Cerebral Aneurysm Surgery

Question 1

Increase in ICP due to aneurysm (effect of hemorrhage and edema) leads to:

Answer 1

Headache
loss of consciousness
possible motor deficits

Question 2

Rising ICP can lead to which reflex?

Answer 2

Cushings-defined by hypertension, bradycardia and (irregular respirations)

Question 3

Rebleeding after aneurysm surgery-when is it most common?

Answer 3

First day!

Question 4

What is TCD? what are its indications?

Answer 4

Its a direct and non-invasive monitor of CBF
Indications:
Determine severity of cerebral vasospasm
Measure CBF during carotid artery clamping in carotid endarterectomy
Detection of emboli after arterial repair or during CPB

Question 5

What are the Hunt and Hess classifications of patients with SAH?

Answer 5

0-unruptured aneurysm
1-asymptomatic or minimal headache and slight nuchal rigidity
2-mod-severe headache, nuchal rigidity, no other neurologic deficit than cranial nerve palsy
3-drowsiness, confusion, or mild focal deficit
4-stupor, early decerebration, moderate to severe hemiparesis
5-deep coma, decerebrate rigidity

Question 6

What is neurogenic pulmonary edema? How do you treat it?

Answer 6

Occurs due to sympathetic activation secondary to the rise in ICP leading to pulmonary and systemic vasoconstriction. This increases pulmonary blood volume, and causes a rise in pulmonary capillary permeability
Treat it with immediate surgical or pharmacologic relief of intracranial hypertension, careful fluid management.

Question 7

Cardiac dysrhythmias and EKG abnormalities during SAH: why? What does it correlate with? How would it look?

Answer 7

Due to excessive catecholamine release triggered by SAH. it correlates with degree of neurologic injury rather than cardiac dysfunction. Will likely have deep wide splayed T wave inversions, long QT, prominent U wave.

Remember to rule out hypotension-as a reason for dysthymia, supply patient wit O2 if you think its necessary

Question 8

What electrolyte abnormalities are you expecting with SAH?

Answer 8

Hyponatremia due to SIADH or CSW
Other electrolyte abnormalities such as hypokalemia, hypocalemia, and hypomagnesemia may occur secondary to diuretic therapy in an attempt to lower ICP with loop or osmotic diuretics.

Question 9

Intraoperatively, How are you trying to induce-what do you want to minimize? how? are its considered full stomach? Induction agent of choice? Other options?

Answer 9

Blunt sympathetic response with IV fentanyl (3 mcg/kg) and IV lidocaine (1.5 mg/kg) Pre-treat with VEC 0.01 mg/kg to prevent associated response of increased ICP (THESE PATIENTS SHOULD BE TREATED AS FULL STOMACH)
Etomidate is induction agent of choice 2/2 hemodynamic stability and decreasing effect on ICP
Thiopental has cerebroprotective effects and can be used, but should be titrated carefully due to its potential to cause hypotension.

Question 10

IV access in cerebral aneurysm/SAH?

Answer 10

At least two large bore IV catheters

Question 11

Monitors during SAH?

Answer 11

CVP can be used for guidance of intravascular volumes in the face of severe cardiac instability

Question 12

What do you want to avoid intraop? Overall goal for intra-op mgmt?

Answer 12

Avoid HTN and resultant aneurysmal rupture.

Ultimate goals for the surgery: avoid aneurysm rupture, maintain cerebral perfusion pressure

Question 13

Would you want neuromonitoring?

Answer 13

it could be beneficial in areas potentially affected by the aneurysm clipping.

Question 14

Postoperative goals at emergence:

Who are you extubating?

Answer 14

avoid coughing, straining, hypercarbia, and hypertension as these will lead to an increase in ICP
Extubation: Those who were Hunt-Hess grades 1 and 2 prep with no intra-op complications
Those who came with altered mental status are going to ICU intubated as well as those who are hemodynamically unstable and/or had a hemorrhage event intra-operatively

Question 15

What do you want to avoid post op?

Answer 15

Extremes. Hypertension (extreme) can lead to cerebral edema or hematoma, leading to increased ICP and vasospasm
Hypotension-decreased BP can cause decreased cerebral perfusion pressure

Question 16

What is formula for Cerebral perfusion pressure?

Answer 16

CPP= MAP-ICP

Question 17

Cerebral vasospasm: we are most concerned about it happening when? How does it present? how will you make the diagnosis?

Answer 17

48 hours after SAH. Presents with neurologic deterioration and drowsiness. Results in cerebral ischemia.

Question 18

Prophylaxis and treatment of vasospasm:

Answer 18

Nimodipine-CCB -improves outcome by unknown mechanism
Triple H therapy: HTN, hypervolemia, and hemodilution
goal is to increase cerebral blood flow, increase CPP, and improve cerebral blood flow with decreased blood viscosity. Can only be done in CLIPPED! SBP raised to 160-200
PAWP 12-18
CVP 10-12
Crit is decreased to 33% to maximize O2 delivery to tissues

Question 19

How can you physically examine someone and know if they have increased ICP?

Answer 19

Regardless, I would perform a·thorough history and physical
looking for signs of elevated ICP, such as headache, papilledema, NN, altered mental
status, and Cushing’s triad of HTN, bradycardia, and a change in respiratory pattern
(some sources· substitute a widened pulse pressure - increased difference between
systolic and diastolic blood pressure - as the third component of the triad, in place of
an irregular respiratory pattern). IfI were still uncertain, I would order a CT, which
would aid in identifying intracranial bleeding, small ventricles, or a midline shift.

Question 20

If you’ve been told that someone has a difficult airway, what are you looking for on physical exam? what are other resources you could use to be ready to intubate?

Answer 20

I would perform a history and physical looking for specific findings
that may suggest a difficult airway such as inability to open the mouth, poor cervical
spine mobility, receding chin, large tongue, prominent incisors, short neck, reduced
thyromental distance(< 6.5 cm), reduced sternomental distance(< 12.5 cm), and a
Mallampati classification of III or IV. I would also question the patient about weight
change and evaluate the patency of his nares to determine whether nasal intubation
would be an acceptable option in an emergent situation .
In addition, I would attempt to obtain the old anesthetic record to further delineate the
difficulty encountered, whether ventilation was difficult, and what steps were taken to
successfully secure the airway. I would then discuss potential intubation plans with
the patient, including the performance of an awake, fiberoptic intubation.

Question 21

If you inadvertently cannulated the carotid artery(-in the neuro case of UBP-you continuing (pt had aneurysm in this case, but wasn’t bleeding)? couldn’t you just place one on the left side?

Answer 21

Ifl inadvertently cannulated the right carotid artery, I would cancel
the case and consult a vascular surgeon. Pulling the cannula from the carotid artery
would lead to bleeding and hematoma formation in the neck potentially leading to
decreased cerebral venous return, decreased cerebral perfusion, and even airway
compromise in this patient with possibly elevated ICP and a known difficult airway.
While I could place a central line in the left internal jugular, this may result in further
impairment of cerebral venous return leading to increased intracranial hypertension
which could further compromise cerebral perfusion.

Question 22

In neuro cases, is there an advantage to a subclavian line over an IJ?

Answer 22

A subclavian approach theoretically avoids the risk of damaging the
internal jugular vein or artery, with subsequent obstruction of cerebral venous return
and/or cerebral perfusion. However, placing a central line using the subclavian
approach is technically more difficult and is associated with a higher risk of
pneumothorax.

Question 23

In patient with difficult airway, what do you want to have in the room?

Answer 23

Difficult airway cart
glide, fiberoptic
ENT surgeon on standby
Surgeon in room

Question 24

Surgeon wants you to lower BP prior to clipping-how are you feeling about this with patients?

Answer 24

We can, but I would also want to discuss the
possibility of temporary clipping of supplying arteries to reduce transmural pressure
in lieu of deliberate hypotension. If the surgeon insisted that deliberate hypotension
was necessary, I would only agree to minimal decreases in blood pressure with
careful monitoring for signs of end-organ ischemia.

Question 25

CAD and the hypotension the surgeon might want-how far are you going? which other conditions lead to cardiac ischemia?

Answer 25

Due to his coronary artery disease, I would only allow the MAP to
decrease about 10-20 mmHg, while carefully monitoring for signs of cerebral and/or
cardiac ischemia as indicated by jugular bulb oximetry, regional cerebral oximetry,
EEG, transcranial Doppler, EKG, or TEE. Additionally, I would avoid conditions
that may contribute to cerebral and/ or cardiac ischemia, such as hyperthermia,
hyperglycemia, anemia, and hypoxemia.

Question 26

The surgeon decides to go ahead and place a temporary clip on the anterior
cerebral artery. Does this alter your management?

Answer 26

Yes, placing a temporary clip on a feeding vessel results in decreased
focal blood flow through the aneurysm, obviating the need for deliberate hypotension.
During temporary occlusion, the mean arterial pressure should be maintained at
higher than normal pressures to support collateral flow of blood.

Question 27

Is there anything you could do to provide protection while the temporary clip
was in place?

Answer 27

The administration of thiopental, etomidate, or propofol, can be
neuroprotective in the setting of focal ischemia secondary to reductions in CMR02.
Other strategies to prevent cerebral ischemia include, maintaining a higher than
normal mean arterial pressure, minimizing occlusion time, utilizing neurophysiologic
monitoring (i.e. EEG and SSEPs ), ensuring brain relaxation (i.e. CSF drainage,
mannitol administration, induced hypocapnia) to facilitate surgery and reduce
required retractor pressure, allowing mild hypothermia (32 -34 °C), and administering
a barbiturate.

Question 28

Burst suppression

Answer 28

periods of high voltage electrical activity alternating with periods of no activity in the brain. Can be seen in GA, coma, or hypothermia

Question 29

Signs of aneurysm rupture intraop: and wyd?

Answer 29

sustained HTN with or without bradycardia. Control ICP while maintaining CPP

Question 30

Could you provide hypothermia to protect during aneurysm clipping?

Answer 30

While the benefits are unproven, mild hypothermia (32-34 °C) may
provide some brain protection from ischemia due to a reduction of oxygen
consumption by 5-7% for every one °C decrease in body temperature. While CMR02
reduction may be as much as 50% with lower temperatures (about 27 °C), deep
hypothermia is not practical for most neurosurgical interventions due to its
association with delayed emergence.

Question 31

You notice ST changes on the EKG. What do you think? What would you do? (during aneurysm surgery)

Answer 31

EKG changes, including ST-segment depression, often occur in the
presence of subarachnoid hemorrhage and have not been shown to increase morbidity
or mortality. These changes are concerning, however, because they suggest that a
previously unruptured aneurysm is now bleeding or, given this patient’s cardiac
history, the patient is experiencing myocardial ischemia. In response, I would look at
the surgical field and ask the surgeon about potential rupture; continue to observe the
EKG, arterial line, pulse-oximeter, and CVP monitor; ensure adequate ventilation
with 100% oxygen; assess hemodynamic status; and order a troponin-I level.

Question 32

The surgeon confirms that the aneurysm has ruptured. What would you do?
Would you raise or lower the BP?

Answer 32

If possible, the surgeon should apply permanent or temporary clips to
control bleeding. If the bleeding were not excessive, I would: (1) correct any
conditions that may contribute to cerebral ischemia, such as hyperthermia,
hyperglycemia, and hypoxemia; (2) induce mild hypotension with sodium
nitroprusside, to facilitate surgical repair; and (3) consider administering
cerebroprotective agents (i.e. volatile agents and/or a barbiturate), understanding that
these actions may increase risk of end-organ ischemia (some practitioners would
avoid deliberate hypotension even in these circumstances). If massive hemorrhage
were occurring, I would: (1) compress the carotid arteries; (2) suggesttemporary
clipping of the vessels proximal and distal to the aneurysm; and (3) prepare for
aggressive resuscitation with fluids and blood products. I would avoid deliberate
hypotension and cerebroprotective agents that would not likely be tolerated. And, if
the surgeon were unable to control bleeding despite these measures, I would talk to
the surgeon about the benefits of cardiopulmonary bypass or cardiac circulatory
arrest.

Consider adenosine, but not until they push me

Question 33

The surgeon places a clip on the anterio:r cerebral artery to get control of the
bleeding and the posterior tibial-to-vertex SSEPs disappear. Is this concerning?

Answer 33

Yes, the loss of SSEPs may be indicative of focal ischemia secondary
to placement of the clip. As long as the bleeding was controlled, I would correct any
hypoxemia, hypotension, hypovolemia, anemia, and hypo/hypercarbia in order to
optimize oxygen delivery; make sure that the depth of anesthesia had remained stable
and was not interfering with the evoked potential readings; and consider increasing
the patient’s MAP in order to improve collateral circulation to the surrounding brain.
If these measures proved ineffective, I would provide a volatile agent, propofol, or a
barbiturate to provide some ischemic brain protection.

Question 34

Mode of ventilation: SIMV

Answer 34

Assuming pulmonary compliance were normal, I would start with
synchronized intermittent mandatory ventilation (SIMV). Like intermittent
mandatory ventilation (IMV), SIMV allows spontaneous respirations while requiring
a preset number of mandatory breaths per minute. SIMV, however, is designed to
time delivery of a mechanical breath with the beginning of a spontaneous effort. This
synchronization prevents “stacking”, in which a mechanical breath is delivered in the
middle of a spontaneous breath, which can result in the delivery of larger than desired
tidal volumes. This mode of ventilation is more comfortable for the patient and
provides a guaranteed baseline of ventilation during the weaning process, when the
patient’s ability to ventilate adequately is in question.

Question 35

What if the patient has reduced pulmonary compliance? Then which mode are you going with?

Answer 35

If pulmonary compliance is impaired due to pulmonary edema or intrinsic disease, a
pressure-controlled mode of ventilation may be more appropriate.

Question 36

Cerebral angiogram reveals diffuse vasospasm. How will you treat this patient?

Answer 36

First, I would secure the airway. Next, I would begin “triple H”
therapy - hypervolemia, hypertension, and hemodilution. The goal is to improve
delivery of blood to ischemic areas with impaired autoregulation by increasing
perfusion pressure and decreasing viscosity. Unfortunately, this treatment may result
in worsening cerebral edema, increasing ICP, pulmonary edema, and hemorrhage.
If the patient proved refractory to “triple-H” therapy, I would discuss with the
surgeon the efficacy of using transluminal angioplasty to dilate major constricted
cerebral vessels. Additionally, I would consider the use of intra-arterial infusion of
verapamil to dilate distal vessels too small for angioplasty.

Question 37

During triple H therapy the patient develops progressive and significant
hypoxia. What do you think is the cause?

Answer 37

Given the volume loading that occurs with “triple-H” therapy, this
progressive hypoxia is most likely due to pulmonary edema following overzealous
fluid administration. However, I would also consider neurogenic pulmonary edema,
myocardial infarction, arrhythmia, congestive heart failure, right mainstem intubation,
pneumothorax, atelectasis, pulmonary embolism, pneumonia, ventilator associated
barotrauma, or acute respiratory distress syndrome (ARDS)

Question 38

What is neurogenic pulmonary edema?

Answer 38

Mechanism not totally understood, but: A massive sympathetic surge generated by the injured CNS results
in generalized vasoconstriction and a redistribution of blood volume to the pulmonary
circulation.

Question 39

Treatment of neurogenic pulmonary edema:

Answer 39

Treatment is primarily aimed at addressing the underlying
neurological condition. For mild cases, in which gas exchange is minimally
impaired, I may just increase the patient’s Fi02. However, in a case such as this one,
where the patient is developing significant hypoxemia, I would: (1) treat the
underlying cause of CNS injury; (2) attempt to reduce intracranial pressure; (3)
mechanically ventilate with tidal volumes between 5-6 mL/k:g (lower volumes would
be utilized to prevent iatrogenic injury); (4) provide PEEP to prevent atelectasis and
improve gas exchange, being careful to avoid excessively high intrathoracic pressures
that could lead to decreased cerebral venous return, increased ICP, and decreased
cerebral perfusion; (5) consider administering diuretics to reduce capillary hydrostatic
pressure and increase colloid osmotic pressure (it is likely that hypervolemia is
contributing to his condition, given the recent treatment of vasospasm ); ( 6) provide
optimal oxygen delivery by ensuring adequate hemoglobin (> 10 g/ dL) and cardiac
output, and carefully monitoring intravascular volume; and (7) consider
pharmacologic intervention with alpha-adrenergic antagonists (i.e. phentolamine ),
beta-adrenergic agonists (i.e. dobutamine ), or dopamine, being very cautious to avoid
significant hypotension that may compromise cerebral perfusion.

Question 40

On post-op day #3, the serum sodium is 125mEq/L. What is your differential?

Answer 40

UBP Answer: With the volume loading that occurs during “triple-H” therapy, this is
most likely dilutional hyponatremia. However, hyponatremia would also be
consistent with cerebral salt wasting syndrome (CSWS) and the syndrome of
inappropriate antidiuretic hormone (SIADH), both of which are often associated with
brain injury, including cerebral aneurysm. The two disorders may be ·differentiated
by the volume status of the patient, since CSWS is usually associated with
hypovolemia, while patients with SIADH are usually euvolemic. In addition, patients
with SIADH exhibit elevated ADH levels and rarely develop urine sodium levels >
100 mEq/L, while patients with CSWS usually have normal ADH levels and often
develop urine sodium levels > 100 mEq/L. The distinction is important because the
water restriction and diuresis often employed to treat SIADH would serve to
exacerbate the hypovolemia associated with CSWS and, in this patient, contribute to
vasospasm. The treatment for CSWS, on the other hand, would entail fluid and
sodium replacement.