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Department of Radiology
Seth G.S. Medical College and K.E.M. Hospital, Mumbai , India
Interventional Case Record
Interventional Case Record
Embolisation of a bleeding AVM in the thigh
Embolisation of a bleeding AVM in the thigh
Contributed by : Armaandeep Singh Aulakh
Contributed by : Armaandeep Singh Aulakh
Introduction:
Introduction:
Arteriovenous malformations (AVMs) can result in dermatological manifestations, such as a reddish, eczematous reaction, angiodermatitis and ulcerations (1,2),. Some cases result in life-threatening congestive heart failure or even intractable bleeding. Some AVMs may lead to skin ulcerations which may bleed due to high flow in the feeder arteries. We report a case of a leg ulcer bleeding profusely due to underlying AVM supplied by branches superficial femoral artery. It was embolised using NBCA glue via transarterial and transvenous approach.
Arteriovenous malformations (AVMs) can result in dermatological manifestations, such as a reddish, eczematous reaction, angiodermatitis and ulcerations (1,2),. Some cases result in life-threatening congestive heart failure or even intractable bleeding. Some AVMs may lead to skin ulcerations which may bleed due to high flow in the feeder arteries. We report a case of a leg ulcer bleeding profusely due to underlying AVM supplied by branches superficial femoral artery. It was embolised using NBCA glue via transarterial and transvenous approach.
Case presentation:
Case presentation:
A 40-year-old man suffering from arteriovenous malformation (AVM) involving the left lower limb presented with bleeding ulcer secondary to trivial trauma along the medial aspect of lower one third of left thigh. Profuse spurt of blood was noted from the base of the ulcer (Fig 10a) . A tight compression dressing was applied to control the bleeding in the emergency surgical services of our hospital. The patient was referred to department of Interventional Radiology, Digital subtraction angiography was performed and subsequent embolization of AVM involving the left lower thigh was planned. Using the right 6F femoral access and Balkin cross over sheath, the left lower limb angiogram was performed. Multiple arterial feeders arising from superficial femoral artery were noted feeding the nidus with femoral vein being the major draining vein ( Fig 1 , 2).
A 40-year-old man suffering from arteriovenous malformation (AVM) involving the left lower limb presented with bleeding ulcer secondary to trivial trauma along the medial aspect of lower one third of left thigh. Profuse spurt of blood was noted from the base of the ulcer (Fig 10a) . A tight compression dressing was applied to control the bleeding in the emergency surgical services of our hospital. The patient was referred to department of Interventional Radiology, Digital subtraction angiography was performed and subsequent embolization of AVM involving the left lower thigh was planned. Using the right 6F femoral access and Balkin cross over sheath, the left lower limb angiogram was performed. Multiple arterial feeders arising from superficial femoral artery were noted feeding the nidus with femoral vein being the major draining vein ( Fig 1 , 2).
Fig 1, 2; Left SFA angiogram shows large AVM involving the thigh with multiple feeders from the branches of the SFA. Early opacification of multiple dilated venous pouches and femoral vein is seen.
Using eV3 Marathon microcatheter and glue of various concentration, trans arterial embolization of the nidus was performed and extensive glue cast involving the nidus was obtained (Fig3 &4).
Using eV3 Marathon microcatheter and glue of various concentration, trans arterial embolization of the nidus was performed and extensive glue cast involving the nidus was obtained (Fig3 &4).
Fig 3: Selective catheterization of arterial feeders done with microcatheter and embolization done using 16 % NBCA (n butyl cyanoacrylate) .
Fig 4: Glue cast in the AVM
However, the patient had blood tinged oozing from the ulcer next day. Hence patient was taken for another session of embolization. A decision was taken to perform the procedure via venous access. An occlusion balloon was inflated and placed in the proximal left SFA to decrease the arterial inflow (Fig 5).
However, the patient had blood tinged oozing from the ulcer next day. Hence patient was taken for another session of embolization. A decision was taken to perform the procedure via venous access. An occlusion balloon was inflated and placed in the proximal left SFA to decrease the arterial inflow (Fig 5).
Fig 5 : Inflation of compliant balloon in SFA to reduced arterial in flow.
Retrograde left great saphenous vein (GSV) access was obtained with a SL10 microcatheter and a microwire was advanced till the AVM nidus (Fig 6 &7).
Retrograde left great saphenous vein (GSV) access was obtained with a SL10 microcatheter and a microwire was advanced till the AVM nidus (Fig 6 &7).
Fig. 6: Retrograde access in the left GSV to reach the nidus via transvenous approach.
Fig 7: Injection of NBCA via transvenous approach
A 16 % NCBA glue- lipiodol mixture was used for embolization. At this step, a decision was taken to release the pressure bandage around the ulcer. On releasing the pressure bandage the glue was seen tracking from the nidus to the bleeding site and subsequent oozing of glue from the bleeding site was noted and the track got sealed (Fig 9 &8)
A 16 % NCBA glue- lipiodol mixture was used for embolization. At this step, a decision was taken to release the pressure bandage around the ulcer. On releasing the pressure bandage the glue was seen tracking from the nidus to the bleeding site and subsequent oozing of glue from the bleeding site was noted and the track got sealed (Fig 9 &8)
Fig 8, 9 : Pressure bandage over the oozing ulcer released to allow glue to track along the flow of blood leading to hemostasis and deeper penetration of AVM.
Final glue cast was noted along the nidus reaching the skin surface and complete haemostasis was achieved (Fig 10a, b).
Final glue cast was noted along the nidus reaching the skin surface and complete haemostasis was achieved (Fig 10a, b).
Fig 10 a, b : Photographs showing spurt of blood from AVM and post embolisation hemostasis.
Fig 11: Final SFA angiogram shows significant obliteration of AVM with glue cast.
The patient was discharged three days post procedure with healthy granulation tissue and non-bleeding ulcer base.
The patient was discharged three days post procedure with healthy granulation tissue and non-bleeding ulcer base.
Discussion:
Discussion:
AVMs are defined as high-flow vascular malformations involving abnormal communication between arterioles and veins (i.e. nidus) without an intervening capillary network. Vascular anomalies are classified into vascular tumors (eg. Haemangiomas) and vascular malformations (4). Vascular malformations arise from aberrant vessel angiogenesis and comprise direct microscopic connections between arteries, veins and lymphatic vessels without a normal capillary bed. They are divided into low-flow or high-flow lesions based on their haemodynamic flow characteristics. AVMs and AVFs, which are vascular malformations with an arterial component, are classified as high-flow lesions. AVMs have a nidus – abnormal channels connecting the arteries and veins – whereas AVFs do not have a nidus. Some vascular malformations appear as part of a familial genetic disorder. Parkes Weber syndrome is a condition characterised by nevus flammeus and AVMs associated with hypertrophy of the soft tissues or bones of the extremities (5), features of which were absent in this case. AVMs are congenital lesions and do not regress (6). AVMs may be classified into four stages using the Schobinger classification (8): Stage 1 is characterised by macular lesions, pink patches or warmth; stage 2 is characterised by a mass with a bruit and thrill, changes of which may mimic Kaposi’s sarcoma in adults; stage 3 is characterised by ulceration, pain or haemorrhage and stage 4 is associated with cardiac compromise from increased preload.
AVMs are defined as high-flow vascular malformations involving abnormal communication between arterioles and veins (i.e. nidus) without an intervening capillary network. Vascular anomalies are classified into vascular tumors (eg. Haemangiomas) and vascular malformations (4). Vascular malformations arise from aberrant vessel angiogenesis and comprise direct microscopic connections between arteries, veins and lymphatic vessels without a normal capillary bed. They are divided into low-flow or high-flow lesions based on their haemodynamic flow characteristics. AVMs and AVFs, which are vascular malformations with an arterial component, are classified as high-flow lesions. AVMs have a nidus – abnormal channels connecting the arteries and veins – whereas AVFs do not have a nidus. Some vascular malformations appear as part of a familial genetic disorder. Parkes Weber syndrome is a condition characterised by nevus flammeus and AVMs associated with hypertrophy of the soft tissues or bones of the extremities (5), features of which were absent in this case. AVMs are congenital lesions and do not regress (6). AVMs may be classified into four stages using the Schobinger classification (8): Stage 1 is characterised by macular lesions, pink patches or warmth; stage 2 is characterised by a mass with a bruit and thrill, changes of which may mimic Kaposi’s sarcoma in adults; stage 3 is characterised by ulceration, pain or haemorrhage and stage 4 is associated with cardiac compromise from increased preload.
In patients with AVMs, two factors contribute to the leg ulcer. First is the steal phenomenon- There is ischaemia of adjacent skin and soft tissue due to shunting of blood into the AVM (steal phenomenon). The second factor is the venous hypertension due to the AVMs leading to stasis of the skin microcirculation.
In patients with AVMs, two factors contribute to the leg ulcer. First is the steal phenomenon- There is ischaemia of adjacent skin and soft tissue due to shunting of blood into the AVM (steal phenomenon). The second factor is the venous hypertension due to the AVMs leading to stasis of the skin microcirculation.
The management of AVM varies, with a conservative approach adopted for patients who are asymptomatic or have minor symptoms. Symptomatic AVMs may be treated using techniques such as percutaneous sclerotherapy, endovascular embolization, or surgery. Complete eradication of the nidus of AVM has been known to be the only option for a potential cure. However, surgical treatment alone can result in massive bleeding during the surgery and can be life-threatening. In addition, surgical trauma and incomplete resection with a remnant nidus can result in the explosive growth of AVM due to a high blood flow between the arteries and the veins. Therefore, to minimize the complications related with surgery, a multidisciplinary approach should be considered. Embolization has been commonly used for reducing the vascularity of extensive AVM before surgery. In our patient, trans arterial route of embolization was employed initially which was not completely successful. Later a superficial venous access was obtained for achieving better penetration of the nidus. Most commonly liquid embolic agents are used to treat a complex AVM, NCBA glue 16 % was used in this case. The embolic agent formed extensive glue cast involving the nidus through both arterial and superficial venous approaches.
The management of AVM varies, with a conservative approach adopted for patients who are asymptomatic or have minor symptoms. Symptomatic AVMs may be treated using techniques such as percutaneous sclerotherapy, endovascular embolization, or surgery. Complete eradication of the nidus of AVM has been known to be the only option for a potential cure. However, surgical treatment alone can result in massive bleeding during the surgery and can be life-threatening. In addition, surgical trauma and incomplete resection with a remnant nidus can result in the explosive growth of AVM due to a high blood flow between the arteries and the veins. Therefore, to minimize the complications related with surgery, a multidisciplinary approach should be considered. Embolization has been commonly used for reducing the vascularity of extensive AVM before surgery. In our patient, trans arterial route of embolization was employed initially which was not completely successful. Later a superficial venous access was obtained for achieving better penetration of the nidus. Most commonly liquid embolic agents are used to treat a complex AVM, NCBA glue 16 % was used in this case. The embolic agent formed extensive glue cast involving the nidus through both arterial and superficial venous approaches.
Important technical point of the case-
Important technical point of the case-
The best result was obtained when a decision was taken to release the pressure bandage over the bleeding ulcer and glue was seen oozing from the bleeding site, subsequently stopping the bleed. A simple step of releasing the pressure generated by the bandage helped in achieving haemostasis.
The best result was obtained when a decision was taken to release the pressure bandage over the bleeding ulcer and glue was seen oozing from the bleeding site, subsequently stopping the bleed. A simple step of releasing the pressure generated by the bandage helped in achieving haemostasis.
To manage AVMs successfully, a careful assessment of the treatment strategy before the treatment is important and there must be a positive balance between subsequent morbidity and treatment gains from a plan. A simple manoeuvre of opening the compression bandage over the ulceration helped the embolizing agent to reach site of bleeding ulcer.
To manage AVMs successfully, a careful assessment of the treatment strategy before the treatment is important and there must be a positive balance between subsequent morbidity and treatment gains from a plan. A simple manoeuvre of opening the compression bandage over the ulceration helped the embolizing agent to reach site of bleeding ulcer.
References:
References:
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