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Interventional Case Record
Interventional Case Record
Embolisation of a popliteal arteriovenous malformation using cyanoacrylate glue
Embolisation of a popliteal arteriovenous malformation using cyanoacrylate glue
Contributed by : Aparna J K
Contributed by : Aparna J K
Introduction:
Introduction:
Arteriovenous malformations (AVMs) are congenital vascular malformations (CVMs) caused by birth defects involving the arterial and venous origins that result in direct communications between vessels of different sizes or primitive reticular networks of dysplastic minute vessels that have failed to mature into “capillary” vessels termed “nidus”. These lesions are characterized by shunting of high-velocity and low-resistance flow from the arterial vasculature into the venous system in various fistulous conditions. The common clinical manifestations of AVMs of the trunk and extremities are a pulsating mass, pain, ulceration, bleeding, tissue necrosis, enlargement of draining vein, and venous hypertension and/or cardiac failure. Because of its biologic nature and its associated high-flow shunting, AVMs are more aggressive, and they are often associated with life- or limb-threatening complications than other types of CVMs (1) . Therefore, early aggressive treatment of AVM is recommended. An inappropriate treatment strategy (e.g., partial excision, ligation, or endovascular occlusion of the feeding artery) only stimulates the AVM lesion into a proliferative state, resulting in aggressive growth with uncontrollable complications. The surgical resection of an AVM lesion carries the risks of extensive intraoperative hemorrhage, incomplete removal of the AVM nidus, surrounding organ or tissue injuries, and high recurrence rates. Therefore, endovascular treatment with various embolic and sclerosing agents has become an accepted option for the management of AVM (2).
Arteriovenous malformations (AVMs) are congenital vascular malformations (CVMs) caused by birth defects involving the arterial and venous origins that result in direct communications between vessels of different sizes or primitive reticular networks of dysplastic minute vessels that have failed to mature into “capillary” vessels termed “nidus”. These lesions are characterized by shunting of high-velocity and low-resistance flow from the arterial vasculature into the venous system in various fistulous conditions. The common clinical manifestations of AVMs of the trunk and extremities are a pulsating mass, pain, ulceration, bleeding, tissue necrosis, enlargement of draining vein, and venous hypertension and/or cardiac failure. Because of its biologic nature and its associated high-flow shunting, AVMs are more aggressive, and they are often associated with life- or limb-threatening complications than other types of CVMs (1) . Therefore, early aggressive treatment of AVM is recommended. An inappropriate treatment strategy (e.g., partial excision, ligation, or endovascular occlusion of the feeding artery) only stimulates the AVM lesion into a proliferative state, resulting in aggressive growth with uncontrollable complications. The surgical resection of an AVM lesion carries the risks of extensive intraoperative hemorrhage, incomplete removal of the AVM nidus, surrounding organ or tissue injuries, and high recurrence rates. Therefore, endovascular treatment with various embolic and sclerosing agents has become an accepted option for the management of AVM (2).
Patients with hand and foot AVMs have more severe ischemic pain, ulceration, and/or necrosis. The treatment outcomes for hand and foot AVMs are relatively poor; they have lower cure and higher complication rates than AVMs in other locations. Hand AVMs involving the fingers had relatively more complications than those without finger involvement. If an AVM is small, it is difficult to puncture or catheterize the nidus or discriminate between AVM and normal vessels on angiography. Moreover, the risk of inevitable embolization or reflux to normal vessels increases, and coil embolization is difficult due to the narrow space and the superficial location. To reduce the complications, meticulous discrimination and infusion techniques that reduce the amount and concentration of embolizing agent are required (2,3).
Patients with hand and foot AVMs have more severe ischemic pain, ulceration, and/or necrosis. The treatment outcomes for hand and foot AVMs are relatively poor; they have lower cure and higher complication rates than AVMs in other locations. Hand AVMs involving the fingers had relatively more complications than those without finger involvement. If an AVM is small, it is difficult to puncture or catheterize the nidus or discriminate between AVM and normal vessels on angiography. Moreover, the risk of inevitable embolization or reflux to normal vessels increases, and coil embolization is difficult due to the narrow space and the superficial location. To reduce the complications, meticulous discrimination and infusion techniques that reduce the amount and concentration of embolizing agent are required (2,3).
Here we discuss the case of a 12-year-old boy, who underwent glue embolization of an AVM from branches of the popliteal artery..
Here we discuss the case of a 12-year-old boy, who underwent glue embolization of an AVM from branches of the popliteal artery..
Case presentation:
Case presentation:
A 12-year-old boy presented with complaints of pain in the left knee with difficulty in walking for the past one year. There is history of fall one year ago when the patient sustained injury to the left knee. There was swelling and tenderness of the left knee with painful extension and restriction of movements. There was no redness or warmth.
A 12-year-old boy presented with complaints of pain in the left knee with difficulty in walking for the past one year. There is history of fall one year ago when the patient sustained injury to the left knee. There was swelling and tenderness of the left knee with painful extension and restriction of movements. There was no redness or warmth.
An MRI of the knee (Figures 1-6) showed multiple dilated tubular flow voids in the Hoffa’s fat pad with adjacent PDFS hyperintensity over the anteromedial aspect of the lateral tibial plateau. Prominent feeding artery was seen arising from the lateral geniculate branch of the popliteal artery with a draining venous channel in the subcutaneous plane along the lateral femoral condyle. The joint space, articular cartilage and underlying bones were normal. These features were suggestive of arteriovenous malformation in the Hoffa’s fat pad of the left knee (4,5).
An MRI of the knee (Figures 1-6) showed multiple dilated tubular flow voids in the Hoffa’s fat pad with adjacent PDFS hyperintensity over the anteromedial aspect of the lateral tibial plateau. Prominent feeding artery was seen arising from the lateral geniculate branch of the popliteal artery with a draining venous channel in the subcutaneous plane along the lateral femoral condyle. The joint space, articular cartilage and underlying bones were normal. These features were suggestive of arteriovenous malformation in the Hoffa’s fat pad of the left knee (4,5).
Figure 1 - 6- Pre embolization MRI left knee
The left lower limb DSA (Video 1, 2) showed a lobular hypervascular lesion (nidus) of approximate size 3.4x2.9cm in the popliteal region with arterial feeders from the inferior lateral and inferior medial genicular arteries and early draining veins, draining into the genicular veins, consistent with high flow arteriovenous malformation. The left anterior tibial, posterior tibial, peroneal arteries were normal and the distal arch was formed.
The left lower limb DSA (Video 1, 2) showed a lobular hypervascular lesion (nidus) of approximate size 3.4x2.9cm in the popliteal region with arterial feeders from the inferior lateral and inferior medial genicular arteries and early draining veins, draining into the genicular veins, consistent with high flow arteriovenous malformation. The left anterior tibial, posterior tibial, peroneal arteries were normal and the distal arch was formed.
Interventional Technique:
Interventional Technique:
Left lower limb DSA (Video 1, 2) had shown a lobular hypervascular lesion (nidus) of approximate size 3.4x2.9cm in the popliteal region with arterial feeders from the inferior lateral and inferior medial genicular arteries and early draining veins, draining into the genicular veins, consistent with high flow arteriovenous malformation. The left anterior tibial, posterior tibial, peroneal arteries were normal and the distal arch was formed.
Left lower limb DSA (Video 1, 2) had shown a lobular hypervascular lesion (nidus) of approximate size 3.4x2.9cm in the popliteal region with arterial feeders from the inferior lateral and inferior medial genicular arteries and early draining veins, draining into the genicular veins, consistent with high flow arteriovenous malformation. The left anterior tibial, posterior tibial, peroneal arteries were normal and the distal arch was formed.
The patient was planned embolization of the left popliteal AVM. Under general anaesthesia, with all aseptic precautions and fluoroscopy guidance right common femoral vein access was secured using 6F paediatric sheath. Using a Terumo glide wire and 4Fr H1 catheter, the distal left SFA was catheterized. An angiogram from this location is shown in Video 1. The 4Fr H1 catheter was exchanged for a 5Fr H1 Envoy catheter and subsequently, a micro catheter was used for selective cannulation of the feeding vessels. Selective cannulation of the feeder from lateral geniculate artery was cannulated (Video 2) and 33% of glue was injected (33% NBCA and 67% lipiodol). Post embolization angiogram showed filling of the nidus via the feeder arising from medial branch of geniculate artery (Video 3). Selective cannulation of this feeder was done (Video 4, 5) and 16% of glue (16% NBC and 84% of lipiodol). Post embolization angiogram showed complete obliteration of feeders and nidus suggestive of isolation of the nidus from circulation with no evidence of early draining vein(Video 6). Figure 10 shows the post embolization glue cast spot film. Patient tolerated the procedure well and was discharged on post operative day 4.
The patient was planned embolization of the left popliteal AVM. Under general anaesthesia, with all aseptic precautions and fluoroscopy guidance right common femoral vein access was secured using 6F paediatric sheath. Using a Terumo glide wire and 4Fr H1 catheter, the distal left SFA was catheterized. An angiogram from this location is shown in Video 1. The 4Fr H1 catheter was exchanged for a 5Fr H1 Envoy catheter and subsequently, a micro catheter was used for selective cannulation of the feeding vessels. Selective cannulation of the feeder from lateral geniculate artery was cannulated (Video 2) and 33% of glue was injected (33% NBCA and 67% lipiodol). Post embolization angiogram showed filling of the nidus via the feeder arising from medial branch of geniculate artery (Video 3). Selective cannulation of this feeder was done (Video 4, 5) and 16% of glue (16% NBC and 84% of lipiodol). Post embolization angiogram showed complete obliteration of feeders and nidus suggestive of isolation of the nidus from circulation with no evidence of early draining vein(Video 6). Figure 10 shows the post embolization glue cast spot film. Patient tolerated the procedure well and was discharged on post operative day 4.
Post operative MRI (Figures 7-9) of the left knee done on post operative day 3 showed heterogeneously hyperintense signal intensity on T2WI in the previously described flow voids suggestive of thrombosis of the nidus.
Post operative MRI (Figures 7-9) of the left knee done on post operative day 3 showed heterogeneously hyperintense signal intensity on T2WI in the previously described flow voids suggestive of thrombosis of the nidus.
Figure 7-9 Post embolization MRI left knee
Figure 10 shows the final cast of the glue in the AVM
Figure 10 shows the final cast of the glue in the AVM
Figure 10 Glue cast
Discussion:
Discussion:
High-flow malformations make up approximately 10% of malformations in the extremities. AVMs and AVFs are typically congenital and acquired malformations, respectively. AVFs are formed by a single vascular channel between an artery and a vein. AVMs consist of feeding arteries, draining veins and a nidus composed of multiple dysplastic vascular channels that connect the arteries and veins, with the absence of a normal capillary bed. Although there are a cluster of channels, there is no significant solid identifiable mass.
High-flow malformations make up approximately 10% of malformations in the extremities. AVMs and AVFs are typically congenital and acquired malformations, respectively. AVFs are formed by a single vascular channel between an artery and a vein. AVMs consist of feeding arteries, draining veins and a nidus composed of multiple dysplastic vascular channels that connect the arteries and veins, with the absence of a normal capillary bed. Although there are a cluster of channels, there is no significant solid identifiable mass.
AVMs are present in a dormant stage during birth but can show rapid growth over a relatively short period of time during childhood or adulthood, as they increase in size proportionally with the growth of the patient. This growth rate can be exacerbated by hormonal changes during puberty or pregnancy or as a result of thrombosis, infection, and trauma. AVMs may be single, multiple or part of a genetic disorder such as hereditary hemorrhagic telangiectasia syndrome (6)
AVMs are present in a dormant stage during birth but can show rapid growth over a relatively short period of time during childhood or adulthood, as they increase in size proportionally with the growth of the patient. This growth rate can be exacerbated by hormonal changes during puberty or pregnancy or as a result of thrombosis, infection, and trauma. AVMs may be single, multiple or part of a genetic disorder such as hereditary hemorrhagic telangiectasia syndrome (6)
The high blood flow in the lesions produces a pulsatile, red, warm mass with a thrill on examinations. If related to joints, they may lead to bone overgrowth, arterial steal phenomenon and cutaneous ischaemia. Ulceration and haemorrhage may be seen in extreme cases. Less commonly, high-output cardiac failure can occur with large arteriovenous shunts.
The high blood flow in the lesions produces a pulsatile, red, warm mass with a thrill on examinations. If related to joints, they may lead to bone overgrowth, arterial steal phenomenon and cutaneous ischaemia. Ulceration and haemorrhage may be seen in extreme cases. Less commonly, high-output cardiac failure can occur with large arteriovenous shunts.
The aim of treatment of high-flow lesions is the complete occlusion of the AVM nidus or fistulous connection. Sclerotherapy has not been shown to be as effective in treating these lesions, in part owing to the rapid outflow of the infused agents. Historically, surgical resection has been considered the treatment of choice. However, due to the significant morbidity and high rate of recurrence associated with surgical resection, endovascular therapy has emerged as a less invasive alternative with comparable efficacy. There is no unified agreement on the ideal treatment of these more complex malformations and a case-by-case basis multidisciplinary approach has been advocated. Based on the angiographic classification of AVMs, the treatment strategies should vary. The treatment strategy for type II AVMs, such as the one described in our patient is as follows: first, reduce the blood flow velocity in the venous segment of the AVM with coils; second, perform ethanol embolotherapy of the residual shunts, because the shunts are located at the venous wall of the draining vein (7)
The aim of treatment of high-flow lesions is the complete occlusion of the AVM nidus or fistulous connection. Sclerotherapy has not been shown to be as effective in treating these lesions, in part owing to the rapid outflow of the infused agents. Historically, surgical resection has been considered the treatment of choice. However, due to the significant morbidity and high rate of recurrence associated with surgical resection, endovascular therapy has emerged as a less invasive alternative with comparable efficacy. There is no unified agreement on the ideal treatment of these more complex malformations and a case-by-case basis multidisciplinary approach has been advocated. Based on the angiographic classification of AVMs, the treatment strategies should vary. The treatment strategy for type II AVMs, such as the one described in our patient is as follows: first, reduce the blood flow velocity in the venous segment of the AVM with coils; second, perform ethanol embolotherapy of the residual shunts, because the shunts are located at the venous wall of the draining vein (7)
A variety of percutaneous sclerotic and transarterial embolizing agents have been advocated in numerous combinations, depending on location, severity and the extent of the malformations. Absolute ethanol, bleomycin, 3% sodium tetradecyl sulfate (STS), polidocanol, ethanolamine oleate, n-butyl cyanoacrylate, polyvinyl alcohol foam and various types of coils and polymer microspheres have all been used.
A variety of percutaneous sclerotic and transarterial embolizing agents have been advocated in numerous combinations, depending on location, severity and the extent of the malformations. Absolute ethanol, bleomycin, 3% sodium tetradecyl sulfate (STS), polidocanol, ethanolamine oleate, n-butyl cyanoacrylate, polyvinyl alcohol foam and various types of coils and polymer microspheres have all been used.
Of the agents described, ethanol sclerotherapy has been the most successfully applied, in suitable low-flow lesions, as single therapy or as part of pre-operative surgery. It has been shown to be an effective means of treating these malformations with a 64–96% response rate, defined as improvement in symptoms or reduction in the size of the lesion (8)
Of the agents described, ethanol sclerotherapy has been the most successfully applied, in suitable low-flow lesions, as single therapy or as part of pre-operative surgery. It has been shown to be an effective means of treating these malformations with a 64–96% response rate, defined as improvement in symptoms or reduction in the size of the lesion (8)
Since the initiation of endovascular therapy for AVMs, ethanol has been the preferred embolic agent because of its strong devascularization effect resulting from endothelial damage of the vessel, serum protein denaturation, and rapid thrombus formation. However, ethanol induces significant pain in the vessel wall vasa nervorum when injected intravascularly. General anesthesia is required to minimize patient discomfort. Post-embolization edema always occurs with the use of ethanol. Pulmonary hypertension is another potentially fatal complication associated with ethanol embolotherapy, and it occurs when a significant amount of ethanol is injected (9)
Since the initiation of endovascular therapy for AVMs, ethanol has been the preferred embolic agent because of its strong devascularization effect resulting from endothelial damage of the vessel, serum protein denaturation, and rapid thrombus formation. However, ethanol induces significant pain in the vessel wall vasa nervorum when injected intravascularly. General anesthesia is required to minimize patient discomfort. Post-embolization edema always occurs with the use of ethanol. Pulmonary hypertension is another potentially fatal complication associated with ethanol embolotherapy, and it occurs when a significant amount of ethanol is injected (9)
Endovascular treatment of AVMs using other liquid embolic agents such as n-butyl cyanoacrylate (NBCA) and Onyx (ethylene vinyl alcohol copolymer, dissolved in dimethyl-sulfoxide (DMSO)) has been reported. The symptomatic improvement in NBCA is good, but the clinical result is not long-lasting. NBCA glue was used mainly for the surgically excisable lesions as preoperative embolo/sclerotherapy to reduce the morbidity during the subsequent surgical therapy. The aim of using it in our patient was the same. Onyx is a more controllable agent, but its reported data are limited, and it is associated with a risk of recanalization and recurrence. The drawbacks of Onyx are high costs, radio-opacity, and residual mass effects (10)
Endovascular treatment of AVMs using other liquid embolic agents such as n-butyl cyanoacrylate (NBCA) and Onyx (ethylene vinyl alcohol copolymer, dissolved in dimethyl-sulfoxide (DMSO)) has been reported. The symptomatic improvement in NBCA is good, but the clinical result is not long-lasting. NBCA glue was used mainly for the surgically excisable lesions as preoperative embolo/sclerotherapy to reduce the morbidity during the subsequent surgical therapy. The aim of using it in our patient was the same. Onyx is a more controllable agent, but its reported data are limited, and it is associated with a risk of recanalization and recurrence. The drawbacks of Onyx are high costs, radio-opacity, and residual mass effects (10)
References:
References:
1. ISSVA Classification of Vascular Anomalies ©2014 International Society for the Study of Vascular Anomalies.
1. ISSVA Classification of Vascular Anomalies ©2014 International Society for the Study of Vascular Anomalies.
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9. Legiehn GM, Heran MK. Classification, diagnosis, and interventional radiologic management of vascular malformations. Orthop Clin North Am. 2006;37(3):435-474, vii-viii.
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10. Mulligan PR, Prajapati HJS, Martin LG, et al. Vascular anomalies: classification, imaging characteristics and implications for interventional radiology treatment approaches. Br J Radiol. 2014;87(1035):20130392.
10. Mulligan PR, Prajapati HJS, Martin LG, et al. Vascular anomalies: classification, imaging characteristics and implications for interventional radiology treatment approaches. Br J Radiol. 2014;87(1035):20130392.