Carotid Occlusion and Near-Carotid Occlusion of the Extracranial Internal Carotid Artery Steven M. Farley and William J. Quinones-Baldrich A diagnosis of an occluded or nearly occluded carotid artery is anxiety provoking for the patient. In these cases, referring physicians often request urgent if not emergent vascular consultation. Because large randomized trials regarding these conditions do not exist, best practices for optimal results require careful history taking, physical examination, appropriate imaging, and careful patient selection. The vascular specialist must have a thorough understanding of the etiology and natural history of an occluded or near-occluded internal carotid artery in order to manage this uncommon presentation of carotid artery disease. Internal Carotid Artery Occlusion Acute Occlusion, Asymptomatic An acute asymptomatic carotid occlusion is difficult, if not impossible, to identify. The asymptomatic patient does not seek medical attention. Moreover, in the absence of symptoms, the timing of the carotid occlusion is difficult to elucidate. Some investigators have attempted to identify changes on computed tomography (CT) that might correlate with a carotid occlusion. Acute Occlusion, Symptomatic An acute extracranial internal carotid artery (ICA) occlusion with neurologic changes represents a challenging clinical dilemma. Symptoms can range from a brief period of lightheadedness to a transient focal neurologic deficit to a massive stroke. Current treatment options include medical management, endovascular therapy, and open surgery. Unlike carotid stenosis, no randomized, controlled trials exist to support exploration with revascularization. The surgical management of an acute carotid occlusion remains controversial. In a majority of cases, the pathogenesis of an acute extracranial carotid occlusion is a high-grade proximal ICA lesion. As a result of plaque rupture or a low-flow state, the internal carotid artery usually thromboses in an antegrade direction to the level of the first branch of the ICA, the ophthalmic artery. However, other causes of an acute internal carotid artery occlusion include embolism, carotid dissection, or retrograde propagation of thrombus from an intracranial source. Medical therapy for symptomatic patients with an acute carotid occlusion is similar to the treatment of an ischemic stroke. The fundamental goals are to minimize neural tissue damage, while controlling complications. Reversible conditions, such as infection, should be treated promptly. Generally, blood pressure is treated if it is extremely high or low. Long-standing hypertension is common in these patients, and aggressive lowering of blood pressure can lead to worse results. In randomized trials, aspirin is the only antiplatelet agent that has been established as effective for the early treatment of acute ischemic stroke. The American College of Chest Physicians does not support the use of anticoagulation for ischemic stroke. However, in subgroup analysis of the Trial of Org 10172 in Acute Stroke Treatment (TOAST) trial, patients with extracranial carotid occlusion or severe stenosis might benefit from anticoagulation. Early treatment with intravenous systemic tissue plasminogen activator (tPA) has been discouraging for extracranial carotid occlusion with low rates of patency restoration (10%). Given the challenges of treating stroke with systemic intravenous tPA, and the poor effectiveness of tPA for extracranial carotid occlusion, endovascular intervention with intraarterial tPA for extracranial carotid occlusion has been limited to small case series. Reports have detailed carotid angioplasty and stenting of acute extracranial carotid occlusion. These techniques require further investigation. With the expansion of carotid endarterectomy in the 1960s, early attempts at open carotid revascularization for acute carotid occlusion were met with hemorrhagic strokes and dismal outcomes. For decades, intervention was not supported. Recent advances in imaging and the demonstrated benefit of early administration of tPA for acute strokes have sparked renewed interest in acute carotid surgery for symptomatic patients. Magnetic resonance imaging (MRI) with perfusion- and diffusion-weighted imaging can time strokes more accurately and identify viable versus nonviable brain tissue. Noninvasive imaging can precisely and quickly assess the intracerebral circulation and characterize the patency of the distal internal carotid artery. Some authors argue that these advances can better identify a subset of symptomatic patients with carotid occlusion who could benefit from more aggressive, early therapy. Modern series emphasize proper patient selection and demonstrate neurologic improvement and restoration of ICA patency in up to 50% and 80% of patients, respectively. Exclusion criteria include large areas of infarcted brain at risk for hemorrhagic transformation, significant neurologic deficit, and thrombosis of the intracranial ICA. The timing of carotid surgery in the setting of carotid occlusion neurologic symptoms remains an area of active debate. Some authors support expedient preoperative assessment and encourage operative intervention as soon as possible, suggesting the best results are seen with surgery within 24 hours. However, recent reports have included patients with neurologic deficits 1 week from initial presentation. This group of patients should not be confused with patient who have acute stroke in the setting of carotid stenosis, in whom current recommendations suggest postponing surgery until neurologic recovery plateaus. The technical aspects of the open operation are important. First, ICA clamping is to be avoided because clamping can fracture the thrombus, making thrombus retrieval difficult and potentially worsening the outcome by creating a distal embolus. In about half of patients, simply opening the ICA after common carotid clamping allows the cerebral back pressure to expel the clot. If this is unsuccessful, a 2-Fr or 3-Fr Fogarty embolectomy catheter can be passed under fluoroscopic guidance into the intracranial ICA. Blood flow should not be reestablished until the patency of the distal ICA is confirmed by angiography. If patency cannot be reestablished, the ICA should be ligated and an external carotid endarterectomy performed. Acute symptomatic internal carotid occlusion caused by carotid dissection is more commonly seen in younger patients, particularly related to trauma. This topic is the subject of another chapter. In a majority of patients, the dissection extends into the intracranial portion of the ICA. Open surgical exploration is perilous. If at exploration an acute carotid dissection is discovered, extensive distal exposure of the ICA may be required to find a healthy endpoint. Traditionally, these patients are treated with anticoagulation, antiplatelet therapy, or both, despite neurologic symptoms. Occasionally, patients refractory to anticoagulation with continued neurologic symptoms are treated with carotid stenting. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Dyslipidemia and Hypertriglyceridemia Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. Join our Telegram channel Join Tags: Current Therapy in Vascular and Endovascular Surgery Aug 25, 2016 | Posted by admin in CARDIOLOGY | Comments Off on Carotid Occlusion and Near-Carotid Occlusion of the Extracranial Internal Carotid Artery Full access? Get Clinical Tree
Carotid Occlusion and Near-Carotid Occlusion of the Extracranial Internal Carotid Artery Steven M. Farley and William J. Quinones-Baldrich A diagnosis of an occluded or nearly occluded carotid artery is anxiety provoking for the patient. In these cases, referring physicians often request urgent if not emergent vascular consultation. Because large randomized trials regarding these conditions do not exist, best practices for optimal results require careful history taking, physical examination, appropriate imaging, and careful patient selection. The vascular specialist must have a thorough understanding of the etiology and natural history of an occluded or near-occluded internal carotid artery in order to manage this uncommon presentation of carotid artery disease. Internal Carotid Artery Occlusion Acute Occlusion, Asymptomatic An acute asymptomatic carotid occlusion is difficult, if not impossible, to identify. The asymptomatic patient does not seek medical attention. Moreover, in the absence of symptoms, the timing of the carotid occlusion is difficult to elucidate. Some investigators have attempted to identify changes on computed tomography (CT) that might correlate with a carotid occlusion. Acute Occlusion, Symptomatic An acute extracranial internal carotid artery (ICA) occlusion with neurologic changes represents a challenging clinical dilemma. Symptoms can range from a brief period of lightheadedness to a transient focal neurologic deficit to a massive stroke. Current treatment options include medical management, endovascular therapy, and open surgery. Unlike carotid stenosis, no randomized, controlled trials exist to support exploration with revascularization. The surgical management of an acute carotid occlusion remains controversial. In a majority of cases, the pathogenesis of an acute extracranial carotid occlusion is a high-grade proximal ICA lesion. As a result of plaque rupture or a low-flow state, the internal carotid artery usually thromboses in an antegrade direction to the level of the first branch of the ICA, the ophthalmic artery. However, other causes of an acute internal carotid artery occlusion include embolism, carotid dissection, or retrograde propagation of thrombus from an intracranial source. Medical therapy for symptomatic patients with an acute carotid occlusion is similar to the treatment of an ischemic stroke. The fundamental goals are to minimize neural tissue damage, while controlling complications. Reversible conditions, such as infection, should be treated promptly. Generally, blood pressure is treated if it is extremely high or low. Long-standing hypertension is common in these patients, and aggressive lowering of blood pressure can lead to worse results. In randomized trials, aspirin is the only antiplatelet agent that has been established as effective for the early treatment of acute ischemic stroke. The American College of Chest Physicians does not support the use of anticoagulation for ischemic stroke. However, in subgroup analysis of the Trial of Org 10172 in Acute Stroke Treatment (TOAST) trial, patients with extracranial carotid occlusion or severe stenosis might benefit from anticoagulation. Early treatment with intravenous systemic tissue plasminogen activator (tPA) has been discouraging for extracranial carotid occlusion with low rates of patency restoration (10%). Given the challenges of treating stroke with systemic intravenous tPA, and the poor effectiveness of tPA for extracranial carotid occlusion, endovascular intervention with intraarterial tPA for extracranial carotid occlusion has been limited to small case series. Reports have detailed carotid angioplasty and stenting of acute extracranial carotid occlusion. These techniques require further investigation. With the expansion of carotid endarterectomy in the 1960s, early attempts at open carotid revascularization for acute carotid occlusion were met with hemorrhagic strokes and dismal outcomes. For decades, intervention was not supported. Recent advances in imaging and the demonstrated benefit of early administration of tPA for acute strokes have sparked renewed interest in acute carotid surgery for symptomatic patients. Magnetic resonance imaging (MRI) with perfusion- and diffusion-weighted imaging can time strokes more accurately and identify viable versus nonviable brain tissue. Noninvasive imaging can precisely and quickly assess the intracerebral circulation and characterize the patency of the distal internal carotid artery. Some authors argue that these advances can better identify a subset of symptomatic patients with carotid occlusion who could benefit from more aggressive, early therapy. Modern series emphasize proper patient selection and demonstrate neurologic improvement and restoration of ICA patency in up to 50% and 80% of patients, respectively. Exclusion criteria include large areas of infarcted brain at risk for hemorrhagic transformation, significant neurologic deficit, and thrombosis of the intracranial ICA. The timing of carotid surgery in the setting of carotid occlusion neurologic symptoms remains an area of active debate. Some authors support expedient preoperative assessment and encourage operative intervention as soon as possible, suggesting the best results are seen with surgery within 24 hours. However, recent reports have included patients with neurologic deficits 1 week from initial presentation. This group of patients should not be confused with patient who have acute stroke in the setting of carotid stenosis, in whom current recommendations suggest postponing surgery until neurologic recovery plateaus. The technical aspects of the open operation are important. First, ICA clamping is to be avoided because clamping can fracture the thrombus, making thrombus retrieval difficult and potentially worsening the outcome by creating a distal embolus. In about half of patients, simply opening the ICA after common carotid clamping allows the cerebral back pressure to expel the clot. If this is unsuccessful, a 2-Fr or 3-Fr Fogarty embolectomy catheter can be passed under fluoroscopic guidance into the intracranial ICA. Blood flow should not be reestablished until the patency of the distal ICA is confirmed by angiography. If patency cannot be reestablished, the ICA should be ligated and an external carotid endarterectomy performed. Acute symptomatic internal carotid occlusion caused by carotid dissection is more commonly seen in younger patients, particularly related to trauma. This topic is the subject of another chapter. In a majority of patients, the dissection extends into the intracranial portion of the ICA. Open surgical exploration is perilous. If at exploration an acute carotid dissection is discovered, extensive distal exposure of the ICA may be required to find a healthy endpoint. Traditionally, these patients are treated with anticoagulation, antiplatelet therapy, or both, despite neurologic symptoms. Occasionally, patients refractory to anticoagulation with continued neurologic symptoms are treated with carotid stenting. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Dyslipidemia and Hypertriglyceridemia Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. Join our Telegram channel Join Tags: Current Therapy in Vascular and Endovascular Surgery Aug 25, 2016 | Posted by admin in CARDIOLOGY | Comments Off on Carotid Occlusion and Near-Carotid Occlusion of the Extracranial Internal Carotid Artery Full access? Get Clinical Tree
