INTRODUCTION — Stroke resulting from cardiac catheterization is relatively common due to the high volume of cardiac procedures performed worldwide. This topic will review periprocedural stroke in the setting of cardiac catheterization, which includes diagnostic and interventional procedures. Other aspects of acute stroke are discussed elsewhere. (See "Initial assessment and management of acute stroke" and "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use".)
MECHANISMS — Patients may experience either ischemic or hemorrhagic stroke in the setting of cardiac catheterization.
Ischemic stroke — In most cases, the mechanism of ischemic stroke is directly related to cardiac catheterization itself, which initially involves advancing catheters over wires into the aorta, generally using either transfemoral or transradial access. Catheter or wire manipulation may dislodge debris made up of thrombus, calcific material, or cholesterol particles from atherosclerotic plaques within the aortic arch and the proximal carotid and vertebral arteries [1-4]. In addition, fresh thrombus material may form at the catheter and guidewire tips. Most cases of ischemic stroke related to cardiac catheterization are caused by such thromboemboli. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)
The mechanism of ischemic stroke is similar between diagnostic and interventional procedures. However, interventional catheters are on average larger than diagnostic catheters and the procedures are often longer and thus there may be a theoretical increase in risk.
Ultimately, one or more catheters end up in one of the cardiac chambers or in the coronary arteries. Catheterization across a degenerated aortic valve may lead to thromboembolism and the risk of stroke may be particularly high in patients with significant valvular aortic stenosis (AS) who undergo retrograde catheterization of the aortic valve [5,6]. This was demonstrated in a study of 152 patients with AS (mean age 71 years) who were randomly assigned to cardiac catheterization with or without catheter passage through the valve [5]. The following findings were noted:
●Brain magnetic resonance imaging obtained before and after the catheterization demonstrated focal lesions consistent with cerebral emboli in 22 percent of those who underwent retrograde catheterization of the aortic valve, but in none of the patients who did not.
●Detailed neurologic examination done before and after the catheterization demonstrated clinically apparent deficits in 3 percent of those who underwent retrograde catheterization, but in none of the other patients.
As a result, catheterization across a degenerated aortic valve should be performed with caution in patients with severe calcific AS and only when the information sought cannot be reliably obtained noninvasively [6].
Less common causes of ischemic stroke related to cardiac catheterization include air embolism, thromboembolism from clot in the left ventricle, periprocedural hypotension, arterial dissection, and fractured guidewire [7,8].
Hemorrhagic stroke — Patients having cardiac catheterization are at increased risk for hemorrhagic stroke because of acquired hemostatic abnormalities induced by thrombolytic, anticoagulant, and/or antiplatelet regimens used in the periprocedural time period [9].
INCIDENCE — Mainly retrospective data suggest that stroke (within 36 hours) occurs at a rate of 0.1 to 0.6 percent in patients undergoing diagnostic cardiac catheterization [10-13]. The higher estimate (0.6 percent) comes from a meta-analysis of studies that performed systematic neurologic evaluation and brain magnetic resonance imaging (MRI) [13]. Among those undergoing percutaneous coronary (artery) intervention (PCI), the rate ranges from 0.07 to 0.96 percent [12,14-20].
Hemorrhagic stroke, most often intracerebral hemorrhage, has accounted for 8 to 46 percent of stroke related to cardiac catheterization in the few registries that distinguish between ischemic and hemorrhagic stroke types [9,12,15,18,19,21]. Subarachnoid hemorrhage following cardiac catheterization is probably uncommon if not rare, with only a few cases reported in the literature [9,22]. However, most studies of invasive cardiac procedures reporting the incidence of intracranial hemorrhage do not distinguish intracerebral hemorrhage from subarachnoid hemorrhage. The risk of hemorrhagic stroke is probably increased for patients undergoing acute coronary interventions because of the intense antithrombotic regimens that are used [9,23].
Compared with procedures on the coronary arteries, the incidence of periprocedural stroke is somewhat higher after aortic valvuloplasty or radiofrequency catheter ablation for atrial fibrillation. (See "Atrial fibrillation: Catheter ablation", section on 'Periprocedural embolic events' and "Transcatheter aortic valve implantation: Complications", section on 'Stroke and subclinical brain injury'.)
Asymptomatic embolism — Asymptomatic cerebral embolism is much more common than clinically manifest stroke, as illustrated by the findings of a 2017 systematic review and meta-analysis of studies reporting brain infarcts on diffusion-weighted MRI in patients undergoing cardiac procedures [13]. All included studies performed neurologic examinations and brain MRI both pre-and post-procedure. Among 833 patients who had diagnostic cardiac catheterization, the incidence of asymptomatic radiographic brain infarcts was 8 percent (95% CI 4.1-12), while the incidence of clinically symptomatic events (ischemic stroke and transient ischemic attack) was 0.6 percent (95% CI 0.1-1.1).
Transcranial Doppler ultrasonography studies reveal an even higher prevalence (up to 100 percent) of microemboli during cardiac catheterization procedures [24-27]. The majority of these microemboli occur during contrast injection, while a smaller number are observed with movement of the catheter/guide wire. Most of the signals that are seen with injection of solutions have profiles consistent with gaseous origin (eg, air bubbles) and are thought to be of no clinical consequence, whereas the microembolic signals that occur during catheter and guide wire manipulation have signal profiles consistent with particulate origin (eg, atheromatous debris), and could result in transient or persistent ischemic brain injury. Nevertheless, most patients are asymptomatic. These observations suggest that catheter manipulation in the diseased aortic root releases small pieces of atherosclerotic debris more commonly than suspected, based upon the low incidence of clinically apparent stroke. (See 'Mechanisms' above.)
In a report of 47 unselected patients in whom transcranial Doppler was used to detect microemboli and MRI to detect new lesions, the median number of solid (ie, not gaseous) microemboli was significantly higher with a transradial compared with a transfemoral access (57 versus 36). New MRI lesions occurred in 5 of 33 patients (15 percent) after transradial catheterization, compared with 0 of 9 after transfemoral catheterization. Most of the patients with new lesions remained asymptomatic [24].
RISK FACTORS — Clinical risk factors for stroke with cardiac catheterization and PCI include the following [3,9,10,12,15,17,18,20,21,28-30]:
●Older age (eg, >75 to 80 years)
●Hypertension
●Diabetes mellitus
●History of stroke
●Renal failure
●Heart failure
●Severity of coronary artery disease, including the presence of triple vessel disease
●Carotid artery disease
Procedural risk factors for stroke include the following [5,9,10,12,15,17,18,20,21,29-31]:
●Emergent catheterization, including acute coronary syndrome
●Longer procedure time
●Greater contrast use
●Retrograde catheterization of the left ventricle in patients with aortic stenosis
●Interventions at bypass grafts
●Use of an intra-aortic balloon pump
●Presence of coronary artery thrombus
The risk of intracerebral hemorrhage is increased in those receiving anticoagulation or thrombolytic therapy for acute myocardial infarction as well as in those with any of the following: age ≥75 years; female sex; systolic blood pressure ≥160 mmHg; being from a Black population; and low body weight (table 1) [32].
PREVENTION — Meticulous attention to technical factors such as wire and catheter exchanges is mandatory in all patients, regardless of risk. Transient neurologic deficits may also result from the injection of high osmolar contrast agents into the carotid or vertebral arteries.
For patients undergoing percutaneous coronary intervention, there is some evidence that radial artery catheterization is associated with a lower risk of stroke compared with femoral artery catheterization.This evidence is reviewed elsewhere. (See "Periprocedural complications of percutaneous coronary intervention", section on 'Radial artery access'.)
CLINICAL PRESENTATION — Most strokes related to cardiac catheterization present during the procedure or within the first 24 hours after the procedure [21,33]. Frequent manifestations of ischemic stroke and intracerebral hemorrhage include visual disturbance, aphasia, dysarthria, hemiparesis, and altered mental status. In contrast, subarachnoid hemorrhage usually presents with headache and global neurologic deficits, mainly altered level of consciousness. A maximal deficit at onset or a fluctuating course suggest ischemic stroke, while gradual worsening of neurologic deficits over minutes to hours and signs of elevated intracranial pressure suggest hemorrhage. However, clinical features alone do not reliably distinguish brain ischemia from hemorrhage, necessitating neuroimaging.
The symptoms and signs of acute ischemic stroke often correspond to recognized stroke syndromes with focal neurologic deficits attributable to ischemia within a vascular territory affecting the cerebral cortex (eg, aphasia and left hemiparesis related to embolic occlusion within the left middle cerebral artery territory), brainstem, or cerebellum. (See "Clinical diagnosis of stroke subtypes".) Monocular visual loss may be caused by retinal embolism [34,35]. Some data suggest that a disproportionate number of ischemic strokes related to cardiac catheterization affect the vertebrobasilar circulation [29,36,37], but other reports suggest that the rate of posterior circulation ischemic stroke is close to 20 percent [15], as might be expected given the percentage of blood that the posterior circulation supplies to the brain. In addition to focal deficits, a nonfocal presentation of ischemic stroke with reduced alertness and encephalopathy can occur as a result of diffuse bilateral cerebral embolization.
EVALUATION AND DIAGNOSIS — The evaluation of the patient who is undergoing or who has recently undergone cardiac catheterization and who is suspected of an acute stroke is presented briefly here. Acute stroke evaluation is discussed in detail separately. (See "Initial assessment and management of acute stroke".)
Important aspects of the evaluation of any patient with periprocedural neurologic deterioration suggestive of stroke include:
●Rapid activation of the stroke team.
●Stabilization of airway, breathing, and circulation.
●Checking serum glucose, as symptoms of hypoglycemia may mimic stroke; low serum glucose (<60 mg/dL [<3.3 mmol/L]) should be corrected rapidly.
●Platelet count and coagulation studies if there is suspicion for thrombocytopenia or coagulopathy.
●Determining symptom onset time or the last time the patient was known to be neurologically normal. (In a sedated patient, this time would be when the patient was last alert enough to be assessed).
●A focused history and examination will help in the development of a differential diagnosis.
●Emergent brain imaging with noncontrast computed tomography (CT) or magnetic resonance imaging (MRI), and concurrent neurovascular imaging with CT angiogram or magnetic resonance (MR) angiogram.
●CT or MR perfusion imaging, if the clinical diagnosis of stroke is uncertain (eg, high suspicion for a seizure with a postictal state). However, caution should be taken not to delay stroke treatment (if indicated) in order to obtain additional tests. Perfusion studies or MRI may also be useful in patients with unknown time of onset or more than 4.5 hours from last known well.
We recommend brain imaging with CT or MRI to rule out hemorrhage as a standard approach. In contrast, some experts have advocated immediate angiography followed by intra-arterial thrombolysis rather than obtaining a head CT or MRI after an acute stroke from cardiac catheterization, because the time needed for brain imaging may significantly delay treatment of a vessel occlusion [38]. However, this approach would require a high level of confidence that intracranial hemorrhage is not causing the stroke symptoms, that any identified vessel occlusion is acute and responsible for the symptoms, and that the risk of hemorrhagic transformation of the acute ischemic stroke is low (eg, the diagnostic procedure was done without the use of full-dose anticoagulation and/or glycoprotein IIb/IIIa inhibitors).
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of acute stroke in this setting includes transient ischemic attack, seizure, migraine, encephalopathy, and toxic-metabolic disturbances such as hypoglycemia. In some cases, the recognition of stroke deficits can be confounded by altered mentation caused by sedative medications used for the procedure or by comorbid medical or neurologic conditions.
An additional but rare consideration in the periprocedural period is that of contrast-induced transient cortical blindness [39-41], which can occur with ionic and nonionic contrast media. Onset is seen within minutes to hours after the procedure, typically beginning with blurred vision that rapidly progresses to complete blindness, usually associated with headache. Additional symptoms may include vomiting, confusion, aphasia, memory impairment, and limb weakness or ataxia. On head computed tomography (CT) performed without additional contrast, there is often enhancement from contrast administered during cardiac catheterization affecting the cortex, particularly the parieto-occipital lobes, as well as the deep gray structures, brainstem, and/or cerebellum. Symmetrical white matter edema in the posterior cerebral hemispheres is another frequent finding. In one affected patient evaluated with brain magnetic resonance imaging, hyperintense signal on T2-weighted sequences was seen in the occipital lobes, thalami, and cerebellum [41]. In nearly all cases, the neurologic impairments and neuroimaging abnormalities gradually resolve over days. Although the mechanism is uncertain, a transient vasculopathy with disruption of the blood-brain barrier is postulated, suggesting that this is a form of posterior reversible encephalopathy syndrome (PRES), also called reversible posterior leukoencephalopathy syndrome [40,42,43]. (See "Reversible posterior leukoencephalopathy syndrome".)
In addition to being associated with the signs and symptoms described above, extravasation of contrast after coronary angiography can sometimes mimic the appearance of subarachnoid hemorrhage [44] and intracerebral hemorrhage [45] on noncontrast head CT scan.
Although visual loss after cardiac catheterization has usually been related to contrast, and therefore reversible, bilateral occipital lobe infarction in this setting may present in a similar manner and must be considered [46].
TREATMENT — Treatment of ischemic stroke is dependent on the time elapsed from stroke onset. As discussed below, we suggest intravenous thrombolytic therapy for eligible patients (table 2) with ischemic stroke in the setting of cardiac catheterization who are within 4.5 hours of last known well and otherwise eligible, and consideration in some patients beyond 4.5 hours with favorable advanced imaging. However, despite the evidence of benefit in many patients, the risk of bleeding is relatively high in these patients compared with the broad population of patients with ischemic stroke due to the recent use of aggressive antithrombotic therapy as well as the potential for significant procedure site and device related (eg, retroperitoneal) bleeding. The benefits and risks of intravenous thrombolytic therapy need to be weighed carefully in potential candidates.
An option for patients who are ineligible for intravenous thrombolysis consists of mechanical thrombectomy (within 6 hours of onset of onset in most patients, and in 6 to 24 hours of onset in selected patients with favorable perfusion imaging). For ischemic stroke, the goal should be to initiate reperfusion therapy within one hour and preferably sooner from the time that symptoms are first noted.
For patients with hemorrhagic stroke (ie, intracerebral hemorrhage or subarachnoid hemorrhage), urgent management issues involve reversal of anticoagulation when feasible, blood pressure control, and treatment of elevated intracranial pressure. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".)
Ischemic stroke — Stroke caused by embolization of fresh thrombus forming on the catheter or guidewire would seem to be ideally suited to thrombolytic treatment. However, theoretical concerns about the utility of thrombolytic therapy for ischemic stroke after cardiac catheterization are based upon the possible composition of some other types of thrombi causing stroke in this setting [47]. For example, dislodged debris from aortic atherosclerotic plaque might be made up primarily of calcific material and therefore not responsive to thrombolysis, or calcific thrombus might undergo partial lysis leading to distal migration of calcific fragments [48]. In addition, air embolism and metallic fragments would be impervious to thrombolytic agents.
Despite these concerns, data from a retrospective, multicenter, observational study evaluating ischemic stroke after cardiac catheterization suggest that tissue plasminogen activator (tPA; alteplase) is safe and efficacious in this setting [47]. Among 66 consecutive cases of ischemic stroke after cardiac catheterization, 12 patients were treated acutely with thrombolysis (7 with intravenous tPA and 5 with intra-arterial tPA), while 54 received no thrombolysis. Patient demographics (age, medical comorbidities, and cardiac procedure characteristics) were similar between the thrombolysis and no thrombolysis groups. Eleven of these 12 treated patients had received periprocedural heparin, and two of the seven who received intravenous tPA had prolonged partial thromboplastin time (PTT). The following observations were made [47]:
●There was a statistically significant improvement in stroke symptoms by predefined end points in patients who received tPA compared with those who did not, including change in the National Institutes of Health Stroke Scale (NIHSS) score from baseline to 24 hours (-6 versus 0) and change in NIHSS score from baseline to seven days (-6.5 versus -1.5).
●There were no significant differences in mortality or bleeding events, including symptomatic intracranial hemorrhage, hemopericardium, and other systemic bleeding causing hemodynamic instability or requiring transfusions.
Additional case reports and case series, while potentially limited by publication bias, also suggest reasonable safety and efficacy of thrombolysis for patients with acute ischemic stroke related to cardiac catheterization [36,49-55].
Therefore, patients should be evaluated for reperfusion therapy based on the time of stroke onset if no hemorrhage is seen on head computed tomography (CT) scan. For eligible patients (table 2) with acute ischemic stroke related to cardiac catheterization, we suggest intravenous tPA (alteplase) therapy, provided that treatment is initiated within 4.5 hours of clearly defined symptom onset, and consider treatment beyond 4.5 hours in selected patients based on advanced imaging (ie, those with an ischemic brain lesion on magnetic resonance imaging (MRI) diffusion-weighted imaging but no corresponding hyperintensity on fluid-attenuated inversion recovery (FLAIR), an imaging mismatch that correlates with a stroke onset time of 4.5 hours or less). (See "Approach to reperfusion therapy for acute ischemic stroke", section on 'Benefit with imaging selection of patients'.)
Furthermore, patients with acute ischemic stroke caused by a large vessel occlusion may be eligible for mechanical thrombectomy if they can be treated within 24 hours of the time they were last known to be at their neurologic baseline (algorithm 1).
The use of intravenous thrombolysis is discussed in greater detail elsewhere, including the management of blood pressure before and during alteplase administration (table 3). (See "Approach to reperfusion therapy for acute ischemic stroke" and "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use".)
Similarly, mechanical thrombectomy for acute ischemic stroke is reviewed separately. (See "Mechanical thrombectomy for acute ischemic stroke".)
Regardless of reperfusion therapy modality, it is imperative to minimize the time to treatment. It is well established that longer times to reperfusion translate to lower likelihoods of good clinical outcome.
Another issue of particular importance to the treatment of patients in the peri- or post-catheterization setting is the use of anticoagulants and antithrombotics:
●A normal PTT should be documented prior to administration of intravenous tPA for ischemic stroke, if heparin was administered within 48 hours. Protamine can be used to reverse the effect of heparin in the setting of hemorrhagic stroke. (See 'Hemorrhagic stroke' below.)
For patients with a prolonged PTT, mechanical embolectomy is the preferred treatment option [56].
●The degree to which glycoprotein IIb/IIIa inhibitor therapy may increase the risk of hemorrhagic complications with intravenous tPA for ischemic stroke is unknown, although preliminary data suggest safety [57-59]. Endovascular interventions are the preferred treatment option in this setting as well.
●Single or dual antiplatelet therapy is not a contraindication to intravenous tPA.
The standard management of acute ischemic stroke is discussed in greater detail separately. (See "Initial assessment and management of acute stroke".)
Hemorrhagic stroke — The management of hemorrhagic stroke following cardiac catheterization follows the same principles as the management of hemorrhagic stroke in other settings. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis" and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Nonaneurysmal subarachnoid hemorrhage", section on 'Management and prognosis'.)
All anticoagulant and antiplatelet drugs should be discontinued acutely, and should not be used until cessation of bleeding is documented by neuroimaging (and possibly longer depending on risk-benefit profile). Anticoagulant effect should be reversed immediately with appropriate agents.
●For patients with unfractionated heparin-associated intracerebral hemorrhage, protamine sulfate is recommended for urgent treatment. Protamine sulfate can be administered by slow intravenous infusion (not greater than 20 mg/min and no more than 50 mg over any 10-minute period). The appropriate dose of protamine sulfate is dependent upon the dose of heparin given and the time elapsed since that dose. For patients with low-molecular weight heparin-associated intracranial bleeding, andexanet alfa or protamine sulfate can be used for anticoagulant reversal. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Unfractionated heparin' and "Reversal of anticoagulation in intracranial hemorrhage", section on 'LMW heparin' and "Heparin and LMW heparin: Dosing and adverse effects", section on 'Reversal'.)
●For patients taking warfarin, aggressive and rapid use of intravenous vitamin K, unactivated prothrombin complex concentrate (also called factor IX complex), and other factors may be necessary. Antidotes to oral factor Xa and direct thrombin inhibitors are discussed elsewhere. (See "Management of bleeding in patients receiving direct oral anticoagulants", section on 'Dabigatran reversal' and "Management of bleeding in patients receiving direct oral anticoagulants", section on 'Factor Xa inhibitors' and "Reversal of anticoagulation in intracranial hemorrhage", section on 'Reversal strategy for specific anticoagulants'.)
Severe elevations in blood pressure may worsen intracerebral hemorrhage by representing a continued force for bleeding. Labetalol, nicardipine, esmolol, enalapril, hydralazine, nitroprusside, and nitroglycerin are useful intravenous agents for controlling blood pressure. Specific recommendations for managing elevated blood pressure in patients with acute intracerebral hemorrhage are reviewed in detail separately. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Blood pressure management'.)
Initial management of elevated intracranial pressure (ICP) includes elevating the head of the bed to 30 degrees and use of analgesia and sedation. Suggested intravenous agents for sedation are propofol, etomidate, or midazolam. Suggested agents for analgesia and antitussive effect are morphine or alfentanil. More aggressive therapies for reducing elevated ICP include osmotic diuretics (eg, mannitol), ventricular catheter drainage of cerebrospinal fluid, neuromuscular blockade, and hyperventilation. We suggest continuous monitoring of ICP and arterial blood pressure when using these aggressive therapies, with the goal of maintaining cerebral perfusion pressure above 70 mmHg. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Intracranial pressure management'.)
For patients with a cerebellar hemorrhage >3 cm in diameter who are deteriorating or who have brainstem compression and/or hydrocephalus due to ventricular obstruction, we recommend surgical removal of hemorrhage. Surgery for supratentorial intracerebral hemorrhage (ICH) is controversial; standard craniotomy might be considered only for those who have lobar clots within 1 cm of the surface. The routine evacuation of supratentorial ICH in the first 96 hours is not recommended. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".)
Supportive care — Important acute stroke management issues, some already mentioned above, include the following:
●Assessing swallowing and preventing aspiration. (See "Initial assessment and management of acute stroke", section on 'Swallowing assessment' and "Complications of stroke: An overview", section on 'Dysphagia'.)
●Optimizing head of bed position; for patients in the acute phase of stroke who are at risk for elevated intracranial pressure, aspiration, cardiopulmonary decompensation, or oxygen desaturation, we suggest keeping the head in neutral alignment with the body and elevating the head of the bed to 30 degrees; for patients in the acute phase of stroke who are not at risk for elevated intracranial pressure, aspiration, or worsening cardiopulmonary status, we suggest keeping the head of bed flat (0 to 15 degree head-of-bed position). (See "Initial assessment and management of acute stroke", section on 'Head and body position'.)
●Managing blood pressure:
•For patients with acute ischemic stroke who will receive thrombolytic therapy or mechanical thrombectomy, antihypertensive treatment is recommended so that systolic blood pressure is ≤180 mmHg and diastolic blood pressure is ≤105 mmHg during and after treatment (table 3). This issue is discussed in detail separately. (See "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use", section on 'Management of blood pressure'.)
•For patients with acute ischemic stroke who are not treated with thrombolytic therapy, we suggest treating high blood pressure only if the hypertension is extreme (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg), or if the patient has another clear indication (active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute renal failure, or pre-eclampsia/eclampsia). When treatment is indicated, we suggest cautious lowering of blood pressure by approximately 15 percent during the first 24 hours after stroke onset. (See "Initial assessment and management of acute stroke", section on 'Blood pressure goals in ischemic stroke'.)
•In both intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH), the approach to blood pressure lowering must account for the potential benefits (eg, reducing further bleeding) and risks (eg, reducing cerebral perfusion). Recommendations for blood pressure management in acute ICH and SAH are discussed in detail separately. (See "Initial assessment and management of acute stroke", section on 'Blood pressure in acute hemorrhagic stroke' and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Blood pressure management' and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Blood pressure control'.)
●Treating hypoglycemia and hyperglycemia. (See "Initial assessment and management of acute stroke", section on 'Hypoglycemia' and "Initial assessment and management of acute stroke", section on 'Hyperglycemia'.)
●Evaluating and treating the source of any fever; for patients with acute stroke, we suggest maintaining normothermia for at least the first several days after an acute stroke. (See "Initial assessment and management of acute stroke", section on 'Fever'.)
●Preventing deep venous thrombosis and pulmonary embolism. (See "Prevention and treatment of venous thromboembolism in patients with acute stroke", section on 'Approach to VTE prevention'.)
PROGNOSIS — Stroke after cardiac catheterization is associated with a high in-hospital and 30-day mortality rate [10,15,17-19,21]. In the largest of these studies, the 30-day mortality rate after percutaneous coronary interventions was 19 percent for patients who experienced an ischemic stroke and 50 percent for those who had a hemorrhagic stroke, versus 2 percent in those without stroke [19]. Few data are available for long-term outcomes among survivors, but among 69 patients with stroke or transient ischemic attack who survived hospitalization in one report, transfers to inpatient rehabilitation, nursing home, or assisted living made up 31 percent of discharges [21]. The high morbidity and mortality associated with these strokes justifies aggressive treatment strategies.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".)
SUMMARY AND RECOMMENDATIONS
●Diagnostic and interventional cardiac catheterization may lead to either ischemic or hemorrhagic stroke. The overall incidence of clinically apparent stroke during or after cardiac catheterization is well under 1 percent in most studies, but may be higher with certain interventional procedures, particularly with aortic valvuloplasty. Stroke in this setting is associated with a high morbidity and mortality rate. (See 'Mechanisms' above and 'Incidence' above and 'Prognosis' above.)
●Most strokes related to cardiac catheterization present during the procedure or within the first 24 hours after the procedure. Frequent manifestations of ischemic stroke and intracerebral hemorrhage include visual disturbance, aphasia, dysarthria, hemiparesis, and altered mental status. (See 'Clinical presentation' above.)
●Important aspects of the management of any patient with periprocedural neurologic deterioration suggestive of stroke include stabilization of airway; breathing and circulation; stroke team activation; emergent brain imaging; determination of symptom onset time; and laboratory tests such as serum glucose and measures of hemostasis. (See 'Evaluation and diagnosis' above.)
●The differential diagnosis of acute stroke includes transient ischemic attack, seizure, migraine, encephalopathy, and other conditions such as hypoglycemia. An additional consideration in the periprocedural period is that of contrast-induced transient cortical blindness. (See 'Differential diagnosis' above.)
●For eligible patients with ischemic stroke who can be treated within 4.5 hours of stroke onset, and selected patients with unknown time of onset and favorable imaging, we suggest intravenous thrombolytic therapy (table 2) (Grade 2C), followed by mechanical thrombectomy for select patients with large vessel occlusions. (See 'Treatment' above and 'Ischemic stroke' above.)
●Patients with acute ischemic stroke caused by a large artery occlusion who can be treated within 24 hours of the time they were last known to be at their neurologic baseline should be evaluated for mechanical thrombectomy (algorithm 1). (See 'Ischemic stroke' above and "Mechanical thrombectomy for acute ischemic stroke".)
●For patients with hemorrhagic stroke (ie, intracerebral hemorrhage or subarachnoid hemorrhage), urgent management issues involve reversal of anticoagulation, blood pressure control, and treatment of elevated intracranial pressure. (See 'Hemorrhagic stroke' above.)
