37: Intracranial and Cerebrovascular Disease

Published on 06/02/2015 by admin

Filed under Anesthesiology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1068 times

CHAPTER 37 Intracranial and Cerebrovascular Disease

Gurdev S. Rai, MD, Luke Osborne, MD

1 What is cerebrovascular insufficiency?

Cerebrovascular insufficiency results from an inadequate supply of blood flow, oxygen, and/or glucose to the brain. Cerebral ischemia develops, and neurologic damage will ensue if the underlying process is not corrected within 3 to 8 minutes.

2 Compare global ischemia with focal ischemia

Global ischemia refers to global hypoxia (respiratory failure, asphyxia) or circulatory arrest wherein the brain is not perfused. Focal ischemia can result from vasospasm, traumatic, hemorrhagic, embolic, or atherosclerotic events. If the underlying cause is reversed rapidly and perfusion and oxygenation are restored, neurologic damage can be avoided.

3 How does cerebrovascular insufficiency manifest itself?

Manifestations include transient ischemic attacks (TIAs) and cerebrovascular accidents (CVAs).

image TIAs are acute in onset, involve neurologic dysfunction for minutes to hours (<24 hours), resolve spontaneously, and are associated with a normal computed tomography (CT) scan.
image CVAs may develop acutely or chronically progress over time (minutes to days). Strokes can be classified as minor, with an eventual full recovery, or major, with severe and permanent disability or death. In addition to cerebrovascular abnormalities, CVAs are associated with other comorbidities, including hypertension, diabetes, coagulopathies, atrial fibrillation, mitral valve disease, endocarditis, and substance abuse.
image A third group of patients experience neurologic dysfunction for longer than 24 hours, with spontaneous and complete recovery within 1 to 2 weeks. This phenomenon is termed reversible ischemic neurologic deficit and should be pathophysiologically grouped with TIAs.

4 What is the etiology of cerebrovascular accidents and transient ischemic attacks?

Atherosclerosis at the bifurcation of the common carotid artery is the source of most cerebral ischemic events. The thrombus itself or more likely embolic plaques and debris can dislodge to the brain, resulting in neurologic injury. Resolution of TIAs within 24 hours is the result of the inherent mechanisms of the body for breaking down such emboli. Ischemia of the brainstem and the temporal and occipital lobes is thought to be caused by a transient decrease in blood flow or blood pressure in the vertebrobasilar system. Hypoperfusion to the brain secondary to the atherosclerotic stenosis itself accounts for less than 10% of ischemic events.

5 Are other factors involved in neurologic outcome following an episode of cerebrovascular insufficiency?

The type and size of plaque or embolus, the site of ischemia, the extent of collateral circulation, the duration of inadequate perfusion, and the inherent response of the brain to the insult all contribute to the neurologic sequelae.

6 List the risk factors for cerebral ischemic events

Hypertension and cigarette smoking are the strongest risk factors. Cardiac diseases (e.g., left ventricular hypertrophy, atrial fibrillation, cardiomyopathy, endocarditis, valvular disease, coronary artery disease) are major risk factors. Other risk factors include age, diabetes, hyperlipidemia, coagulopathies, vascular disease elsewhere, and a maternal history of stroke. The 5-year risk of stroke in a patient who has had a TIA is nearly 35%.

7 Who is a candidate for carotid endarterectomy?

Asymptomatic bruits are heard in 5% to 10% of the adult population. A 1989 prospective study of 566 patients with asymptomatic carotid bruits revealed a 1-year stroke or TIA rate of 2.5% compared with a rate of 0.7% in patients without carotid bruits. The European Carotid Surgery Trial (ECST) demonstrated that carotid endarterectomy (CEA) is not indicated for most patients with moderate (30% to 69%) stenoses, even if they are symptomatic. However, the rate of stroke or TIA increases dramatically with increasing stenosis, reaching a 1-year stroke or TIA rate of 46% for stenoses greater than 80%. It is well accepted that symptomatic patients and asymptomatic patients with a stenosis >70% are candidates for CEA.

Carotid stenting is now available for patients who fit these criteria but are high-risk surgical candidates. Stenting is an alternative to CEA in this select patient population and involves only local anesthesia and a small femoral incision.

8 Define cerebral autoregulation. How is it affected in cerebrovascular disease and what are the anesthetic implications?

Cerebral autoregulation is the ability of the brain to maintain cerebral blood flow relatively constant (40 to 60 ml/100 g/min) over a wide range (50 to 150 mm Hg) of arterial pressures. Stenosis or obstruction in the internal carotid artery causes a pressure drop beyond the obstruction. In an effort to maintain cerebral blood flow, the cerebral vasculature dilates. As the degree of carotid obstruction progresses, the cerebral vasculature distal to the obstruction maximally dilates. At this point the cerebral vasculature loses its autoregulatory ability. Cerebral blood flow becomes passive and depends on systemic blood pressure. It thus becomes critically important to maintain the blood pressure of patients with carotid stenosis because they have minimal or no autoregulatory reserve to counter anesthetic-induced reductions in blood pressure.

9 How are the cerebral responses to hypercapnia and hypocapnia altered in cerebrovascular disease? What are the anesthetic implications?

Normal cerebral vessels are highly sensitive to arterial carbon dioxide partial pressure (PaCO2), dilating in response to hypercapnia and constricting in response to hypocapnia. However, in ischemic and already maximally vasodilated areas of the brain, this relationship breaks down, and responses to hypercapnia and hypocapnia may be paradoxical. Because cerebral vessels in an area of ischemia are already maximally dilated, hypercapnia may result in dilation of only normally responsive vessels outside the area of ischemia. This phenomenon, termed steal, may divert blood flow away from the ischemic area, further compromising perfusion. On the other hand, hypocapnia may cause vessels in normal areas to undergo constriction, diverting blood to marginally perfused areas. This phenomenon is termed the Robin Hood or inverse steal effect. Therefore it is generally recommended that normocapnia be maintained in patients undergoing endarterectomy.

10 What is normal cerebral blood flow? At what level is cerebral blood flow considered ischemic?

Normal cerebral blood flow in humans is 40 to 60 ml/100 g/min (15% of cardiac output). The cerebral metabolic rate for oxygen in adults is 3 to 4 ml/100 g/min (20% of whole-body oxygen consumption). The cerebral blood flow at which ischemia becomes apparent on electroencephalogram (EEG), termed the critical regional cerebral blood flow, is 18 to 20 ml/100 g/min.

11 How do inhalational anesthetics affect cerebral perfusion and cerebral metabolic rate?

In the normal brain cerebral blood flow varies directly with the cerebral metabolic rate for oxygen. Inhalational agents are said to uncouple this relationship. They decrease the cerebral metabolic rate for oxygen but concurrently cause dilation of cerebral blood vessels, thus increasing cerebral blood flow.

12 How should patients having carotid endarterectomy be monitored?

In addition to standard monitoring, intra-arterial blood pressure monitoring is indicated to continuously monitor blood pressure. Carotid surgery does not involve large fluid shifts, and monitoring central venous or pulmonary artery pressures is rarely necessary. Since the potential for uncontrolled carotid arterial bleeding always exists, large-bore intravenous access is recommended. Additional intravenous lines dedicated for the use of vasoactive and anesthetic agents is also recommended.

13 Is regional or general anesthesia preferred for the endarterectomy patient?

No controlled, randomized, prospective study exists that demonstrates a long-term benefit of one technique over the other. Ultimately the choice between regional and general anesthesia is based on patient suitability and preference, surgeon and anesthesiologist experience and expertise, and the availability of cerebral perfusion monitoring.

14 What are the advantages of regional anesthesia for carotid endarterectomy?

The main advantage of regional anesthesia is the ability to perform continuous neurologic assessment of the awake, cooperative patient and thus evaluate the adequacy of cerebral perfusion. However, this can become a disadvantage if the patient develops cerebral ischemia. Cerebral ischemia in this setting may lead to disorientation, inadequate ventilation and oxygenation, and a disrupted surgical field. Providing maximal cerebral protection often requires conversion to a general anesthetic, but endotracheal intubation in this setting may prove difficult. Sedation may impair the value of the awake neurologic assessment and must be titrated carefully. There is some evidence that 30-day mortality and postoperative hemorrhage are reduced with regional anesthesia.

15 What are the advantages and disadvantages of general anesthesia for patients undergoing carotid endarterectomy?

Advantages of general anesthesia include control of the airway, a quiet operative field, and the ability to maximize cerebral perfusion if ischemia develops. The main disadvantage of general anesthesia is loss of the continuous neurologic evaluation that is possible in the awake patient.

16 What methods of monitoring cerebral perfusion during general anesthesia are available?

Available techniques include stump pressure monitoring, intraoperative EEG, monitoring of somatosensory-evoked potentials, monitoring of jugular venous or transconjunctival oxygen saturation, transcranial Doppler, and tracer wash-out techniques. Newer methods include transcutaneous cerebral oximetry. None of the methods has been demonstrated to improve outcome, and none has gained widespread acceptance as the monitor of choice.

17 Do stump pressures provide reliable cerebral perfusion information?

No. The stump pressure is the pressure in the portion of the internal carotid artery immediately cephalad to the carotid cross-clamp. This pressure is presumed to represent pressure transmitted from the contralateral carotid and vertebral arteries via the circle of Willis. Stump pressures have no correlation with flow. Some patients with stump pressures less than 50 mm Hg are adequately perfused, whereas some patients with “adequate” stump pressures have suffered ischemic injury.

18 Does intraoperative electroencephalogram provide clinically useful information during carotid endarterectomy?

No data show that EEG during CEA results in improved patient outcomes. Although the EEG is a highly sensitive and an early indicator of global cortical ischemia, it is not highly specific and results in many false-positive (though few false-negative) warnings. Other concerns include the time of ischemia needed before detecting EEG changes. The issue is that, once EEG changes occur, irreversible damage might have already taken place.

19 What are the common postoperative complications of carotid endarterectomy?

image Hypotension: A common complication that is believed to be caused by an intact carotid sinus responding to higher arterial pressures after removal of the atheromatous plaque. Such hypotension responds well to fluid administration and vasopressors.
image Hypertension: Also common but less understood. Obviously the high incidence of preoperative hypertension, particularly when it is poorly controlled, may result in labile postoperative hypertension. It may also be the result of denervation or trauma to the carotid sinus. Given the high association of postoperative hypertension with onset of new neurologic deficit, postoperative hypertension must be monitored and treated with some consideration given to the patient’s baseline blood pressures.
image Cerebral hyperperfusion: After correction of the stenosis, blood flow may increase by as much as 200%. Poorly controlled hypertension contributes to this complication. Symptoms and side effects of hyperperfusion are headache, face and eye pain, cerebral edema, nausea and vomiting, seizure, and intracerebral hemorrhage. The blood pressure of such patients should be very carefully controlled, preferably without the use of cerebral vasodilators.
image Airway obstruction: This could result from hematomas and tissue edema. Treatment involves reestablishing an airway, possibly requiring intubation, opening the incision, and draining the hematoma. Respiratory problems also may result from vocal cord paralysis caused by damage to recurrent laryngeal nerves and from phrenic nerve paresis after cervical plexus block. The chemoreceptor function of the carotid bodies is predictably lost in most patients after CEA, as evidenced by a complete loss of the respiratory response to hypoxia and an average increase in the resting PaCO2 of 6 mm Hg.
image Most strokes associated with CEA occur after surgery as a result of surgical factors involving carotid thrombosis and emboli from the surgical site. Immediate and progressive postoperative strokes are a surgical emergency and require prompt exploration.

20 What are the major causes and presentations of spontaneous subarachnoid hemorrhage?

Intracranial aneurysm rupture is the most common cause of subarachnoid hemorrhage (SAH) (75% to 80%). Risk factors are smoking and systemic hypertension. Rupture depends on the size, with a 6% chance per year if the aneurysm is 25 mm or larger. Arteriovenous malformation (AVM, ≈5%), idiopathic (≈14%), hemorrhagic tumors, and vasculitides are other causes. SAH often presents as a severe frontal or occipital headache, often with associated neurologic deficits, photophobia, stiff neck, and nausea/vomiting. SAH may also manifest as temporary loss of consciousness or even death. Changes in the electrocardiogram (T wave and ST segment changes) and signs of pulmonary edema within 2 days of the bleed are the result of catecholamine release. Establishing the diagnosis and quick intervention decreases the patient’s morbidity and mortality.

21 List the Hunt-Hess classification of neurologic status following spontaneous subarachnoid hemorrhage

image Grade I: Asymptomatic, minimal headache and/or nuchal rigidity
image Grade II: Moderate-to-severe headache/nuchal rigidity; cranial nerve palsy (often cranial nerve III)
image Grade III: Confusion, drowsiness, or mild focal deficit
image Grade IV: Stupor, hemiparesis, early decerebrate rigidity, vegetative disturbances
image Grade V: Moribund, deep coma, decerebrate rigidity

22 Describe the management of intracranial aneurysms following spontaneous subarachnoid hemorrhage

Early surgical intervention (aneurysm clipping) within the first 72 hours of the initial bleed improves neurologic outcome, but early treatment may be technically difficult secondary to cerebral edema and unstable concomitant medical conditions. Surgery is often delayed until the risk of maximal vasospasm has decreased. Initial treatment includes close hemodynamic monitoring and stabilization, stool softeners to prevent straining, bed rest, and analgesia. Anticoagulation, if present, should be reversed. If a patient does not have any neurologic deficits, is alert and appropriate, and has appropriate cerebral perfusion pressure (CPP), antihypertensive therapy may be used; but most hypertensive patients are left untreated so as to maintain CPP.

When blood pressure control is necessary, usually nitroprusside or nitroglycerin is avoided because it increases cerebral blood flow; labetalol is an acceptable alternative. The use of fibrinolytics is controversial and discouraged. Glucocorticoids confer neither a benefit nor a risk. If the patient is stuporous, has decerebrate posturing, or is in a coma, interventional radiologic procedures, ventriculostomy, or burr holes may be indicated. Patients chosen for aneurysmal coiling often have a number of uncontrolled comorbidities. Interventional radiologic procedures have become the treatment of choice for selected patient groups after cerebral aneurysm rupture.

23 Why is early surgical clipping so critical in the management of spontaneous subarachnoid hemorrhage resulting from aneurysm rupture?

Rebleeding and vasospasm are two devastating early complications of SAH. Rebleeding, the principal cause of death in patients after SAH, can be seen years after the initial bleed. Yet 20% of aneurysms rebleed in the first 2 weeks, with the highest risk posed on postbleed day 1. Surgical intervention prevents rebleeding, thus the reason for early clipping. Vasospasm causes delayed cerebral ischemia following SAH. It can present on a neurologic continuum from drowsiness to stroke. The etiology is believed to be subarachnoid blood around the circle of Willis in the basal cisterns. Such blood can be removed at the time of surgical clipping to decrease the incidence of vasospasm. Signs/symptoms of vasospasm are seen in roughly 30% of patients 4 to 14 days following aneurysm rupture.

24 How is vasospasm diagnosed? Who is at risk?

Patients at risk for vasospasm include those with hypertension on admission, age >60, decreased level of consciousness, a large amount of blood in subarachnoid space on CT scan, hydrocephalus, and overall poor health. Intravascular volume depletion, hydrocephalus, sepsis, and electrolyte abnormalities must be considered as alternative causes of acute neurologic deterioration. Vasospasm is most clearly demonstrated by angiography and involves the middle cerebral artery 75% of the time. The pathophysiology of vasospasm is complex and not well understood, but it is thought to be related to products released by the breakdown of erythrocytes in the subarachnoid space. Autoregulation is lost in the vasospastic vessels. Surgery is often delayed if vasospasm is suspected.

25 Describe the treatment options if vasospasm is suspected following an spontaneous subarachnoid hemorrhage

Traditionally vasospasm has been treated with hypertensive, hypervolemic, hemodilution (HHH). Hypervolemia is achieved with colloid administration, with a goal of central venous pressure of 8 to12 mm Hg or pulmonary artery wedge pressure of 18 to 20 mm Hg. The desired level is a hematocrit of 27 to 30, thereby reducing viscosity and improving microcirculation. If the aneurysm is clipped, vasopressors (dopamine, phenylephrine) can be used to induce hypertension, with the goal being a mean arterial pressure approximately 20 to 30 mm Hg greater than baseline systolic pressure. Increased perfusion pressure will attenuate any cerebral ischemia and promote blood flow to transitional areas of injury (known as the penumbra). Calcium channel blockers (CCBs) are usually started empirically following SAH. CCBs have not been found to be consistent in decreasing the incidence of vasospasm (either angiographically or clinically). The CCB nimodipine has been shown to improve outcomes in SAH and should be used with appropriate monitoring. The overall mechanism of action in this setting is unknown, but decreased platelet aggregation, dilation of small arterioles, and reduction of calcium-mediated excitotoxicity are considered possible etiologies. Angioplasty can be performed, and papaverine infused if segmental vasospasm is present on angiogram.

KEY POINTS: Intracranial and Cerebrovascular Disease image

1. Atherosclerosis at the bifurcation of the common carotid artery is the source of most cerebral ischemic events.
2. Cerebral autoregulation usually maintains cerebral blood flow relatively constant over a wide range of arterial pressures. It is critically important to maintain the blood pressure of carotid endarterectomy patients because they have minimal or no autoregulatory reserve to counter anesthetic-induced reductions in blood pressure.
3. Normal cerebral vessels are highly sensitive to PaCO2, dilating in response to hypercapnia and constricting in response to hypocapnia. However, in ischemic and already maximally vasodilated areas of the brain, this relationship breaks down, and responses to hypercapnia and hypocapnia may be paradoxical.
4. In the normal brain cerebral blood flow varies directly with the cerebral metabolic rate. Inhalational agents are said to uncouple this relationship in that they decrease the cerebral metabolic rate while concurrently dilating cerebral blood vessels and increasing cerebral blood flow.
5. No particular anesthetic technique for CEA has been shown to improve outcome.
6. None of the methods of monitoring cerebral blood flow during CEA has been demonstrated to improve outcome, and none has gained widespread acceptance as the monitor of choice.
7. The key to SAH management is early diagnosis and surgical treatment within 72 hours. Vasospasm should be treated with HHH therapy.

26 How can surgical exposure be improved and the brain be protected during aneurysm surgery?

Hypocapnia can be used to relax the brain, but cerebral ischemia to marginally perfused regions is a concern and usually is best avoided. Mannitol is usually given after the dura is opened to facilitate exposure and relax the brain. Lumbar cerebrospinal fluid (CSF) drains can be placed, and CSF can be drained off after the dura has been opened. Glucose must be maintained between 80 and 120 mg/dl to prevent further neurologic insult. Neurosurgeons commonly place temporary occlusion clips on the parent artery that feeds the aneurysm before clipping it. Most studies have shown that this is tolerated for 10 to 14 minutes. The risk of ischemic injury increases up until 31 minutes of temporary clipping, at which time the chance of ischemic insult is nearly 100%. Induced hypertension, mild hypothermia, and burst suppression with high-dose barbiturates should be considered during temporary occlusion to protect against cerebral ischemia. EEG should be used to monitor the effects of occlusion and/or burst suppression. Overall maintaining CPP and minimizing the time of vessel occlusion best protect the brain.

27 What is a cerebral arteriovenous malformation?

AVMs are congenital vascular abnormalities that usually arise during the fetal stage of development as capillary beds are formed. The development of capillary beds is arrested, and direct communications between arteries and veins are formed. As the brain develops, the AVM acquires increased arterial blood flow and becomes a shunt system of high flow and low resistance. AVMs increase in size as they acquire further blood supply.

28 How do arteriovenous malformations typically present?

Most AVMs are symptomatic by the age of 40, usually with the presentation of hemorrhage (nearly 50%), seizure (17% to 50%), or headache (7% to 45%). Less commonly focal neurologic deficits, increased intracranial pressure, and high-output heart failure are the presenting features. Hemorrhage, epilepsy, and neurologic deficits are the traditional indications for surgery, but newer techniques (endovascular and microsurgical/radiation) have allowed for more aggressive surgical intervention in nonruptured aneurysms. Age is also an important factor in the decision to operate.

29 What are the common treatment modalities for arteriovenous malformations?

Conservative treatment is reserved for inoperable AVMs. Inoperable AVMs (e.g., because of size, location) can now be treated with radiosurgery or endovascular embolization. Radiosurgery directs radiation to the AVM to induce fibrosis and obliteration of the communicating vessels. Embolization is often used to decrease the size of an AVM before surgery, decreasing the risks of intraoperative bleeding and postoperative hyperemia. Surgical resection remains the definitive treatment for AVMs, virtually eliminating the risk of hemorrhage following excision.

30 Describe the anesthetic management for surgical excision of an arteriovenous malformation

Most important, acute hypertensive episodes must be avoided. Intra-arterial blood pressure monitoring and large-bore intravenous access are imperative because of the potential for rapid and massive blood loss. Such blood loss can be decreased by preoperative embolization. Some surgeons still advocate high-dose barbiturates, hypocapnia, hypothermia, and deliberate hypotension for cerebral protection.

31 What is normal perfusion pressure breakthrough?

This phenomenon of cerebral edema is also called autoregulation breakthrough. It is commonly seen following AVM resection or embolization. With large AVMs the high-flow, low-resistance shunt can lead to underperfusion of adjacent brain tissue so the vessels supplying the underperfused region of brain lose the ability to autoregulate. Once the shunt is excised, all of the blood flow is diverted to the previously marginally perfused tissues, and the maximally dilated vessels are unable to vasoconstrict. This leads to the potential of cerebral edema, hyperperfusion, and hemorrhage into surrounding areas. The precise mechanism of how and why this occurs is not clear. Neurologic dysfunction following such episodes is a major cause of morbidity and mortality following AVM surgery. Treatment modalities of hyperperfusion include hyperventilation, osmotic diuresis (mannitol), head-up positioning, cautious use of deliberate hypotension, barbiturate coma, and moderate hypothermia.

SUGGESTED READINGS

1. Rabinstein A.A., Wijdicks E.F. Cerebral vasospasm in subarachnoid hemorrhage. Curr Treat Options Neurol. 2005;7:99-107.

2. Roubin G.S., Iyer S. Realizing the potential of carotid artery stenting: proposed paradigms for patient selection and procedural technique. Circulation. 2006;113:2021-2030.

3. Sacco R.L. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke. Stroke. 2006;37:577-617.

4. Suarez J.I., Tarr R.W., Selman W.R. Aneurysmal subarachnoid hemorrhage. N Engl J Med. 2006;354:387-396.

5. van Gijn J., Kerr R.S., Rinkel G.J. Subarachnoid haemorrhage. Lancet. 2007;369:306-318.

Related posts:

58: Congenital Heart Disease 59: Fundamentals of Obstetric Anesthesia 46: Malignant Hyperthermia and Other Motor Diseases 5: Electrolytes 76: Electroconvulsive Therapy 41: Acute Respiratory Distress Syndrome (ARDS)