9.1 The Acute Stroke Patient

Providing anesthesia in the neuroendovascular suite can be challenging for a number of reasons. This location is designed to facilitate a wide range of neuroendovascular procedures. However, unlike an operating room, anesthesia is often not involved, and therefore physical space and ergonomic design for anesthesia personnel and equipment is suboptimal. ² Furthermore, anesthetizing in remote locations can be hazardous. Compared with operating room patients, those receiving anesthesia in remote locations are generally older and sicker. An analysis the American Society of Anesthesiologists (ASA) Closed Claims Project Database reveals adverse respiratory events during monitored anesthesia care in remote nonoperating room locations poses a significant risk to patients. ³ Vigilance and care must be taken to avoid oversedation in this patient population. It is important to maintain the same monitoring standards in the neuroendovascular suite as the operating room.

AIS is a neurologic emergency, and the anesthesia preprocedure evaluation is time limited. Additionally, these patients often present with altered mental status, which makes obtaining a history difficult. However, there are diagnostic tests and patient information that should be acquired before the patient arrives to the endovascular suite. Age, vital signs, allergies, medications, comorbidities, onset of stroke symptoms, and neurologic status, including National Institute of Health Stroke Scale (NIHSS) score, should be known. ⁴ Recommended test results include EKG, chest X-ray, computed tomography (CT) of vessel occlusion, serum glucose, CBC, platelet count, and coagulation studies. ⁵ This information, along with a rapid airway evaluation, is often the extent of an anesthesiologist’s preprocedure evaluation.

9.2 Airway Management

The decision as to whether a patient will receive conscious sedation or a general anesthetic is often predicated upon the patient’s airway patency and their ability to maintain effective ventilation while being positioned supine. If the patient is unable to lie without obstructing their airway, it is prudent to induce general anesthesia and secure the airway before starting the procedure. The anesthesiologist should be able to anticipate potential problems based upon patient characteristics. Male sex, obesity, and sleep apnea are risk factors for difficult mask ventilation. ^{6 ,​ 7} Risk factors for difficult tracheal intubation include limited mouth opening, large neck circumference, short thyromental distance, neck immobility, and the inability to visualize the hypopharynx. ⁸ As neuroendovascular suites are often in a remote location, there should be dedicated difficult intubation equipment readily available.

9.3 Physiologic Monitoring

Monitoring of the AIS patient should meet, at the minimum, ASA standards. The patient’s oxygenation, ventilation, circulation, and temperature should be continuously evaluated. All fluid lines, monitoring cables, and breathing circuits should be long enough to allow safe movement of the angiographic table. Pulse oximetry, placed on the great toe of the leg that will receive the femoral introducer sheath, can qualitatively assess oxygenation and provide early warning of femoral artery occlusion or thrombus. Continuous EKG and blood pressure measurement at least every 3 minutes can detect arrhythmias and any decreases in perfusion. ⁹ Placement of intra-arterial catheter for continuous blood pressure monitoring is helpful but should not delay endovascular treatment. The side port on the femoral artery introducer sheath can also be used to continuously measure the patient’s blood pressure. This method will underestimate systolic and overestimate diastolic pressures due to the catheter within the sheath, but the mean arterial pressures will be accurate.

9.4 Fluid Management

Isotonic crystalloid solutions are recommended for AIS. Patients with chronic hypertension are often volume contracted. This relative hypovolemic state makes these patients prone to hypotension under general anesthesia. Euvolemia should be the therapeutic goal. Hemodilution and hypervolemia has not shown benefit in ischemic stroke. ¹⁰ Hypotonic solution such as lactated ringers should be avoided due to increased risk of cerebral edema. Colloids, particularly albumin, have been proposed as being neuroprotective. However, human trials of albumin in acute stroke have shown no neurologic improvement and increased rates of intracerebral hemorrhage and pulmonary edema. ¹¹ Dextrose-containing fluids should be avoided unless the patient is hypoglycemic.

9.5 Temperature

In animal models, mild hypothermia (33–34° C) has been proven to be effective in reducing the brain’s vulnerability to ischemic injury. In humans, clinical trials for aneurysm surgery and head-injured patients failed to show benefit for induced hypothermia. However, hypothermia has been shown to improve neurologic outcomes following cardiac arrest. ¹² There is yet to be a large randomized clinical trial studying hypothermia in the setting of ischemic stroke. ¹³ What is well established however, is that even mild increases in temperature dramatically worsen ischemic brain injury. Therefore, normothermia should be maintained between 35 and 37° C during endovascular treatment. Patients should be treated with antipyretics and cooling blankets if febrile. Shivering should be treated with meperidine.

9.6 Blood Glucose

Hyperglycemia is an independent risk factor for poor clinical outcomes in ischemic stroke. Hyperglycemia worsens acidosis in the ischemic penumbra through anaerobic glucose metabolism and lactic acid production. Blood glucose level of > 140 mg/dL have been associated with increased mortality and complications, such as intracerebral hemorrhage, in stroke patients receiving thrombolytic therapy. ¹⁴ However, intensive insulin therapy is not without risks. Hypoglycemia can worsen brain injury. It can be difficult to safely administer intensive insulin therapy in the setting of endovascular stroke treatment, as patients are transported between different critical care units and multiple providers. Nevertheless, insulin treatment for hyperglycemia should be initiated for blood glucose levels greater than 140 mg/dL. Blood glucose levels below 50 mg/dL should be treated with dextrose infusion for a target blood glucose level greater than 70 mg/dL. ⁵

9.7 Arterial Carbon Dioxide and Oxygen Tension

Manipulation of arterial carbon dioxide (CO₂) tension is an effective means of altering cerebral physiology. Hyperventilation and hypocapnia will rapidly decrease cerebral blood flow, cerebral blood volume, and intracranial pressure. Hypocapnia has been shown to worsen ischemic and traumatic brain injury. Hypercapnia will have the opposite, increased effect, on cerebral blood flow and intracranial pressure. ¹⁵ There are no clinical studies supporting hypercapnia in ischemic stroke. Normocapnia should be the goal for these patients.

Acute stroke patients are at risk for hypoxia due to stroke symptomatology. Respiratory drive may be impaired as well as the ability to clear secretions and protect the airway. Hyperoxia has been suggested as a neuroprotective therapy and a method to increase the therapeutic time window for revascularization. However, hyperbaric oxygen therapy has failed to improve ischemic stroke outcomes in multiple clinical trials. Supplemental oxygen is indicated during sedation of the stroke patient. ¹⁶ Continuous pulse oximetry should be used, with a target SpO2 of greater than 92%. In patients whom oxygenation and ventilation are inadequate, tracheal intubation and mechanical ventilation are indicated until their condition improves.

9.8 Intraprocedural Complications

Complications during endovascular treatment of thromboembolic stroke are rare events that must be recognized early and treated rapidly to minimize injury to the patient. The most serious complications are vessel perforation and intracerebral hemorrhage. Communication between the anesthesiologist and the neuroendovascular surgeon is critical. The first signs of hemorrhage may be contrast extravasation, abrupt neurologic decline, or bradycardic response to increased intracranial pressure (ICP). If sedation, the case should be converted to a general anesthetic, allowing greater control of the patient’s hemodynamics and ventilation. Vessel injury should be repaired endovascularly. The minimum safe blood systolic blood pressure is 140 mm Hg. ¹⁷ Relative hypotension increases the risk of worsening cerebral ischemia. A fast-acting, easily titratable antihypertensive such as nicardipine is appropriate. Normocapnia should be maintained. If bleeding continues and the patient has received tissue plasminogen activator (tPA), cryoprecipitate can be given to raise fibrinogen levels. Antifibrinolytics, such as tranexamic acid, can also be given to bind plasminogen and inhibit fibrin degradation. Further resuscitation and treatment ICP may include rapid infusion of mannitol, titration of anesthetic to burst suppression, passive cooling, and placement of an external ventricular drain. ⁴

9.9 Hemodynamic Management

Blood pressure management during and after AIS is a controversial subject. The majority of acute ischemic patients present with elevated blood pressures. This is primarily due to underlying baseline hypertension. However, there is also an early hypertensive response to cerebral ischemia which further elevates blood pressures in these patients. Systemic blood pressure rises in an attempt to perfuse ischemic regions of the brain. Within the ischemic penumbra there is maximal arteriole dilation, and autoregulation is impaired as cerebral blood flow becomes directly proportional to blood pressure. ^{18 ,​ 19} This hypertensive response slowly resolves over the next 12 to 24 hours following the stroke.

Ischemic stroke patients have a U-shaped mortality pattern in relation to their admission blood pressures. ²⁰ Both low and high blood pressures are associated with worse outcomes. ²¹ In patients treated with tPA, elevated blood pressures are associated with lower recanalization rates. ^{22 ,​ 23} Similarly, in patients treated by mechanical thrombectomy, elevated systolic blood pressures are associated with lower recanalization rates. ²⁴ The exact neuroprotective mechanism blood pressure plays in the ischemic penumbra is not yet clear. It appears that the hypertensive response, which improves perfusion of the collateral circulation, at some point become inversely correlated to favorable reperfusion therapy outcomes. ²⁵ Whether blood pressure is itself an independent predictive factor or an active contributor affecting clot retrieval is unknown.

Currently, the accepted body of thinking is that during the AIS periprocedural period, moderate hypertension is of benefit, providing perfusion to ischemic regions. ²⁶ Systolic blood pressure less than 140 mm Hg have been associated with worse outcome in patients undergoing endovascular treatment of AIS with general anesthesia. ^{27 ,​ 28} Induced hypertension is reasonable during AIS treatment with a systolic blood pressure goal > 140. Phenylephrine is a good first line choice. A potent alpha-agonist, phenylephrine causes peripheral vasoconstriction, raising blood pressure with few cardiac side effects. However, blood pressure augmentation must be balanced by the possibility that hypertension may result in cerebral hyperemia and edema formation. (Induced hypertension, especially in the setting of tPA administration, could result in catastrophic hemorrhage. Once given tPA, AIS patient blood pressure goals should be less than 180/105 mm Hg to decrease risk of hemorrhage. Calcium channel blockers such as nicardipine or clevidipine, short-acting dihydropyridines, are the preferred agents. This class of drugs is selective for vascular smooth muscle, with little effect on heart rate or contractility. ²⁹ Once thrombectomy has been achieved, the patient’s blood pressure should be brought to below 160 mm Hg systolic to decrease risk of hyperemia and hemorrhage.