Sunday, March 21, 2021

Anesthesia for Intracranial Aneurysm Case File

Posted By: Medical Group - 3/21/2021 Post Author : Medical Group Post Date : Sunday, March 21, 2021 Post Time : 3/21/2021
Anesthesia for Intracranial Aneurysm Case File
Lydia Conlay, MD, PhD, MBA, Julia Pollock, MD, Mary Ann Vann, MD, Sheela Pai, MD, Eugene C. Toy, MD

Case 30
A 50-year-old woman presents for an elective ligation/clipping of an aneurysm at the bifurcation of the internal carotid artery. She recently presented to the emergency room with an unrelenting headache and
neck pain. An evaluation of the headache included a CT scan and an MRI, which showed a 3-mm aneurismal dilatation at the bifurcation of the internal carotid artery and the posterior communicating artery at the circle of Willis. There was no evidence of subarachnoid hemorrhage. 

The patient’s past medical history is significant for systemic hypertension well controlled with atenolol. She has no known drug allergies. She has no focal neurologic deficits or cranial nerve involvement.

➤ What is necessary for the preoperative evaluation of this patient?

➤ What are the specific anesthetic goals for the clipping of an intracranial aneurysm?

➤ What is the management of intraoperative aneurysm rupture?

➤ What are the anesthetic implications of cerebral vasospasm?


ANSWERS TO CASE 30:
Anesthesia for Intracranial Aneurysm

Summary: A 50–year-old woman with a symptomatic 3-mm aneurysm of the bifurcation of the internal carotid artery presents for craniotomy and elective clipping of aneurysm.

Preoperative evaluation: In a patient with an aneurysm, the evaluation includes the determination of the Hunt and Hess classification score in addition to the customary anesthesia preoperative examination. A higher score is associated with poorer preexisting neurological function, and a higher surgical risk. In addition, myocardial stress is a common occurrence after a subarachnoid bleed. Patients with preexisting heart disease need cardiac evaluation, if time permits. Remarkable ECG changes, particularly with the ST segments, occur in most patients following an intracranial bleed. These changes are associated with life-threatening arrhythmias, and a poor outcome. Autonomic dysfunction also frequently accompanies a subarachnoid hemorrhage.

Specific anesthetic goals for intracranial aneurismal surgery: Carefully control systemic blood pressure to minimize the risk of intraoperative aneurysm rupture, to control intracranial pressure, and to provide optimal operating conditions.

Management of intraoperative aneurysm rupture: Aneurysmal rupture can be catastrophic. The sudden, massive blood loss hinders the surgeon’s ability to visualize and control the bleeding. While the overall goal is to maintain a normal blood pressure to ensure optimal collateral circulation, the rapid induction of hypotension, even to a pressure of 40 to 50 mm Hg for a short period, improves surgical visualization and can be lifesaving. A brief, manual compression of the ipsilateral carotid artery may also be helpful for this purpose. Blood transfusions may be needed to replace acute surgical blood loss.

Implications of cerebral vasospasm: This is a major complication following aneurysm rupture. It usually occurs 5 to 9 days post hemorrhage. Hypotension should be avoided at this stage, since in the face of vasospasm, hypotension can be associated with reduced cerebral perfusion and a resultant neurologic deficit. Hypervolemia, hemodilution, and nimodipine, a calcium channel blocker, are used to treat cerebral vasospasm and to improve cerebral perfusion.


ANALYSIS

Objectives
1. Understand the elements of the preoperative evaluation for elective craniotomy for clipping of cerebral aneurysm, including the Hess and Hunt classification of cerebral aneurysms.
2. Discuss pharmacology of commonly used antihypertensives used for induced hypotension.
3. Briefly describe the anesthetic goals for clipping of cerebral aneurysm.
4. Know the management of intraoperative aneurysm rupture and of cerebral vasospasm.


Considerations
The preoperative evaluation of this 50-year-old patient should include an examination of the airway, the patient’s mental status, and presence of any focal neurologic deficit. This patient has history of systemic hypertension, so a thorough cardiac evaluation is essential. A stress echocardiogram with radionuclide imaging provides a guide to whether the patient’s myocardial blood supply is adequate to tolerate induced hypotension which is often required for aneurysm clipping. Assessment should include laboratory tests including complete blood count, coagulation profile, chemistry panel, and an electrocardiogram. The patient should be cross-matched for at least two units of packed red cells.

Anesthetic plan and technique: This patient has presented for elective clipping of an intracranial aneurysm which has not yet bled. Her symptoms are headache and nuchal rigidity, with no focal neurological or cranial nerve involvement. She falls under grade 1 in Hess and Hunt scale, and has a good prognosis from surgical clipping.

Preoperative preparation includes placement of two large-bore intravenous cannulae and an arterial line for blood pressure monitoring. The arterial transducer is positioned at the level of her external auditory canal to precisely report the arterial pressure in the head (as opposed to placing the transducers at the height of the heart, to measures pressures at heart level). This patient does not require a central venous line for this procedure.

A vasodilator or vasodilators are prepared and ready for administration prior to induction, and can profoundly affect blood pressure. Nicardipine, sodium nitroprusside (nitroprusside), and nitroglycerin are most commonly used. These drugs should also be prepared for administration as a bolus prior to starting the infusion.

The induction of anesthesia is carefully begun using sodium thiopental or propofol. Intubating doses of a nondepolarizer are used for muscle relaxation. Lidocaine, administered intravenously or locally to the trachea, as well as an opiate and/or esmolol attenuate any sudden elevations in blood pressure from laryngoscopy, intubation, or the application of surgical pins to the skull.

Anesthesia is maintained with a combination of oxygen and air, and an inhalational anesthetic. Muscle paralysis is monitored closely with a twitch monitor to prevent a patient’s coughing or “bucking” while in head pins. A normal PaCO2 is maintained until the dura is opened, to prevent any sudden reductions in intracranial pressure. Vasodilators are administered as necessary to control any elevations in blood pressure that occur.

Mild hypotension, such as a mean arterial pressure around 60 mm of Hg, is usually desirable to shrink the size of the aneurysm and reduce its transluminal pressures. This, in turn, improves surgical visualization and the ease with which the aneurysm can be manipulated. Mild hypotension is accomplished by increasing the level of the anesthetic and using a nicardipine infusion.

During emergence from anesthesia, surges in blood pressure, elevations in intracranial pressure, and coughing must be avoided. Remifentanil, an opiate, and lidocaine may suppress the cough reflex during emergence. A vasodilator infusion and/or esmolol provide strict blood pressure control and avoidance of tachycardia.


APPROACH TO
Anesthesia for Intracranial Aneurysm

DEFINITIONS
MEAN ARTERIAL PRESSURE = Diastolic pressure + 1/3 pulse pressure
PULSE PRESSURE = Systolic pressure − Diastolic pressure
HUNT AND HESS CLASSIFICATION OF ANEURYSM: A grading scale of 1 to 5 which correlates patient symptoms on presentation with outcome (see Table 30–1).
TRANSMURAL ANEURISMAL PRESSURE: The pressure differential between the interior of the aneurismal sac and the intracranial pressure.
TRIPLE THERAPY FOR VASOSPASM: Forced hypertension, hemodilution, and hypervolemia to overcome vasospasm and preserve cerebral perfusion.


CLINICAL APPROACH
The incidence of subarachnoid hemorrhage is approximately 7 per 100,000, accounting for almost 10% of all cerebrovascular accidents. Sixteen percent of patients die within minutes of a subarachnoid hemorrhage. Of the patients who survive to be admitted to the hospital, 25% will die following admission.

Table 30–1 HUNT AND HESS CLASSIFICATION

Grade 1

Asymptomatic or minimal headache with slight nuchal rigidity

Grade 2

Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy

Grade 3

Drowsiness, confusion, or mild focal deficit

Grade 4

Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity, and vegetative disturbances

Grade 5

Deep coma, decerebrate rigidity, moribund appearance


Left untreated, 50% of aneurysms will re-rupture within 6 months. The incidence of aneurismal rupture during the induction of anesthesia is between 0.5% and 6%, and carries a mortality of 75%. Only about 50% of patients recover fully. The anesthetic management of unruptured intracranial aneurysm is presented in Table 30–2

The surgery for an intracranial aneurysm may be scheduled as an elective procedure, or as an emergency, following a subarachnoid hemorrhage. The goals of the anesthetic for intracranial aneurismal surgery are: to carefully control systemic blood pressure to minimize the risk of intraoperative aneurysm rupture, to provide optimal operating conditions, and to control intracranial pressure. The risk of re-bleeding is highest between day 1 and day 4. Thus strict blood pressure control is imperative to prevent a re-bleed, especially during this period.

Before the dura is opened, any reductions in ICP can actually increase the aneurysm’s transmural pressures, thus increasing the risk of rupture. For this reason, the PaCO2 is maintained at a normal level. Once the dura is opened, 

Table 30–2 ANESTHETIC MANAGEMENT FOR AN UNRUPTURED INTRACRANIAL ANEURYSM

• Assignment of Hunt and Hess grading of neurological status.

• Evaluation of comorbidities (emphasis on whether patient can tolerate deliberate hypotension, volume loading).

• Two large-bore i.v. access; central line/PA catheter if necessary.

• Arterial line.

• Strict control of blood pressure, possibly including deliberate hypotension .

• Risk of hypertension is highest during laryngoscopy and intubation, placement of surgical pins, craniotomy and manipulation of dura, and during emergence.

• Patient should be monitored in an intensive care setting in the postoperative period.


mild hyperventilation may be useful to improve operating conditions. Manipulation of the dura is quite painful, and can suddenly increase blood pressure, particularly in the face of light anesthesia. Anticipation of this event can minimize any changes.

The risk of vasospasm is highest between days 5 and 9. The treatment for vasospasm is forced hypertension, hemodilution, and hypervolemia, also known as triple therapy, and used to relieve vasospasm and preserve cerebral perfusion. Infusions of phenylephrine or norepinephrine are typically used to elevate blood pressure. Nimodipine, a calcium channel blocker which causes cerebral vasodilatation, is also be added to this regimen.

After hemorrhage, any blood remaining in the cisterns can contribute to the development of obstructive hydrocephalus. This may require the placement of a temporary ventricular drain or a ventriculo-peritoneal shunt.


Deliberate Hypotension
Deliberate or induced hypotension is useful in minimizing blood loss especially in orthopedic and neurological procedures. In patients with no systemic disease (including hypertension), a MAP of 50 mm of Hg can be tolerated without adverse effects. For the elderly and patients with coexisting systemic disease even in the absence of obvious end-organ damage, it is probably more appropriate to maintain MAP at 60 mm Hg or above. In patients with endorgan involvement such myocardial ischemia, impaired kidney function or those with diabetes, deliberate hypotension is relatively contraindicated. If absolutely required for the aneurysm surgery, it should be utilized cautiously and only for intermittent short periods.

The medications used for deliberate hypotension for intracranial aneurysm surgery, particularly when near the aneurysm, include:

Nicardipine, a calcium channel blocker which can be used as an infusion or as a bolus. Nicardipine dilates arteries and veins, and is not typically associated with as potent reflex tachycardia than some of the other infusions.

Nitroglycerine, a potent venodilator, reduces blood pressure by reducing venous return. It has a rapid onset and rapid offset. But as with any venodilator, nitroglycerine increases intracranial pressure. It also causes reflex tachycardia which can be treated with beta blockers. Nitroglycerine causes cerebral venodilation and increases in ICP. It is best used after the dura is opened and should be avoided in patients with poor intracranial compliance.

Sodium nitroprusside is an arterial and venodilator, which also increases intracranial pressure. Nitroprusside breaks down and releases nitric oxide which activates guanylate cyclase. This increases the concentration of cyclic guanosine monophosphate which causes smooth muscle relaxation. It has a rapid onset and rapid offset. It reduces blood pressure by reducing afterload. A major side effect is cyanide toxicity. The treatment of cyanide toxicity includes cessation of the SNP infusion and specific antidotes such as inhalation of amyl nitrate, sodium nitrate 5 mg/kg i.v., or sodium thiosulfate 150 mg/kg.

If nitroprusside is chosen as the vasodilator, it’s worth noting that the sudden cessation of nitroprusside infusion can cause rebound hypertension, so nitroprusside needs to be weaned off gradually. Nitroprusside has five cyanide molecules and cyanide toxicity can occur if doses exceed > 7 mg/min. The signs of toxicity include increasing tolerance and metabolic acidosis.

Hydralazine, a direct acting vasodilator, acts independently of the adrenergic or cholinergic receptors. The peak effect is in 15 to 20 minutes and the halflife is up to 4 hours. Hydralazine causes reflex tachycardia.

Labetalol, a mixed alpha- and beta-receptor antagonist. The ratio of beta to alpha receptor blockade is 3:1 with oral administration and 7:1 with intravenous administration. Labetalol decreases the peripheral vascular resistance and reduces mean arterial pressure. It does not cause reflex tachycardia and has no effect on intracranial pressure.

Esmolol, a selective beta-1-adrenergic-receptor antagonist. Esmolol is rapidly metabolized by red cell esterases. It has a rapid onset, peak effect in 5 minutes, and a short duration of action. The half-life is 9 minutes. It is invaluable in the perioperative period due to its rapid onset and offset. It can be used even in patients with reactive airway disease.

The complications of deliberate hypotension include: myocardial ischemia, cerebral ischemia, oliguria and/or renal failure, metabolic acidosis, rebound hypertension, visual impairment (especially in the prone position and in diabetics). Deliberate hypotension is contraindicated in patients with preexisting coronary/cerebral or renal vascular insufficiencies, hypovolemia, and anemia.


Comprehension Questions

30.1. Which of the following symptoms is most closely associated with an intracranial aneurysm?
A. Headache and neck stiffness
B. Severe episodes of headache that are intermittent
C. Headache associated with photophobia
D. Headache that improves on lying down

30.2. Which of the following statements regarding “deliberate hypotension” is accurate?
A. Deliberate hypotension is a safe, effective way to reduce blood pressure in patients undergoing aneurysm surgery.
B. Deliberate hypotension can cause acute renal failure.
C. Deliberate hypotension has not been associated with visual disturbances.
D. Deliberate hypotension is a treatment for cerebral vasospasm.

30.3. Treatment of cerebral vasospasm includes which of the following?
A. Maintaining an hematocrit of 45%
B. Calcium channel blocker
C. Diuretics
D. An infusion of a local anesthetic such as lidocaine


ANSWERS
30.1. A. Symptoms of an intracranial aneurysm include a severe headache, neck stiffness, and changing neurological signs including hemiparesis. Headache from an aneurysm is usually relentless and constant. It is accompanied by nuchal rigidity, cranial nerve involvement, and sometimes even coma. Answer C, a headache accompanied by photophobia, is more characteristic of migraines. Answer D, a postural headache, is typical of post dural puncture headaches.

30.2. B. Deliberate hypotension can cause acute renal failure. It can also cause myocardial ischemia, renal failure, and visual disturbances including blindness and even stroke. The treatment of cerebral vasospasm is induced hypertension.

30.3. B. Nimodipine is a calcium channel blocker which has been used to treat cerebral vasospasm. Hemodilution aims for an hematocrit of 30% not 45%, and hypovolemia and intentional hypertension are part of the triple therapy used to treat vasospasm.


Clinical Pearls
➤ Blood pressure control is crucial in preventing rupture and re-bleed of cerebral aneurysms.
➤ A sudden reduction in intracranial pressure prior to the opening of the dura can increase the transluminal pressure of the aneurysm, and precipitate rupture.
➤ The intraoperative rupture of an aneurysm is a catastrophic event, which can occur at the induction of anesthesia. Acute management includes induced hypotension to enable surgical visualization.
➤ In a patient with vasospasm, even relative hypotension can be associated with neurological changes.
➤ Subarachnoid hemorrhage is associated with ECG changes and life-threatening arrhythmias.

References

Cucchiara RF, et al. Anesthesia for intracranial procedures. In: Barash PG, ed. Clinical Anesthesia. 4th ed. Philadelphia, PA: Lippincott; 1989]. 

Hoff RG. Hypotension in anesthetized patients during aneurysm clipping: Not as bad as expected. Acta Anaesthesiologica Scandinavica. 2008;52(7):1006-1011. E pub 2008 May 20. 

Newfield, Phillippa, Cottrell, James E. Handbook of Neuroanesthesia. 4th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2007:143-172. 

Priebe HJ. Aneurismal subarachnoid hemorrhage and the anaesthetist. Br J Anesthesiol. 2007;99(1):102-118. E pub 2007 May 23. Review.

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