Carotid angioplasty and stenting in carotid artery stenosis: neuroscience nursing implications.
Stenosis of the internal carotid artery due to atherosclerosis can cause embolic stroke or cerebral ischemia, both of which may result in significant morbidity, mortality, and long-term disability. Although the endovascular technique with balloons and stents to relieve arterial (i.e., coronary) stenosis has allowed a nonsurgical approach to the management of atherosclerotic disease for many years, its use in carotid vessels has only recently gained popularity. In addition, improvements in endovascular access systems have extended the use of carotid angioplasty and stenting (CAS), especially since the advent of cerebral emboli protection devices. Nowadays, CAS is emerging as an intervention for high-risk surgical patients with high-grade carotid artery stenosis. Nursing care of these patients before, during, and after CAS is challenging. Patients and family need to be educated about the aim and consequences of the procedure and its complications. To care for these patients, the nurse must understand the techniques of CAS. The purpose of this article was briefly to review the etiology of stroke, the current treatments to relieve carotid stenosis, and the basic steps of CAS. The nursing management throughout the procedure, the patient preparation before the procedure, and most importantly, the postprocedure nursing care are discussed.
In Western countries, stroke is the third leading cause of death and can cause permanent disability. Atherosclerotic carotid artery disease is linked directly to 20%-30% of all strokes, so the embolization to the brain vessels resulting from atherosclerotic carotid artery narrowing (stenosis) is a significant healthcare issue (Frizzell, 2005). Atherosclerotic carotid artery stenosis is characterized by vessel wall thickening, plaque formation, and a progressive narrowing of the carotid artery. Stenosis is most significant at the carotid bifurcation, also known as the carotid bulb, where the common carotid artery branches into the internal and external carotid arteries.
Surgical removal of plaque is the typical means of managing patients with high-grade carotid artery stenosis. Although intravascular stents have long been used in the peripheral arteries (Palmaz et al., 1988), carotid stenting has attracted attention recently after introduction of the embolic protection devices. The purpose of this article was to provide neuroscience nurses with information about the atherosclerotic carotid artery disease and carotid angioplasty and stenting (CAS), a relatively new but evolving minimal invasive treatment option.
Background of Current Problems
Several risk factors are clearly associated with atherosclerotic carotid artery disease and stroke (Table 1). It is very important to remember these risk factors as a means of decreasing the risk of stroke recurrence after the removal of carotid plaque. To date, the only approved nonmedical treatment method of carotid stenosis is carotid endarteractomy (CEA); stenting is currently reserved only for those patients who fall into the high-risk category (Centers for Medicare and Medicaid Services, 2008). The importance of CAS in the high-risk surgical patients appears to be gaining ground, but the question as to the application of this procedure in the much larger population of standard-risk patients remains unanswered. One important U.S. trial, Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST), is currently underway and will likely add to the increasing understanding of CAS in this population. CREST is a prospective, randomized, multicenter clinical trial of CEA versus CAS as prevention for stroke in patients with symptomatic carotid stenosis greater than 50% (Hobson, 2000). A recent lead-in phase analysis (749 patients) of this trial has shown encouraging results, with a 30-day stroke and/or death rate of 4.4% in the CAS arm (Hobson et al., 2004). The final data, however, are needed to compare the CAS versus CEA.
Detection and Diagnostics
Carotid artery stenosis may be either symptomatic or asymptomatic. Symptomatic patients present with transient ischemic attack (TIA), stroke in evolution, or completed stroke. A TIA is a neurological event that may last from several seconds to 24 hours. It is not associated with residual neurological deficits, but it may be a forerunner of stroke. A stroke in evolution occurs when the neurological deficit progresses or fluctuates but never returns to normal. A completed stroke progresses to a stable deficit without a change in degree of symptoms; the deficit lasts for more than 24 hours. An ischemic stroke usually manifests as an infarct on computed tomography (CT) or magnetic resonance imaging (MRI). In case of acute ischemia (less than 24 hours), CT may not detect a new ischemic area; MRI detects a new infarct even within an hour after ictus. In hemorrhagic stroke, both CT and MRI detect hemorrhage clearly.
Asymptomatic carotid artery stenosis may be identified during routine physical examination by the presence of a carotid bruit (on auscultation) or during carotid duplex ultrasonography screening of high-risk patients, such as coronary artery disease, congestive heart failure, and hypertension, because atherosclerosis is frequently manifest at multiple sites of cardiovascular system (see Table 1). Presence of a bruit is not a reliable criterion with which to independently diagnose carotid artery stenosis; however, its presence indicates the need for further investigation by duplex ultrasonography, CT angiography, and MRI angiography. Not all asymptomatic carotid plaques occurring with the same narrowing ratio on radiological imaging have the similar rupture and cerebral emboli risk. Some narrowings have irregular ulcerated (vulnerable) plaque with relatively high embolic tendency, which generally require invasive intervention. The smooth (stable) plaques generally possess a smaller risk and may be amenable to medical management instead.
If a patient presents with signs and symptoms of TIA or stroke, the cause must be identified. Causes other than atherosclerotic carotid artery stenosis may underlie cerebral ischemia. Knowing all causes is crucial not only in getting accurate diagnosis but also in giving optimum treatment. Differential diagnosis is not the scope of this article; however, it is heavily (but not completely) based on the imaging of the brain, carotid (and other neck) arteries, and heart. In a typical patient, after a thorough history and physical examination, a brain CT or MRI is obtained. This usually differentiates causes of stroke as embolic, microvascular nonembolic, hemorrhagic, and others such as tumor or encephalitis. In case of embolic stroke, the patient should undergo imaging of the carotid vessels by duplex ultrasonography, CT angiography, MRI angiography, or catheter angiography.
Established Treatment Options
Treatment for patients with carotid artery stenosis depends on the severity of the stenosis and the individual's presenting signs and symptoms. During the 1980s, two prospective randomized clinical trials (i.e., North American Symptomatic Carotid Endarterectomy Trial [NASCET] and European Carotid Surgery Trial) studied plaque removal with carotid endarterectomy versus best medical management for the treatment of patients with ipsilateral carotid artery stenosis (European Carotid Surgery Trialists' Collaborators Group, 1991; NASCET Collaborators, 1991). On the basis of these earlier and other more recent studies (CAVATAS Investigators, 2001; Executive Committee for the Asymptomatic Carotid Atherosclerosis Study, 1995), agreement has been reached to support the benefit of carotid revascularization (regaining the carotid artery patency by removing the plaque surgically or by applying angioplasty-stenting endovascularly) over medical management for symptomatic patients with documented ipsilateral carotid stenosis greater than 60% as a cause of cerebral ischemia. Revascularization is also more effective than medical management for asymptomatic patients with carotid stenosis greater than 80% (CAVATAS Investigators, 2001; NASCET Collaborators, 1991). All other patients who do not meet these criteria should be treated medically. The goal of medical treatment is to minimize symptoms and more importantly reduce risk of future stroke in both symptomatic and asymptomatic patients while optimally controlling concurrent disease such as hypertension, diabetes mellitus, cardiac disease, and hyperlipidemia. Management of patients also includes weight reduction, smoking cessation, limiting alcohol consumption, and antiplatelet therapy (Sillesen, 2008). The latter measures are not only limited to patients managed medically, but they should also be employed for all patients treated with carotid revascularization by either surgical or endovascular routes.
An Emerging Treatment Option: CAS
Endovascular techniques have continued to evolve even in supra-aortic vessels, and CAS has provided an alternative treatment for patients with carotid artery stenosis (CAVATAS Investigators, 2001). The most significant improvement in CAS safety outcomes has been the development and utilization of devices that protect brain tissue from emboli (Kastmp et al., 2003). CAS is emerging as an equivalent and even better alternative to carotid endarterectomy in the management of carotid artery stenosis in high-risk surgical patients according to a recent trial (Yadav et al., 2004). The Food and Drag Administration has approved this procedure in the treatment of high-risk surgical patients (Table 2; Centers for Medicare and Medicaid Services, 2008; Higashida et al., 2004). However, CAS likely will remain a procedure with limited availability until ongoing investigations definitively prove its value as compared with endarterectomy in the standard-risk population. The underlying purpose of the ongoing CREST trial is to determine its equivalency or superiority to CEA in both standard- and high-risk categories. Although CREST results are not available yet, preliminary 30-day stroke and death rate of CAS arm in lead-in phase are comparable with two well-known CEA trials, namely, the NASCET and European Carotid Surgery Trial (Hobson et al., 2004). Asymptomatic Carotid Trial I is another ongoing (sponsored by Abbot Vascular) study randomizing standard-risk surgical patients to either CAS with cerebral filter protection or endarterectomy. The Transatlantic Asymptomatic Carotid Intervention Trial study has been in development for several years and contains a modern medical therapy arm in addition to revascularization arms as CAE and CAS. These studies currently underway will hopefully make the technique more available to a broader base of patients, assuming equal safety and efficacy. Although CAS is rapidly evolving worldwide, there is limited nursing literature on the technique (Bassler, 2003; Kougias et al., 2006; Lopez & Roper, 2008; Macari-Hinson, Moore, & Morley, 2006; Morelli & Davis, 2007; Tarolli, 2007).
Carotid endarterectomy is an open surgical procedure, typically performed under general anesthesia, in which atherosclerotic plaque is completely removed from the artery through the incision of vessel wall. During CAS, the plaque is simply displaced against the vessel wall by a self-expanding stent reinforced with in-stent balloon inflation (angioplasty); the treatment does not require general anesthesia. Timing of the carotid revascularization after a stroke is a matter of debate. Early intervention may precipitate hemorrhage in the infracted area (Riggs & DeWeese, 1998); therefore, it is recommended at least 4 weeks after stroke, unless emergency intervention is indicated.
Preparation of the patient for a typical CAS procedure starts with premedication (i.e., aspirin and clopidogrel). Medication associated with a CAS procedure is summarized in Table 3. The medication management may vary according to the physician's preference and the patient's clinical status. The procedure is very similar to the approach in which the patient is taken to the angiographic catheterization suit, the femoral artery (rarely axillobrachial artery) is accessed, and a guide catheter is passed to the affected common carotid artery. The carotid narrowing is then evaluated under angiographic visualization. A cerebral protection device (it is usually a filter) is passed across the area of stenosis and deployed distal to the carotid narrowing to catch any debris dislodged from the stenotic area during the procedure. Subsequently, a self-expanding carotid stent is placed across the stenosis. The interventionalist may perform balloon angioplasty before and alter stenting; finally, the filter is removed. Stent patency and absence of intracerebral embolization are confirmed by completion angiography. The length of the procedure is usually 30 to 60 minutes; thereafter, the patient is admitted to the hospital for observation. Most patients are discharged approximately 48 hours later and will continue to receive dual platelet therapy. Because of the invasiveness of this technique using the endovascular route or the patient's inherent clinical conditions, patients may present some contraindications to an elective CAS. It is imperative that a thorough assessment be performed prior to this endovascular treatment (Table 4).
Although CAS is an evolving minimally invasive treatment option not related to open surgery, it can have complications as well. Some of these complications can occur during the procedure, and others can occur up to a week later (Tan et al., 2003). Assessing for these complications is important to prevent further injury. In addition, patients and families should be educated on signs and symptoms of these complications.
Stroke and TIA
Stroke and TIA remain risks of CAS even when embolic protection devices are used (Tan et al., 2003). Plaque can be dislodged with subsequent embolization into the cerebral circulation before the embolic protection device is placed. Some plaque fragment may even go through the struts of the filter into the brain. Stroke can occur after an uncomplicated procedure due to acute or subacute thrombus formation within the stent; however, this is uncommon because of dual antiplatelet therapy. Unlike plaque fragment dislodged during the procedure, acute or subacute stent thrombosis and its cerebral embolic complication may benefit from the emergency intra-arterial thrombolytic therapy with tissue plasminogen activator. In case of plaque dislodgement with subsequent cerebral embolization, a clot retrieval device may also be used in selected patients.
Bradycardia, related to manipulation of the carotid sinus baroreceptors located in the carotid bulb, may occur during the procedure just after the stent implantation and/or balloon angioplasty (Martinez-Fernandez et al., 2008). Routine intravenous infusion of 1 mg atropine 1 minute before the inflation of angioplasty balloon can prevent this potentially dangerous complication. Atropine is infused only after the physician's order; it therefore should always be kept on hand. Even after premedication with atropine, symptomatic bradycardia (less than 40 beats/minute) or asystole for a short period may also occur; instruct the patient to cough or take a deep breath in such conditions because this can be effective. Additional atropine and temporary pacers must be available if needed.
Hypotension may occur immediately after stent implantation and last a few hours. It may continue up to 12 hours and rarely lasts more than 24 hours. Persistent hypotension can be caused by the effect of the stent on the carotid sinus baroreceptors (Trocciola et al., 2006). Check to see if patient took an antihypertensive because this could be another contributing factor for persistent hypotension.
Initial treatments include lowering the head of the bed and administering crystalloid intravenous fluids or volume expanders such as hydroxyethyl starch boluses as ordered. Inability to keep the mean arterial pressure greater than 75 mm Hg necessitates administration of additional medications that increase systemic blood pressure, such as dopamine. In addition, sudden loss of blood from the femoral access site or retroperitoneal hematoma may also present with hypotension. Nurses must routinely check the access site and monitor for signs and symptoms of retroperitoneal hematoma (flank, back, groin, or abdominal pain; hypotension; tachycardia; hypovolemic shock; and decrease in hematocrit level).
This is a rare complication of carotid revascularization independent of the mode of treatment (surgical or endovascular) that carries with it very high morbidity and mortality rates. It is thought to be the result of an impaired autoregulation of cerebral blood flow, which results from long-standing decreased cerebral perfusion pressure that occurs with carotid artery disease. When normal perfusion pressure is restored after carotid revascularization, the cerebral arterioles lose their ability to constrict and the hyperperfusion syndrome occurs (Abou-Chelb et al., 2004). Signs and symptoms include severe temporal headache, hypertension, seizures, and focal neurological deficits. The syndrome may be associated with intracranial hemorrhage. It may occur within 1 hour of the postprocedural period up to 24 hours or even 1 week later. Patients at high risk for this complication include those with severe bilateral carotid stenosis and hypertension.
Typically, a patient is discharged 1 to 2 days postprocedurally when hemodynamic status and neurological function are stable. The patient will have a follow-up appointment within 2-4 weeks to assess the femoral access site and clinical status. Carotid duplex ultrasonography is the most common imaging study used in postoperative surveillance of carotid stents (Armstrong & Bandyk, 2007). Follow-up duplex studies are performed 6 and 12 months then yearly after CAS to show possible recurrent stenosis in the stent. The incidence of restenosis after CAS is still unclear, but it is well below 10% (Groschel, Riecker, Schulz, Ememann, & Kastrup, 2005). In-stent restenosis is usually treated first with angioplasty rather than stent removal--the stents often embed themselves in the arterial wall after time.
Teaching and care monitoring are two key aspects to which the nurse must attend when caring for this patient population. Patient care monitoring by the nurse includes preprocedural, intraprocedural, and postprocedural activities. Teaching can take place at any time while the nurse is monitoring the patient.
Patient care monitoring activities start with the preparation (Table 5). Patients with recent stroke require a baseline CT to exclude intracranial hemorrhage and a thorough neurological evaluation. Preoperative laboratory examination such as blood count, blood chemistry, and coagulation profile must be completed. Likewise, the nurse should check the patient's medical regiment and obtain signed consent.
The CAS procedure takes place in the angiography room (interventional radiology and cardiology). A typical CAS team consists of an interventionalist, nurse, and technician. Intraprocedural patient care monitoring activities are maintained by the angiography nurses. Patient's vital signs, neurological status, and any evidence of complications are monitored continuously. The preparation of medications needed in CAS and administration of specific medication as ordered are important responsibilities of nurses during the procedure. For example, pressure on the carotid baroreceptors from balloon dilation or stent deployment commonly causes sudden bradycardia or transient asystole. The nurse should be ready to give intravenous atropine as ordered to treat this complication. In Table 6, specific activities are included for periprocedural nursing management.
Postprocedural care monitoring usually takes place again in the primary hospital clinic and therefore by the same nurses. Even after successful CAS procedures, patients are still subjected to some complications. For more accurate management, nurses must understand the procedure and be aware of the complications. Continuous monitoring of the vital signs, neurological status, and groin is mandatory especially in the first 12 hours after CAS. Nursing guidelines following CAS procedure are summarized in Table 7.
The word stroke can evoke terrifying images in the minds of patients and their families. Patients generally have many questions, fears, and concerns. Teach your patients to recognize and report immediately signs and symptoms of stroke and TIA, a medical emergency that should be treated as soon as possible. Moreover, stent may be a new term introduced to the patient and family. It is therefore important to clearly define stent and to stress that CAS is an interventional treatment used to open the vessel narrowing rather than an open surgery. Explanation of the procedure and expectations of treatment must be clear and free from medical jargon. Therefore, teaching is an ongoing process. Continual reinforcement and clarification are necessary to assist the patient and family in their comprehension of the therapy. Postprocedure education should include a review of activity levels, diet, medications, and signs that need to be reported to the healthcare provider.
Tell the patient to avoid sitting for prolonged periods for the next few days and not to perform heavy lifting (heavier than 10 pounds) for a week. The patient should contact his or her healthcare provider if he or she notices drainage, increased pain, or swelling at the access site. The most problematic complication in this site is the formation of pseudoaneurysm, which may necessitate surgical repair of the femoral artery.
Teach the patient to recognize and report signs and symptoms of gastrointestinal bleeding related to dual antiplatelet medication prescribed routinely after CAS. These are tarry stool, dark urine, and unusual or prolonged fatigue with minimal activity. The patient also should seek immediate medical attention if he or she develops confusion, visual disturbances, slurred speech, paresthesia, or weakness in the arms or legs. These may be signs and symptoms of stroke or TIA related to the acute in-stent thrombus formation, which is one of the important complications after CAS even dual antiplatelet medication. Under angiographic control, emergency intra-arterial infusion ofthrombolytics may be lifesaving (see Table 3). The patient should be alert for a sudden temporal headache because this may be an initial finding of hyperperfusion syndrome, which may occur even 2 weeks after CAS. The patient also should be taught to recognize other signs and symptoms of hyperperfusion syndrome, such as uncontrolled hypertension, seizures, and even focal neurological deficits. Encourage the patient to make lifestyle changes, including regular exercise, a healthy diet, weight loss if indicated, and cessation of smoking. The patient also should be encouraged to take his or her hypertension, diabetes, and high-cholesterol medications.
Starting with transferring bed until discharge from the hospital, a patient may encounter a set of complications after CAS (Table 8). A neuroscience nurse may be the first medical person who notices the symptoms of these complications. Loss of consciousness and sudden hemiparesis are the two most serious neurological complications associated with cerebral embolism or hemorrhage after CAS. Hypotension, bradycardia, hypoglycemia, and hemorrhage from groin should also be considered in case of consciousness after CAS. Cerebral hemorrhage due to hyperperfusion syndrome may present with new-onset severe headache, seizure, hemiparesis, and eventual consciousness. Stenting itself induces baroreceptors located in the carotid bulb, which in turn results in persistence of bradycardia and hyopotension in some cases. In case of complication, clinical (checking blood pressure and searching groin hemorrhage), laboratory (checking ECG and blood glucose level), and radiological (cranial CT) diagnostic tools are indicated. Most of these complications should be managed in an emergency condition, so a nurse should keep in mind all these details to prevent time loss. The CAS procedure is on the horizon for nonsurgical treatment of carotid artery stenosis with encouraging clinical and long-term results. By understanding details of the procedure, neuroscience nurses will be able to help patients more accurately on the road to recovery.
Abou-Chelb, A., Yadav, J. S., Reginelli, J. P., Bajzer, C., Bhatt, D., & Krieger, D. W. (2004). Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting. Risk factors, prevention, and treatment. Journal of American College of Cardiology, 43, 1596-1601.
Armstrong, P., & Bandyk, D. (2007). Duplex ultrasound surveillance after carotid stent angioplasty: When to follow-up and what to look for. Vascular Disease Management, 4, 73-77.
Bassler, S. K. (2003). Carotid stents: Is the gold standard ready for change? Journal of Vascular Nursing, 21, 132-138.
CAVATAS Investigators. (2001). Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS): A randomised trial. Lancet, 357, 1729-1737.
Centers for Medicare and Medicaid Services. (2008). NCA tracking sheet for percutaneous transluminal angioplasty of the carotid artery concurrent with stenting. Retrieved December 2, 2008, from http://www.cms.hhs.gov/mcd/ viewtrackingsheet.asp?id=194
European Carotid Surgery Trialists' Collaborators Group. (1991). MRC European Carotid Surgery Trial: Interim results for symptomatic patients with severe (70-90%) or with mild (0-29%) carotid stenosis. Lancet, 337, 1235-1243.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. (1995). Endarterectomy for asymptomatic carotid artery stenosis. JAMA, 273, 1421-1428.
Frizzell, J. P. (2005). Acute stroke. Pathophysiology, diagnosis and treatment. AACN Clinical Issues, 16, 421-440.
Groschel, K., Riecker, A., Schulz, J. B., Ememann, U., & Kastrup, A. (2005). Systematic review of early recurrent stenosis after carotid angioplasty and stenting. Stroke, 36, 367-373.
Higashida, R. T., Meyers, P. M., Phatouros, C. C., Connors, J. J. 3rd., Barr:, J. D., Sacks, D., et al. (2004). Reporting standards for carotid artery angioplasty and stent placement. Stroke, 35, e112-e134.
Hobson, R. W. II. (2000). CREST (Carotid Revascularization Endarterectomy Versus Stent Trial): Background, design, and current status. Seminars in Vascular Surgery, 13, 139-143.
Hobson, R. W. II, Howard, V. J., Roubinn, G. S., Brott, T. G., Ferguson, R. D., Popma, J. J., et al. (2004). Carotid artery stenting is associated with increased complications in octogenarians: 30-Day stroke and death rates in the CREST lead-in phase. Journal of Vascular Surgery, 40, 1106-1111.
Kastrup, A., Groschel, K., Krapf, H., Brehm, B. R., Dichgans, J., & Schulz, J. B. (2003). Early outcome of carotid angioplasty and stenting with and without cerebral protection devices. A systematic review of the literature. Stroke, 34, 813-819.
Kougias, P., Lin, P. H., Bush, R. L., Peden, E. K., Zhou, W., & Lumsden, A. B. (2006). Carotid artery stenting. Perioperative Nursing Clinics, 1, 99-110.
Lopez, A. C., & Roper, L. D. (2008). New techniques in carotid stenting. Nurse Practitioner, 33, 43-47.
Macari-Hinson, M., Moore, C., & Morley, M. (2006). Carotid artery stenting: New hope for blocked vessels. Critical Care Insider, 36(Suppl.), 14-20.
Martinez-Fernandez, E., Garcia, F. B., Gonzalez-Marcos, J. R., Peralta, A. G., Garcia, A. G., & Deya, A. M. (2008). Clinical and electroencephalographic features of carotid sinus syncope induced by internal carotid artery angioplasty. AJNR. American Journal of Neuroradiology, 29, 269-272.
Morelli, P., & Davis, K. L. (2007). Stenting fights carotid disease. Nurse Practitioner, 32, 49-52.
North American Symptomatic Carotid Endarterectomy Trial Collaborators. (1991). Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. New England Journal of Medicine, 325, 445-453.
Palmaz, J. C., Richter, G. M., Noeldge, G., Schatz, R. A., Robison, P. D., Gardiner, G. A., et al. (1988). Intraluminal stents in atherosclerotic iliac artery stenosis: Preliminary report of a multicenter study. Radiology, 168, 727-731.
Riggs, P. N., & DeWeese, J. A. (1998). Carotid endarterectomy. Surgical Clinics of North America, 78, 881-900.
Sillesen, H. (2008). What does best medical therapy really mean? European Journal of Vascular and Endovascular Surgery, 35, 139-144.
Tan, K. T., Cleveland, T. J., Berezi, V., McKevitt, F. M., Venables, G. S., & Gaines, P. A. (2003). Timing and frequency of complications after carotid artery stenting: What is the optimal period of observations? Journal of Vascular Surgery, 38, 236-243.
Tarolli, K. A. (2007). Percutaneous interventions. Critical Care Nursing Quarterly, 30, 12-19.
Trocciola, S. M., Chaer, R. A., Lin, S. C., Ryer, E. J., De Rubertis, B., Morrissey, N. J., et al. (2006). Analysis of parameters associated with hypotension requiring vasopressor support after carotid angioplasty and stenting. Journal of Vascular Surgery, 43, 714-720.
Yadav, J. S., Wholey, M. H., Kuntz, R. E., Fayad, P., Katzen, B. T., Mishkel, G. J., et al. (2004). Protected carotid artery stenting versus endarterectomy in high-risk patients (SAPPHIRE). New England Journal of Medicine, 351, 1493-1501.
Questions or comments about this article may be directed to Nazan Tuna Oran, PhD, at email@example.com. She is an assistant professor at the Ege University Izmir Ataturk School of Health, Izmir, Turkey.
Ismail Oran, MD, is a professor at the Ege University Medical School Department of Radiology, Izmir, Turkey.
TABLE 1. Common Risk Factors Associated With Atherosclerotic Carotid Artery Disease and Stroke Nonmodifiable Modifiable Age [greater than or equal to] 80 years Hypertension Male gender Hyperlipidemia Presence of CAD Smoking Presence of CHF Diabetes mellitus Positive family history Obesity Note. CAD = coronary artery disease; CHF = congestive heart failure. TABLE 2. High-Risk Surgical Patients With Carotid Stenosis (Higashida et al., 2004) Anatomical Risk Factors Comorbidity Risk Factors Previous carotid Patients older than 80 years endarterectomy Myocardial infarction within Contralateral carotid artery the previous 6 months occlusion Unstable angina Previous radical neck dissection or radiation Requires concurrent coronary therapy to neck region artery bypass grafting, abdominal aortic aneurysm Target lesion above second repair, or peripheral vascular cervical vertebra surgery Low cervical carotid lesions New York Heart Association class III or IV heart failure Dissection Chronic obstructive pulmonary Inability to extend neck disease with FFV1 <30% (i.e., cervical osteoarthritis and mobility limitations) History of liver failure with elevated prothrombin time Tandem lesions [greater than or equal to] 70% stenosis, intracranial stenosis, or occlusion Contralateral laryngeal palsy At risk for wound infection Tracheostomy Note. FEV1 = forced expiratory volume 1. TABLE 3. Medications Associated With CAS Medications Comments Preprocedural Aspirin 100-300 mg/day PO Prescribe at least 3-5 days before CAS Clopidogrel (Plavix) 75 Prescribe at least 3-5 days mg/day PO before CAS Personal medications (a) As ordered Periprocedural Heparin 75-100 unit/kg Administer after femoral sheath IV bolus insertion Atropine 1 mg IV bolus Just before the inflation of angioplasty balloon Regular IV fluids and/or IV In case of hypotension, as ordered 9l volume expanders Nimodipine 0.25-0.5 mg In case of carotid artery spasm due to the balloon or filter device manipulations, the physician administers it with intra-arterial slow infusion. tPA In case of acute stent thrombosis, the physician administers it with intra-arterial route. Postprocedural Heparin IV or subcutaneous To keep anticoagulation up to 12-24 hours, as ordered Clopidogrel 75 mg/day PO 1-3 months Aspirin 100-300 mg/day PO Indefinitely Regular IV fluids and/or IV In case of hypotension, as ordered volume expanders Dopamine IV infusion In case of persistent hypotension, as ordered Blood transfusion In case of groin or retroperitoneal hemorrhage Personal medications As ordered Note. CAS = carotid angioplasty and stenting; PO = orally; IV = intravenous; tPA = tissue plasminogen activator. (a) Skipping or shifting morning dose of antihypertensive drugs may be ordered by physician to preclude the complication of postprocedural persistent hypotension. TABLE 4. Contraindications to Elective CAS Contraindication to anticoagulant or antiplatelet therapy Uncorrected bleeding disorders Hemorrhagic transformation of cerebral ischemia on CT at the time of procedure Free-floating fresh thrombus inside the carotid lumen Occlusion of carotid artery Severe tortuosity in arcus aorta and carotid artery Extreme calcification within the carotid stenosis Early (not later than 4 weeks) CAS in patients with cerebral infarct on CT/MRI (a) Bradycardia less than 40/minute Renal insufficiency (due to using contrast media during CAS) Note. CAS = carotid angioplasty and stenting; CT = computed tomography; MRI = magnetic resonance imaging. (a) Early (within 1 month) revascularization may precipitate hemorrhage in the infracted area (Riggs & DeWeese, 1998). Table 5. Preprocedural Nursing Considerations Calculate time period between date of stroke and endovascular treatment; notify the physician if it is less than 1 month. Obtain baseline cranial CT scan to exclude intracranial hemorrhage especially in patients with recent stroke (less than 4 weeks); if hemorrhage is present, postpone the procedure (see Table 4). Verify if consent was signed properly. Check patient's medical file. Exclude other etiologies causing stroke. Verify more than 60% carotid stenosis for symptomatic and more than 80% stenosis for asymptomatic patients. Notify any contraindications (see Table 4). Notify any renal insufficiency (creatinine greater than 2.0 mg/dl). Notify any coagulation abnormalities (platelet count, prothrombin time, and partial thromboplastin time). Check patient's medication regiment (see Table 3). Assess and document baseline neurological condition: Consciousness Verbal responses Motor (leg and arm) function Prep bilateral groin areas. Insert IV line and administer IV fluids. Prep monitoring of patient: oxygen saturation, ECG, and blood pressure Note. CAS = carotid angioplasty and stenting; CT = computed tomography; IV = intravenous; ECG = electrocardiogram. TABLE 6. Intraprocedural Nursing Considerations Document baseline patient assessment: Pulse rate Cardiac rhythm Blood pressure Oxygen saturation Have the following medications available and administer as ordered: Atropine and antiarrhythmic medications Antihypertensive medication Medications to treat hypotension Thrombolytic medications Administer medication as ordered (see Table 3). Continuous neurological monitoring; notify any difference from baseline. Continuous cardiovascular monitoring; notify physician of the following: Oxygen saturation less than 92% Pulse rate less than 40/minute Systolic blood pressure less than 90 mm Hg or greater than to 160 mm Hg Be alert of sudden bradycardia, asystole just after the stent implantation, or balloon angioplasty. Be alert of sudden hypotension just after the stent implantation and balloon angioplasty. TABLE 7. Postprocedural Nursing Considerations Assist patient transfer from stretcher to bed without flexion of extremity. Keep femoral sheath in place for about 30 minutes; confirm unchanged neurological status before sheath removal. Perform patient assessment every 15 minutes x 4, every 30 minutes x 2, and hourly up to first 12 hours: Blood pressure Heart rate Neurological examination After sheath removal, monitor femoral access site for hematoma formation and assess peripheral pulses and the color distal to access at least four times within the first 12 hours. Closely monitor the patient for any signs and symptoms of postprocedural complications: Worsened neurological status (stroke and TIA) Symptomatic bradycardia Persistent hypotension Hyperperfusion syndrome Hematoma in access site or retroperitoneal space In case of complications Notify the physician. Administer medication as ordered. Contact the radiology unit to obtain emergency CT or duplex ultrasonography scan if radiological confirmation is needed. Be ready for emergency insertion of cardiac pacemaker. Transfer the patient to intensive care unit. Note. TIA = transient ischemic attack; CT = computed tomography. TABLE 8. Problem Solving Related to CAS Signs and Symptoms Causes Diagnostic Tools Loss of conscious Hypotension Check blood pressure Bradycardia Check heart rate, obtain ECG Search for signs of circulatory collapse Hypoglycemia (in Check glucose level diabetes patients) Blood loss Check groin/flank and check (hemorrhage) hematocrit level Cerebral embolism Emergency cranial CT; if it is okay, then conduct emergency carotid duplex ultrasonography to exclude stent thrombosis Hyperperfusion Emergency cranial CT to syndrome exclude hemorrhage Sudden hemiparesis Hyperperfusion Emergency cranial CT to (without other syndrome exclude hemorrhage signs of stroke) Cerebral embolism Emergency cranial CT then carotid duplex ultrasonography to exclude stent thrombosis Seizure Hyperperfusion Check blood pressure syndrome Emergency cranial CT to exclude hemorrhage Sudden headache Hyperperfusion Check blood pressure syndrome Emergency cranial CT to exclude hemorrhage Hypotension Stretching the -- carotid bulb with stent Blood loss Check groin/flank (hemorrhage) Check hematocrit level to confirm the diagnosis Bradycardia Stretching Obtain an ECG the carotid bulb with stent Search for signs and symptoms of circulatory collapse to exclude cardiac insufficiency Note. CAS = carotid angioplasty and stenting; ECG = electrocardiogram; CT = computed tomography.
|Printer friendly Cite/link Email Feedback|
|Author:||Oran, Nazan Tuna; Oran, Ismail|
|Publication:||Journal of Neuroscience Nursing|
|Article Type:||Clinical report|
|Date:||Feb 1, 2010|
|Next Article:||Reliability and validity of the adult alpha functional independence measure instrument in England.|