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Phlebology OnlineFirst, published on July 25, 2014 as doi:10.1177/0268355514543940

Short report

Arteries masquerading as varicose veins: A trap for phlebologists

Phlebology 0(0) 1–7 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0268355514543940 phl.sagepub.com

L Jones1 and K Parsi1,2,3

Abstract Ultrasound guided sclerotherapy may be complicated by intra-arterial injections resulting in significant tissue necrosis. Here, we present a 69-year-old man with a history of right small saphenous vein ‘‘stripping’’, presenting for the treatment of symptomatic lower limb varicose veins. Duplex ultrasound of the right lower limb outlined the pathway of venous incompetence. Despite the history of ‘‘stripping’’, the small saphenous vein was present but the sapheno-popliteal junction was ligated at the level of the knee crease. No other unusual findings were reported at the time. During ultrasound guided sclerotherapy, subcutaneous vessels of the right posterior calf were noted to be pulsatile on B-mode ultrasound. Treatment was interrupted. Subsequent angiography and sonography showed absence of the right distal popliteal artery. A cluster of subcutaneous vessels of the right medial and posterior calf were found to be arterial collaterals masquerading as varicose veins. Injection sclerotherapy of these vessels would have resulted in significant tissue loss. This case highlights the importance of vigilance at the time of treatment and the invaluable role of ultrasound in guiding endovenous interventions.

Keywords Sclerotherapy, foam sclerotherapy, duplex ultrasound, varicose veins

Case report A 69-year-old man presented for treatment of symptomatic bilateral varicose veins. He complained of cramps in the right (R) leg during exercise and bilateral lower limb swelling but no rest pain. A (R) small saphenous vein (SSV) ‘‘stripping’’ undertaken 10 years before was complicated by excessive post-operative pain, swelling and slow wound healing. There was a concurrent history of hypertension and dyslipidemia but no history of peripheral vascular, cardiac or cerebrovascular disease, deep vein thrombosis (DVT) or pulmonary embolism (PE). He was a smoker for 40 years. His concurrent medications included atorvastatin and ramipril. On examination, this gentleman presented with bilateral lower limb varicose veins. Typical changes of chronic venous hypertension were evident in the (R) medial ankle area and consisted of corona phlebectatica paraplantaris, pigmentation and atrophie blanche (Figure 1). The capillary return time was normal (less than 2 s) suggesting normal perfusion of the nail beds. The clinical stage of his CEAP (clinical, aetiological, anatomical and pathological) classification was C4b. Continuous-wave (CW) Doppler examination of the sapheno-femoral junction (SFJ) and sapheno-popliteal junction (SPJ) and clinically prominent tributaries of

both lower limbs was performed. Reflux was detected in the examined varicosities but no other abnormal findings were detected at the time. Routine pre-operative duplex ultrasound venous incompetence mapping of both lower limbs was undertaken by an experienced vascular sonographer following standard protocols.1 Our protocol includes assessment of both deep and superficial venous systems in the erect position. The vessels are examined in the B-mode for morphology and compressibility. Spectral and Colour Doppler is used to assess flow. Reflux is defined as retrograde flow greater than 0.5 s. 1

Dermatology, Phlebology and Fluid Mechanics Research Laboratory, St. Vincent’s Centre for Applied Medical Research (AMR), St. Vincent’s Hospital, Sydney, Australia 2 Phlebology Vascular Laboratory, Sydney Skin and Vein Clinic, Sydney, Australia 3 St. Vincent’s Clinical School, Faculty of Medicine, University of New South Wales, Sydney, Australia Corresponding author: Kurosh Parsi, Dermatology, Phlebology and Fluid Mechanics Research Laboratory, St. Vincent’s Hospital Centre for Applied Medical Research, Level 8, Lowy-Packer Building, 405 Liverpool Street, Darlinghurst, NSW 2010, Australia. Email: [email protected]

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Venous incompetence mapping of the (R) leg demonstrated reflux in the posterior arch vein and inter-saphenous tributaries of the great saphenous vein (Figure 2(a)). The trunk of the (R) SSV measured 2.1 mm in diameter and was found to be competent (Figure 2(b)). The vein appeared to be ligated near the junction at the knee crease. A cluster of superficial vessels measuring 1–2 mm in diameter were located in the posterior calf. The femoral vein demonstrated mild reflux in the mid segment and distally. The popliteal

Figure 1. A 69-year-old man presented with typical changes of chronic venous hypertension in the right medial ankle area which consisted of corona phlebectatica paraplantaris, pigmentation and atrophie blanche. (a) post-calf view, (b) right medial ankle.

vein, the medial and lateral gastrocnemius veins were incompetent. No other unusual features were reported at the time of this scan. The venous incompetence study protocol does not include assessment of the arterial system and hence no arterial pathology was investigated in this study. Following a second consultation, informed consent to treat the lower limb varicose veins with foam ultrasound guided sclerotherapy (UGS) was obtained. Incompetent veins of the left lower limb were treated in three sessions uneventfully and the patient was brought back for the first treatment on the (R) leg. As the patient was being prepped, the assisting sonographer noted pulsatile flow in the vessels of the (R) posterior calf. Treatment was interrupted and further investigations were arranged to exclude a traumatic arterio-venous fistula (AVF). Further sonography revealed absence of the (R) distal popliteal artery (Figure 3(a)). The (R) medial gastrocnemius artery (MGA) originated from the mid-segment of the (R) popliteal artery (Figure 3(b)) and was significantly enlarged at 4.3 mm (largest diameter) compared with the contralateral vessel at 2.6 mm (Figure 4). Perforating arteries arising from the (R) MGA crossed the fascia to communicate with the subcutaneous vessels in the posterior calf which measured 1–2 mm in diameter and demonstrated monophasic pulsatile flow (Figure 4).

Figure 2. (a) Venous incompetence mapping of the right lower limb demonstrating reflux in the calf tributaries of the great saphenous vein, ligation of the sapheno-popliteal junction and cluster of vessels in the posterior calf. Circles denote perforating veins and arrows point to direction of flow. (b) Duplex ultrasound of the right small saphenous vein showing antegrade flow on augmentation. GSV, great saphenous vein; PAV, posterior arch tributary of the GSV; Rt, right; SATV, superficial anterior tibial vein; SSV, small saphenous vein.

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Angiography confirmed absence of the distal popliteal artery (Figure 5). The collateral circulation in the calf reconstituted flow in the distal posterior tibial and anterior tibial arteries (Figure 6). These collateral arteries had a superficial and tortuous course, mimicking subcutaneous varicosities. The vascular tree on the contralateral leg and proximal to the popliteal artery was absolutely free from lesions. Ankle brachial index (ABI) pressure measurements were obtained which demonstrated moderately severe peripheral vascular disease on the (R) side, with an

index of 0.71 at dorsalis pedis and 0.86 at the posterior tibial artery. The left side demonstrated a normal ABI. A review of the angiographic and ultrasonic findings suggested a possible iatrogenic cause for the absence of the distal popliteal artery, possibly an inadvertent event during the ligation of the SPJ. This could not be verified as the medical records dating back to the operation date were reported to be destroyed. He was referred for further vascular review and was commenced on anti-platelet agents and a regular exercise program which included daily walking.

Figure 3. (a) B-mode ultrasound image demonstrating a sharp termination to the popliteal artery. Arrow points to the tapered end of the vessel. POP a, popliteal artery; POP v, popliteal vein; OCCL, occluded. (b) Colour Doppler demonstrating the origin of the right (Rt) MGA from the mid-section of the popliteal artery.

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Figure 4. Duplex ultrasound images of the right calf. (a) Right medial gastrocnemius (R) MGA demonstrating an enlarged diameter. (b–e) Perforating arteries arising from the (R) MGA communicating with subcutaneous vessels of the medial calf. (f) Subcutaneous collateral arteries demonstrating monophasic pulsatile flow.

On follow-up three years later, he remained well with no ongoing lower limb symptoms.

Discussion Serious complications of sclerotherapy are rare.2 The more severe adverse events include DVT, PE, stroke3 and intra-arterial injection leading to critical ischaemia. A recent review of the literature revealed that intraarterial injection resulted in critical ischaemia requiring amputation in 52.5% of cases.4 Intra-arterial injections may be due to inadvertent administration of the sclerosing agent into a normal artery or arteriole, or an undetected AVM.2,5 Proximity of certain arteries to veins targeted during sclerotherapy presents a risk for

intra-arterial injections, highlighting the necessity of ultrasound in guiding sclerotherapy.6,7 In particular, the small saphenous artery lies in close proximity to the SSV and may be the target of inadvertent injections.6–8 Arteries accompanying perforating veins are other potential targets. Finally, pulsatile varicose veins are found secondary to right heart failure and tricuspid regurgitation. These vessels, however, demonstrate a velocity profile which essentially remains venous superimposed with a pulsed systolic flow.9 In the present case, due diligence was exercised at the time of the procedure, the treatment was interrupted and no inadvertent intra-arterial injection occurred. However, the current case demonstrates another potential situation where arteries may be confused with

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Figure 5. Digital subtraction angiography of lower limbs. Sequence of radiograms demonstrating absence of the right distal popliteal artery and formation of collateral circulation. Arrows indicate the normal flow in the left popliteal (a), peroneal (b) and posterior tibial (c) arteries and collateral vessels in the right calf (d).

Figure 6. Digital subtraction angiography of the right lower limb. Sequence of radiograms demonstrating reconstitution of flow in the anterior tibial (a) and posterior tibial (b) arteries.

varicose veins and targeted during sclerotherapy. Collaterals arteries by-passing occluded arterial trunks are usually found in muscular tissues below the deep fascia and subcutaneous collateral arteries are at least

exceptional. In the present case, we first identified these vessels on duplex ultrasound and further confirmed their collateral nature on angiography. Absence of the distal popliteal artery was shown on duplex ultrasound

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Phlebology 0(0) Table 1. Ultrasonic features of small arterial and venous vessels.

B-mode

Doppler

Arterial

Venous

Profile Vessel wall Compressibility

Circular (erect or supine) Echogenic, thicker Non-compressible

Pulsatilitya Velocity Profile Max Velocities

Pulsatile Pulsed systolic flow High

Circular (erect) Circular to oval (supine) Non-echogenic, thinner Compressible Non-pulsatile Non-phasicb Low

a

Pulsatility detected on transverse view after applying probe pressure. Feature of lower limb venous flow with the exception of flow detected in the common femoral vein which is normally in phase with respiration. Continuous low resistance flow (monophasic) would indicate a proximal obstruction. b

and further confirmed on angiography. Superficial collateral vessels were traced to perforating arteries arising from the (R) MGA. Enlarged septal arteries were also observed to communicate with the subcutaneous vessels. The collateral nature of the subcutaneous vessels was demonstrated on angiography with flow reconstitution in the anterior and posterior tibial arteries. As a differential diagnosis, we considered a traumatic AVF communicating with subcutaneous veins. A small AVF could explain an arterialized flux into a calf varicose vein. AVFs can be readily diagnosed on duplex examination with direct and indirect signs such as high velocities and systole-diastolic flux in the feeding artery and arterialization of the draining vein flux. However, these duplex features were not present in this case. In addition, typical angiographic features of an AV communication such as early venous filling10–12 were not present. Despite the clinical assessment and venous incompetence mapping by an experienced vascular sonographer, the arterial pathology was initially missed in this case. Cramps during exercise are suggestive of arterial claudication, especially in a patient presenting with risk factors such as hypertension, dyslipidemia and history of smoking. However, this patient was referred by his family physician for the management of venous disease and hence was only assessed for the venous presentation. In retrospect, ABI pressure measurements and a peripheral arterial duplex ultrasound should have been performed during the initial assessment. Arterial and venous pathology coexist commonly in the elderly men. Both should be investigated in selected patients presenting with signs or symptoms of peripheral vascular disease. A comprehensive clinical examination, CW-Doppler assessment and duplex ultrasound examination of both arterial and venous systems is essential in detecting an unusual vascular pathology such as that presented here. While colour Doppler provides a qualitative assessment

of flow, pulsed wave Doppler offers a quantitative analysis of the velocity profile which allows differentiation of venous from arterial flow. Venous flow in the lower limbs is characterized by no-flow or low-velocity continuous flow that appears or increases during augmentation manoeuvers such as calf compression. Arterial flow is characterized by pulsed systolic flow with a diastolic flow that varies depending on vascular resistance in the corresponding territory. AVFs are characterized by high amplitudes and a low resistance diastolic flow. In general, the combination of B-mode features and pulsed wave Doppler flow characteristics can distinguish between the arterial and venous nature of vessels (Table 1).13,14 Spectral and colour Doppler are not as sensitive as Power Doppler which provides a non-directional assessment of blood flow.15,16 Small superficial arteries may demonstrate velocities as low as 1 cm/s. To detect flow in such vessels, many Doppler features such as the pulse repetition frequency, velocity scale, wall filter and the angle of interrogation have to be optimized.17 In addition, motion artefacts due to probe movement or breathing can make Doppler assessment of small vessels difficult. Hence, due diligence must be exercised when assessing such vessels and all ultrasound capabilities (B-mode and Doppler) should be used to prevent an inadvertent intra-arterial injection. In the present case, the initial suspicion that these vessels were arterial was based on their B-mode features. Duplex features of arterial vessels include echogenic walls, partial to non-compressibility, circular profile on cross section and pulsatility.18,19 In our experience, pulsatility on B-mode, while maintaining probe pressure on the vessel, is helpful to detect small arteries. Following adequate optimization, colour and pulsed wave Doppler should be used to confirm arterial flow. Our patient reported the onset of (R) leg symptoms to coincide with his stripping procedure 10 years prior. Duplex ultrasound and subsequent angiography demonstrated absence of the distal (R) popliteal artery.

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Furthermore, despite the history of (R) SSV ‘‘stripping’’, the vein was present but ligated at the knee crease. An attempt was made to obtain further information about this procedure and any documented complications. In New South Wales, Australia, medical records are kept by-law for 7 years and hospital paper records are destroyed after this period. Hospital and private medical records of this procedure were not available to the authors and hence we could not confirm whether an inadvertent event was documented at the time of the procedure. In summary, we report a patient presenting with subcutaneous collateral arteries of the (R) posterior calf masquerading as varicose veins. This paper demonstrates that unusual pathology can be missed during the initial assessment. In this case, an adverse outcome was not experienced by the patient due to vigilance at the time of treatment: a key message of this case report. Ultrasound guidance at the time of treatment is mandatory to reduce the risk of intra-arterial injections. Care and vigilance should be maintained at all times during UGS of superficial vessels to avoid intra-arterial injections. Acknowledgments We thank our vascular sonographers, Kaye Rubis who first identified the pathology described in this case report and Yana Parsi for further sonographic characterisation of the collateral pathway. We are grateful to Prof. Lourens Bester, interventional radiologist, for advice on the angiographic images and David Du for assistance with the manuscript.

Conflict of interest None declared.

Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

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5. Grommes J, Franzen EL, Binnebosel M, et al. Inadvertent arterial injection using catheter-assisted sclerotherapy resulting in amputation. Dermatol Surg 2011; 37: 536–538. 6. Schadeck M. Sclerotherapy of the small saphenous vein: how to avoid bad results? [Article in French]. Phlebology 2004; 57: 165–169. 7. Parsi K, Exner T, Connor DE, et al. In vitro effects of detergent sclerosants on coagulation, platelets and microparticles. Eur J Vasc Endovasc Surg 2007; 34: 731–740. 8. Lemasle P, Uhl JF and Gillot C. Small saphenous artery: embryology, anatomy and therapeutic considerations [Article in French]. Phlebology 2006; 59: 35–45. 9. Abbas M, Hamilton M, Yahya M, et al. Pulsating varicose veins!! The diagnosis lies in the heart. ANZ J Surg 2006; 76: 264–266. 10. Gonza´lez SB, Busquets JC, Figueiras RG, et al. Imaging arteriovenous fistulas. Am J Roentgenol 2009; 193: 1425–1433. 11. Valji K. Pathogenesis of vascular diseases. In: Valji K (ed.) Vascular and interventional radiology, 2nd ed. Maryland Heights, USA: Saunders, 2006. 12. Tayama K, Akashi H, Hiromatsu S, et al. Acquired arteriovenous fistula of the right forearm caused by repeated blunt trauma: a report of a rare case. Ann Thorac Cardiovasc Surg 2005; 11: 59–62. 13. Hennerici M and Neuerburg-Heusler D. Extracranial cerebral arteries. Vascular diagnosis with ultrasound: clinical references with case studies. Germany: Grammlich, Pliezhausen, 1998, p.43. 14. Stojanovich L and Djokovic A. Tomography and blood vessels in Hughes syndrome. Lupus 2014; 23: 337–341. 15. Barth RA and Shortliffe LD. Normal pediatric testis: comparison of power Doppler and color Doppler US in the detection of blood flow. Radiology 1997; 204: 389–393. 16. Fortunato SJ. The use of power Doppler and color power angiography in fetal imaging. Am J Obstet Gynecol 1996; 174: 1828–1831. 17. Marsha M and Neumyer BS. Nonimaging physiologic tests for assessment of lower extremity arterial disease. In: Pellerito J and Polak JF (eds) Introduction to vascular ultrasonography: expert consult. Philadelphia, PA: Elsevier, Saunders, 2012, p.245. 18. Moore C, Piccirillo B, Buonocore D, et al. Differentiating arteries from veins. AIUM practice guideline for the use of ultrasound to guide vascular access procedures. American Institute of Ultrasound in Medicine, 2012, p.5. Available online http://www.aium.org/resources/ guidelines/usgva.pdf. 19. Scoutt LM, Cruz J and Hamper UM. Ultrasound diagnosis of lower extremity venous thrombosis. In: Pellerito J and Polak JF (eds) Introduction to vascular ultrasonography: expert consult. Philadelphia, PA: Elsevier, Saunders, 2012, p.385.

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Arteries masquerading as varicose veins: A trap for phlebologists.

Ultrasound guided sclerotherapy may be complicated by intra-arterial injections resulting in significant tissue necrosis. Here, we present a 69-year-o...
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