Anaesthesia For Aneurysm Flashcards
(47 cards)
1
Q
What is the blood supply to the brain?
A
2
Q
Label the diagram
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3
Q
What is the common location of aneurysms of the circle of Willis?
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4
Q
What is the clinical presentation of aneurysm?
A
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.
5
Q
How are aneurysms graded?
A
Hunt and Hess grade
•World Federation of Neurologic Surgeons’ grade
6
Q
What are the parameters of hunt and hess grading
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0: Unruptured aneurysm
I: Asymptomatic or minimal headache and slight nuchal rigidity
ii Moderate to severe headache, nuchal rigidity, but no neurologic deficit other than cranial nerve palsy
iii Drowsiness, confusion, or mild focal deficit
IV Stupor, mild to severe hemiparesis, possible early decerebrate rigidity, vegetative disturbance
V Deep coma, decerebrate rigidity, moribund appearance
7
Q
What is the WFNS grading?
A
8
Q
What is the pathophysiology of aneurysmal rupture and SAH?
A
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 the SAH. A gradual reduction in ICP and an increase in CBF indicate improved cerebral function and possibly a return to consciousness. A persistent increase in ICP (perhaps resulting from thrombi in the cranial cisterns), however, results in a persistent no-flow pattern with acute vasospasm, cell swelling, and death.
9
Q
What are the cardiovascular effects of SAH?
A
- 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 STsegment 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.
- 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 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 found that reversible neurogenic cardiac dysfunction was associated with a troponin level of 0.22 to 0.25ng per mL and an ejection fraction of less than 40% by echocardiography.
10
Q
How is the diagnosis of SAH made?
A
- 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 and currently is used to determine whether an aneurysm is amenable to coiling or requires surgical clip placement. 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 to further delineate the intracranial vasculature.
11
Q
What are some concerns in going to the interventional neuroradiology suite in the midst of an angiogram to be followed immediately with coiling of an aneurysm?
A
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.
12
Q
What type of anesthesia is required for coiling of an aneurysm?
A
Although there is a case series of aneurysm coiling undermonitored anesthesia care with dexmedetomidine infusion without loading dose, in most institutions, general anesthesia is required for coiling of an intracranial aneurysm. First, intraoperative neurologic testing is generally not required. Second, immobility is very important not only when the coils or stent are actually deployed but also while the interventionist is navigating the intracranial vessels to reach the aneurysm.
13
Q
What is the risk for rebleeding for a patient with SAH?
A
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.
14
Q
What types of emergencies can occur during coiling of an aneurysm, and how should they be managed?
A
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 bythe ICP.
- As the technology of endovascular therapy has advanced to include balloon- or stent-assisted coiling, treatment of more complex aneurysms has increased.
- The rate of intraprocedural rupture (IPR) has increased as well. The rate of IPR may be as high as 7.5% in ruptured aneurysms and 2.5% in unruptured aneurysms. IPR may lead to significant clinical deterioration in previously unruptured aneurysms but does not appear to have a severe an impact in patients undergoing endovascular treatment for SAH.
- In the case of catheter-induced thrombosis, induced hypertension is usually desirable while tissue plasminogen activator or antiglycoprotein IIb/IIIa therapy is considered. If a coil was malpositioned, anticoagulation would be continued while the interventional radiologist attempts to snare the coil. As with thrombosis, it may be desirable to augment the blood pressure.
15
Q
What other modalities of endovascular therapy are available?
A
Flow diverting devices (stents) have been utilized as an endovascular treatment for wide necked and fusiform aneurysms, which are otherwise not amenable to coiling. When these procedures are planned, the patient is prepared with acetylsalicylic acid (ASA) and clopidogrel to prevent stent
16
Q
Should surgery be postponed because of the patient’s elevated troponin and CPK-MB fractions?
A
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. 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, noninvasive cardiac output monitor, 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. In a study by Bulsara et al., 2.9% of patients had severe cardiac dysfunction, and neurogenic left ventricular dysfunction resolved over 4 to 5 days.
17
Q
Would you premedicate this patient before craniotomy?
A
No. When the patient is in a Hunt and Hess grade III to V state, anxiety is unlikely. Furthermore, heavy sedation may decreaseventilation, raising PaCO2 and increasing CBF and ICP, which, at the very least, may hinder preoperative and postoperative neurologic evaluation. If patients are Hunt and Hess grade I to II and it appears that preoperative anxiety might lead to hemodynamic instability, a small dose of a benzodiazepine may be appropriate. Medications such as calcium channel blockers (nicardipine), anticonvulsants, and corticosteroids should be continued preoperatively on the day of surgery. If the patient is at risk for aspiration, medications to decrease gastric acidity and volume are appropriate. Most patients will already be receiving a histamine-2 blocker or proton pump inhibitor if they are receiving a glucocorticoid.
18
Q
What are the goals of the induction and maintenance of anesthesia for this patient?
A
- The primary goal is to prevent aneurysm rupture, either on induction or intraoperatively, while maintaining adequate CPP.
- The goal of matching anesthetic depth to surgical stimulation is more important than the specific drugs used.
- In general, the anesthesiologist should provide for rapid and reversible titration of blood pressure, maintain CPP, and protect against cerebral ischemia.
- An additional goal is to provide a relaxed brain for ease of surgical exposure with minimal brain retraction.
- Finally, the anesthetic should be planned to achieve a rapid, smooth emergence, allowing prompt neurologic assessment. This can be accomplished with a combination of balanced anesthesia, muscle relaxation, and sympathetic blockers as well as with totalintravenous anesthesia.
19
Q
Is placement of an arterial catheter necessary for induction of anesthesia in this patient in the interventional neuroradiology suite?
A
In this case, because a femoral sheath is in place at the time that anesthesia is induced, one may transduce femoral arterial pressure during induction. However, because the patient has two aneurysms and because the sheath will be removed at the end of the procedure, an additional arterial catheter should be placed before the removal of the sheath. When a large coaxial catheter is placed through the femoral sheath, systolic pressure is underestimated, but mean pressure should be accurate. Studies have suggested that the placement of an arterial catheter prior to induction is not essential when an unruptured aneurysm is to be coiled.
20
Q
How would you assess fluid status in this patient?
A
Several issues in interventional radiology complicate fluid management. First, contrast material acts as an osmotic diuretic. Often, these patients have had a CT scan with contrast in addition to an angiogram and may become intravascularly depleted. Second, the femoral sheath and other catheters are constantly flushed with a heparinized saline solution. It is not uncommon for a patient to receive 1,000 mL or more of flushfluid during the case. This must be taken into account when calculating fluid balance.
21
Q
Would monitoring central venous pressure (CVP) be useful for craniotomy and aneurysm clipping in this patient?
A
Many have suggested that CVP monitoring is essential in assessing volume replacement needs because urine output will be affected by osmotic or loop diuretics administered to facilitate surgical exposure.
- In addition, should vasoactive medication become necessary, it may be most effectively administered through a central venous catheter.
- One disadvantage of CVP monitoring in the neurosurgical patient is catheter placement. Some clinicians are concerned that placement of an internal jugular venous CVP will compromise venous outflow of the head, thereby predisposing to bleeding or brain swelling, although this remains controversial. A “longarm” or peripheral antecubital CVP catheter may be more difficult to insert and have a higher incidence of thrombophlebitis. Multiple studies have shown the complication rate of central catheter placement to be as high as 14%. When including failure to place the catheter, the complication rate rises to 54%. Nevertheless, use of an ultrasound-guided approach to placement of central venous catheters reduces the complication rates to less than 2% to 5% and should be the standard of care whenever possible.
- Finally, a poor correlation between CVP and left ventricular end-diastolic pressure has been documented in SAH, so a pulmonary artery catheter may be more useful in assessing volume status as well as providing a monitor of cardiac output in those patients who have had preoperative cardiac problems.
- Patients who are expected to be candidates for hypertensive hypervolemic hemodilution (HHH) therapy for vasospasm or fordrug-induced coma may also benefit from placement of a pulmonary artery catheter.
- Central pressure monitoring is usually instituted after the patient is anesthetized to minimize patient stress.
- One should be careful to use the minimal degree of head-down tilt necessary to access the central circulation because the Trendelenburg position can increase ICP and thereby decrease CPP.
• Based on the risk and benefits of central venous and pulmonary artery access, placement of CVP and pulmonary artery catheters is reserved for patients who have documented cardiac dysfunction, cerebral vasospasm or poor peripheral intravenous access. Volume status may be assessed by noninvasive monitors that calculate stroke volume or by careful assessment of the arterial waveform utilizing calculated pulse pressure variation available on many monitoring systems.
22
Q
What other forms of monitoring would you consider?
A
Electroencephalography (EEG) and somatosensory evoked potentials (SSEPs) have been advocated by some, although they are not standard monitoring in most hospitals.
- Although EEG has been used to monitor cerebral ischemia, scalp electrodes may not reflect activity of brain areas most at risk. Cortical electrodes, such as those used in epilepsy surgery, may avoid the problem of attenuation of the scalp electroencephalographic signal by CSF drainage and air between scalp electrodes and brain surface during surgery. EEG is useful in a titrating intravenous anesthetic infusion if burst suppression is desiredduring temporary clipping.
- SSEPs may detect reversible ischemia during temporary vessel occlusion, but they may not detect ischemia in subcortical structures and motor cortex. Furthermore, SSEPs have relatively high false-positive (38% to 60%) and false-negative (5% to 34%) rates.
- Brainstem auditory evoked responses may be useful for monitoring during posterior circulation aneurysm clipping.
- Motor evoked potentials may be superior in detecting subcortical ischemia. The use of SSEP and motor evoked potential monitoring usually warrants use of total intravenous anesthesia and avoidance of muscle relaxants.
- Microvascular Doppler ultrasound evaluation may detect inadvertent vessel occlusion, but it cannot assess the adequacy of collateral perfusion.
- Monitoring of ICP is common, with the probability of increased ICP being greatest 24 to 48 hours after SAH. An intraventricular catheter not only allows for ICP monitoring but also allows for CSF drainage to improve operating conditions. If an intraventricular catheter is not present, lumbar spinal drain may be placed. One must be careful not to allow substantial CSF drainage before dural opening because this may decrease ICP leading to an increase in transmural pressure and possible rupture.
- Intraoperative angiography is one means to assess complete obliteration of the aneurysm without clip occlusion of the parent artery or perforating branches. Its use has increased with the installation of hybrid operating rooms that are fully equipped with advanced angiography equipment.
23
Q
What are your specific concerns during induction of anesthesia in this patient?
A
If an aneurysm ruptures during anesthetic induction, mortality is high (approximately 75%). Therefore, precise control of transmural pressure is important in preventing aneurysm rupture.
Transmural pressure = CPP = MAP – ICP or CVP (whichever is greater), where MAP = mean arterial pressure
On the other hand, one does not want CPP to be so low that ischemia develops, especially in areas of vasospasm.
24
Q
How would you accomplish a smooth and safe induction and intubation in this patient?
A
- Assuming that evaluation of the airway indicated that tracheal intubation is unlikely to be difficult, induction would begin with preoxygenation followed by propofol 1.5 to 2.5 mg per kg, thiopental 3 to 5 mg per kg, or etomidate 0.5 to 1 mg per kg, which have similar effects on CBF and cerebral metabolic rate. Given that this patient had no other medical problems, propofol is a reasonable choice.
• One may want to avoid ketamine for induction because of its potential to increase in CBF and ICP. Thiopental is not presently available in North America but may be available elsewhere.
- After loss of consciousness and apnea, care must be taken to maintain a normal PaCO2. Vigorous hyperventilation will lower PaCO2, decreasing CBF.
• This may lower ICP to such a degree that if MAP is maintained or increased, transmural pressure may be increased, leading to rupture of the aneurysm. - A nondepolarizing muscle relaxant, which has no effect on ICP or CBF, should be given to facilitate tracheal intubation.
•The neuromuscular junction should be monitored to ensure that paralysis is adequate to avoid coughing with intubation. - Fentanyl 3 to 5 μg per kg, sufentanil 0.5 to 1 μg per kg, or remifentanil 0.25 to 1 μg per kg can be given 3 to 5 minutes before laryngoscopy to blunt the hemodynamic response.
• Isoflurane, desflurane, or sevoflurane can be used to deepen the anesthetic. - Finally, approximately 90 seconds before laryngoscopy, lidocaine 1.5 to 2 mg per kg or esmolol 0.5 mg per kg can be given to blunt the hemodynamic response to intubation. • Lidocaine decreases both CBF and cerebral metabolic rate for oxygen (CMRO2), and at high concentrations can cause seizures.
• Esmolol and labetalol have no effect on CBF and ICP, even in brain areas where autoregulation may not be intact.
• Extreme reductions in MAP (greater than 35%) may compromise CPP in patients with increased ICP.
25
Would you perform a rapid sequence induction and tracheal intubation for this patient?
No indication is seen for a rapid sequence induction and intubation in this patient. Overall risk of aspiration during general anesthesia has been estimated at 0.05%; however, the risk of aneurysm rupture during induction is 1% to 2%. Therefore, unless a clear indication exists for rapid sequence induction, it is best avoided. If a rapid sequence induction is indicated, one may consider using vecuronium 0.15 to 0.20 mg per kg or rocuronium 0.9 to 1.2 mg per kg rather than succinylcholine. Succinylcholine may increase in ICP, although some recent studies have noted no increase in ICP with administration of succinylcholine, but rather with intubation. The increase in ICP can be attenuated or eliminated by deep anesthesia or prior defasciculation. Succinylcholine, more importantly, may lead to hyperkalemia and possibly ventricular fibrillation in those patients presenting with motor deficits following SAH or in those patients who have been bedridden for some time. In the case of a full stomach or an anticipated difficult airway, an awake fiberoptic intubation, with the use of appropriate sedation and topical application of local anesthesia, may be an appropriate alternative. Under such circumstances, it is useful to have an assistant so that while one person is securing the airway, the other is solely focused on controlling the hemodynamics with titration of appropriate medication. Videolaryngoscopy may reduce the need for awake fiberoptic intubation. In addition, the use of a supraglottic devices to maintain an airway during a difficult intubation may be useful in patients with an unanticipated difficult airway.
26
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)?
Each millimeter of mercury increase in PaCO2 increases CBF 3% to 4%, when PaCO2 is in the range of 20 to 80 mmHg. In addition, hypoxemia will ensue if the airway is not secured in a timely manner and will also cause an increase in CBF once arterial oxygen partial pressure (PaO2) is less than 60 mmHg
27
Draw theChange in CBF as a function of PaCO2 and PaO2 tension curve
28
What is optimal fluid management for aneurysm clipping? Would you use a dextrose-containing solution?
Maintenance fluid requirements and blood loss should be replaced.
One wants to avoid profound hypovolemia not only for its detrimental cardiovascular effects but also because it is associated with cerebral ischemia and perioperative neurologic deficits resulting from vasospasm.
Some authors advocate mild hypervolemia to maximize cerebral CBF and minimize vasospasm; however, one must keep in mind the possibility of cerebral edema as well as acute congestive heart failure.
In general, dextrose-containing solutions should be avoided because an increased incidence of neurologic deficits associated with glucose administration has been found in experimental models of focal cerebral ischemia.
Blood glucose should be maintained less than 180 mg per dL.
Use of crystalloid versus colloid for fluid management and which type of crystalloid solution has long been a matter of controversy. Although some authors advocate colloid solutions to diminish the risk of brain swelling, evidence exists that the solution may predispose to brain edema and contribute to hyponatremia, which may increase the incidence of delayed ischemic neurologic deficits.
Hypotonic crystalloid solutions are avoided in the neurosurgical patient; acceptable solutions include normal saline and balanced electrolyte solutions such as Normosol® and Plasma-Lyte®.
A moderate degree of hemodilution to a hematocrit of 30% to 35% usually lowers blood viscosity, thereby increasing CBF.
The goal is to increase oxygen delivery by increasing CBF, without allowing the hematocrit to decrease to a degree that reduction in oxygen content negates the increase in CBF.
* Hematocrit, serum sodium, and serum osmolality measurements may be used to guide fluid therapy.
* Serum sodium should be maintained within normal limits, both to maintain serum oncotic pressure and to avoid the hyponatremia associated with cerebral salt wasting.
29
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?
Any method that rapidly decreases ICP before dural opening may suddenly increase transmural pressure and lead to aneurysm rupture. After dural opening, one of the fastest ways to decrease cerebral blood volume and improve exposure is through hyperventilation. Mild hypocarbia (PaCO2 = 30 to 35 mmHg) can usually be established before dural opening, with moderate hypocarbia (PaCO2 = 25 to 30 mmHg) after dural opening. Because of the risk of cerebral ischemia secondary to diminished CBF, normocarbia should be maintained whenever possible in patients with vasospasm. Mannitol is the most frequently used diuretic to reduce brain swelling. It is given as an infusion to a total dose of 0.7 g per kg (0.25 to 1 g per kg). Its immediate effect is a transient rise in intravascular volume, which may pose problems in patients with impaired ventricular function. In addition, too rapid infusion can lead to decreases in systemic vascular resistance. Its onset of diuretic action is in 10 to 15 minutes, with peak effect occurring at 60 to 90 minutes. If mannitol does not produce the desired brain relaxation and the serum osmolality is greater than 320 mOsm, additional mannitol is unlikely to produce additional effect. In those patients who may not tolerate the initial effects of mannitol, intravenous furosemide 0.1 to 0.3 mg per kg can besubstituted. Both medications can cause derangements in fluid status and serum electrolytes that require close monitoring. Drainage of CSF from either a lumbar drain or an intraventricular catheter is usually effective in optimizing surgical exposure. One must be careful to avoid significant CSF drainage before dural opening to prevent either brainstem herniation or a sudden decrease in transmural pressure. Similarly, hemodynamic instability can ensue if CSF is drained too rapidly at any point in the operation. If tight brain remains a problem, one must ascertain that there is no hypoxemia or hypercarbia. In addition, one should consider eliminating nitrous oxide (N2O) and reducing the amount of volatile anesthetic because all inhalational agents are cerebral vasodilators and may potentially increase ICP. Of course, if inhaled agents are reduced, appropriate intravenous agents should be substituted to ensure adequate anesthesia. Total intravenous anesthesia may be useful in this situation. One may give a bolus of propofol or thiopental to decrease CMRO2 and CBF; nevertheless, one must maintain MAP to maintain CPP. At the time of patient positioning, one must ensure that no impediment exists to venous outflow of the brain (i.e., extreme flexion or rotation of the head should be avoided and no monitor cables [electrocardiogram] should be draped across the neck). Even 10 degrees of head-up positioning has been found to be effective at reducing ICP.
30
How might transmural pressure be decreased to allow for aneurysm clip placement?
The most widely accepted method for producing a slackaneurysm to allow for clip placement is the use of temporary clip occlusion of one or more parent vessels. For example, to place a permanent clip on an anterior communicating artery aneurysm, a temporary clip can be placed on either the right or left anterior cerebral artery or both.
* Advantages of temporary clip use include a greater reduction in transmural pressure, a greater ease in clipping, a decreased incidence of intraoperative rupture, and the avoidance of controlled hypotension.
* The maximal duration of temporary clip application before a neurologic deficit occurs is unknown, but it is probably related to the location of the aneurysm and distribution of perforating vessels distal to the temporary clip. White matter and major deep nuclei are likely to be more susceptible than gray matter to temporary ischemia.
* Risk factors for neurologic deficit following temporary clip placement include poor preoperative neurologic condition, age older than 61 years, and distribution of perforating arteries in distal basilar and horizontal segments of middle cerebral artery.
• Recent studies suggest that there are regional differences in brain oxygenation during temporary clip occlusion, with the middle cerebral artery distribution being more susceptible to ischemia than the anterior cerebral artery distribution.
In addition, patients who underwent multiple brief periods of temporary occlusion had less ischemia than those who underwent a single temporary artery occlusion of greater than 10 minutes.
• Adenosine-induced temporary flow arrest has also been reported as a mechanism to produce a slack aneurysm to facilitate clipping.
31
What is the purpose of controlled hypotension, and how is it achieved?
In the past, controlled hypotension was used to decrease transmural pressure, making the aneurysm neck slack enough to allow placement of a clip without vessel rupture. Various agents were used to achieve controlled hypotension, including volatile agent, nitroprusside, esmolol, labetalol, nitroglycerin, and trimethaphan.
* Specific agents were selected based on the patient’s preexisting medical conditions, especially coronary ischemia or poor ventricular function. In an otherwise healthy patient, sodium nitroprusside infusion may be used for its rapid onset, easy titratability, and quick offset.
* An esmolol infusion can be added to augment hypotension and counteract the reflex tachycardia; by decreasing the amount of nitroprusside needed to induce hypotension, the likelihood of cyanide toxicity diminishes. Side effects of nitroprusside include cyanide toxicity, rebound hypertension, and intrapulmonary shunting.
* Direct measurement of CVP is useful when planning to use controlled hypotension in these patients.
•During controlled hypotension, MAP is usually maintained at a minimum of 50 mmHg in previously normotensive individuals.
Neurologic function monitors (EEG, SSEP, brainstem auditory evoked response, and cerebral oximetry) may be useful in guiding target level of MAP.
32
What are some of the drawbacks of controlled hypotension?
The main drawback of controlled hypotension is that it leads to a global decrease in CPP.
* CPP is then further diminished in the presence of vasospasm or in areas of brain retraction.
* In a retrospective study, multiple regression analysis indicated that patients who underwent even limited periods of controlled hypotension had a worse outcome, both in terms of Glasgow Outcome Scale (multiple regression) and higher incidence and severity of vasospasm. Although further studies indicated that this effect was not seen when corrected for age, controlled hypotension usually is avoided in neurosurgery.
33
What methods of cerebral protection might you use during this operation?
Cerebral protection has long been a matter of much investigation and controversy. Barbiturate loading has been shown in animals to be protective against focal ischemia, although no controlled human studies have been performed. Barbiturates decrease cerebral metabolic rate for glucose and oxygen and lower CBF and ICP. The dose is usually titrated to electroencephalographic silence or burst suppression. At doses used to suppress electroencephalographic activity, the patient may experience cardiovascular depression. The dose of barbiturate traditionally used for cerebral protection may also prolong emergence and hinder postoperative neurologic evaluation. Although barbiturates were originally thought to protect against ischemia through metabolic depression, other factors such as redistribution of blood flow to ischemic areas, blockade ofsodium channels and glutamate receptors, attenuation of Nmethyl D-aspartate (NMDA), and α-amino-3-hydroxy-5-methyl4-isoxazole propionic acid (AMPA) receptor-mediated glutamate toxicity all play a role. Propofol has also been used as an alternative to thiopental sodium. Cerebral protection from propofol is thought to result from scavenging of free radicals, inhibition of glutamate release, and prevention of lipid peroxidation. In studies involving both volatile anesthetics and propofol, apoptotic cell death was delayed, but not prevented, if the ischemic result is mild.
* Propofol may be titrated to burst suppression on EEG monitoring.
* Etomidate decreases cerebral metabolic rate at electroencephalographic burst suppression and prevents an increase in excitatory neurotransmitters during cerebral ischemia in animal models; nevertheless, it has been associated with a greater volume of injured brain than thiopental and control groups in focal ischemia in hypertensive rats.
* Deliberate mild hypothermia (32.5°C to 35.5°C), although promising in animal models, did not demonstrate efficacy with patients with good-grade aneurysm in the Intraoperative Hypothermia for Aneurysm Surgery Trial (IHAST) 2, although there was a suggestion of a trend toward benefit in subgroup analysis.
Although many pharmacologic targets for cerebral protection, including magnesium, lidocaine, and others, have shown promising results in laboratory analysis, none have consistently proven effective in the clinical setting.
34
Would you induce mild hypothermia as a means of cerebral protection?
Hypothermia causes a greater reduction in cerebral metabolic rate for glucose and oxygen than the level attained at electroencephalographic silence because its reduction of metabolism is caused by a reduction in both neuronal electrical activity and enzyme activity related to maintenance of cellular function.
* Hypothermia also reduces the release of excitatory neurotransmitters.
* Significant reduction in infarct size after global and focal ischemia has been demonstrated in several animal studies. Unfortunately, these advantages have not been documented in clinical trials.
* The IHAST study showed no differences in Glasgow Outcome Scale at 3 months in patients who present with good neurologic grade.
* Disadvantages of unintentional hypothermia documented in the literature include an increased incidence of myocardial ischemia in peripheral vascular surgery, increased incidence of postoperative wound infection in abdominal surgery, coagulopathy, prolonged drug clearance, and hyperglycemia.
* In the IHAST study, the hypothermic group had a small increase in infection rate. The effect of hypothermia in poor clinical grade patients is unknown.
35
What are the indications for deep hypothermic circulatory arrest?
Hypothermic circulatory arrest at body temperature less than 22°C (71.6°F) is reserved for giant aneurysms, difficult basilar artery aneurysms, and anatomically complex aneurysms that are not clippable without complete cessation of blood flow and are not amenable to the use of temporary clips.
• Deep hypothermic circulatory arrest requires cooperation between several services, including anesthesiology, neurosurgery, cardiac surgery, and perfusionists. In addition to the concerns mentioned regarding anesthesia for the person with an intracranial aneurysm and the need for prompt awakening for ease of neurologic assessment, deep hypothermic circulatory arrest adds concerns regarding institution of and separation from cardiopulmonary bypass, systemic heparinization and protamine reversal, and, of course, rewarming from profound hypothermia.
This is rarely performed now that coil embolization is possible for many of these aneurysms.
Giant and complex aneurysms that are not amenable to coiling may be managed with flow diversion endovascular therapy.
36
What steps should be taken in the case of intraoperative rupture of an intracranial aneurysm?
The incidence of intraoperative rupture is 2% to 19%. The stageof the operation at which rupture occurs affects outcome, with rupture at induction being the worst.
After induction, the most common times for rupture are when the dura mater or arachnoid mater are being opened, during intracranial hematoma removal, and, of course, during dissection exposure of the aneurysm.
At any point in the operation, a sudden sustained increase in blood pressure with or without bradycardia is suggestive of rupture.
If rupture is suspected on induction, one must institute measures to control ICP while maintaining CPP. If rupture occurs during surgical dissection, mortality is lower.
The primary concern is to control bleeding while maintaining systemic perfusion.
Bleeding is controlled by placement of temporary clips or by clamping or compression of the ipsilateral carotid artery in the neck if the aneurysm is too proximal.
• If bleeding is not controlled in a timely manner and a significant amount of blood accumulates in the subarachnoid space, severe brain swelling that is refractory to all treatment may develop.
37
How would you plan the emergence from an anesthetic for aneurysm clipping?
The goal is to have a patient comfortable and not coughing or straining or subject to hypercarbia or wide variations in blood pressure.
After discontinuing all anesthetic agents and reversing neuromuscular blockade, the use of a lidocaine 1.5 mg per kg bolus may minimize coughing and reaction to the endotracheal tube.
Strict control of blood pressure must be observedespecially in the presence of ischemic heart disease or in patients suspected of having multiple aneurysms.
One should keep the blood pressure within 20% of the patient’s normal measurement.
38
Would you extubate the patient postoperatively?
Most patients who are in Hunt and Hess grades I and II can be extubated postoperatively with no need for airway support. Patients in grades IV and V usually require mechanical ventilation postoperatively, whereas grade III patients may or may not require intubation and mechanical ventilation. Patients with vertebral or basilar artery aneurysms may require airway protection secondary to cranial nerve damage and loss of protective reflexes. If this patient is able to follow commands, is clinically recovered from the effects of muscle relaxants, and has established an adequate ventilatory pattern with return of protective airway reflexes, extubation would be appropriate.
39
What would be the differential diagnosis if the patient did not return to her preoperative neurologic condition?
If the patient had a focal neurologic deficit on awakening in the operating room, the cause most likely would be a surgical one, although new-onset vasospasm is also a possibility. If the patient failed to regain consciousness, the first step would be to ensure that all inhalational and infused anesthetics had been discontinued. Second, one should make sure that neuromuscular blockade was fully reversed. In addition, ensure that the patient is not hypothermic as hypothermia can prolongthe duration of action of intravenous medications. While considering reversal of benzodiazepines and opioids, one should rule out other causes such as hypoxia, hypercarbia, hyponatremia, and hypoglycemia. One should consider the possibility of intraoperative seizure, with delayed emergence resulting from a postictal state. If after reversal of all anesthetic agents, the patient has not awakened, a CT scan should be obtained to rule out subdural hematoma, intracranial hemorrhage, hydrocephalus, and pneumocephalus. An angiogram may also be obtained to rule out vascular occlusion. An electroencephalogram might be appropriate to rule out subconvulsive status epileptics.
40
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?
If transcranial Doppler is available, an increased value for cerebral arterial flow velocity would be suggestive for vasospasm, leading to delayed cerebral ischemia/infarction. Tissue oximetry may also be useful as a monitor for vasospasm. Angiography is the gold standard for diagnosis of cerebral vasospasm and should be performed to confirm the diagnosis and characterize the number and location of the vessels involved. Cerebral vasospasm may be localized to the area of aneurysm rupture or in an area of the brain remote from SAH. The worst prognosis is in those patients in whom vasospasm is diffuse. Of course, as these studies are being done, laboratory values shouldbe checked to make sure no new or worsening metabolic derangement is contributing to the neurologic deterioration.
41
What is cerebral vasospasm, and what causes it?
Vasospasm, which occurs in 35% of patients with SAH, is a segmental or diffuse narrowing of the lumen of one or more intracranial arteries. It is the most common cause of delayed cerebral ischemia/infarction and may be seen angiographically in 60% of patients, even if clinical manifestations are not apparent. The severity of vasospasm may be related to the amount and location of subarachnoid blood. Injection of blood into the subarachnoid space causes vasospasm in experimental animals and antifibrinolytics apparently worsen the spasm. On a molecular level, one theory is that oxyhemoglobin causes the production of superoxide radicals that lead to a decrease in nitric oxide levels in endothelial cells. This decrease in nitric oxide increases protein kinase C and intracellular calcium, resulting in myofilament activation and vasospasm. Other theories involve prostaglandins and lipid peroxidases. There may also be a genetic predisposition to development of vasospasm. Preliminary studies suggest that patients with the polymorphism of haptoglobin (α1α1) may be protected against vasospasm compared to patients with haptoglobin α2α2, which is less effective at neutralizing free radical formation by free hemoglobin. It is clear that endothelial dysfunction is present, particularly in the microcirculation. The risk of vasospasm decreases with advancing age, with patients younger than 50 years old at a fivefold greater risk than older patients.
42
What are pathophysiologic changes seen in cerebral vasospasm?
Structurally, leukocytes, red blood cells, and macrophages are seen in arterial walls. Inflammatory mediators, such as eicosanoids, interleukin 1, and immune complexes, are increased. Eventually, the vessel wall thickens, and smooth muscle proliferation and collagen deposition accompany degenerative changes in the tunica intima and media. Functionally, carbon dioxide reactivity is impaired, and autoregulation is often impaired, perhaps correlating to the degree of delayed cerebral ischemia/infarction. CBF in some areas appears to be pressure dependent, hence the reasoning behind hypertensive therapy.
43
How is the diagnosis of cerebral vasospasm made?
The clinical diagnosis of cerebral vasospasm is made when the patient experiences an altered level of consciousness (drowsiness, disorientation) or a new focal neurologic deficit. These may be accompanied by increasing headache, meningismus, and fever. Vasospasm is rare in the first 3 days following SAH. It reaches peak incidence at 3 to 10 days and usually resolves by 10 to 14 days after SAH. In this patient, the new onset of hemiplegia suggests that the middle cerebral artery is involved. If vessels in the posterior fossa are involved, respiratory and hemodynamic abnormalities may develop. The differential diagnosis includes rebleeding, hydrocephalus, seizure, hyponatremia, and drug effects. Transcranial Doppler CBF velocity greater than 120 cm per second in association with a new focal neurologic deficit are usually sufficient to make the diagnosis of cerebral vasospasm; however, a change intranscranial Doppler values over time may be more useful than an absolute value. CBF velocity greater than 200 cm per second is associated with a high risk of cerebral infarct, whereas a velocity less than 100 cm per second indicates that cerebral vasospasm is unlikely. Recent evidence shows that transcranial Doppler had only 63% sensitivity in identifying delayed cerebral ischemia/infarction, with a positive predictive value of only 22% in grade II and III patients. Cerebral perfusion imaging may be necessary in patients of poor grade who are unable to participate in neurologic examination. Angiographic cerebral vasospasm can be found in 60% of patients following SAH, but only 50% of these patients develop clinical focal neurologic deficits.
44
What steps can be taken to prevent cerebral vasospasm?
Calcium channel blockers are standard prophylactic therapy to prevent vasospasm. The mechanism is unknown, but presumably, calcium channel blockers aid in maintaining cellular integrity by preventing calcium entry into ischemic cells. Nimodipine, taken orally, improves neurologic outcome. Patients given nimodipine have no change in overall incidence of vasospasm, but they have a lower incidence of severe narrowing. In addition, although no improvement is found in mortality, there is improvement in outcome for survivors. Use of nicardipine, an intravenous agent, showed a lower incidence of vasospasm, but no improvement in outcome versus a placebo group; both groups received HHH therapy. The maincomplication of calcium channel blocker therapy is hypotension (0% to 8%), which may make this therapy difficult to achieve. Intravenous nimodipine is not available in the United States, although patients are given nimodipine orally or via nasogastric tube every 4 hours. The incidence of vasospasm does not differ significantly from open surgical repair to endovascular procedures. In addition, although calcium channel blockers cross the blood–brain barrier, the dose needed to achieve significant levels at the site necessary may be limited by systemic hypotension. Prolonged-release nicardipine implants placed at the time of surgical clipping were shown to reducing the incidence of vasospasm, improving outcome. In order to deliver calcium channel blockade intrathecally, nicardipine nanoparticles administered via external ventricular drains reduced delayed cerebral ischemia and improved clinical outcome. The microparticles appeared safe and there was no significant hypotension. In addition, there was a reduction in delayed cerebral ischemia/infarction and an improvement in clinical outcome. Other steps to limit cerebral vasospasm include the removal of subarachnoid blood as quickly as possible, instillation of thrombolytic agents (e.g., tissue plasminogen activator), and use of pharmacologic agents to reduce inflammatory response (highdose glucocorticoids, ibuprofen). In Europe and Japan, protease inhibitors have been used in the treatment of vasospasm.
45
What treatments can be undertaken once a diagnosis of cerebral vasospasm is made?
Treatment for cerebral vasospasm is multifactorial and includes continuation of prophylactic measures. In the past, HHH therapy was used to augment CBF past the stenotic areas. It begins with hypervolemic hypertension, with intravascular volume expansion with crystalloid or colloid to increase cardiac output. Some recommended target values are CVP of 10 to 12 mmHg, pulmonary artery occlusion pressure of 15 to 18 mmHg, cardiac index of 3.0 to 3.5 L/min/m2, and hematocrit of 30% to 35%. Various blood pressure targets have been reported, but a reasonable plan is systolic blood pressure 160 to 200 mmHg if the aneurysm is clipped and 120 to 150 mmHg if unclipped. Vasoactive infusions are added if hypervolemia alone is inadequate. End points of therapy are resolution of neurologic deficits or occurrence of complications of therapy, such as pulmonary edema (26%), myocardial ischemia, and rebleeding or rupture of a secondary aneurysm. A pulmonary artery catheter is often indicated. Fluid used for HHH should be isotonic and have enough sodium to avoid hyponatremia. Vasopressin, fludrocortisone, or hydrocortisone can be administered to counteract excessive sodium and fluid loss. Recent literature has proven the benefit of maintenance of euvolemia with induced hypertension in contrast to strict HHH. Other treatments for vasospasm, including intra-arterial vasodilators or angioplasty, are utilized if the patient does not demonstrate prompt improvement with hypertensive therapy. In spite of all attempted therapy, the outcome in patients withsignificant vasospasm is often poor. Most medications investigated to ameliorate the devastating consequences of vasospasm have limited efficacy. Nimodipine has been found to have some efficacy in treating vasospasm and improving outcome. A recent target of pharmacologic therapy has been endothelin, a potent long-lasting vasoconstrictor. Clazosentan, an endothelin receptor antagonist, reduced angiographic vasospasm but did not improve clinical outcome in two appropriately powered trials.
46
What are other neurologic complications following SAH and aneurysm clipping?
What are other neurologic complications following SAH and aneurysm clipping?
47
What other organ systems may manifest problems postoperatively in aneurysm clipping patients?
The lungs can be affected by pneumonia or neurogenicpulmonary edema, in which disruption of the pulmonary capillary membrane occurs secondary to increased sympathetic nervous system activity. Because of inactivity, patients may be predisposed to developing deep venous thrombosis (DVT) and pulmonary embolism. Patients (approximately 5%) may develop heparin-induced thrombocytopenia, possibly due to heparin exposure during angiography. These patients tend to have increased rates of both vasospasm and DVT. In general, heparin prophylaxis is often avoided in patients after SAH due to concerns for aneurysmal rebleeding, surgical site bleeding or new bleeding around a ventriculostomy catheter. The incidence of venous thromboembolism in neurocritical care patients may be as high as 14%. There appears to be a relationship between the use of hypertonic saline in the SAH patient and the incidence of acute kidney injury. Patients may have a fever secondary to subarachnoid blood, which may make the workup of postoperative infection more difficult. Finally, as in most patients with head injury, those with SAH may have increased metabolic rate.
