Cerebral Aneurysm
Patricia Fogarty Mack
A 43-year-old woman presented to the emergency room 2 days ago, complaining of severe headache, nausea, and vomiting, followed by a witnessed 3-minute loss of consciousness. On regaining consciousness, the patient was noted by her family to be confused. A computed tomography (CT) scan showed subarachnoid bleeding. You are called to the angiography suite because four-vessel angiography has revealed an 18-mm basilar tip aneurysm and a 10-mm right middle cerebral artery aneurysm. The interventional neuroradiologist wishes to coil the basilar tip aneurysm but believes the middle cerebral artery aneurysm will require a craniotomy and clipping. At present, she was oriented only to person. She had no previous medical history; however, she had smoked one pack of cigarettes per day for the last 20 years. Her blood pressure was 130/80 mm Hg, pulse 90 beats per minute, and respiration 18 breaths per minute. She had no focal neurologic deficits. Laboratory examination revealed normal electrolytes and complete blood count but elevated CPK-MB and troponin. Electrocardiogram demonstrated normal sinus rhythm with flipped T waves throughout the precordium.
A. Medical Disease and Differential Diagnosis
What are the incidence, prevalence, and causes of subarachnoid hemorrhage (SAH) and what are the risk factors associated with rupture of intracranial aneurysms?
What are common sizes and locations of intracranial aneurysms?
What is the pathophysiology of aneurysmal rupture and SAH?
What are symptoms and signs of SAH?
How does one assess the severity of SAH?
What are the cardiovascular effects of SAH?
How is the diagnosis of SAH made?
What is the risk for rebleeding for a patient with SAH?
B. Preoperative Evaluation and Preparation
What are some concerns in going to the interventional neuroradiology suite in the midst of an angiogram to follow immediately with coiling of an aneurysm?
What type of anesthesia is required for coiling of an aneurysm?
Should one proceed with induction of general anesthesia under these circumstances?
What types of emergencies can occur during coiling of an aneurysm and how should they be managed?
A craniotomy is planned for the following day to clip the middle cerebral artery aneurysm. Should surgery be postponed because of the patient’s elevated troponin and creatine phosphokinase (CPK) myocardial-bound (MB) fractions?
Would you premedicate this patient before craniotomy?
C. Intraoperative Management
What are the goals of the induction and maintenance of anesthesia for this patient?
Is placement of an arterial line necessary for induction of anesthesia in this patient in the interventional neuroradiology suite?
How would you assess fluid status in this patient?
Would monitoring central venous pressure (CVP) be useful in this patient for craniotomy for clipping?
What other forms of monitoring would you consider?
What are your particular concerns during induction of anesthesia in this patient?
How would you accomplish a smooth and safe induction and intubation in this patient?
Would you perform a rapid sequence induction and intubation on this patient?
What are the effects of hypoxemia and hypercapnia, such as would be seen with loss of the airway on induction, on cerebral blood flow (CBF)?
What is optimal fluid management for aneurysm clipping? Would you use a dextrose-containing solution?
After the bone plate was removed and as the dura was being opened, the surgeon complained that the brain was “tight.” What could you do to achieve better brain relaxation and facilitate surgical exposure?
How might transmural pressure be decreased to allow for aneurysm clip placement?
What is the purpose of controlled hypotension and how is it achieved?
What are some of the drawbacks of controlled hypotension?
What methods of cerebral protection might you use during this operation?
Would you induce mild hypothermia as a means of cerebral protection?
What are the indications for deep hypothermic circulatory arrest?
What steps should be taken in the case of intraoperative rupture of an intracranial aneurysm?
How would you plan the emergence from an anesthetic for aneurysm clipping?
D. Postoperative Management
Would you extubate the patient postoperatively?
What would be the differential diagnosis if the patient did not return to her preoperative neurologic condition?
On postoperative day 2, the patient became disoriented and developed hemiplegia. A CT scan was obtained, which shows no new intracranial bleeding. What other diagnostic studies should be performed?
What is cerebral vasospasm and what causes it?
What are pathophysiologic changes seen in cerebral vasospasm?
How is the diagnosis of cerebral vasospasm made?
What steps can be taken to prevent cerebral vasospasm?
What treatments can be undertaken once a diagnosis of cerebral vasospasm is made?
What are other neurologic complications following SAH and aneurysm clipping?
What other organ systems may manifest problems postoperatively in aneurysm clipping patients?
A. Medical Disease and Differential Diagnosis
A.1. What are the incidence, prevalence, and causes of subarachnoid hemorrhage (SAH) and what are the risk factors associated with rupture of intracranial aneurysms?
The prevalence of SAH is 2% to 5% with an incidence of 10 to 15 per 100,000 people. Each year, 25,000 cases of SAH occur in the United States, comprising 5% to 10% of all cases of
stroke. In China and South America, the incidence is only 2 to 4 cases per 100,000 people, whereas higher rates of 19 to 23 per 100,000 are reported in Finland and Japan. Sixty percent of the cases occur in young individuals between the ages of 40 and 60 years. Therefore, a poor neurologic outcome is a devastating condition to be endured over a potentially long period.
stroke. In China and South America, the incidence is only 2 to 4 cases per 100,000 people, whereas higher rates of 19 to 23 per 100,000 are reported in Finland and Japan. Sixty percent of the cases occur in young individuals between the ages of 40 and 60 years. Therefore, a poor neurologic outcome is a devastating condition to be endured over a potentially long period.
Approximately one-third of patients die as a result of the acute bleed. Of the two-thirds who survive the acute bleed, one-half (one-third of total) later die or are severely disabled and half (one-third of total) have an acceptable outcome.
Cerebral aneurysms account for 75% to 80% of SAH; arteriovenous malformations are the cause in 4% to 5%, whereas no specific cause can be found in 15% to 20% of SAH. Other causes of SAH include trauma, mycotic aneurysm, sickle cell disease, cocaine use, and coagulation disorders.
The four strongest independent predictors of aneurysmal SAH are smoking (OR 6.0; 95% CI 4.1 to 8.6), family history of aneurysmal SAH (4.0; 95% CI 2.3 to 7.0), hypertension (2.4; 95% CI 1.5 to 3.8), and hypercholesterolemia (0.2; 95% CI 0.1 to 0.4) according to a recent case control study. Other risk factors include pregnancy and vascular abnormalities (e.g., type III collagen deficiency and elastase abnormalities). One-third of patients with polycystic kidney disease have been found to have intracranial aneurysms at autopsy. Genetic predisposition plays a role: Seven percent of berry aneurysms are familial, and 5% to 10% of patients with a ruptured aneurysm have a first-order relative with a ruptured aneurysm. The rupture rate for aneurysm has been estimated at 0.14% per year for a 5-mm lesion to 1.1% per year for a 10-mm lesion.
Smoking and alcohol abuse also appear to predispose to aneurysm formation and rupture. Smoking at any time and female gender are related to the presence of multiple intracranial aneurysms as well as accelerated aneurysm growth. Cocaine abuse and resultant episodic hypertension may predispose to aneurysmal rupture at an early age.
Death and disability are primarily due to the initial bleed, vasospasm, and rebleeding. Other causes include surgical complications, parenchymal hemorrhage, hydrocephalus, and complications of medical therapy.
Chang HS. Simulation of the natural history of cerebral aneurysms based on data from the International Study of Unruptured Intracranial Aneurysms. J Neurosurg. 2006;104:188-194.
Cottrell JE, Young WL, eds. Cottrell and Young’s Neuroanesthesia. 5th ed. Philadelphia, PA: Mosby Elsevier; 2010:218-246.
de Rooij NK, Linn FH, van der Plas JA, et al. Incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends. J Neurol Neurosurg Psychiatry. 2007;78(12):1365-1372.
Vlak MH, Rinkel GJ, Greebe P, et al. Lifetime risks for aneurysmal subarachnoid haemorrhage: multivariable risk stratification. J Neurol Neurosurg Psychiatry. 2013;84(6):619-623.
Yoshimoto Y. A mathematical model of the natural history of intracranial aneurysm: quantification of the benefit of prophylactic treatment. J Neurosurg. 2006;104:195-200.
A.2. What are common sizes and locations of intracranial aneurysms?
Small (less than 12 mm) aneurysms make up 78% of the total, whereas large (12 to 24 mm) are 20%, and giant (greater than 24 mm) comprise 2%. Most aneurysms are located in the anterior circulation, with the junction of the anterior communicating and anterior cerebral arteries being the most common (39%). Thirty percent of aneurysms occur in the internal carotid artery, 22% in the middle cerebral artery, and 8% in the posterior circulation (posterior cerebral, basilar, and vertebral arteries).
Kasell NF, Torner JC, Haley C, et al. The international cooperative study on the timing of aneurysm surgery. Part 1: overall management results. J Neurosurg. 1990;73:18-32.
A.3. What is the pathophysiology of aneurysmal rupture and SAH?
On the basis of experimental models, aneurysmal rupture leads to the leakage of arterial blood and a rapid increase in intracranial pressure (ICP), approaching diastolic blood pressure in the proximal intracerebral arteries. This increase in ICP causes a decrease in cerebral perfusion pressure (CPP) and a fall in CBF, leading to a loss of consciousness. The decrease in CBF diminishes bleeding and stops the SAH. A gradual reduction in ICP and an
increase in CBF indicates improved cerebral function and possibly a return to consciousness. A persistent increase in ICP (perhaps resulting from thrombi in the cranial cisterns), however, indicates a persistent no-flow pattern with acute vasospasm, cell swelling, and death.
increase in CBF indicates improved cerebral function and possibly a return to consciousness. A persistent increase in ICP (perhaps resulting from thrombi in the cranial cisterns), however, indicates a persistent no-flow pattern with acute vasospasm, cell swelling, and death.
A.4. What are symptoms and signs of SAH?
Headache occurs in 85% to 95% of patients. Often, a brief loss of consciousness occurs, followed by diminished mentation; consciousness may be impaired to any degree or may be unaffected at the time of presentation. Symptoms secondary to subarachnoid blood may be similar to those of infectious meningitis (nausea, vomiting, and photophobia). The patient may also experience motor and sensory deficits, visual field disturbances, and cranial nerve palsies. Finally, blood in the subarachnoid space may cause an elevated temperature.
Cottrell JE, Young WL, eds. Cottrell and Young’s Neuroanesthesia. 5th ed. Philadelphia, PA: Mosby Elsevier; 2010:218-246.
A.5. How does one assess the severity of SAH?
Two grading scales are commonly used to assess neurologic status following SAH, the Hunt and Hess grade (Table 21.1) and the World Federation of Neurologic Surgeons’ grade (Table 21.2), based on the Glasgow Coma Scale. The scales are useful in identifying a baseline neurologic status from which any acute changes should be assessed. In addition, the scales may correlate with physiologic status. Patients who are Hunt and Hess grades I and II have near-normal cerebral autoregulation and ICP.
Drake CG. Report of World Federation of Neurological Surgeons committee on a universal subarachnoid hemorrhage grading scale. J Neurosurg. 1988;68:985-986.
Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg. 1968;28:14-20.
A.6. What are the cardiovascular effects of SAH?
Injury to the posterior hypothalamus from SAH causes the release of norepinephrine from the adrenal medulla and cardiac sympathetic efferents. Norepinephrine can cause an increase in afterload and direct myocardial toxicity, leading to subendocardial ischemia. Pathologic analysis of the myocardium of patients who have died of acute SAH has revealed microscopic subendocardial hemorrhage and myocytolysis.
Electrocardiographic abnormalities are present in 50% to 80% of patients with SAH. Most commonly, these involve ST-segment changes and T-wave inversions but also include prolonged QT interval, U waves, and P-wave changes. ST-T wave changes are usually scattered and not related to a particular distribution.
TABLE 21.1 Modified Hunt and Hess Clinical Grades | ||||||||||||||||||
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TABLE 21.2 World Federation of Neurological Surgeons (WFNS) Grading Scale | |||||||||||||||||||||
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Dysrhythmias occur in 80% of patients, usually in the first 48 hours. Premature ventricular contractions are the most common abnormality, but any type of dysrhythmia is possible. They include severely prolonged QT interval, torsades de pointes, and ventricular fibrillation. In one series, 66% of the arrhythmias were considered mild, 29% moderate, and 5% severe. In addition to increased catecholamine secretion, hypercortisolism and hypokalemia have been suggested as causes for the dysrhythmias seen with SAH.
Ventricular dysfunction, possibly leading to pulmonary edema, is present in approximately 30% of patients with SAH.
Cardiac troponin I predicts myocardial dysfunction in SAH with a sensitivity of 100% and a specificity of 91%. This compares with a sensitivity and specificity of 60% and 94% for CPK-MB in predicting myocardial dysfunction. In order to plan optional anesthetic management, it is important to determine if any cardiac dysfunction is due to a myocardial infarction or reversible neurogenic left ventricular dysfunction. A retrospective study from Duke determined that reversible neurogenic cardiac dysfunction was associated with a troponin level of 0.22 to 0.25 ng per mL and an ejection fraction of less than 40% by echocardiogram.
Bulsara KR, McGirt MJ, Liao L, et al. Use of peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage. J Neurosurg. 2003;98:524-528.
Cottrell JE, Young WL, eds. Cottrell and Young’s Neuroanesthesia. 5th ed. Philadelphia, PA: Mosby Elsevier; 2010:218-246.
A.7. How is the diagnosis of SAH made?
Noncontrast CT scan can determine the magnitude and location of the bleed. It may also be useful in assessing ventricular size and aneurysm location. High-resolution CT (CT angiogram) with contrast can more precisely determine the location of the aneurysm.
Lumbar puncture can be used to diagnose SAH if CT is negative, especially when the patient presents more than 1 week after an initial bleed. Xanthochromia, a yellow discoloration of the cerebrospinal fluid (CSF) after centrifugation, is present from 4 hours to 3 weeks after SAH. A lumbar puncture can cause herniation or rebleeding. Therefore, a CT scan should be performed first if the patient presents within 72 hours of suspected SAH.
Four-vessel angiography (right and left carotid and vertebral arteries) has been considered the gold standard in the diagnosis of a intracranial aneurysm; however, CT angiography has been used with increasing frequency. The goal is to visualize all of the intracranial vessels, to localize the source of bleeding, and to rule out multiple aneurysms (5% to 33% of patients). Three-dimensional reconstructive angiograms and magnetic resonance angiography also may be used.
Guy J, McGrath BJ, Borel CO, et al. Perioperative management of aneurysmal subarachnoid hemorrhage: part 1. Operative management. Anesth Analg. 1995;81:1060-1072.
Zhang LJ, Wu SY, Niu JB, et al. Dual energy CT angiography in the evaluation of intracranial aneurysms: image quality, radiation dose, and comparison with 3D rotational digital subtraction angiography. AJR Am J Roentgenol. 2010;194:23-30.
A.8. What is the risk for rebleeding for a patient with SAH?
The risk of rebleeding from a ruptured aneurysm is highest, 4%, in the first 24 hours after the initial bleed and 1.5% per day thereafter. The cumulative risk is 19% in 14 days and 50% at 6 months. After 6 months, the rebleeding risk is 3% per year.
Kassell NF, Torner JC. Aneurysmal rebleeding: a preliminary report from the Cooperative Aneurysm Study. Neurosurgery. 1983;13:479-481.
B. Preoperative Evaluation and Preparation
B.1. What are some concerns in going to the interventional neuroradiology suite in the midst of an angiogram to follow immediately with coiling of an aneurysm?
Whenever an anesthesiologist assumes care of a patient when the patient is already sedated, it may be more difficult to obtain an accurate medical history. In addition, the physical examination will be limited by the patient’s position for the diagnostic study. Finally, the patient’s capacity to consent may also be impaired by previous sedation.
B.2. What type of anesthesia is required for coiling of an aneurysm?
In most institutions, general anesthesia is required for coiling of an intracranial aneurysm. First, intraoperative neurologic testing is generally not required. Second, akinesis is very important not only when the coils are actually deployed but also while the interventionist is navigating the intracranial vessels to reach the aneurysm.
B.3. Should one proceed with induction of general anesthesia under these circumstances?
Obliteration of the aneurysm with coils has become the standard of care for basilar tip aneurysm, and it would be best for the patient to have this done in the same setting as the angiography, provided there were no contraindications to induction of general anesthesia (e.g., hemodynamic instability).
Cottrell JE, Young WL, eds. Cottrell and Young’s Neuroanesthesia. 5th ed. St. Louis, MO: Mosby; 2010:218-246.
Lee CZ, Young WL. Anesthetic considerations for interventional neuroradiology. In: ASA Refresher Courses in Anesthesiology. 2005;33:145-154.
B.4. What types of emergencies can occur during coiling of an aneurysm and how should they be managed?
Basically, intraoperative emergencies can be divided into two categories—hemorrhage and thrombosis. Appropriate management requires constant communication between the radiologist, surgeon, and anesthesiologist. If an intracranial hemorrhage occurs, the interventionalist may try to “glue” the hole in the aneurysm or embolize the parent vessel. If this is not possible, heparin should be rapidly reversed with protamine, and a ventriculostomy will generally be placed by the surgical team. Management of arterial carbon dioxide partial pressure (PaCO2) can then be guided by the ICP. In the case of catheter-induced thrombosis, induced hypertension is usually desirable while tissue plasminogen activator or glycoprotein IIb/IIIa therapy is considered.
If a coil is malpositioned, anticoagulation would be continued while the interventional radiologist attempts to snare the coil. As with a thrombosis, it may be desirable to augment the blood pressure.
B.5. A craniotomy is planned for the following day to clip the middle cerebral artery aneurysm. Should surgery be postponed because of the patient’s elevated troponin and creatine phosphokinase (CPK) myocardial-bound (MB) fractions?
Fifty percent of patients will have an increase in CPK-MB fraction; however, CPK-MB per total CPK fraction is usually not consistent with a transmural myocardial infarction. As discussed previously, troponin I levels are more sensitive. In addition, although some patients (0.7%) do sustain a myocardial infarction in the setting of SAH, little correlation is found between electrocardiographic abnormalities and ischemia in this population.
An echocardiogram may be useful in determining the severity of reversible neurogenic left ventricular dysfunction. If left ventricular function is found to be depressed, a pulmonary artery catheter or intraoperative transesophageal echocardiography may be helpful for intraoperative management.
The desire to delay surgery because of cardiac abnormalities must be weighed against the risk of rebleeding and vasospasm. In most cases, the risk of recurrent hemorrhage outweighs the risk of perioperative myocardial infarction. Furthermore, even if coronary artery disease is present, these patients are not candidates for angioplasty or myocardial revascularization, which requires heparinization. If pulmonary edema or malignant dysrhythmias are present, it may be prudent to postpone surgery until such problems are controlled medically. However, if these problems are not present, then clipping of the aneurysm may be indicated. Bulsara et al. found that 2.9% of patients had severe cardiac dysfunction. In this study, neurogenic left ventricular dysfunction resolved over 4 to 5 days.
Bulsara KR, McGirt MJ, Liao L, et al. Use of peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage. J Neurosurg. 2003;98:524-528.
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