Intracranial arteriovenous malformations (AVMs) are now a recognized entity because of improvements in imaging diagnosis. They are relatively uncommon but can cause serious neurological symptoms or death. We report a case of a 22- year-old man who presented with left parietal hemorrhage and on cerebral angiography was found to have a small AVM in the left middle cerebral artery (MCA) territory. Glue embolization followed by immediate surgical resection of the AVM was carried out, resulting in complete cure

Azeemuddin, Muhammad

Haq, Tanveer ul

Jooma, Rashid

Rehman, Imaad ur

Sajjad, Zafar

English

eCommons@AKU

Pakistan Journal ofNeurological Sciences (PJNS)Volume 3 | Issue 1 Article 34-2008Embolization of An IntracranialarteriovenousMalformation Followed Byimmediate SurgicalResection: A Case ReportImaad ur RehmanAga Khan UniversityTanveer ul HaqAga Khan UniversityRashid JoomaAga Khan UniversityMuhammad AzeemuddinAga Khan UniversityZafar SajjadAga Khan UniversityFollow this and additional works at: https://ecommons.aku.edu/pjnsRecommended CitationRehman, Imaad ur; Haq, Tanveer ul; Jooma, Rashid; Azeemuddin, Muhammad; and Sajjad, Zafar (2008) "Embolization of AnIntracranialarteriovenous Malformation Followed Byimmediate Surgical Resection: A Case Report," Pakistan Journal of NeurologicalSciences (PJNS): Vol. 3 : Iss. 1 , Article 3.Available at: https://ecommons.aku.edu/pjns/vol3/iss1/3Arteriovenous malformations (AVMs) consist of tangles ofvessels of different wall thickness and diameter associatedwith arteriovenous shunting. In AVMs, arterioles andvenules communicate directly without the interposition ofa capillary bed. Ninety percent of intracranial AVMs aresupratentorial.1 They often have associated aneurysms.2Hemorrhage is the most dreaded presentation. Treatmentand complete cure is challenging, especially for Spetzlergrade IV and V.3 Glue embolization offers cure in somecases but most of the time it is adjuvant to surgery orgamma knife therapy. The following case report shows acomprehensive multidisciplinary approach to treat AVM inwhich embolization was immediately followed by surgicalresection under the same anesthesia.CASE REPORTA 22-year-old man presented with headache, right sidedweakness and slurred speech for one week. CT scanshowed hemorrhage in the left parietal lobe (Figure 1).Cerebral angiography showed Spetzler Grade II AVM in theleft parietal region. He was referred to our facility forelective embolization of AVM. During embolization, the initial angiographic run revealedan approximately 1.2 cm-sized AVM nidus supplied by twoV O L .  3 ( 1 )   J A N - M A R  2 0 0 8P A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S  9C A S E R E P O R TEMBOLIZATION OF AN INTRACRANIALARTERIOVENOUS MALFORMATION FOLLOWED BYIMMEDIATE SURGICAL RESECTION: A CASE REPORTImaad ur Rehman,1 Tanveer ul Haq,1 Rashid Jooma,2 Muhammad Azeemuddin1 and Zafar Sajjad1Departments of Radiology1 and Surgery, 2 Aga Khan University Hospital, Karachi, PakistanCorrespondence to: Dr. Haq, Associate Professor of Radiology, Aga Khan University Hospital, Karachi 74800, Pakistan. Email: tanveer.haq@aku.eduABSTRACTIntracranial arteriovenous malformations (AVMs) are now a recognized entity because of improvements in imagingdiagnosis. They are relatively uncommon but can cause serious neurological symptoms or death. We report a case of a 22-year-old man who presented with left parietal hemorrhage and on cerebral angiography was found to have a small AVM inthe left middle cerebral artery (MCA) territory. Glue embolization followed by immediate surgical resection of the AVM wascarried out, resulting in complete cure.Pak J Neurol Sci 2008; 3(1):9-11Figure 1. Left parietal hemorrhage.V O L .  3 ( 1 )   J A N - M A R  2 0 0 8P A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S  10branches of the left middle cerebral artery (MCA) that wasdraining into a superficial cortical vein (Figure 2). With thehelp of a flow-guided microcatheter, the nidus wasoccluded via the major feeder with Histoacryl glue. Refluxof glue was noted into the draining vein (Figure 3).A subsequent angiographic run revealed part of the niduspersistently filling up by a tiny proximal branch from theleft MCA (Figure 4). It was not possible to manipulate thecatheter through this tiny vessel despite multiple attempts.Due to reflux of glue into the draining vein, the risk of re-hemorrhage was significantly increased and immediatesurgery was planned. The atient was shifted to theoperating room where left fronto-parietal craniotomy wasperformed under general anesthesia and successfulexcision of the left parietal AVM was done (Figure 5),along with evacuation of left parietal hematoma. Following surgery, the patient was hemodynamicallystable. Although he continued to have right-sidedweakness and slurred speech, he was fol lowingcommands (pre-procedural state). No endovascular orsurgical complication was observed. Figure 2. AVM with two arterial feeders (majorand minor), a small nidus, and a draining vein.Figure 4. Post-embolization: tiny arterial feeder isstill supplying the nidusFigure 3. Histoacryl glue seen in AVM with refluxin draining vein.Figure 5. Surgically excised AVM specimen.DISCUSSIONArteriovenous malformations (AVMs) are the mostcommon intracranial vascular malformation. Incidence ofAVMs is one-seventh to one-tenth that of aneurysms, andAVMs occur in about 0.02% to 0.05% of the population.Varying degrees of thrombosis and calcification may beseen. Atrophy of the surrounding parenchyma caused bysteal can be seen.The usual presenting symptoms are seizures, progressiveneurologic deficit, intractable headache, intracranialhemorrhage and hydrocephalus. About 64% of casespresent by 40 years of age; 30% to 50% presentsecondary to hemorrhage. The risk of death from bleedingin a patient with an AVM is about 29%; an additional 20%to 30% of patients suffer neurologic deficits. Eachbleeding episode carries a mortality rate of 10% to15%.4,5 Hemorrhage from an AVM is usually related to anassociated aneurysm, outflow restriction, or pure deepvenous drainage.For treatment of AVMs, the nidus of the lesion must beremoved or obliterated. Surgical resection is the mainstayof treatment. Only when the surgical approach or actualremoval of the AVM is risky is endovascular therapycontemplated. Because the endovascular cure rate forAVMs is only 5% to 10%, endovascular therapy usually isused for preoperative assistance, or to shrink the mass asmuch as possible before radiosurgery, which is anothertherapeutic option.Embolization is a good adjuvant to surgery. Although avery large range of materials have been used to try andembolize intracranial AVMs, it was the introduction ofacrylate adhesive agents that have had the most impact.Acrylate-based glues are now the mainstay of intracranialAVM embolization. Endovascular therapy for intracranial AVMs is nowemployed widely with a high degree of success andrelatively infrequent complications. Recently, the morepredictable embolic agent onyx has been introduced whichallows targeted delivery to the nidus. Risks associated withthe use of these agents include stroke or cranial nervedysfunction due to unintended branch occlusions,hemorrhage, obstruction of venous outflow due to reflux inthe draining vein, and cementing of catheter in thevessel.6In our case, reflux in the draining vein occurred whichoccluded outflow while inflow was still present by the othertiny arterial feeder. The patient’s blood pressures werekept low during the procedure and there was a highprobability that as soon as blood pressures returned tonormal, hemorrhage would recur. Therefore it wasimperative that immediate surgery was planned for theresection of the AVM. Through this report, we also wish tohighlight the multidisciplinary approach that mustunderpin any effective clinical approach to AVMs. REFERENCES1. Al-Rodhan NRF, Sundt TM, Piepgras DG, et al. Occlusive hyperemia: A theory for the hemodynamiccomplications following resection of intracerebral arteriovenous malformations. J Neurosurg 1993; 78:167-175.2. Brown RD, Wiebers DO, Torner JC, O’Fallon WM. Incidence and prevalence of intracranial vascular malformations in Olmsted County, Minnesota, 1965to 1992. Neurology 1996; 340:1812-18.3. Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformation. J Neurosurgery1986; 65:476-7864. Jessurun GA, Kamphuis DJ, Zande FH, et al. Cerebral arteriovenous malformations in the Netherland Antilles: high prevalence of hereditary hemorrhagic telangiectasia-related single and multiple cerebral arteriovenous malformations. Clin Neurol Neurosurg 1993; 95:193-198.5. Albert P, Salgado H, Polaina M, et al. A study on thevenous drainage of 150 cerebral malformations as related to hemorrhagic risks and size of the lesion. Acta Neurochir (Wein) 1990; 103:30-34.6. Debrun GM, Aletich V, Ausman JI, et al. Embolization of nidus of brain arteriovenous malformations with n-butylcyanoacrylate. Neurosurgery 1997; 40:112-21.V O L .  3 ( 1 )   J A N - M A R  2 0 0 8P A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S  11

Embolization of An Intracranialarteriovenous Malformation Followed Byimmediate Surgical Resection: A Case Report

Ul Haq, Tanveer

eCommons@AKU Department of Radiology Medical College, Pakistan 1-1-2008 Embolization of an intracranial arteriovenous malformation followed by immediate surgical resection: A case report Imaad ur Rehman Tanveer Ul Haq Rashid Jooma Muhammad Azeemuddin Zafar Sajjad Follow this and additional works at: https://ecommons.aku.edu/pakistan_fhs_mc_radiol  Part of the Neurology Commons, Neurosurgery Commons, Radiology Commons, and the Surgery Commons Arteriovenous malformations (AVMs) consist of tangles ofvessels of different wall thickness and diameter associatedwith arteriovenous shunting. In AVMs, arterioles andvenules communicate directly without the interposition ofa capillary bed. Ninety percent of intracranial AVMs aresupratentorial.1 They often have associated aneurysms.2Hemorrhage is the most dreaded presentation. Treatmentand complete cure is challenging, especially for Spetzlergrade IV and V.3 Glue embolization offers cure in somecases but most of the time it is adjuvant to surgery orgamma knife therapy. The following case report shows acomprehensive multidisciplinary approach to treat AVM inwhich embolization was immediately followed by surgicalresection under the same anesthesia.CASE REPORTA 22-year-old man presented with headache, right sidedweakness and slurred speech for one week. CT scanshowed hemorrhage in the left parietal lobe (Figure 1).Cerebral angiography showed Spetzler Grade II AVM in theleft parietal region. He was referred to our facility forelective embolization of AVM. During embolization, the initial angiographic run revealedan approximately 1.2 cm-sized AVM nidus supplied by twoV O L .  3 ( 1 )   J A N - M A R  2 0 0 8P A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S  9C A S E R E P O R TEMBOLIZATION OF AN INTRACRANIALARTERIOVENOUS MALFORMATION FOLLOWED BYIMMEDIATE SURGICAL RESECTION: A CASE REPORTImaad ur Rehman,1 Tanveer ul Haq,1 Rashid Jooma,2 Muhammad Azeemuddin1 and Zafar Sajjad1Departments of Radiology1 and Surgery, 2 Aga Khan University Hospital, Karachi, PakistanCorrespondence to: Dr. Haq, Associate Professor of Radiology, Aga Khan University Hospital, Karachi 74800, Pakistan. Email: tanveer.haq@aku.eduABSTRACTIntracranial arteriovenous malformations (AVMs) are now a recognized entity because of improvements in imagingdiagnosis. They are relatively uncommon but can cause serious neurological symptoms or death. We report a case of a 22-year-old man who presented with left parietal hemorrhage and on cerebral angiography was found to have a small AVM inthe left middle cerebral artery (MCA) territory. Glue embolization followed by immediate surgical resection of the AVM wascarried out, resulting in complete cure.Pak J Neurol Sci 2008; 3(1):9-11Figure 1. Left parietal hemorrhage.V O L .  3 ( 1 )   J A N - M A R  2 0 0 8P A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S  10branches of the left middle cerebral artery (MCA) that wasdraining into a superficial cortical vein (Figure 2). With thehelp of a flow-guided microcatheter, the nidus wasoccluded via the major feeder with Histoacryl glue. Refluxof glue was noted into the draining vein (Figure 3).A subsequent angiographic run revealed part of the niduspersistently filling up by a tiny proximal branch from theleft MCA (Figure 4). It was not possible to manipulate thecatheter through this tiny vessel despite multiple attempts.Due to reflux of glue into the draining vein, the risk of re-hemorrhage was significantly increased and immediatesurgery was planned. The atient was shifted to theoperating room where left fronto-parietal craniotomy wasperformed under general anesthesia and successfulexcision of the left parietal AVM was done (Figure 5),along with evacuation of left parietal hematoma. Following surgery, the patient was hemodynamicallystable. Although he continued to have right-sidedweakness and slurred speech, he was fol lowingcommands (pre-procedural state). No endovascular orsurgical complication was observed. Figure 2. AVM with two arterial feeders (majorand minor), a small nidus, and a draining vein.Figure 4. Post-embolization: tiny arterial feeder isstill supplying the nidusFigure 3. Histoacryl glue seen in AVM with refluxin draining vein.Figure 5. Surgically excised AVM specimen.DISCUSSIONArteriovenous malformations (AVMs) are the mostcommon intracranial vascular malformation. Incidence ofAVMs is one-seventh to one-tenth that of aneurysms, andAVMs occur in about 0.02% to 0.05% of the population.Varying degrees of thrombosis and calcification may beseen. Atrophy of the surrounding parenchyma caused bysteal can be seen.The usual presenting symptoms are seizures, progressiveneurologic deficit, intractable headache, intracranialhemorrhage and hydrocephalus. About 64% of casespresent by 40 years of age; 30% to 50% presentsecondary to hemorrhage. The risk of death from bleedingin a patient with an AVM is about 29%; an additional 20%to 30% of patients suffer neurologic deficits. Eachbleeding episode carries a mortality rate of 10% to15%.4,5 Hemorrhage from an AVM is usually related to anassociated aneurysm, outflow restriction, or pure deepvenous drainage.For treatment of AVMs, the nidus of the lesion must beremoved or obliterated. Surgical resection is the mainstayof treatment. Only when the surgical approach or actualremoval of the AVM is risky is endovascular therapycontemplated. Because the endovascular cure rate forAVMs is only 5% to 10%, endovascular therapy usually isused for preoperative assistance, or to shrink the mass asmuch as possible before radiosurgery, which is anothertherapeutic option.Embolization is a good adjuvant to surgery. Although avery large range of materials have been used to try andembolize intracranial AVMs, it was the introduction ofacrylate adhesive agents that have had the most impact.Acrylate-based glues are now the mainstay of intracranialAVM embolization. Endovascular therapy for intracranial AVMs is nowemployed widely with a high degree of success andrelatively infrequent complications. Recently, the morepredictable embolic agent onyx has been introduced whichallows targeted delivery to the nidus. Risks associated withthe use of these agents include stroke or cranial nervedysfunction due to unintended branch occlusions,hemorrhage, obstruction of venous outflow due to reflux inthe draining vein, and cementing of catheter in thevessel.6In our case, reflux in the draining vein occurred whichoccluded outflow while inflow was still present by the othertiny arterial feeder. The patient’s blood pressures werekept low during the procedure and there was a highprobability that as soon as blood pressures returned tonormal, hemorrhage would recur. Therefore it wasimperative that immediate surgery was planned for theresection of the AVM. Through this report, we also wish tohighlight the multidisciplinary approach that mustunderpin any effective clinical approach to AVMs. REFERENCES1. Al-Rodhan NRF, Sundt TM, Piepgras DG, et al. Occlusive hyperemia: A theory for the hemodynamiccomplications following resection of intracerebral arteriovenous malformations. J Neurosurg 1993; 78:167-175.2. Brown RD, Wiebers DO, Torner JC, O’Fallon WM. Incidence and prevalence of intracranial vascular malformations in Olmsted County, Minnesota, 1965to 1992. Neurology 1996; 340:1812-18.3. Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformation. J Neurosurgery1986; 65:476-7864. Jessurun GA, Kamphuis DJ, Zande FH, et al. Cerebral arteriovenous malformations in the Netherland Antilles: high prevalence of hereditary hemorrhagic telangiectasia-related single and multiple cerebral arteriovenous malformations. Clin Neurol Neurosurg 1993; 95:193-198.5. Albert P, Salgado H, Polaina M, et al. A study on thevenous drainage of 150 cerebral malformations as related to hemorrhagic risks and size of the lesion. Acta Neurochir (Wein) 1990; 103:30-34.6. Debrun GM, Aletich V, Ausman JI, et al. Embolization of nidus of brain arteriovenous malformations with n-butylcyanoacrylate. Neurosurgery 1997; 40:112-21.V O L .  3 ( 1 )   J A N - M A R  2 0 0 8P A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S  11View publication stats

Embolization of an intracranial arteriovenous malformation followed by immediate surgical resection: A case report

https://ecommons.aku.edu/cgi/viewcontent.cgi?article=1384&context=pakistan_fhs_mc_radiol

Embolization of An Intracranialarteriovenous Malformation Followed Byimmediate Surgical Resection: A Case Report

Abstract

Similar works

Full text

Available Versions

eCommons@AKU

eCommons@AKU