56INTERVENTIONAL RADIOLOGY

DAVID SUTTON

DAVID SUTTON PICTURES

DR. Muhammad Bin Zulfiqar PGR-FCPS III SIMS/SHL

Fig. 56.1 Intra-arterial thrombolysis. Left internal carotid injection (A) in a patient who suffered an acute stroke during a coronary angiogram showing an abrupt change in caliber of the horizontal (M1) portion of the left middle cerebral artery with occlusion of some M2 branches. Angiogram through microcatheter (B) that had been advanced into the acute middle cerebral artery clot. Superselective angiogram during thrombolysis (C) with urokinase shows re-opening of previously occluded MCA branches. Left internal carotid injection following the procedure (D) shows successful lysis of the acute left MCA thrombus. (Courtesy of Dr James Jackson.)

• Fig. 56.1 Intra-arterial thrombolysis. Left internal carotid injection (A) in a patient who suffered an acute stroke during a coronary angiogram showing an abrupt change in caliber of the horizontal (M1) portion of the left middle cerebral artery with occlusion of some M2 branches. Angiogram through microcatheter (B) that had been advanced into the acute middle cerebral artery clot. Superselective angiogram during thrombolysis (C) with urokinase shows re-opening of previously occluded MCA branches. Left internal carotid injection following the procedure (D) shows successful lysis of the acute left MCA thrombus. (Courtesy of Dr James Jackson.)

• Fig. 56.2 Angioplasty of vasospasm. Right ICA angiogram following clipping of a right MCA aneurysm, which had bled, demonstrates severe vasospasm of the M1 segment of the right MCA (A). An unsubtracted image taken during balloon dilatation (B) demonstrates the inflated angioplasty balloon and aneurysms clip. Postangioplasty right ICA angiogram (C) demonstrating a normal caliber of the M1 segment.

• Fig. 56.2 Angioplasty of vasospasm. Right ICA angiogram following clipping of a right MCA aneurysm, which had bled, demonstrates severe vasospasm of the M1 segment of the right MCA (A). An unsubtracted image taken during balloon dilatation (B) demonstrates the inflated angioplasty balloon and aneurysms clip. Postangioplasty right ICA angiogram (C) demonstrating a normal caliber of the M1 segment.

• Fig. 56.3 Carotid stenting. The preceding common carotid artery angiogram (A) demonstrates a severe stenosis at the origin of the internal carotid artery. An unsubtracted image during the procedure (B) shows a self-expandable stent placed across the stenosis with a residual waist at level of stenosis. The postprocedure right CCA angiogram (C) demonstrates successful treatment of the stenosis.

• Fig. 56.4 Balloon embolisation of caroticocavernous fistula. Internal carotid artery angiogram (A) demonstrating a traumatic caroticocavernous fistula shunting into the ophthalmic veins and petrosal venous sinuses. Note the absence of opacification of the ipsilateral intracranial vessels due to steal through the shunt. Unsubtracted image (B) at the end of the procedure shows an inflated balloon, filled with contrast medium, within cavernous sinus. The postprocedure internal carotid angiogram (C) demonstrates complete closure of the fistula with normal anterograde opacification of the ipsilateral intracranial vessels.

• Fig. 56.4 Balloon embolisation of caroticocavernous fistula. Internal carotid artery angiogram (A) demonstrating a traumatic caroticocavernous fistula shunting into the ophthalmic veins and petrosal venous sinuses. Note the absence of opacification of the ipsilateral intracranial vessels due to steal through the shunt. Unsubtracted image (B) at the end of the procedure shows an inflated balloon, filled with contrast medium, within cavernous sinus. The postprocedure internal carotid angiogram (C) demonstrates complete closure of the fistula with normal anterograde opacification of the ipsilateral intracranial vessels.

• Fig. 56.5 Coil embolisation of superior cerebellar artery aneurysm. Left vertebral angiogram (A) demonstrating right superior cerebellar artery aneurysm. Note the caudal fusion and the origin of the perforating vessels off the more rostrally located P1 segment. Despite the broad neck and involvement of the superior cerebellar artery origin, it was decided to attempt endovascular treatment because of the posterior fossa location. A 3D GDC coil has been deployed (B) in good position, forming a basket across the aneurysm neck, avoiding the region of the superior cerebellar artery origin and the laterally projecting nipple, presumed to be the site of rupture. Final angiogram (C) demonstrating complete exclusion of the aneurysm without compromise of the adjacent vessels.

• Fig. 56.5 Coil embolisation of superior cerebellar artery aneurysm. Left vertebral angiogram (A) demonstrating right superior cerebellar artery aneurysm. Note the caudal fusion and the origin of the perforating vessels off the more rostrally located P1 segment. Despite the broad neck and involvement of the superior cerebellar artery origin, it was decided to attempt endovascular treatment because of the posterior fossa location. A 3D GDC coil has been deployed (B) in good position, forming a basket across the aneurysm neck, avoiding the region of the superior cerebellar artery origin and the laterally projecting nipple, presumed to be the site of rupture. Final angiogram (C) demonstrating complete exclusion of the aneurysm without compromise of the adjacent vessels.

• Fig. 56.6 Coil embolisation of bilateral intracranial aneurysms. Left ICA angiogram (A) demonstrating a terminal carotid aneurysm. Note the nipple pointing medially, an angiographic sign often seen in acutely ruptured aneurysms. Right ICA angiogram (B) demonstrating a posterior communicating segment aneurysm. CT (not shown) had revealed the greatest density of subarachnoid blood to lie in this region. Because of the disparity between the angiographic and CT findings, it was not certain which of the two aneurysms had bled. It was therefore decided to treat both in a single sitting, despite the risk of intervention in two different arterial territories. Bilateral surgical intervention was not considered to be a safe option. Left ICA angiogram (C) demonstrates the terminal carotid aneurysm to be excluded by coils. Right ICA angiogram (D) demonstrates the posterior communicating segment aneurysm to be excluded by coils. Unsubtracted image (E) shows the position of the coils.

• Fig. 56.6 Coil embolisation of bilateral intracranial aneurysms. Left ICA angiogram (A) demonstrating a terminal carotid aneurysm. Note the nipple pointing medially, an angiographic sign often seen in acutely ruptured aneurysms. Right ICA angiogram (B) demonstrating a posterior communicating segment aneurysm. CT (not shown) had revealed the greatest density of subarachnoid blood to lie in this region. Because of the disparity between the angiographic and CT findings, it was not certain which of the two aneurysms had bled. It was therefore decided to treat both in a single sitting, despite the risk of intervention in two different arterial territories. Bilateral surgical intervention was not considered to be a safe option. Left ICA angiogram (C) demonstrates the terminal carotid aneurysm to be excluded by coils. Right ICA angiogram (D) demonstrates the posterior communicating segment aneurysm to be excluded by coils. Unsubtracted image (E) shows the position of the coils.

• Fig. 56.7 Coil embolisation of of wide-necked aneurysm with balloon remodelling. Subtracted and unsubtracted left internal carotid angiography before (A,B) and after (C,D) balloon remodelling assisted GDC coiling. The large supraclinoid aneurysm has a very wide neck (a). A remodelling balloon was placed across the neck of the aneurysm, seen on the unsubtracted image (B). Also note the microcatheter tip placed within the aneurysm lumen. The remodelling balloon was inflated for short periods during the coil deployment to prevent coil prolapse into the internal carotid artery. This enabled complete exclusion of the aneurysm, without compromise of lumen of the internal carotid artery (C). The dense coil mass is seen on the final unsubtracted image (D).

• Fig. 56.7 Coil embolisation of of wide-necked aneurysm with balloon remodelling. Subtracted and unsubtracted left internal carotid angiography before (A,B) and after (C,D) balloon remodelling assisted GDC coiling. The large supraclinoid aneurysm has a very wide neck (a). A remodelling balloon was placed across the neck of the aneurysm, seen on the unsubtracted image (B). Also note the microcatheter tip placed within the aneurysm lumen. The remodelling balloon was inflated for short periods during the coil deployment to prevent coil prolapse into the internal carotid artery. This enabled complete exclusion of the aneurysm, without compromise of lumen of the internal carotid artery (C). The dense coil mass is seen on the final unsubtracted image (D).

• Fig. 56.8 Rupture during coil embolisation of intracranial aneurysms. Left vertebral angiogram (A) demonstrating extravasation of contrast from ruptured basilar tip aneurysms during coil placement. Note coils within aneurysm and extravasated contrast around the basilar artery in the interpeduncular and pre-pontine cisterns. Left vertebral angiogram (B) demonstrating cessation of extravasation after reversal of heparin with protamine and further packing of the aneurysm, to exclusion. The patient suffered no adverse consequences.

• Fig. 56.9 Arterial occlusion due to coil embolisation of intracranial aneurysms. Left ICA angiogram (A) demonstrating coils within an aneurysm arising at the right side of the large anterior communicating artery and the origin of the right A2 segment. Note the good filling of the A2 segment. Left ICA angiogram (B) demonstrating occlusion of the A2 segment after deployment of a subsequent coil. The coil was successfully retrieved before detachment, but the vessel remained occluded. Fortunately, the patient rapidly developed collateral flow from the posterior cerebral artery and suffered no adverse consequences.

• Fig. 56.10 Vermian AVM embolisation. Pre-embolisation left vertebral angiogram (A) demonstrating vermian arteriovenous malformation supplied by vermian branches of the superior cerebellar arteries. Microcatheter NBCA injection (B) into arteriovenous malformation nidus. Postembolisation of both major pedicles, left vertebral angiography (C) demonstrates almost complete obliteration of the nidus.

• Fig. 56.10 Vermian AVM embolisation. Pre-embolisation left vertebral angiogram (A) demonstrating vermian arteriovenous malformation supplied by vermian branches of the superior cerebellar arteries. Microcatheter NBCA injection (B) into arteriovenous malformation nidus. Postembolisation of both major pedicles, left vertebral angiography (C) demonstrates almost complete obliteration of the nidus.

Fig. 56.11 Embolisation of vein of Galen aneurysmal malformation. Left lateral angiogram (A) demonstrating aneurysmal dilatation of the vein of Galen and rapid arteriovenous shunting into a persistent falcine sinus. A microcatheter was passed into one of the feeding pedicles (B) and NBCA rendered radiopaque with Tantalum was injected (C) through it. This achieved complete closure of the shunt (D). (Courtesy of Dr W. Taylor.)

• Fig. 56.11 Embolisation of vein of Galen aneurysmal malformation. Left lateral angiogram (A) demonstrating aneurysmal dilatation of the vein of Galen and rapid arteriovenous shunting into a persistent falcine sinus. A microcatheter was passed into one of the feeding pedicles (B) and NBCA rendered radiopaque with Tantalum was injected (C) through it. This achieved complete closure of the shunt (D). (Courtesy of Dr W. Taylor.)

• Fig. 56.12 Embolisation of cortical vein dural arteriovenous shunt presenting with parenchymal haemorrhage. CT without contrast at presentation (A) demonstrating right parenchymal haematoma. Right external carotid angiogram (B) showing arteriovenous shunting into a cortical vein in the region of the haematoma. Microcatheter angiogram from a distal position within a frontal branch of the right middle meningeal artery (C) better demonstrating the dural arteriovenous shunt into a cortical vein. There were several additional branches to the dural shunt off the left middle meningeal artery (not shown). NBCA/ Lipiodol was injected from this position (D). This achieved complete closure with no arteriovenous shunting evident from either external carotid artery (E,F). The internal carotid injection (G) demonstrates preservation of the superior sagittal sinus. CT without contrast after embolisation (H) demonstrates the dense glue cast and the evolving haematoma.

• Fig. 56.12 Embolisation of cortical vein dural arteriovenous shunt presenting with parenchymal haemorrhage. CT without contrast at presentation (A) demonstrating right parenchymal haematoma. Right external carotid angiogram (B) showing arteriovenous shunting into a cortical vein in the region of the haematoma. Microcatheter angiogram from a distal position within a frontal branch of the right middle meningeal artery (C) better demonstrating the dural arteriovenous shunt into a cortical vein. There were several additional branches to the dural shunt off the left middle meningeal artery (not shown). NBCA/ Lipiodol was injected from this position (D). This achieved complete closure with no arteriovenous shunting evident from either external carotid artery (E,F). The internal carotid injection (G) demonstrates preservation of the superior sagittal sinus. CT without contrast after embolisation (H) demonstrates the dense glue cast and the evolving haematoma.

• Fig. 56.12 Embolisation of cortical vein dural arteriovenous shunt presenting with parenchymal haemorrhage. CT without contrast at presentation (A) demonstrating right parenchymal haematoma. Right external carotid angiogram (B) showing arteriovenous shunting into a cortical vein in the region of the haematoma. Microcatheter angiogram from a distal position within a frontal branch of the right middle meningeal artery (C) better demonstrating the dural arteriovenous shunt into a cortical vein. There were several additional branches to the dural shunt off the left middle meningeal artery (not shown). NBCA/ Lipiodol was injected from this position (D). This achieved complete closure with no arteriovenous shunting evident from either external carotid artery (E,F). The internal carotid injection (G) demonstrates preservation of the superior sagittal sinus. CT without contrast after embolisation (H) demonstrates the dense glue cast and the evolving haematoma.

• Fig. 56.12 Embolisation of cortical vein dural arteriovenous shunt presenting with parenchymal haemorrhage. CT without contrast at presentation (A) demonstrating right parenchymal haematoma. Right external carotid angiogram (B) showing arteriovenous shunting into a cortical vein in the region of the haematoma. Microcatheter angiogram from a distal position within a frontal branch of the right middle meningeal artery (C) better demonstrating the dural arteriovenous shunt into a cortical vein. There were several additional branches to the dural shunt off the left middle meningeal artery (not shown). NBCA/ Lipiodol was injected from this position (D). This achieved complete closure with no arteriovenous shunting evident from either external carotid artery (E,F). The internal carotid injection (G) demonstrates preservation of the superior sagittal sinus. CT without contrast after embolisation (H) demonstrates the dense glue cast and the evolving haematoma.

• Fig. 56.13 Embolisation of dural arteriovenous shunt causing cortical venous congestion. CT with contrast (A) demonstrating dilated cortical and deep veins, including the septal vein. Right ECA angiogram (B) demonstrating a dural fistula of right transverse sinus supplied by meningeal and transosseous branches with retrograde cortical venous reflux. Unsubtracted image (C) showing NBCA glue cast at the site of the fistula. Note how the glue has penetrated the venous side of the fistula, with the cast corresponding to the zone of shunting demonstrated in (B). Right ECA angiogram (D) demonstrating complete occlusion of the fistula. Note the decrease in calibre of the occipital artery on this follow-up angiogram. (Courtesy of Prof. P. Lasjaunias.)

• Fig. 56.13 Embolisation of dural arteriovenous shunt causing cortical venous congestion. CT with contrast (A) demonstrating dilated cortical and deep veins, including the septal vein. Right ECA angiogram (B) demonstrating a dural fistula of right transverse sinus supplied by meningeal and transosseous branches with retrograde cortical venous reflux. Unsubtracted image (C) showing NBCA glue cast at the site of the fistula. Note how the glue has penetrated the venous side of the fistula, with the cast corresponding to the zone of shunting demonstrated in (B). Right ECA angiogram (D) demonstrating complete occlusion of the fistula. Note the decrease in calibre of the occipital artery on this follow-up angiogram. (Courtesy of Prof. P. Lasjaunias.)

• Fig. 56.14 Embolisation of glomus jugulare tumour. External carotid angiogram (A) showing a hypervascular tumour at the level of the jugular foramen. Superselective catheterisation of the ascending pharyngeal artery (B) prior to embolisation demonstrates that this vessel provides the main vascular supply to the mass, a typical finding in glomus jugulare tumours. The external carotid artery angiogram following particle embolisation (C) shows almost complete obliteration of the vascular supply. There is also some vasospasm near the catheter tip.

• Fig. 56.14 Embolisation of glomus jugulare tumour. External carotid angiogram (A) showing a hypervascular tumour at the level of the jugular foramen. Superselective catheterisation of the ascending pharyngeal artery (B) prior to embolisation demonstrates that this vessel provides the main vascular supply to the mass, a typical finding in glomus jugulare tumours. The external carotid artery angiogram following particle embolisation (C) shows almost complete obliteration of the vascular supply. There is also some vasospasm near the catheter tip.

• Fig. 56.15 Palliative embolisation of malignant extra-axial tumour. A contrast enhanced T1 -weighted MRI (A) demonstrates a markedly enhancing metastasis with extradural and extracranial extension (presumed to be from a known neuroendocrine primary). Superselective angiography of the left internal maxillary artery (B) confirms marked hypervascularity of the mass. Injection of the same vessel following particle embolisation (C) shows devascularisation of the tumour. A contrast enhanced MRI after one week (D) shows large non-enhancing necrotic areas within the tumour.

• Fig. 56.15 Palliative embolisation of malignant extra-axial tumour. A contrast enhanced T1 -weighted MRI (A) demonstrates a markedly enhancing metastasis with extradural and extracranial extension (presumed to be from a known neuroendocrine primary). Superselective angiography of the left internal maxillary artery (B) confirms marked hypervascularity of the mass. Injection of the same vessel following particle embolisation (C) shows devascularisation of the tumour. A contrast enhanced MRI after one week (D) shows large non-enhancing necrotic areas within the tumour.

• Fig. 56.16 Spinal dural arteriovenous fistula. Spinal angiogram in a patient with progressive leg weakness and sphincter disturbance. Selective injection of right thoracic intercostal vessels shows a dural arteriovenous fistula shunting into perimedullary veins, which drain superiorly and inferiorly.

• Fig. 56.17 Vertebral haemangioma biopsy and embolisation. T2-weighted axial MRI (A) of a vertebral haemangioma causing cord compression. CT-guided core biopsy (B). The biopsy needle was placed through the pedicle of the vertebral body to decrease the chance of causing haemorrhage within vertebral canal. Pre-embolisation right intercostal artery angiogram (C) demonstrating the hypervascular haemangioma. Postembolisation angiogram (D) demonstrating almost complete devascularisation after embolisation with PVA particles.

• Fig. 56.17 Vertebral haemangioma biopsy and embolisation. T2-weighted axial MRI (A) of a vertebral haemangioma causing cord compression. CT-guided core biopsy (B). The biopsy needle was placed through the pedicle of the vertebral body to decrease the chance of causing haemorrhage within vertebral canal. Pre-embolisation right intercostal artery angiogram (C) demonstrating the hypervascular haemangioma. Postembolisation angiogram (D) demonstrating almost complete devascularisation after embolisation with PVA particles.

• Fig. 56.18 Percutaneous vertebroplasty. Fluoroscopic images in frontal (A) and lateral (B) projections showing transpedicular course of cannulas prior to first injection of PMMA. Note marked osteopenia and loss of height of vertebral bodies in this patient with multiple myeloma. Subsequently cannulas were placed (C) in the other severely affected levels. A total of three levels were treated (D). The patient was able to cease morphine after the procedure. (Courtesy of Professor Juergen Reul.)

• Fig. 56.18 Percutaneous vertebroplasty. Fluoroscopic images in frontal (A) and lateral (B) projections showing transpedicular course of cannulas prior to first injection of PMMA. Note marked osteopenia and loss of height of vertebral bodies in this patient with multiple myeloma. Subsequently cannulas were placed (C) in the other severely affected levels. A total of three levels were treated (D). The patient was able to cease morphine after the procedure. (Courtesy of Professor Juergen Reul.)

• Fig. 56.19 Photodynamic therapy of carcinoma tongue. Sagittal (A) and axial (B) T1-weighted scans performed on an 'open' interventional MR scanner of a patient with a carcinoma of the base of tongue causing airway obstruction. MR-compatible guiding needles, which appear as low-signal intensity structures, were inserted into the tumour using MR guidance. Palliative treatment with PDT was carried out by inserting optic fibres through these needles.