause of limb pain can be diagnosed after performing non-invasive arterial studies in patients with arterial insufficiency. Acute deep vein thrombosis (DVT) can illustrate a similar calf pain presentation in the majority of patients. Non-invasive imaging studies can be used to diagnose DVT, but the physician faces a conundrum if the non-invasive studies suggest both severe PAD and acute DVT. One questions which of the two is the major contributor for the presentation.

Case report

A 63-year-old female with a past medical history of systemic Lupus Erythematosus and chronic kidney disease presented to our hospital complaining of left lower extremity pain. The pain was diffuse but more prominent in her thigh. She also reported left lower extremity swelling. On physical examination, the patient only had minimal tenderness to palpation without erythema, left lower extremity pulses were absent, and Homan’s Sign was negative. The differential diagnosis at this time was narrowed into two diagnoses: PAD or acute DVT. Hence, a lower extremity Doppler ultrasound and ankle-brachial index (ABI) test were ordered to further assess these diagnoses. The patient's left lower extremity ultrasound was consistent with an acute DVT in the distal left femoral vein. Furthermore, her ABI returned as 0.26 (Figure 3), a value consistent with critical PAD. The DVT was believed to be the acute clinical event that caused the patient's symptoms with a sudden onset of swelling of the extremity. Therefore, enoxaparin medical therapy was initiated and bridged with warfarin to attain a therapeutic INR. However, the patient continued to have severe limb pain and her treatment became more controversial. The DVT was being treated with anticoagulation and perhaps the arterial insufficiency was contributing to her symptoms. Conversely, she had been diagnosed with chronic PAD and her new venous thrombosis was currently severely limiting venous outflow, further compromising arterial flow. After peer discussion, a venous thrombectomy was performed to provide immediate relief of her symptoms. Left popliteal venous access was obtained under ultrasound guidance, with the patient placed in a prone position. Next, a 6 Fr sheath was inserted, and a venogram was performed confirming the presence of an occlusive thrombus (Figure 1). Following this, the Angiojet (Bayer) Solent Omni catheter was used in Power Pulse mode to infuse 10 mg tPA with a dwell time of 10 minutes. This was followed by rheolytic thrombectomy with the Angiojet catheter. The final angiographic images demonstrated elimination of the clot and excellent flow (Figure 2). The patient had resolution of her symptoms and a consequent ABI of 0.87 (Figure 4).

Figure 1. Angiogram before thrombectomy (click thumbnail to view larger image).

Figure 2. Angiogram after thrombectomy (click thumbnail to view larger image).

Figure 3. ABI before thrombectomy (click thumbnail to view larger image).

Figure 4. ABI after thrombectomy (click thumbnail to view larger image).

Discussion

PAD and DVT can both lead to severe disruptions in a patient’s Ankle Brachial Index. This occurs by two very distinct mechanisms.^2,3 In PAD, the change in ankle pressure is inversely proportional to the radius of the artery raised to the fourth power. In healthy individuals with no peripheral arterial pathology, the change in pressure across this index is minuscule given the absence of stenosis. However, with the smallest area of stenosis and a reduction in the radius of a peripheral artery, a drastic change in pressure is seen. This is elegantly illustrated by the

Poiseuille Law: ∆P = 8µLQ/πr⁴

Therefore, it is apparent that minor changes in the radius of the artery will, in turn, dampen the ankle pressure and result in a low ABI in this context.

In DVT, flow (Q) is the major contributor for the alteration in the ABI.

Flow is directly proportional to the change in pressure. It would take a great amount of flow reduction and loss of collateral venous outflow to cause a decrease in the ABI. For this reason, patients will have an array of presentations depending on the reduction of flow. The term phlegmasia cerulea dolens (PCD) was introduced in 1938 to help distinguish it from the less severe form known as phlegmasia alba dolens. PCD was described as a syndrome of massive venous occlusion in a limb with intense violaceous woody edema, ecchymosis, loss of arterial pulsations, and sometimes gangrene.⁴ This is in contrast to phlegmasia alba dolens, which was introduced in the literature in the 17th century to describe painful white swelling in the lower extremity without the loss of arterial pulsations.^5,6 In this condition, the venous outflow is still maintained by collateral flow and therefore arterial ischemia does not

occur. PCD is a rare entity and therefore there are no established guidelines to gauge proper treatment options.⁷ Nevertheless, multiple modalities have been historically used for the treatment of PCD. The use of anticoagulation has been paramount in the non-invasive treatment of PCD. If anticoagulation therapy fails to improve symptoms, then an invasive approach can be selected. Previously, surgical thrombectomy with or without fasciotomy was the most popular treatment among myriad other treatments. Recently, endovascular thrombectomy has been gaining popularity. In a recent study by Erdoes et al, 20 patients with PCD were successfully treated with pharmacomechanical thrombolysis and endovascular techniques.⁸ Besides Angiojet, other popular thrombectomy devices that are used today are the Trellis (Bacchus Vascular) and the Ekos catheters (Ekos Corporation).

The use of one modality over another is governed by the patient’s presenting symptoms, comorbidities, and hospital expertise. Therefore, larger studies are needed on this rare yet fatal syndrome to help reduce limb ischemia, gangrene, massive pulmonary emboli and ultimately death.

In our case, which in retrospect was consistent with phlegmasia cerulea dolens, it was early recognition, evaluation, and intervention that helped treat this patient in a timely fashion. The clinical question of the etiology of the patient’s pain was answered and further morbidity was reduced. It is rare that an acute DVT can decrease the ABI very drastically and thus, identification of a DVT rather than PAD as the primary cause of severe reduction in ABI becomes difficult to ascertain. It was the acuity of illness which lead to prompt treatment that helped precisely identify the acute DVT as the major contributor of the extreme reduction in ABI.

References

1. Criqui MH, Fronek A, Barrett-Connor E, Klauber MR, Gabriel S, Goodman D. The prevalence of peripheral arterial disease in a defined population. Circulation. 1985;71(3):510-515.
2. Bazan ER. Management of bilateral phlegmasia cerulea dolens in a patient with subacute splenic laceration. Ann Vasc Dis. 2008;1(1):45-48.
3. Rooke TW, Hirsch AT, Misra S, et al. 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline). A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. J Am Coll Cardiol. 2011;58(19):2020-2045.
4. Gregoire R. La phlebite bleue (phlegmatia caerulea dolens). Presse Med. 1938;46:1313-1315.
5. Malsbary, Geo. Southern California Practitioner. 30. Los Angeles: University of California Medical Center Library, 1919. eBook
6. Phlegmasia cerulea dolens. Brit Med J. 1967;1(5542):714.
7. Weaver FA, Meacham PW, Adkins RB, Dean RH. Phlegmasia cerulea dolens: therapeutic considerations. South Med J. 1988;81(3):306-312.
8. Erdoes LS, Ezell JB, Myers SI, Hogan MB, LeSar CJ, Sprouse LR 2nd. Pharmacomechanical thrombolysis for phlegmasia cerulea dolens. Am Surg. 2011;77(12):1606-1612.

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From the Department of Cardiology, West Suburban Medical Center, Oak Park, Illinois.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted June 22, 2012, provisional acceptance given July 16, 2012, final version accepted August 6, 2012.

Address for correspondence: Asif Serajian, DO, FACC, FSCAI, Department of Cardiology, West Suburban Medical Center, 3 Erie Court, Oak Park, IL 60302. Email: aserajian1@gmail.com