- Email: [email protected]
Chronic refractory venous ulcer exacerbated by a congenital pelvic arteriovenous malformation successfully treated by transarterial Onyx embolization
Chronic refractory venous ulcer exacerbated by a congenital pelvic arteriovenous malformation successfully treated by transarterial Onyx embolization Naiem Nassiri, MD, RPVI,a Dustin T. Crystal, BS,b Catherine Hoyt, DPM, RN,c and Randy Shafritz, MD, RPVI,d New Brunswick, NJ
Congenital arteriovenous malformations (AVMs) are an important but often neglected cause of lower extremity venous hypertension. A case of a chronic refractory venous stasis ulcer of the lower extremity exacerbated by a pelvic AVM is presented. Healing of the ulcer was achieved at 2 months without recurrence at 1 year after superselective ethylene vinyl alcohol copolymer (Onyx 34; ev3, Covidien, Plymouth, Minn) embolization of the AVM nidus. Chronic venous arterialization should be considered in cases of refractory, nonhealing venous ulcers. Embolotherapy in addition to standard of care therapy can be a therapeutic measure. Modification of the Clinical, Etiology, Anatomy, and Pathophysiology (CEAP) classification to include AVMs as a contributing pathophysiologic process is suggested. (J Vasc Surg: Venous and Lym Dis 2017;-:1-4.)
Congenital arteriovenous malformations (AVMs) are high-flow vascular malformations that represent pathologic connections between arteries and veins anywhere upstream of capillary level. This premature shunting of blood away from high-resistance arterioles and capillaries into the venous system exposes the draining veins to arterial pressures and can result in morbid venous hypertension. This is one of the earliest manifestations of symptomatic extremity AVMs.1-3 In severe cases, venous ulceration can develop in classic locations, which is often refractory to standard therapeutic modalities such as paste boot (Unna boot) compression, superficial and perforator venous ablation, and local wound care. Herein, we highlight this underappreciated phenomenon by a rare case report of a successfully treated venous ulceration exacerbated by a congenital pelvic AVM. The patient consented to this case presentation.
CASE REPORT A 67-year-old, relatively healthy African American woman was referred to the Vascular Anomalies & Malformations Program (VAMP) for evaluation of left pelvic hypervascularity detected on magnetic resonance venography (MRV) as part of the workup for a chronic refractory left lateral malleolar and distal leg stasis ulceration initially measuring 4.3 4 0.2 cm (Fig 1). Circumferential leg lipodermatosclerosis and 2þ pitting edema of the leg and thigh were noted. Venous duplex ultrasound interrogation had shown chronic femoral deep venous thrombosis (DVT) with deep system reflux. There was no evidence of popliteal and femoral level venous arterialization. The patient had previously undergone a full course of oral anticoagulation without recurrence of acute DVT. Pulse examination and ankle-brachial indices were within normal limits bilaterally. Biopsy of the ulcer was not performed. The patient had diligently followed up at a wound care facility for more than a year with weekly sharp débridement, dressing changes, and paste boot compression therapy. Despite these measures, the ulcer had expanded to 10.5 4.5 0.2 cm. MRV
From the Vascular Anomalies & Malformations Program (VAMP) at the Division
was obtained by the referring physician to rule out May-Thurner
of Vascular Surgery, Department of Surgery, Rutgers Robert Wood Johnson
syndrome as a possible cause of the nonhealing ulcer. However,
Medical School, Robert Wood Johnson University Hospital, Bristol-Myers
MRV showed considerable left pelvic hypervascularity and
Squibb Children’s Hospitala; Rutgers Robert Wood Johnson Medical Schoolb;
soft tissue redundancy (Fig 2). There was prompt shunting of
Director for the Center for Wound Healing at Robert Wood Johnson Univer-
gadolinium into the large network of draining veins throughout
c
sity Hospital ; and Division of Vascular Surgery, Department of Surgery, The Center for Wound Healing, Rutgers Robert Wood Johnson Medical School, Robert Wood Johnson University Hospital.d
the pelvis and abdomen. VAMP consultation was obtained. The patient had no history of pelvic trauma, surgery, instru-
Author conflict of interest: none.
mentation, or infection. There was no personal or family history
Correspondence: Naiem Nassiri, MD, RPVI, Assistant Professor, Vascular Surgery,
of epistaxis or telangiectatic rashes that would have suggested
Division of Vascular Surgery, Department of Surgery, Founding Director,
Osler-Weber-Rendu syndrome as the cause of the AVM. She
Vascular Anomalies & Malformations Program (VAMP), Rutgers Robert Wood Johnson Medical School, Robert Wood Johnson University Hospital,
denied blood per rectum and vaginal bleeding. She did have
Bristol-Myers Squibb Children’s Hospital, One Robert Wood Johnson Place,
complaints of left pelvic and lower abdominal throbbing
MEB 541, New Brunswick, NJ 08901 (e-mail: [email protected]).
discomfort that was exacerbated by activity. She was deemed a C6SECSADSPRO, with the pathophysiologic component requiring further explanation than just post-thrombotic reflux.
The editors and reviewers of this article have no relevant financial relationships to disclose per the Journal policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. 2213-333X
A congenital pelvic AVM was suspected and confirmed on
Copyright Ó 2017 by the Society for Vascular Surgery. Published by Elsevier Inc.
angiographic interrogation (Fig 3, A and B) performed through
http://dx.doi.org/10.1016/j.jvsv.2016.12.001
contralateral femoral puncture. 1
2
Nassiri et al
Journal of Vascular Surgery: Venous and Lymphatic Disorders ---
2017
Fig 1. A-C, Progressive stasis ulceration along the anterolateral aspect of the left mid to distal leg with surrounding pitting edema and lipodermatosclerosis. D, Resolution of ulcer within 2 months after embolization without recurrence at approximately 1-year follow-up. Selective left iliac angiography confirmed presence of a Yakes
There were no perioperative complications. She was dis-
IIa AVM4 fed by multiple arterial feeders arising from the main
charged home the same day as the procedure and continued
bifurcation of the left internal iliac artery. A coaxial system was
follow-up at the wound care facility with local wound care mea-
assembled and used to superselectively microcatheterize the
sures and weekly paste boot compression. She had complete
AVM nidus through various arterial feeders. Superselective
healing of the ulcer within 2 months after embolization, with
embolization was performed with ethylene vinyl alcohol copol-
prompt relief of pelvic pain and discomfort noted postopera-
ymer (Onyx 34; ev3, Covidien, Plymouth, Minn; Fig 3, C-E). There was excellent penetration of Onyx into the AVM nidus with
tively. There was no ulcer recurrence at 1-year follow-up. She was maintained on compression stockings.
cast formation and no evidence of nontarget embolization. Postembolization angiography revealed considerably dimin-
DISCUSSION
ished arteriovenous shunting (Fig 3, F).
The International Society for the Study of Vascular Anomalies classifies congenital vascular malformations on the basis of their flow properties into slow-flow venous and lymphatic malformations, high-flow AVMs, and congenital mixed syndromes, which can include combinations thereof.5 Congenital high-flow AVMs represent a short circuit of sorts that shunts blood prematurely from high-resistance arterioles and capillaries into draining veins. Classically, congenital AVMs of the extremities contain a nidusda convoluted conglomerate of blood vessels with poorly differentiated endothelial cells situated between the feeding artery and the draining vein. This nidus acts as a low-pressure sump that is a potent stimulator of angiogenesis. Not all extremity AVMs are congenital; in fact, a significant portion of pathologic connections between the arteries and the veins of the extremities are acquired and secondary to neoplastic changes, trauma, catheterization, and instrumentation. While there have been a handful of case reports that
Fig 2. Magnetic resonance venography (MRV) delineating engorged and promptly enhancing venous drainage of the left pelvis, upper thigh, and abdomen as a result of venous arterialization.
Journal of Vascular Surgery: Venous and Lymphatic Disorders Volume
-,
Number
Nassiri et al
3
-
Fig 3. A and B, Flush aortography demonstrates enlarged left internal iliac artery with multiple arterial feeders supplying the nidus of a Yakes IIa arteriovenous malformation (AVM) with numerous draining veins. C, Superselective microcatheter angiography of individual arterial feeders confirms shunting into an intervening nidus. D and E, Onyx embolization of the AVM nidus with formation of an occlusive cast is demonstrated. F, Postembolization angiography showing diminished AVM nidus filling with significantly reduced pathologic venous flow.
have suggested secondary arteriovenous fistulization after extensive extremity venous thrombosis,6-8 these types of pathologic connections are vastly different angiographically from the congenital varieties of AVMs. The former represent what is often referred to as cavernous transformation of the affected veins to provide collateral draining outflow. There may be erosion of these collateral channels into adjacent arterioles. These can be easily differentiated angiographically from the classic congenital AVM containing a much more convoluted nidus. The current case features the incidental presence of a congenital high-flow AVM arising from branches of the internal iliac artery in the setting of chronic iliofemoral DVT. Unlike in popular belief, digital ischemia and tissue loss as a result of an attributed steal phenomenon represent a rare and extremely late manifestation of large, widespread congenital extremity AVMs. The resultant venous hypertension is one of the earliest and most profound manifestations of symptomatic extremity AVMs.1-3 This can either, in and of itself, contribute to venous insufficiency or alternativelydas was the case in the current scenariodexacerbate concomitant post-thrombotic or
reflux symptoms. Awareness is the most important element that leads to timely investigative measures. However, as demonstrated here, AVMs are often discovered serendipitously as part of a workup for other more commonly encountered disease. Symptoms of AVM-mediated venous insufficiency are often indistinguishable from those of the isolated variety with edema, lipodermatosclerosis, and, in severe cases, tissue loss. In the absence of pre-existing thromboembolic disease, close inspection of color flow Doppler and spectral waveform analysis can provide subtle but important clues that suggest venous arterialization. These can include turbulent flow and pulsatility of the venous waveforms. In this case, the location of the AVM in the more cephalad pelvic circulation and the preexisting thrombotic burden, albeit chronic, precluded identification by duplex ultrasound interrogation. AVMs can have idiosyncratic and highly variable angioarchitectural profiles that complicate therapy. With the exception of direct arteriovenous fistulas, all other congenital AVMs require nidus penetration for adequate treatment. Although tempting because of ease of therapy, all other attempts at more proximal
4
Nassiri et al
Journal of Vascular Surgery: Venous and Lymphatic Disorders ---
occlusion of the AVM, such as coils, plugs, covered stents, and surgical ligation, are futile without superselective nidus penetration.1,4,9-11 Unfortunately, proximal occlusion methods remain commonly practiced, with inevitable recurrence of symptoms in a more hostile AVM configuration that renders superselective nidus access considerably more difficult and at times impossible. In this case, prompt referral to the VAMP on discovery of pelvic hypervascularity led to prompt angiographic interrogation with appropriate delivery of superselective embolotherapy. Ulcer healing was achieved within weeks after more than a year of refractory measures with added costs, the patient’s and provider’s frustration, and compromised quality of life of the patient. The American Venous Forum’s Clinical, Etiology, Anatomy, and Pathophysiology (CEAP) classification provides an excellent schematic platform for evaluation, risk stratification, therapeutic approach, and clinical monitoring of patients with chronic venous disease.12,13 We suggest a slight expansion of the pathophysiology (P) portion of the classification to include venous arterialization caused by AVMs as a contributing factor. This can provide increased awareness among treating personnel with a lower threshold for appropriate imaging protocols in patients with debilitating refractory venous disease. We recommend close evaluation of readily available and easy to obtain venous duplex ultrasound scans to check for color flow Doppler and spectral waveform findings suggestive of venous arterialization. In addition, magnetic resonance angiography can be obtained to verify suspicious clinical or duplex ultrasound findings. In the absence of readily available magnetic resonance imaging protocols, computed tomography angiography can be a useful screening modality.
2017
REFERENCES 1. Rosen RJ, Nassiri N, Drury JE. Interventional management of high-flow vascular malformations. Tech Vasc Interv Radiol 2013;16:22-38. 2. Lee BB, Do YS, Yakes W, Kim DI, Mattassi R, Hyon WS. Management of arteriovenous malformations: a multidisciplinary approach. J Vasc Surg 2004;39:590-600. 3. Yakes WF, Baumgartner I. Interventional treatment of arteriovenous malformations. Gefässchirurgie 2014;19:325-30. 4. Yakes WF. Yakes’ AVM classification system. J Vasc Interv Radiol 2015;26:S224. 5. Dasgupta R, Fishman SJ. ISSVA Classification. Semin Pediatr Surg 2014;23:158-61. 6. Link DP, Garza AS, Monsky W. Acquired peripheral arteriovenous malformations in patients with venous thrombosis: report of two cases. J Vasc Interv Radiol 2010;21:387-91. 7. Labropoulos N, Bhatti AF, Amaral S, Leon L, Borge M, Rodriguez H, et al. Neovascularization in acute venous thrombosis. J Vasc Surg 2005;42:515-8. 8. Varnagy D, Labropoulos N. The issue of spontaneous arteriovenous fistulae after superficial thrombophlebitis, endovenous ablation, and deep vein thrombosis: an unusual but predictable finding. Perspect Vasc Surg Endovasc Ther 2006;18:247-50. 9. Nassiri N, Cirillo-Penn NC, Thomas J. Evaluation and management of congenital peripheral arteriovenous malformations. J Vasc Surg 2015;62:1667-76. 10. Yakes W. Endovascular management of high-flow arteriovenous malformations. Semin Intervent Radiol 2004;21:49-58. 11. Lee BB, Baumgartner I, Berlien HP, Bianchini G, Burrows P, Do YS, et al. Consensus Document of the International Union of Angiology (IUA)d2013. Current concept on the management of arterio-venous management. Int Angiol 2013;32:9-36. 12. Porter JM, Moneta GL; International Consensus Committee on Chronic Venous Disease. Reporting standards in venous disease: an update. J Vasc Surg 1995;21:635-45. 13. Eklof B, Rutherford RB, Bergan JJ, Carpentier PH, Gloviczki P, Kistner RL, et al. Revision of the CEAP classification for chronic venous disorders: consensus statement. J Vasc Surg 2004;40:1248-52.
Submitted Aug 10, 2016; accepted Dec 27, 2016.
Congenital arteriovenous malformations (AVMs) are an important but often neglected cause of lower extremity venous hypertension. A case of a chronic refractory venous stasis ulcer of the lower extremity exacerbated by a pelvic AVM is presented. Healing of the ulcer was achieved at 2 months without recurrence at 1 year after superselective ethylene vinyl alcohol copolymer (Onyx 34; ev3, Covidien, Plymouth, Minn) embolization of the AVM nidus. Chronic venous arterialization should be considered in cases of refractory, nonhealing venous ulcers. Embolotherapy in addition to standard of care therapy can be a therapeutic measure. Modification of the Clinical, Etiology, Anatomy, and Pathophysiology (CEAP) classification to include AVMs as a contributing pathophysiologic process is suggested. (J Vasc Surg: Venous and Lym Dis 2017;-:1-4.)
Congenital arteriovenous malformations (AVMs) are high-flow vascular malformations that represent pathologic connections between arteries and veins anywhere upstream of capillary level. This premature shunting of blood away from high-resistance arterioles and capillaries into the venous system exposes the draining veins to arterial pressures and can result in morbid venous hypertension. This is one of the earliest manifestations of symptomatic extremity AVMs.1-3 In severe cases, venous ulceration can develop in classic locations, which is often refractory to standard therapeutic modalities such as paste boot (Unna boot) compression, superficial and perforator venous ablation, and local wound care. Herein, we highlight this underappreciated phenomenon by a rare case report of a successfully treated venous ulceration exacerbated by a congenital pelvic AVM. The patient consented to this case presentation.
CASE REPORT A 67-year-old, relatively healthy African American woman was referred to the Vascular Anomalies & Malformations Program (VAMP) for evaluation of left pelvic hypervascularity detected on magnetic resonance venography (MRV) as part of the workup for a chronic refractory left lateral malleolar and distal leg stasis ulceration initially measuring 4.3 4 0.2 cm (Fig 1). Circumferential leg lipodermatosclerosis and 2þ pitting edema of the leg and thigh were noted. Venous duplex ultrasound interrogation had shown chronic femoral deep venous thrombosis (DVT) with deep system reflux. There was no evidence of popliteal and femoral level venous arterialization. The patient had previously undergone a full course of oral anticoagulation without recurrence of acute DVT. Pulse examination and ankle-brachial indices were within normal limits bilaterally. Biopsy of the ulcer was not performed. The patient had diligently followed up at a wound care facility for more than a year with weekly sharp débridement, dressing changes, and paste boot compression therapy. Despite these measures, the ulcer had expanded to 10.5 4.5 0.2 cm. MRV
From the Vascular Anomalies & Malformations Program (VAMP) at the Division
was obtained by the referring physician to rule out May-Thurner
of Vascular Surgery, Department of Surgery, Rutgers Robert Wood Johnson
syndrome as a possible cause of the nonhealing ulcer. However,
Medical School, Robert Wood Johnson University Hospital, Bristol-Myers
MRV showed considerable left pelvic hypervascularity and
Squibb Children’s Hospitala; Rutgers Robert Wood Johnson Medical Schoolb;
soft tissue redundancy (Fig 2). There was prompt shunting of
Director for the Center for Wound Healing at Robert Wood Johnson Univer-
gadolinium into the large network of draining veins throughout
c
sity Hospital ; and Division of Vascular Surgery, Department of Surgery, The Center for Wound Healing, Rutgers Robert Wood Johnson Medical School, Robert Wood Johnson University Hospital.d
the pelvis and abdomen. VAMP consultation was obtained. The patient had no history of pelvic trauma, surgery, instru-
Author conflict of interest: none.
mentation, or infection. There was no personal or family history
Correspondence: Naiem Nassiri, MD, RPVI, Assistant Professor, Vascular Surgery,
of epistaxis or telangiectatic rashes that would have suggested
Division of Vascular Surgery, Department of Surgery, Founding Director,
Osler-Weber-Rendu syndrome as the cause of the AVM. She
Vascular Anomalies & Malformations Program (VAMP), Rutgers Robert Wood Johnson Medical School, Robert Wood Johnson University Hospital,
denied blood per rectum and vaginal bleeding. She did have
Bristol-Myers Squibb Children’s Hospital, One Robert Wood Johnson Place,
complaints of left pelvic and lower abdominal throbbing
MEB 541, New Brunswick, NJ 08901 (e-mail: [email protected]).
discomfort that was exacerbated by activity. She was deemed a C6SECSADSPRO, with the pathophysiologic component requiring further explanation than just post-thrombotic reflux.
The editors and reviewers of this article have no relevant financial relationships to disclose per the Journal policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. 2213-333X
A congenital pelvic AVM was suspected and confirmed on
Copyright Ó 2017 by the Society for Vascular Surgery. Published by Elsevier Inc.
angiographic interrogation (Fig 3, A and B) performed through
http://dx.doi.org/10.1016/j.jvsv.2016.12.001
contralateral femoral puncture. 1
2
Nassiri et al
Journal of Vascular Surgery: Venous and Lymphatic Disorders ---
2017
Fig 1. A-C, Progressive stasis ulceration along the anterolateral aspect of the left mid to distal leg with surrounding pitting edema and lipodermatosclerosis. D, Resolution of ulcer within 2 months after embolization without recurrence at approximately 1-year follow-up. Selective left iliac angiography confirmed presence of a Yakes
There were no perioperative complications. She was dis-
IIa AVM4 fed by multiple arterial feeders arising from the main
charged home the same day as the procedure and continued
bifurcation of the left internal iliac artery. A coaxial system was
follow-up at the wound care facility with local wound care mea-
assembled and used to superselectively microcatheterize the
sures and weekly paste boot compression. She had complete
AVM nidus through various arterial feeders. Superselective
healing of the ulcer within 2 months after embolization, with
embolization was performed with ethylene vinyl alcohol copol-
prompt relief of pelvic pain and discomfort noted postopera-
ymer (Onyx 34; ev3, Covidien, Plymouth, Minn; Fig 3, C-E). There was excellent penetration of Onyx into the AVM nidus with
tively. There was no ulcer recurrence at 1-year follow-up. She was maintained on compression stockings.
cast formation and no evidence of nontarget embolization. Postembolization angiography revealed considerably dimin-
DISCUSSION
ished arteriovenous shunting (Fig 3, F).
The International Society for the Study of Vascular Anomalies classifies congenital vascular malformations on the basis of their flow properties into slow-flow venous and lymphatic malformations, high-flow AVMs, and congenital mixed syndromes, which can include combinations thereof.5 Congenital high-flow AVMs represent a short circuit of sorts that shunts blood prematurely from high-resistance arterioles and capillaries into draining veins. Classically, congenital AVMs of the extremities contain a nidusda convoluted conglomerate of blood vessels with poorly differentiated endothelial cells situated between the feeding artery and the draining vein. This nidus acts as a low-pressure sump that is a potent stimulator of angiogenesis. Not all extremity AVMs are congenital; in fact, a significant portion of pathologic connections between the arteries and the veins of the extremities are acquired and secondary to neoplastic changes, trauma, catheterization, and instrumentation. While there have been a handful of case reports that
Fig 2. Magnetic resonance venography (MRV) delineating engorged and promptly enhancing venous drainage of the left pelvis, upper thigh, and abdomen as a result of venous arterialization.
Journal of Vascular Surgery: Venous and Lymphatic Disorders Volume
-,
Number
Nassiri et al
3
-
Fig 3. A and B, Flush aortography demonstrates enlarged left internal iliac artery with multiple arterial feeders supplying the nidus of a Yakes IIa arteriovenous malformation (AVM) with numerous draining veins. C, Superselective microcatheter angiography of individual arterial feeders confirms shunting into an intervening nidus. D and E, Onyx embolization of the AVM nidus with formation of an occlusive cast is demonstrated. F, Postembolization angiography showing diminished AVM nidus filling with significantly reduced pathologic venous flow.
have suggested secondary arteriovenous fistulization after extensive extremity venous thrombosis,6-8 these types of pathologic connections are vastly different angiographically from the congenital varieties of AVMs. The former represent what is often referred to as cavernous transformation of the affected veins to provide collateral draining outflow. There may be erosion of these collateral channels into adjacent arterioles. These can be easily differentiated angiographically from the classic congenital AVM containing a much more convoluted nidus. The current case features the incidental presence of a congenital high-flow AVM arising from branches of the internal iliac artery in the setting of chronic iliofemoral DVT. Unlike in popular belief, digital ischemia and tissue loss as a result of an attributed steal phenomenon represent a rare and extremely late manifestation of large, widespread congenital extremity AVMs. The resultant venous hypertension is one of the earliest and most profound manifestations of symptomatic extremity AVMs.1-3 This can either, in and of itself, contribute to venous insufficiency or alternativelydas was the case in the current scenariodexacerbate concomitant post-thrombotic or
reflux symptoms. Awareness is the most important element that leads to timely investigative measures. However, as demonstrated here, AVMs are often discovered serendipitously as part of a workup for other more commonly encountered disease. Symptoms of AVM-mediated venous insufficiency are often indistinguishable from those of the isolated variety with edema, lipodermatosclerosis, and, in severe cases, tissue loss. In the absence of pre-existing thromboembolic disease, close inspection of color flow Doppler and spectral waveform analysis can provide subtle but important clues that suggest venous arterialization. These can include turbulent flow and pulsatility of the venous waveforms. In this case, the location of the AVM in the more cephalad pelvic circulation and the preexisting thrombotic burden, albeit chronic, precluded identification by duplex ultrasound interrogation. AVMs can have idiosyncratic and highly variable angioarchitectural profiles that complicate therapy. With the exception of direct arteriovenous fistulas, all other congenital AVMs require nidus penetration for adequate treatment. Although tempting because of ease of therapy, all other attempts at more proximal
4
Nassiri et al
Journal of Vascular Surgery: Venous and Lymphatic Disorders ---
occlusion of the AVM, such as coils, plugs, covered stents, and surgical ligation, are futile without superselective nidus penetration.1,4,9-11 Unfortunately, proximal occlusion methods remain commonly practiced, with inevitable recurrence of symptoms in a more hostile AVM configuration that renders superselective nidus access considerably more difficult and at times impossible. In this case, prompt referral to the VAMP on discovery of pelvic hypervascularity led to prompt angiographic interrogation with appropriate delivery of superselective embolotherapy. Ulcer healing was achieved within weeks after more than a year of refractory measures with added costs, the patient’s and provider’s frustration, and compromised quality of life of the patient. The American Venous Forum’s Clinical, Etiology, Anatomy, and Pathophysiology (CEAP) classification provides an excellent schematic platform for evaluation, risk stratification, therapeutic approach, and clinical monitoring of patients with chronic venous disease.12,13 We suggest a slight expansion of the pathophysiology (P) portion of the classification to include venous arterialization caused by AVMs as a contributing factor. This can provide increased awareness among treating personnel with a lower threshold for appropriate imaging protocols in patients with debilitating refractory venous disease. We recommend close evaluation of readily available and easy to obtain venous duplex ultrasound scans to check for color flow Doppler and spectral waveform findings suggestive of venous arterialization. In addition, magnetic resonance angiography can be obtained to verify suspicious clinical or duplex ultrasound findings. In the absence of readily available magnetic resonance imaging protocols, computed tomography angiography can be a useful screening modality.
2017
REFERENCES 1. Rosen RJ, Nassiri N, Drury JE. Interventional management of high-flow vascular malformations. Tech Vasc Interv Radiol 2013;16:22-38. 2. Lee BB, Do YS, Yakes W, Kim DI, Mattassi R, Hyon WS. Management of arteriovenous malformations: a multidisciplinary approach. J Vasc Surg 2004;39:590-600. 3. Yakes WF, Baumgartner I. Interventional treatment of arteriovenous malformations. Gefässchirurgie 2014;19:325-30. 4. Yakes WF. Yakes’ AVM classification system. J Vasc Interv Radiol 2015;26:S224. 5. Dasgupta R, Fishman SJ. ISSVA Classification. Semin Pediatr Surg 2014;23:158-61. 6. Link DP, Garza AS, Monsky W. Acquired peripheral arteriovenous malformations in patients with venous thrombosis: report of two cases. J Vasc Interv Radiol 2010;21:387-91. 7. Labropoulos N, Bhatti AF, Amaral S, Leon L, Borge M, Rodriguez H, et al. Neovascularization in acute venous thrombosis. J Vasc Surg 2005;42:515-8. 8. Varnagy D, Labropoulos N. The issue of spontaneous arteriovenous fistulae after superficial thrombophlebitis, endovenous ablation, and deep vein thrombosis: an unusual but predictable finding. Perspect Vasc Surg Endovasc Ther 2006;18:247-50. 9. Nassiri N, Cirillo-Penn NC, Thomas J. Evaluation and management of congenital peripheral arteriovenous malformations. J Vasc Surg 2015;62:1667-76. 10. Yakes W. Endovascular management of high-flow arteriovenous malformations. Semin Intervent Radiol 2004;21:49-58. 11. Lee BB, Baumgartner I, Berlien HP, Bianchini G, Burrows P, Do YS, et al. Consensus Document of the International Union of Angiology (IUA)d2013. Current concept on the management of arterio-venous management. Int Angiol 2013;32:9-36. 12. Porter JM, Moneta GL; International Consensus Committee on Chronic Venous Disease. Reporting standards in venous disease: an update. J Vasc Surg 1995;21:635-45. 13. Eklof B, Rutherford RB, Bergan JJ, Carpentier PH, Gloviczki P, Kistner RL, et al. Revision of the CEAP classification for chronic venous disorders: consensus statement. J Vasc Surg 2004;40:1248-52.
Submitted Aug 10, 2016; accepted Dec 27, 2016.