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Principles III > Anesthesia for Neurosurgery > Flashcards

Anesthesia for Neurosurgery Flashcards

1
Q

What vasculature supplies blood to the brain?

A

internal carotid artery and the vertebral arteries

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2
Q

Where do the 2 vertebral arteries branch off of and how do they get to the brain?

A

they branch off of the subclavian artery and enter the base of the skull through the foramen magnum, run along the medulla, and join in the pons to form the basilar artery, the basilar artery then branches into 2 posterior cerebral arteries which primarily supply the occipital lobes of the brain

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3
Q

What do the internal carotid arteries branch into?

A
  • middle cerebral artery: supplies lateral surface of the brain and runs between frontal and temporal lobes
  • posterior communicating artery
  • anterior cerebral artery: supplies the frontal lobe
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4
Q

What and where is the circle of willis?

A

located at the base of the brain and forms an anastomotic ring that includes vertebral (basilar) and internal carotid flow

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5
Q

What happens if one portion of cerebral blood flow becomes obstructed in the circle of willis?

A

other blood flow will compensate and give collateral flow

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6
Q

Where is the most common site of aneurysm and atherosclerosis in the circle of willis?

A

middle cerebral artery

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7
Q

What vessel provides majority of blood flow to the brain?

A

internal carotid artery (85%), supplies anterior 2/3 surface of brain

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8
Q

How much blood flow comes from the vertebral arteries?

A

15%, supplies posterior 1/3 of brain

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9
Q

What is normal cerebral blood flow?

A

50 mL/100 gm brain tissue/minute (750 mL/min or 15-20% of CO)

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10
Q

At what level of decreased cerebral blood flow classifies cerebral impairment?

A

decreased flow by 50% (20-25 mL/100 gm/min)

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11
Q

What cerebral flow rate would indicate isoelectric eeg?

A

6-15 mL/100 gm/min

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12
Q

What cerebral flow rate would indicate neuronal death?

A
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13
Q

How do you calculate cerebral perfusion pressure?

A

CPP = MAP - ICP (or CVP)

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14
Q

What is normal CPP?

A

80-100 mmHg

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15
Q

What is an acceptable low CPP?

A

50 mmHg

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16
Q

What CPP would indicate slowing EEG?

A
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17
Q

What CPP would indicate flat EEG?

A

25-40 mmHg

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18
Q

What CPP would indicate brain damage?

A
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19
Q

What is CPP primarily dependent on?

A

MAP since ICP is normally

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20
Q

What metabolic factors regulate CBF?

A
  • H+ ions
  • CO2
  • oxygen tension
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21
Q

What is the most potent determinant of CBF?

A

CO2, directly proportional relationship between PaCO2 and CBF with PaCO2 tensions between 20-80 mmHg

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22
Q

What happens to your CBF as your PaCO2 increases?

A

increased arterial CO2 —> increased cerebral vasodilation —> increased cerebral blood flow

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23
Q

How much does CBF increase or decrease for every 1 mmHg change in PaCO2?

A

1-2 mL/100 gm/min

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24
Q

Will you CBF change of your PaCO2 is

A

no, no more vasoconstricting effects below 20 mmHg, may cause cerebral impairment

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25
Q

How much will CBF change for changes in PaO2?

A

CBF only affected by marked changes in PaO2, PaO2

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26
Q

Will a high PaO2 cause changes in CBF?

A

NO

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27
Q

How do H+ ions affect CBF?

A

increased H+ concentration depresses neuronal activity and increases CBF, which helps to carry away H+ and CO so that normal activity can be restored

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28
Q

How does temperature regulate CBF?

A
  • CBF changes 5-7% per 1 degree Celsius
  • hypothermia decreases CBF
  • hyperthermia increases CBF
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29
Q

At what temperature is EEG isoelectric?

A

20 degrees Celsius

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30
Q

At what temperature does O2 activity begin to decrease and cell damage may occur?

A

42 degrees Celsius

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31
Q

How does viscosity affect CBF?

A
  • decreased Hct causes decreased viscosity and can improve CBF; however, reductio in Hct also decreases O2 carrying capacity
  • increased Hct (polycythemias) causes increased viscosity and can reduce CBF
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32
Q

What is the optimum Hct for neurosurgery?

A

30-34%

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33
Q

What are autonomic influences on CBF?

A
  • cerebral circulation has extensive sympathetic nervous innervations
  • conditions that cause very strong sympathetic activity, the cerebral vasoconstrictor activity may become apparent, especially in large cerebral vessels
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34
Q

What MAP range is the brain able to autoregulate CBF?

A

50-150 mmHg

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35
Q

What happens of the MAP falls out of the range for cerebral autoregulation?

A

CBF becomes pressure dependent, if MAP falls below 50 mmHg CBF is compromised and if MAP>150 mmHg BBB may be disrupted and cerebral edema or hemorrhage may result

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36
Q

What happens to the cerebral autoregulation curve in patients with chronic HTN?

A

shifts to the right so higher pressures are necessary to maintain CBF

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37
Q

How is the overall metabolic rate of the brain compared to the metabolic rate of the rest of the body?

A

cerebral metabolism 7 times greater than the average metabolic rate of the body

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38
Q

How much of the body’s total O2 does the brain consume?

A

20%

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39
Q

What is the average CMRO2?

A

3.5 mL O2/100 gm/min (50 mL/min)

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40
Q

What happens if you have relatively high O2 consumption and absence of O2 reserves?

A

unconsciousness within 10 seconds with interruption of cerebral perfusion

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41
Q

Can the brain be supplied by anaerobic glycolysis?

A

No, because the metabolic rate of the neurons is too great

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42
Q

What is the average brain glucose consumption?

A

5 mg/100gm/min

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43
Q

What becomes a major energy substitute for the brain during starvation?

A

ketone bodies

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44
Q

How does hyperglycemia affect the brain?

A

can exacerbate global hypoxic brain injury by accelerating cerebral acidosis and cellular injury

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45
Q

How do volatiles affect your CMRO2?

A

decrease CMRO2

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46
Q

How do volatiles affect CBF?

A

greatly increase CBF

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47
Q

How are the junctions between vascular endothelial cells in cerebral capillaries different?

A

near fused together (tight-junctions) which creates the blood brain barrier

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48
Q

What substances are able to pass through the BBB?

A

lipid-soluble substances (CO2, O2, most anesthetics, alcohol) but restricts movement of ions, proteins, and large molecules

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49
Q

Can mannitol cross the BBB?

A

No, but used when vasculature osmolality increases and causes sustained decrease in brain H2O content and thus decreases brain volume

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50
Q

What can disrupt the BBB?

A

severe HTN, CVA, head trauma, cerebral infection

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51
Q

Where is CSF found?

A

within the ventricles of the brain, in the cisterns around the brain, and in the subarachnoid space surrounding the brain and spinal cord

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52
Q

What is the major function of CSF?

A

protect the CNS against trauma

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53
Q

What is the normal rate of CSF production per day?

A

~21 mL/hr, but total CSF volume is only 150 mL

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54
Q

Where is ICP measured?

A

in the subarachnoid space over the cerebral cortex or in the lateral ventricles

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55
Q

What is the normal ICP range?

A

5-15 mmHg

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56
Q

What is the Monro-Kellie doctrine?

A

any increase in one component must be offset by an equivalent decrease in another to prevent a rise in ICP

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57
Q

How are increases in volume initially compensated for in the brain?

A
  • initial displacement of CSF from the cranial to the spinal compartment
  • increase in CSF absorption by the arachnoid villi, which acts as “pressure valves” that open up when ICP increases
  • decrease in CSF production
  • decrease in cerebral blood volume, primarily venous
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58
Q

What is intracranial HTn?

A

a point is eventually reached in which further increases produce precipitous rises in ICP, producing intracranial HTN

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59
Q

What range is mild intracranial HTN?

A

15-25 mmHg

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60
Q

What range is moderate intracranial HTN?

A

25-40 mmHg

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61
Q

What range is severe intracranial HTN?

A

> 40 mmHg

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62
Q

What are signs of increased ICP?

A
  • HA
  • NV
  • blurred vision
  • unilateral pupillary dilation
  • papilledema
  • confusion, altered LOC
  • lethargy
  • seizures
  • Cushing’s triad (HTN, bradycardia, irregular respirations)
  • posturing
  • oculomotor nerve (III) paralysis (inability to adduct eye)
  • abducens nerve (VI) (inability to abduct eye)
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63
Q

How can you manage increased ICP?

A
  • hyperventilate to PaCO2 30-35 mmHg
  • diuretics (Manitol 0.25-1.0 gm/kg or lasix)
  • corticosteroid to decrease edema
  • restrict fluids
  • elevate HOB 30 degrees, keep head midline
  • control BP
  • cool pt to 34 degrees Celsius
  • ventriculostomy
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64
Q

Why do anesthetic agents have luxury perfusion?

A

combination of decreased metabolic demand and increased cerebral blood flow, allows for great perfusion during induced hypotension or cases that increase risk of global ischemia

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65
Q

What is circulatory steal?

A
  • in ischemic brain regions, blood vessels are maximally dilated, in non-ischemic regions, blood vessels have tone
  • vasodilators (volatile agents, NTG, SNP) and hypercarbia from hypoventilation cause vessels in non-ischemic regions to dilate so flow to ischemic brain decreases
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66
Q

What is the robin hood effect or inverse steal?

A
  • barbituates and hyperventilation (hypocarbia) cause cerebral vasoconstriction in normal or healthy areas of the brain
  • blood flow is thus shunted to the diseased areas
  • good for patients with focal ischemia or tumors
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67
Q

What are some strategies for cerebral protection?

A
  • hypothermia
  • anesthetic agents
  • methylprednisolone
  • avoid hyperglycemia
  • maintain normocarbia
  • maintain O2 carrying capacity
  • maintain normal or slightly increased BP
68
Q

What is the most important mechanism for protecting the brain during focal and global ischemia?

A

hypothermia, decreases basal and electrical metabolic requirements throughout the brain

69
Q

Why are anesthetic agents beneficial for cerebral protection?

A

barbiturates produce inverse steal and acts as an anticonvulsant

70
Q

Why is methylprednisolone beneficial for cerebral protection?

A

decreases inflammation and free radical production

71
Q

What are general preoperative considerations for neurosurgery?

A
  • neurologic evaluation (LOC, reflexes, motor/sensory function, document s/s of increased ICP, document preexisting neurological deficits)
  • assess if pt is on anticonvulsants (increases NDNMB requirements, will need to continue intraop, assess therapeutic levels)
  • premeds (may want to avoid if need to do postop neuro assessment and fentanyl will dec. RR which will inc. CBF)
  • monitoring
  • blood available
  • antibiotics
72
Q

What kind of induction do you want for neurosurgery?

A

smooth induction essential to avoid increases in ICP

73
Q

What are unique positioning needs for neurosurgery?

A

bed turned 90-180 degrees so have extensions on all lines/tubes

74
Q

What should you consider with ICP intraop?

A

maintain low ICP or implement strategies to lower ICP

75
Q

What solutions should you use for fluid management?

A

NS (308 mOsm) or LR (273 mOsm), AVOID GLUCOSE CONTAINING SOLUTIONS

76
Q

What should you remember regarding emergence?

A

must be smooth, especially if they did anastomosis of blood vessels

77
Q

What are the types of intracranial mass lesions?

A
  • congenital
  • neoplastic (benign vs malignant)
  • infectious (abcess or cyst)
  • vascular (hematoma or arteriovenous malformation)
78
Q

What symptoms indicate an intracranial mass lesion?

A
  • HA
  • seizures
  • general decline in neurological function
  • focal neurological deficits
79
Q

What are primary intracranial tumors?

A
  • glial cells (astrocytoma, oligodendroglioma, glioblastoma)
  • ependymal cells (ependymoma)
  • supporting tissues (meningioma, schwannoma, choroidal papilloma)
80
Q

What are secondary intracranial tumors?

A

evolve from lesions that metatizes from primary cancers in the lungs, breast, or skins

81
Q

What are major considerations for patients with intracranial lesions?

A
  • tumor location (determines position, EBL, risk for hemodynamic changes intraoperatively)
  • growth rate and size (slow growing tumors are often asymptomatic)
  • is ICP elevated
82
Q

What are anesthetic goals for patients with intracranial lesions?

A
  • control ICP
  • maintain CPP
  • protect from position-related injuries
  • rapid emergence for neuro assessment
  • will almost always extubate after surgery
83
Q

What are intraoperative monitoring considerations for a patient with an intracranial lesion during induction?

A
  • maintain normal CPP and avoid inc. ICP with slow, smooth induction
  • good preoxygenation
  • induction agents (thiopental, propofol, etomidate, paralytic, opioid, lidocaine)
  • hyperventilate
  • smooth laryngoscopy and intubation
  • be prepared to treat rapid changes in BP (treat HTN with esmolol or by deepening anesthetic, treat HoTN with incremental doses of phenylephrine or ephedrine rather than IVF boluses)
  • secure ETT away from the surgical field
  • consider use of reinforced tube if head will be flexed or turned lateral
  • secure breathing circuit
  • eye protection
  • OG tube, esophageal probe
84
Q

What are intraoperative positioning conditions for a patient with an intracranial lesion?

A
  • anticipate turning HOB 90-180 degrees
  • insure ability to access all vital equipment (adequate IV extensions, Aline extensions, long breathing circuit, PNS often on lower extremities)
  • HOB often elevated 10-15 degrees
  • pt may be supine, lateral, prone, or sitting
  • risk of unrecognized disconnects may be increased since patient and breathing circuit are almost completely covered by the surgical drapes
  • anticipate sympathetic response with placement of Mayfield head tongs
85
Q

What are intraoperative maintenance considerations for a patient with an intracranial lesion?

A
  • no set rules for best technique (N2O, opioid, NDNMR; or N2O, opioid, TIVA, NDNMB; or forane and opioid)
  • moderate hyperventilation
  • if cerebral edema occurs, discontinue agents that may increase cerebral blood volume (N2O and volatiles); TIVA may be necessary
86
Q

What are intraoperative fluid management considerations for the patient with an intracranial mass?

A
  • use glucose-free isotonic crystalloid (LR or NS) or colloid solutions
  • maintain normovolemia
  • fluid replacement will be below calculated maintenance requirements (usually
87
Q

How can you control ICP intraop in someone with an intracranial mass?

A
  • control BP and CVP (low normal)
  • PaO2>100 mmHg
  • Limit IVF to 10 mL/kg + UOP
  • Decrease volatile anesthetic concentration
  • Steroids
  • Hyperventilate
  • Mannitol +/- lasix (remember to assess K+ level)
  • HOB elevated
  • Ventriculostomy
88
Q

What should you consider regarding emergence in a patient with an intracranial mass?

A
  • consult with surgeon regarding extubation at end of case
  • if pt is to remain intubated, keep sedated and paralyzed; transport to ICU
  • if planning to extubate, must avoid wide swings in BP, HR, or ICP, must be slow and controlled, straining or bucking on ETT can cause intracranial hemorrhage or worsen cerebral edema
  • once head dsg is applied and anesthesia has full access to pt’s airway, discontinue anesthetic agents and reverse neuromuscular blocking agents
  • IV lidocaine or small doses of propofol may be used to prevent coughing whiel suctioning oropharynx
  • rapid awakening for neuro assessment is desirable
  • antiemetics necessary
  • monitor closely for occult blood loss
  • replace blood loss with blood or colloids
  • blood loss varies on site and type of lesion; typically 25-500 mL
89
Q

What are postop management considerations for the patient with an intracranial mass?

A
  • admit to ICU for observation
  • transport with HOB elevated
  • manage HTN
  • O2 for transport
  • minimal pain post craniotomy
  • observe for seizures, neuro deficits, increased ICP
90
Q

What areas of the brain are involved with surgery for posterior fossa lesions?

A
  • cerebellum (movement and equilibrium)
  • brainstem (ANS, CV and resp. centers, RAS, motor/sensory pathways)
  • CN I-XII
  • large venous sinuses
91
Q

What should you remember regarding anesthesia for posterior fossa lesions in the brainstem?

A
  • risk injury to cranial nerves, resp. centers, circ. centers
  • communication with surgeon is critical
  • bradycardia and HTN = trigeminal nerve stimulation (Cushing’s reflex)
  • bradycardia and HoTN = glossopharyngeal or vagus nerve stimulation
  • resp. centers may be damaged and necessitate mechanical ventilation postoperatively
  • tumors around glossopharyngeal and vagus nerves may impair gag reflex and increase risk of aspiration
  • CN IX, X, and XI control pharynx and larynx
92
Q

What positioning can be done for posterior fossa lesions?

A
  • Sitting, modified lateral, or prone
  • Sitting position preferred by surgeon (back is elevated 60 degrees while the legs are elevated with the knees flexed, head is fixed in a three-point holder with neck flexed, arms remain at sides with hands resting on top)
93
Q

What are the advantages of the sitting position for posterior fossa lesions?

A
  • improved surgical exposure
  • more anatomically “correct”
  • less retraction and tissue damage
  • less bleeding
  • less cranial nerve damage
  • better resection of the lesion
  • access to airway, chest, extremities
94
Q

What are cardiovascular complications with the sitting position for a posterior fossa surgery?

A

postural hypotension
arrhythmias
venous pooling

95
Q

How can you prevent cardiac compromise in the sitting position for a posterior fossa surgery?

A
  • light anesthesia during positioning
  • paralysis
  • volume load; vasopressors
  • leg wraps/compression stockings
  • move pt into position slowly
96
Q

What is a major sitting position complication to consider with an open dura?

A

pneumocephalus

97
Q

What is pneumocephalus?

A

an open dura causes CSF leak and air enters, after dural closure air can act as a mass lesion as CSF accumulates, usually resolves spontaneously but may cause tension pneumocephalus needing Burr holes to relieve

98
Q

What are symptoms of pneumocephalus?

A

delayed awakening, HA, lethargy, confusion

99
Q

How can you change your anesthetic to help prevent pneumocephalus?

A

discontinue N2O before dural closure

100
Q

What are potential nerve injuries from the sitting position for a posterior fossa surgery?

A
  • ulnar compression (arms across abdomen, pad elbows)
  • sciatic nerve stretch (pillow under knees)
  • lateral peroneal compression (pad knees)
  • brachial plexus stretch (pad under arms to support shoulders)
101
Q

When does a VAE occur?

A

occurs when the pressure within an open vein is subatmospheric, occurs when the level of the incision is >5 cm higher than the heart (the larger the gradient the higher the risk); veins higher than the right atrium have a lower intravascular pressure than the heart, patients with PFO can have entry of air into arterial circulation

102
Q

What is the incidence of VAE in the sitting position?

A

25-50%

103
Q

What is the incidence of VAE in the prone, lateral, or supine position?

A

12%

104
Q

What is a VAE?

A

large bubbles enter and lodge in the SVC, RA, or RV which impedes flow thru the heart, slow increase in PAP causing cardiovascular collapse

105
Q

What is a paradoxical air embolism?

A
  • air enters the left side of the heart and travels to systemic circulation (coronary and cerebral circulations most at risk)
  • occurs with right heart pressure is > L heart pressure
106
Q

How can you help prevent paradoxical air embolism?

A
  • monitor PAP/CVP
  • don’t allow R>L gradient
  • assess for murmur preoperatively; echo as indicated
107
Q

With which patients are paradoxical air embolisms common?

A

patients with a PFO, 10-25% incidence

108
Q

What are signs and symptoms of a VAE?

A
  • millwheel murmur
  • decreased EtCO2
  • increased PaCO2
  • decreased SaO2 and PaO2
  • detection of ET nitrogen
  • dysrhythmias
  • hypotension
  • sudden appearance of vigorous spontaneous ventilation
109
Q

What monitoring can you use for VAE?

A
  • precordial doppler
  • capnography
  • CVP/PA line
110
Q

Should you rely on only one monitor alone to diagnose VAE?

A

NO!!!! use 2 or 3 monitors of varying sensitivity to confirm diagnosis

111
Q

What is the sensitivity of the TEE monitor for VAE?

A

5-10 times more sensitive than doppler

detects 0.25 mL air

112
Q

What is the sensitivity of the precordial doppler monitor for VAE?

A

position over right atrium, less sensitive than TEE

113
Q

What is the sensitivity of the EtCO2 monitor for VAE?

A

decreases with 15-25 mL of air

114
Q

What is the sensitivity of the PAP monitor for VAE?

A

increases with 20-25 mL of air

115
Q

What monitors for VAE are the least sensitive?

A

PaCO2

MAP (hypotension seen with 50-60 mL of air)

116
Q

What monitors can be used for detection of VAE?

A 
TEE
precordial doppler
EtCO2
PAP
MAP
PaCO2
CVP
117
Q

What is the treatment of VAE?

A
  • 100% O2, discontinue N2O
  • notify surgeon to flood field or pack wound
  • call for help
  • aspirate from CVP line (have stopcock close to insertion site; aspirate with 30-60 mL syringe)
  • volume load
  • inotropes/vasopressors
  • jugular vein compression
  • PEEP
  • position pt LLD with slight Trendlenberg
  • CPR if necessary
118
Q

What is the leading cause of non-traumatic intracranial hemorrhage?

A

cerebral aneurysms

119
Q

Where do cerebral aneurysms predominantly occur?

A

branch of a large cerebral artery, base of the brain in the anterior Circle of Willis

120
Q

What are symptoms of an unruptured cerebral aneurysm?

A
  • headache
  • unsteady gait
  • visual disturbances (loss, diplopia, photophobia)
  • facial numbness
  • pupil dilation
  • drooping eyelid
  • pain above or behind eye
121
Q

What are symptoms of a ruptured cerebral aneurysm?

A
  • sudden, extremely severe HA
  • N/V
  • LOC, prolonged coma
  • focal neuro deficits
  • hydrocephalus
  • seizure
  • s/s of increased ICP
122
Q

What is the treatment for cerebral vasospasm?

A

Triple H therapy

  • HTN (SBP 160-200 mmHg)
  • Hemodilution (Hct ~33% provides balance between O2 carrying capacity and viscosity)
  • Hypervolemia (aggressive IV infusion of colloids and crystalloids for CVP >10 mmHg or PCWP 12-20 mmHg
123
Q

What is the rationale behind triple H therapy?

A
  • increase CBF in areas that become ischemic due to intense vascular narrowing
  • normally, inc. CBF would not result from inc. BP; however, with vasospasm, the vascular bed becomes passive
  • therefore, inc. CPP by inc. volume or by systemic administration of vasoactive drugs may reverse symptoms of cerebral ischemia inc.
124
Q

How can you diagnose a cerebral aneurysm?

A
  • H&P
  • CT
  • MRI
  • angiography
125
Q

What is the emergency treatment for cerebral aneurysm?

A
  • early diagnosis
  • airway management
  • control of ICP
  • hemodynamic stabilization
  • seizure prophylaxis
126
Q

What is the most common surgical treatment for cerebral aneurysm?

A
  • microsurgical clip ligation
  • craniotomy aproach; parent vessel giving rise to aneurysm is identified
  • aneurysm neck is isolated, and a clip is placed across the neck, excluding it from circulation
  • deep circulatory arrest may be necessary with giant aneurysms (>2.5 cm)
127
Q

What is involved with the preoperative management of a patient with an intracranial aneurysm?

A
  • thorough neurological assessment and documentation
  • identify other coexisting diseases, especially those that may be aggravated by induced hyper/hypotension
  • EKG studies
  • lab studies
  • radiological studies
128
Q

What are some of the anesthesia goals with patients with an intracranial aneurysm?

A
  • maintain optimum CPP, but be prepared to decrease CPP rapidly if intracranial hemorrhage occurs during surgical clipping
  • maintain transmural pressure
  • decrease intracranial volume (blood and tissue); provide “slack” brain
  • minimize CMRO2
129
Q

What should you do for preinduction with patients with an intracranial aneurysm?

A
  • limit sedation to avoid hypercapnia
  • Aline for induction
  • 2 large bore PIV’s
  • type and cross 2-4 units PRBCs ( blood loss can be >1 L)
  • remember HOB will be turned 90-180 degrees
  • positioning concerns
130
Q

What should you do for an induction with a patient with an intracranial aneurysm?

A
  • same goals for smooth induction as with tumor resection

- aggressive BP and HR control (esmolol, narcotic, deepen anesthetic)

131
Q

How should you consider for maintenance for someone with an intracranial aneurysm?

A
  • may use TIVA or anesthetic gases
  • STP gtt 20-30 mg/kg over 2 hours if brain protection is necessary due to temporary occlusion of a cerebral artery
  • maintain BP 15-20% below baseline to prevent vasospasm, dec. EBL, and allow for better surgical exposure and visualization
  • employ methods for cerebral protection and to reduce ICP if necessary
132
Q

How should fluid management be done for someone with an intracranial aneurysm?

A
  • run pt dry (
133
Q

How should you control BP for someone with an intracranial aneurysm?

A
  • control of BP is critical to successful outcome of case (inc. BP = inc. TMP across aneurysmal wall = rupture of aneurysm)
  • surgeon may ask for temporary inc. in MAP to 80-100 mmHg (or 20-30% overbaseline) to provide for collateral flow if a feeder vessel is clamped for a short period to allow for clipping of aneurysm
  • post-clipping, MAP is usually kept at 80-100 mmHg
134
Q

What is the major complication of cerebral aneurysm surgery?

A

aneurysm rupture

135
Q

When are the likely times for cerebral aneurysm rupture during repair?

A
  • dural incision
  • excessive brain retraction
  • aneurysm dissection
  • during clipping or releasing of clip
136
Q

What is the treatment of cerebral aneurysm rupture?

A
  • immediate, aggressive fluid resuscitation and replacement of blood loss
  • decrease MAP to 40-50 mmHg (SNP, labetalol, esmolol)
  • STP boluses (15-20 mg/kg over 30 mins) for brain production, to decrease MAP, and decrease blood loss
  • surgeon may apply temporary clip on parent vessel to control bleeding; restore BP after clipping to improve collateral flow
137
Q

What should you remember with emergence with patients with an intracranial aneurysm?

A
  • discuss with surgeon possibility for extubation
  • rapid neuro assessment
  • similar considerations as with intracranial lesions
138
Q

What is Guglieimi Detachable Coil (GDC) used for?

A
  • inserted into cerebral aneurysm and prevents flow of blood, thus preventing rupture
  • standard arteriogram is performed to locate aneurysm
  • catheter is passed, often through femoral vessels, and coil is advanced
  • advantages include shorter stay, less anesthetic requirements, uncomplicated positioning, minimally invasive
139
Q

What are complications of coiling?

A
  • aneurysm rupture/subarachnoid hemorrhage (rapid transport to OR for clipping is necessary)
  • vasospasm
  • CVA
  • incomplete coiling
140
Q

What are anesthetic implications for endovascular therapy for cerebral aneurysms?

A
  • GETA with complete muscle paralysis
  • control CPP
  • minimal narcotic needs since minimally invasive
  • a line preferred
  • minimal to no blood loss
  • heparin may be used for ACT 200-250
  • same postop concerns and with clipping
141
Q

What is an AVM?

A

congenital abnormality that involves a direct connection from an artery to a vein without a pressure modulating capillary bed which leads to high risk for SAH or intracerebral hemorrhage

142
Q

What is the treatment for AVM?

A

intravascular embolization
surgical excision
radiation

143
Q

What are preop considerations for a patient with an AVM?

A

same as with aneurysm

144
Q

What are anesthetic considerations for someone with an AVM?

A

similar to aneurysms, but potential for significant blood loss is much higher (upwards of 3 L), so large bore IV access is crucial

145
Q

What is the significance of a head injury dependent on?

A

extent of irreversible neuronal damage at time of injury as well as occurrence of secondary insults

146
Q

What are some secondary insults that can occur from head trauma?

A
  • systemic factors such as hypoxemia, hypercapnia, or hypotension
  • formation and expansion of an epidural, subdural, or intracerebral hematoma
  • sustained intracranial HTN
147
Q

What does the presence of a skull fracture indicate?

A

increased likelihood of significant intracranial lesion

148
Q

What are linear skull fractures associated with?

A

subdural or epidural hematomas

149
Q

What are basilar skull fractures with?

A

CSF rhinorrhea, pneumocephalus, and cranial nerve palsies

150
Q

What are depressed skull fractures associated with?

A

brain contusion

151
Q

What can deceleration injuries produce?

A

coup and contrecoup lesions

152
Q

What is the range for the Glasgow coma scale?

A

3-15

153
Q

What does a glasgow coma scale score

A

~35% mortality, “less than 8 intubate”

154
Q

What are anesthetic considerations unique to head trauma patients?

A
  • assess for and consider other traumatic injuries in treatment regimen
  • assume C-spine injury until otherwise proven radiographically
  • in-line stabilization should be used during airway manipulation and management; maintain head in neutral position
  • intubate early
  • full stomach precautions
  • awake FOI if difficult airway is anticipated
  • hypotension common with spinal cord injuries
  • maintain Hct>30%
  • seizure prophylaxis
  • DIC with severe head trauma, treat with FFP and platelets
  • monitor for diabetes insipidus
  • recovery from head injury unpredictable, generally advisable to leave pt intubated at end of procedure
155
Q

Should you ever do a blind nasal intubation in someone with a basilar skull fracture?

A

NO, would avoid in anyone with CSF rhinorrhea, otorrhea, hemotympanum, or ecchymosis into periorbital tissues (raccoon’s sign) or behind the ear (Battle’s sign)

156
Q

When are VP shunt procedures done?

A

conditions like hydrocephalus in which there is obstruction in flow of CSF or decreased absorption of CSF, VP shunt systems have one-way, pressure-dependent valves to regulate flow of CSF

157
Q

How is the patient positioned for a VP shunt procedure and where are the incisions?

A

positioned so that the cranial incision and abdominal incision are aligned in the same plane (often supine with head turned to contralateral side), cranial incision is made over region of ventricular cannulation and burr hole is made in the cranium, pocket is created for the valve (usually behind the ear), a separate incision is made in the abdomen and dissection is carried down to level of peritoneum, catheter is them passed subcutaneously from abdominal incision to cranial incision using special tunneling instrument

158
Q

What are anesthetic considerations for VP shunt procedures?

A
  • patient is to be treated as if they have inc. ICP
  • GETA with controlled ventilation
  • avoid hyperventilation and hypocarbia because they make cannulation of the ventricle more difficult for the surgeon
  • may be helpful to hand ventilate during catheter tunneling as positive pressure ventilation could increase risk for pneumothorax
  • EBL 5-25 mL
159
Q

What is stereotactic neurosurgery?

A
  • applies simple rules of geometry to radiologic images to allow for precise localization within the brain, providing up to 1 mm accuracy
  • allows surgeons to perform certain intracranial procedures less invasively
  • radiologically, small markers (fudicals) are affixed to the scalp and forehead with adhesive; important that these fudicials do not move between the time of imaging and entry into the OR
160
Q

What is an awake craniotomy done for?

A
  • used for epilepsy surgery and resection of tumors in frontal lobes and temporal lobes when speech and motor are to be assess intraoperatively
  • intraoperative neurological testing allows optimal tumor resection with minimal postoperative neurological dysfunction
161
Q

How is anesthesia done for an awake craniotomy?

A
  • pt often put under GA for opening of dura and exposure of tumor (LMA inserted with controlled ventilation, TIVA technique with precedex or propofol and remifentanil is often employed; TIVA meds are adjusted according to hemodynamics and BIS scores)
  • once the tumor is exposed, remifentanil is decreased until spontaneous ventilation returns
  • LMA discontinued
  • Propofol is discontinued and pt is allowed to awaken
  • continue low dose remifentanil to provide analgesia during awake period
  • nasal trumpets with O2 may be helpful to prevent hypoxia
  • when tumor resection is complete, GA is induced and LMA is placed, ventilation is then controlled until the end of surgery
162
Q

What are the most common symptoms of enlarging pituitary tumors?

A

frontal or temporal HA

163
Q

What approach is done for pituitary surgery?

A

transsphenoidal approach done for tumors under 10 mm in diameter, bifrontal craniotomy approach is done for tumors >20 mm in diameter

164
Q

What are some preop considerations for pituitary surgery?

A
  • hyperglycemia
  • Cushing’s disease
  • Addison’s disease
  • acromegaly
  • diabetes insipidus
165
Q

What are anesthetic considerations for pituitary surgery?

A
  • transsphenoidal approach necessitates HOB elevated 10-20 degrees
  • airway is shared with surgeon; oral RAE tube useful
  • protect patient’s eyes
  • avoid hyperventilation because reduction in ICP result in retraction of pituitary into the sella tursica making surgical access difficult
  • consider potential for mass hemorrhage as the carotid arteries lie adjacent to the suprasellar area
  • epinephrine and cocaine may be used as a topical to vasoconstrict vessels (epi and cocaine may cause HTn adn dysrhythmias, avoid halothane)
  • mouth and throat pack is placed to absorb glottic blood and minimize postoperative vomiting of blood
  • surgeon may inject air or saline to delineate suprasellar margins; if air is injected, discontinue N2O
166
Q

What complication is common after pituitary surgery and how would you treat it?

A

diabetes insipidus, usually self-limiting and resolves within 7-10 days, can treat with vasopressin or desmopressin

Principles III (12 decks)

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