Anesthesia For Neurosurgery Barash 37 Flashcards Preview

Advanced Principles III > Anesthesia For Neurosurgery Barash 37 > Flashcards

Flashcards in Anesthesia For Neurosurgery Barash 37 Deck (275)
Loading flashcards...
1
Q

Basal Ganglia is made of

A
1-Caudate Nucleus
2-Substantia Nigeria
3-Red Nucleus 
4-Globus Pallidus 
5- Putamen
2
Q

Dysfunction if Extrapyramidal System lead to

A

Parkinson’s
Essential Tremors
Ataxia

3
Q

Supratentorium contains

A

1) Paired Cerebral Hemispheres

2) Diencephalon : Thalamus and Hypothalamus

4
Q

What makes the extrapyramidal system

A

Basal Ganglia
Cerebellum
Auditory and Vestibular system

5
Q

Where the diencephalon located

A

Cephalad to the midbrain

6
Q

Thalamus role

A

Sensory and motor Relay station

Connect the cortex and the rest of the nervous system functionally and physically

7
Q

Hypothalamus located where? It’s function ? It is connected to ?

A

Below the thalamus
Autonomic and Endocrine function
Connected to the pituitary glad via the Infundibulum

8
Q

Limbic play a role in (3)

A

1) Cognitve
2) Memory
3) Emotional

9
Q

The limbic system components are :

A

Amygdala
Hippocampus
Some regions of the Cortex : Insular region example
Part of the hypothalamus

10
Q

Brain stem has nuclei for CN 3 and 12 . true or False ?

A

True

11
Q

Brain receives 70 % blood from and 30 % from

A

70% from Two internal carotid arteries .

30% from vertebral arteries posteriorly forming the basilar artery , subsequently converge to for circle of willin

12
Q

Common carotid emerges from the

A

Aortic arch and divides at the level of the thyroid cartilage in the internal and the external carotid arteries

13
Q

The internal carotid artery traverse the ____through the ____and subsequently travels through the _____and into the _____

A

The skull though foreman lace rum

The cavernous sinus and into the carotid groove .

14
Q

Bil vertebral arteries originate from the_____and converge to form the ____at the _____junction

A

From the Subclavian arteries
Form the basilar artery
At the pontmedullary junction

15
Q

Basilar reached midbrain and divides into the

A

Posterior cerebral arteries and anastomoses with the PCOMs = completes the circle of Willis .

16
Q

Less than ___% of people demonstrate a complete circle of Willis

A

50 %

17
Q

All the sinus Darin into the

A

Sigmoid sinus and thereafter the internal jugular veins

18
Q

CSF is produced mostly by choroid Plexus of lateral and third ventricle. True or False ?

A

True

19
Q

Average volume of CSF in an adult is

A

150 ml ( approx)

20
Q

CSF is created at a rate of ___ and moves from

A

15- 20 ml .hr

Moves from the ventricles via the aqueduct of sylvius to the fourth ventricle .

21
Q

CSF flow

A

Choroid plexus of third and lateral ventricle(aqueduct of Sylvius )&raquo_space;4th ventricle» ( Foramen of Magendie and lateral foramina of Lushka)&raquo_space;Subarachnoid space of the cranium .

22
Q

Primary sinus where CSF gets reabsorbed

A

Superior Sagittal Sinus via arachnoid villi and granulations

23
Q

Some CSF traverses the Foramen Magnum , enters the subarachnoid space of the spinal column . This movement is important how?

A

Acute and chronic compensation in elevated ICP

24
Q

How vertebraes

A
33 vertebrae 
7 C
12 T 
5L
9 fused sacral (5) And coccygeal (4)
25
Q

Dorsal Columns containing tracts responsible for :

A

Proprioception, light touch

Central gray Matter *

26
Q

Lateral Spinothalamic Tract responsible for

A

Pain and temperature

Central gray matter *

27
Q

The outer white mater contains the ______Tract

A

lateral Corticospinal

28
Q

Lateral gray column contain the cell bodies of the ______neurons that enter the _____chain , running on either side of the vertebral bodies , arising from

A

Preganglionic
Sympathetic chain
Arsing from T1 to L2/L3

29
Q

Spinal cord ends

A

L1 or L2 in adults

Conus medullaris and film terminale

30
Q

Spinal cord receives blood from :

A

1 anterior spinal

2 posterior spinal arteries

31
Q

The anterior spinal artery originates from

A

6 - 8 major radicular arteries derived from the aorta.

32
Q

The largest of the radicular arteries in the anterior spinal artery is the

A

Artery of Adamkiewicz

Occurs at T11/T12 but supplies T8 to conus medullaris terminus

33
Q

Artery of Adamkiewicz is responsible for supplying blood to the _______of the spinal cord

A

Anterior 2/3 of the spinal cord

34
Q

The posterior Spinal arteries supply the ______and ______and feeds ______of the spinal cord

A

Dorsal horn and the white matter

Posterior 1/3 of the spinal cord.

35
Q

Brain is ___% of total body weight and ___% of O2 consumption and ____% of total body glucose consumption

A

2% Total Body weight
20% O2 consumption
25% total glucose consumption

36
Q

brain glucose consumption

A

5mg/100g/min

37
Q

CMRO2 normal is

A

3 - 3.8 ml/100g/min

38
Q

Normal CBF

A

50ml/100g/min or 750 ml/min .therefore the brain receives 15% of the cardiac output

39
Q

Irreversible Brain injury will occur how long after lack of O2 supply ?

A

4 to 5 minutes of global ischemia

40
Q

CBF is regulated by …

A

Flow- metabolism coupling

41
Q

CPP is the

A

≠ between MAP and ICO or CVP depends on which is bigger

42
Q

CBF itself equal to

A

CPP/CVR

43
Q

Cerebral auto regulation remain intact between MAP of ___ and it function by ___

A

*60 -1 60 mmHg ( approx)
Lower limit autoregulation is > 60 mmHg, changes throughout the day , differs per individual.

*Functions by altering CVR on the order of 5 to 60 seconds ( within a minute)

44
Q

In health brains the LLA may be as high as MAP of

A

80 mmHg

45
Q

Altering CVR is accompanied by ( 2 things )

A

Rapid phase aka dynamic autoregulation (: pulsatile changes link to SBP

Slow phase aka Static autoregulation ( phenomenon that accommodate to changes in MAP over longer time intervals

46
Q

Above the Upper Limit and Lower to the LLA CBF is

A

Pressure dependant

47
Q

Below the LLA what occurs?

A

Max cerebral vasodilation and Ischemia

48
Q

Above the autoregulation upper limit , what occurs ?

A

Max vasoconstriction

Increased perfusion pressure&raquo_space; disrupted BBB» Cerebral edema or cerebral hemorrhage.

49
Q

Chronic HTN, autoregulatory curve is shifted

A

Right

50
Q

Anesthetics do what to your autoregulation ?

A

Anesthetics, especially the potent ones have a dose dependent DECREASE in autoregulation

51
Q

What physiologic parameters play important role in regulating CBF ? Which is most important ?

A

A)MAP
B)PaCO2 : most important **
CBF is linear to PaCO2 ( but the PaCO2 must be between 20 and 80 mmHg )
C) Temp

52
Q

Hypoventilation does what to the CBF ?

A
Increase 
Remember CO2 ( vasodilates you )
53
Q

What does hyperventilation to your CBF ?

A

Decrease

Remember low CO2= vasoconstriction

54
Q

A change in PaCO2 of ___mmHG correlates with changes in ___of _____

A

PaCO2 change of 1 mmHg = same change in CBF of 1- 2 ml/100g/min

55
Q

What happens is PaCO2 is lower than 20 mmHG

A

Max cerebral vasoconstriction&raquo_space; Tissue hypoxia&raquo_space;> reflex vasodilation.

That’s why you start hyperventilating when your ICP is acutely elevated. But that reflex vasodilation can cause ischemia.

56
Q

The effects of hyperventilation on CBF and ICP only sustainable for how long ?

A

only 6 hours .

BC Phof CSF will renormalize

57
Q

When does PaO2 have effect on CBF ?

A

Marked hypoxia aka PaO2 < 50 mmHg

CBF increases dramatically!

58
Q

When can PaO2 cause vasoconstriction

A
When > 350 mmHg 
Slight vasoconstriction ( to protect itself from O2 toxicity ( O2 free radical formation )
59
Q

How does Temp affect CBF ?

A

6- 7% DECREASE in CBF per 1 º C DECREASE in core temp .

60
Q

Regional CBF is governed by

A

Humoral and Neurogenic factors

61
Q

Catecholamines and mediators involved in regional cerebral vasoconstriction are

A

A1 agonists
Ionic Ca+
Endothelium
Thromboxane A2

62
Q

Catecholamines and mediators involved in regional cerebral vasodilation are

A

B2 agonist
Nitric Oxide
Adenosine
PGs

63
Q

Neurogenic influence over local CBF regulation :

A

Ach
Dopamine
Serotonin
Substance P

64
Q

What the effects of Anesthetics on CBF ? ( not autoregulation)

A

Profound effect !!!

65
Q

IV anesthetic effects on CBF

A

Propofol, Etomidate, Benzodiazepines, Thiopental DECREASE CBF bc&raquo_space; decrease in CRMO2&raquo_space; flow-metabolism coupling .
* Autoregulation and PaCO2 remain intact with those !

66
Q

Ketamine effects on CBF, CMRO2 , Autoregulation, PaCO2 ( 2)

A

1) Increases CBF and CMRO2

2) Little effect in autoregulation and PaCO2

67
Q

Volatile anesthesic effects on CBF and autoregulation .

A

1) Potent volatiles Sevo, ISO and Des = DIRECT cerebral vasodilators ! but&raquo_space; decrease CRMO2&raquo_space; flow-metabolism coupling&raquo_space; offset CBF = none to min. Increase in CBF at lower dose , but at high doses&raquo_space;max suppression of CRMO2» major vasodilation» increased CBF Therefore we say they have **dose- dependent effects of CBF
2) Autoregulation is inhibited : but vessels can still response to PaCO2 changes .

68
Q

N2O effects on CBF

A

Direct cerebral vasodilator +
Minimal effect on CRMO2 +
Variable effect on cerebral autoregulation capacity
Propofol + N2O = preserved autoregulation
Sevo+ N2)= impaired autoregulation

69
Q

Spinal Cord Perfusion Pressure SCPP=

A

MAP- SSSP ( Spinal subarachnoid Space pressure )

70
Q

Volume of brain

A

1400 ml

71
Q

volume of CSF in cranium

A

150 ml

72
Q

CBV ( cerebral volume )

A

150 ml

73
Q

Monroe Kellie Doctrine

A

Increase in the volume of one will lead to a rise in ICP unless it is matched by an equal reduction in the volume of another compartment.
Brain can’t compress so CSF and CBV adjust to maintain ICP

74
Q

CBV decrease how ?

A

Reflex arterial vasoconstriction + increase venous Efflux from brain and venous sinuses .

75
Q

Care of elevated ICP patients

A

1) Avoid Hypoventilation
2) Maintain CPP
3) Reduce intracranial volume : Mannitol, CSF 4)diversion, Cerebral vasoconstricting anesthetics ????
5) Consider decompression craniectomy

76
Q

Normal ICP is

A

7 - 15 mmHg ( 5-15 mmHg PP)

77
Q

Poor neurological outcome is from ICP above

A

20 - 25 mmHg

78
Q

High ICP does what to CBF ?

A

Decrease

79
Q

Intracranial elastance curve

A

Visualizing the ICP -Volume relationship

80
Q

Cerebral elastance formula

A

E= dP/dV

Lumbardrain, extraventricular drain.

81
Q

“Flat of the curve “( intracranial elastance curve means :

A

Elastance is low

In normal brain , changes in volume compensated for easily by CSF and CBV

82
Q

Elbow of the curve ( intracranial elastance curve )means :

A

Elastance increases

Small increase in volume = rapid rise in ICP

83
Q

Most common cause of elevated ICP is

A

**Cerebral edema **
Cytotoxic : increase intracellular water i.e Post ischemia.
Vasogenic: loss of integrity of BBB. Happens in tissue around tumors, abcess, contusion. Dexamethasone*
Interstitial : increase extrecellular fluids + intact BBB i.e hydrocephalus

84
Q

Why dexamethasion only can treat vasogenic edema ?

A

BC it upregulates the proteins responsible for the integrity of the tight junctions

85
Q

How can increase CBV increase ICP ?

A

Increase arterial inflow plus decreased venous efflux = rise in ICP

86
Q

What can increase arterial inflow ?

A

Vasodilators
Hypercapnia
Severe hypoxemia/ Acidosis

87
Q

What can cause decreased Venous efflux ? Thus increasing ICP

A

Jugular vein obstruction

Elevated pressure within the airways

88
Q

Clinical symptoms of elevated Intracranial Hypertension.

A

Headache
N/V
Papilledema

89
Q

As ICP continues to increase you will see what ?

A

Cushing Triad
1 HTN
2 Bradycardia
3 Irregular respiration

90
Q

Signs of herniation

A
Depends on structures herniating 
Pupillary Dilation 
Oculomotor weakness 
Absent light reflex 
Cardiorespirations
91
Q

CT results of elevated ICP

A

Effacement of Sulci
Compression of ventricles
Midline shift
Even possible ventriculomegaly

92
Q

In acute phase of spinal cord injury , what are the s/s ?

A

Flaccid paralysis and hypotension

93
Q

Flaccid paralysis and Hypotension are seen in which phase of spinal injury ?

A

Acute

94
Q

Spastic , Pain and risk for autonomic hyperreflexia are seen in which phase spinal cord injury ?

A

Chronic

95
Q

Both chronic and acute spinal injury may have what s/s ?

A

Loss of sensory, motor, autonomic function below the level of injury.

96
Q

Most important monitor of CNS function is

A

Neuro exam of an an awake and responsive patient.

97
Q

BAEP and VEPs are less commonly used. True or False ?

A

True

98
Q

Amplitude is measured in ____ for SSEP and BAEP and measured in _____for MEPs

A

Microvolts

Millivots

99
Q

Latency is measured in ___ refers to the _____

A

Milliseconds

Refers to The delay in peak signal following stimulation and reflects transit time along the neural pathway.

100
Q

SSEP elicited from ____and is measured at the level of ______

A

A peripheral nerve

Subcortex : upper cervical spine , inion and cortex : scalp.

101
Q

SSEP stimuli travel through

A

Posterior Column/ Medial Lemnicus pathway in the CNS

102
Q

SSEP is useful for monitoring integrity of

A
Peripheral Nerves 
Dorsal Column 
Brainstem 
Subcortex ( upper cervical spine, inion)
Sensory cortex of the brain
103
Q

SSEP stimuli are recorded in the contralateral side scalp because

A

Sensory tracts crosses at the brainstem before getting through the thalamus and up the sensory Cortex

104
Q

SSEP are used during

A

Spine Surgery

Neurovascular brain surgery : cerebral aneurysm clipping.

105
Q

Significant changes in SSEP means

A

Decrease amplitude by 50%

Increase Latency by 50%

106
Q

MEPs are produced at the level of the

A

Cortex by direct stimulation of the cerebral cortex or by

Indirect stimulation of the scalp

107
Q

Lower extremity SSEP which artery ?

A

ACA

108
Q

Upper extremity SSEP which artery ?

A

MCA

109
Q

MEPs for assessing what ?

A

Motor cortex and anterolateral spinal cord ( containing the corticospinal tracts )

110
Q

MEPs how is stimulation produced ?

A

Indirect electrical stimulation of motor cortex via scalp electrodes&raquo_space;pulses travel caudad» depolarization of upper motor neurons in spinal cord» accumulating in the ventral horn&raquo_space; alpha motor neurons&raquo_space;motor endplates» muscle movement

111
Q

Muscles relaxant effects on SSEP vs MEPs

A

SSEP muscle relaxants helpful to remove artifacts by the EMG activity
MEP muscle relaxants inhibit measurement of muscle response

112
Q

Change Latency of MEPs less worrisome change than in SSEPs

A

True

113
Q

EMG sensitive to what type of injury ?

A

Mechanical and Thermal

Does not monitor ischemia ,

114
Q

Is EMG sensitive to muscle relaxant ?

A

Yes !

115
Q

What are BAEPs used for ?

A
Integrity of 
Auditory Canal 
Tympanic membrane 
Hair cells
Spiral ganglion 
Vestibulocochlear nerve 
Cochlear nuclei 
Superior Oliver’s complex
Lateral lemniscus 
Inferior Colliculus 
Medial geniculate thalamic nuclei
116
Q

VEPs and anesthetics ?

A

Exquisitely sensitive to almost any anesthetic regimen , diff to obtain and interpret the signals = they are not used often

117
Q

Potent volatile and N2O causes what to SSEPs

A

Greatest inhibition&raquo_space; Decreased amplitude , increase latency

118
Q

IV anesthetics , limited effect on SSEPS unless?

What about opioids ?

A

Very high doses

Opioids Salem unless a bolus = decrease amplitude.

119
Q

N2O affects amplitude or latency more ?

A

Amplitude

120
Q

Etomidate and Ketamine effects on SSEP

A

Increases amplitude!!! Even are used to enhance SSEP

121
Q

Scalp MEPs are sensitive to

A

Anesthesia
Potent volatile greatly inhibitory
But can still use Mac of 0.5

122
Q

TIVA for MEPs is the usual . True or False ?

A

True

123
Q

BAEPS are ____ regardless of anesthetic regimen being used . Deep anesthesia may cause _____ but ______will cause some increase in interweave latencies

A

Robust !
Small increase in latency
Cold irrigation of fluid at the brainstem

124
Q

Most sensitive neuromonitoring modality to anesthesia ?

A

Very
Inhalation w/ or w/o N2O > TIVA
Use opioids TIVA, muscle relaxant and BIS

125
Q

TCD measures

A

Blood Flow Velocity

126
Q

Decrease arterial diameter does what to blood flow velocity ?

A

Decrease

127
Q

Normal ICP

A

7 to 15 mmHg

Monitoring begins when ICP > 20 mmHg

128
Q

What ICP values means severe life threatening Intracranial hypertension?

A

ICP > 40mmHg

129
Q

The presence of characteristic Lindbergh waves provides

A

State of brain

130
Q

How many Lindbergh waves ? What are they ?

A

(3 ) A, B, C waves

131
Q

A waves are

A

(1) Plateau waves
(2) Happen when compensatory mechanism for elevated ICP are severely exhausted.
(3) Due to intense vasodilation in response to decreased CPP
* Are ALWAYS pathologic.

132
Q

B waves are

A

(1) Elevated ICP 20 - 30 mmHg above baseline , occurring 1 or 2 times a minute.
(2) reflects changes in vascular tome when CPP is at the LLA ( lower limit autoregulation)

133
Q

C waves are

A

Small oscillation , 4 to 8 times a minute ,
ICO is Normal
Reflects systemic changes in vasomotor tone, with LITTLE pathologic significance

134
Q

Most commonly use ICP monitoring device

A

Ventriculostomy or
External Ventricular Drain aka EVD ( transducer is zeroed at the auditory meatus )
Connected to lateral ventricle

135
Q

What is the gold standard ICP monitoring ?

A

Ventriculostomy or EVD placed int the lateral ventricle

136
Q

A ventriculostomy can

A

Monitor ICP
Drain CSF
Deliver drugs ( i.e ABX, thrombolytic)

137
Q

EVDs have great risk for

A

Infection,

CSF sepsis

138
Q

What is SjVO2 ? What tool measures it ?

A

Mixed cerebral O2 tension
Indicative of brain’s global O2 consumption/extraction.

Jugular bulb venous oximetry , most commonly used technique,
catheter place in internal jugular, in the jugular bulb , X-ray confirms it at level of mastoid process

139
Q

SjVO2 less than 55%=

A

Cerebral ischemia in the setting of hypotension or marked elevated ICP

Useful during hyperventilation which may cause vasoconstriction, so goal to keep it above 55%

140
Q

Other measures of cerebral metabolism are brain tissue oxygen monitor and microdialysis catheter ?

A

True

141
Q

Brain tissue o2 monitor measure what ?

A

Partial pressure of O2 ( PbtO2) in a portion of brain interstitium , directly or indirectly , via Clark-type electrode

142
Q

What is normal PbtO2 ?

A

25 to 48 mmHg

Reflects balance between O2 supply vs demand in the region around the electrode

143
Q

What affects PbtO2?

A
FIO2
PaO2
CO
Hemoglobin concentration
Local O2 extraction
CBF
144
Q

In pathologic brain state , PbtO2 less than … are considered significant

A

PbtO2< 20 mmHg

145
Q

What does SjVO2 80 - 85 % mean?

A

Low O2 extraction or high O2 delivery

146
Q

When do we monitor brain tissue Oxygen ?

A

TBI and SAH

147
Q

Glutamate level means ____and glycerol level means____ measured by cerebral microdialysis

A
Glutamate = ischemic neuronal stress
Glycerol= cell membrane degradation
148
Q

Cerebral Oximerty is

A

Transcutaneous measurement of REGIONAL cerebral blood oxygenation ( rSO2) over the frontal cortices bilaterally.

149
Q

Cerebral oximetry reflect arterial or venous blood ?

A

Both

Bc Oxygenation is given as a %tage of maximum hemoglobin saturation. Oxymoglobin and deoxymoglobin

150
Q

Significant hypoxia in cerebral oximetry is when

A

A decreased of at least 20 % from baseline

151
Q

Cerebral Oximetry relies on pulsatile flow , True or False ?

A

False ! Pulse oximetry relies on pulsatile flow not cerebral oximetry

152
Q

When you have low cerebral oximetry what factors can prevent long term injury

A

Increasing the systemic BP
increasing the CO
Increasing the FIO2
increasing the PaCO2 : fix the vasoconstriction
RBC transfusion= increase O2 carrying capacity

153
Q

Brain is susceptible to rapid ischemic injury because?

A

1) High rate O2 and Glucose consumption
2) can’t store substrates
3) cant dispose of toxic metabolites quick
4) intracellular Calcium builds up when ischemic = quick neuro damage + lactic acid accumulates

154
Q

Focal ischemia vs global ischemia

A

Focal due to regional insult ( embolus, arterial disruption . Treat by restoring perfusion to the region» restore O2 and substrate the ischemic penumbra . The penumbra around the necrotic core is salvageable!

Gobal is due to severe hypotension, severe anemia. Treat by restoring Cerebral perfusion, O2 delivery i.e CPR , RBC transfusion ,

155
Q

Saving the Penumbra

A

Increase CPP and reduce brain edema

156
Q

Repercussion injury of the brain

A

Reperfusing ischemic brain tissue leads to worse neuro outcome bc of free radicals from O2, mediators of inflammation and repeat of Injury of microvasculature when the flow is restored

157
Q

Hypothermia and cerebral protection

A

In theory should be protective to brain and spinal cord , it lowers CRMO2 . But also , even 1ºC decrease protects , so other pathway beside decrease CRMO2 may be involved
But works best for global ischemia not so much focal ischemia

158
Q

27 ºC is

A

Profound hypothermia used in cold- cardiopulmonary bypass

159
Q

12 to 18 ºC is

A

Deep hypothermia used in circulatory arrest

160
Q

Cerebral hyperthermia is good or bad

A

Detrimental !
Ischemia tripled 1ºC in animals
Must be avoided in cerebral ischemia

161
Q

Satins upregulate

A

Nitric oxide synthase.

162
Q

How are volatiles cerebral protectors (5) ?

A

1) Reduce ischemia-induced glutamate release
2) Increase antiapoptotic mediators
3) Activate ATP- dependent K channel
4) Reduce excitotoxic stressors
5) Increase CBF

163
Q

What is the only subtstrate that can be aerobically metabolized by the brain under normal conditions ?

A

Glucose

164
Q

Is glucose stored in the CNS ?

A

No
When no sugar bc of limited cerebral circulation&raquo_space; no ATP&raquo_space; energy requirement not supplied&raquo_space; cellular injury quickly ensues .

165
Q

Cerebral glucose consumption normal value is _____and it parallels what ?

A

5mg/100g/min

Cerebral Glucose Consumption parallels CRMO2

166
Q

Hypoxemia or hypoglycemia , which is more detrimental to brain ?

A

Roughly EQUALLY detrimental

167
Q

Define hyperglycemia ___ and what effect on neuro outcome .

A

BG> 180mg/dL
Worsen neuro outcome
By worsening cerebral acidosis in an anaerobic setting (bc the glucose converts to lactic acid !)

168
Q

Temporary clipping of cerebral vessel what anesthetic you give ?

A

Propofol 1- 2 mg/kg followed by 150 mcg.kg.min to induce “Burst suppression” prior to the planned ischemia

169
Q

Deep hypothermia in what cardiac and neuro sx to protect nervous system?

A

Aortic arch repair or giant basilar aneurysm clipping - 12ºC to 18 ºC

170
Q

Prior to throracoabdominal aortic aneurysm repair what can be done for neuro protection?

A

Placement of a lumbar CSF drain&raquo_space;to lower the CSF and maintain spinal cord perfusion when radicular arteries from the aorta are at surgical risk

171
Q

Preop of patient with Intracranial mass lesions what is the most important thing to ascertain ?

A

Ascertain presence or extent of Intracranial Hypertension , this should be assumed until proven otherwise .
get this info from H&P, CT , MRI, ICP measurements.

172
Q

What do patients with elevated ICP complain of ?

A
Headache 
Dizziness
Visual or gait disturbances 
N/V
Seizures
173
Q

What do patients with elevated ICP show on physical exams?

A
Altered LOC 
Confusion
Papilledema 
Loss of strength or sensation
Cranial nerve dysfunction
174
Q

Radiology studies quantify degree of ICP showing

A

Slit ventricles or

Shift of midline brain > 5 mm = advanced pathology

175
Q

What lab may accompany elevated ICP ?

A

Electrolyte disturbances due to pituitary pathology SIADH

Or due to diuretics , steroids, anticonvulsants

176
Q

Premedication with Benzo and opioids even in small doses can lead to what ?

A

Elevated ICP bc they depress respirations&raquo_space; elevated PaCO2» ICH

177
Q

What meds to continue preop with these patients with elevated ICP?

A

Corticosteroids ( i.e Dexamethasone ) and anticonvulsants

178
Q

Preop for Spine surgery , especially acute focus on

A

Airway exam
Hemodynamics
Level of injury
The degree of injury : complete vs non complete

179
Q

Induction of GA and airway mngmt in elevated ICP , unsecured aneurysm , cervical spinal cord injury focus on

A

Hemodynamics
Slow and controlled induction for high ICP patients with constant blood pressure maintenance

Avoid HYPOTENSION

Opioid and Lidocaine to blunt the systemic response to DL

Avoid HHYPOVENTILATION and HYPOCAPNEA

Should give a muscle relaxant after induction but Sux be careful
Avoid HYPOTENSION and low CPP

Cervical spine sx: not only maintain MAP , but techniques to prevent further compromise

180
Q

What does SUX do to ICP ?

A

Increased ICP but short acting
Use it with caution in patients with motor deficits bc upregulation of nicotinic receptors at the NMJ lead to increased risk Hyperkalemia

181
Q

During intubation of pt with high ICP

A

Rapid rise in arterial BP will worsen ICP esp when autoregulation fails , or pt w. Unsecured aneurysm

182
Q

Maintenance of GA in intracranial sx with high ICP what is paramount until the dura mater is opened?

A

ICP control

183
Q

Once Mayfield fixation and head positioned safely give

A

Mannitol 0.5 1.5 mg/kg if you need to control the ICP
Give dexamethasone 10 mg
Sometimes give anticonvulsant prophylactic

184
Q

High ICP, volatile MAC is limited to ___if used at all

A

0.5 MAC

Instead give IV anesthetic i.e.propofol w/ or w/o opioids short acting i.e. remifentanil or Alfentanil

185
Q

> 0.5 MAC may interfere with SSEP and MEPs true or false ?

A

True

186
Q

Why is N2O avoided in elevated ICP cases ?

A

Mild vasodilating effect
Potential intradural air
Or can interfere with monitoring

187
Q

MEP and EMG you can give muscle relaxants , what can you use instead ?

A

Remifentanil infusion 0.2 mcg/kg/min

188
Q

Have you vasopressor on board to maintain the

A

CPP

189
Q

When autoregulation is inhibited either bc of the disease or the anesthetic , what does CBF depends on

A

MAP

So that means avoid hypertension

190
Q

Ventilation Management in neurosurgery , Intracranial sx , what is Tidal Volume and peak pressure goal ?

A

Maintain at 6- 8 mL/kg = minimize inflammatory lung injury
Peak pressure < 40 cmH2O
Esp patients with SAH and TBI
And esp patient w/ ALI , ARDS

191
Q

Why do you avoid PEEP in elevated ICP pts

A

( unless you need it for better oxygenation )

Bc : increase intrathoracic pressure&raquo_space; impede cerebral venous drainage

192
Q

What mode is used in neuro sx ?

A

PPV ( positive pressure ventilation) bc it allows direct control of PaCO2 !!!
Esp in sitting craniotomy where negative intrathoracic pressure&raquo_space; VAE ( venous air embolism )

193
Q

Primary goal of fluid management in neuro surgery is to

A

Maintain cerebral perfusion , not to dry them out !, keep euvolemic . Give isotonic solution if you have to give large amount
AVOID hypotonic such as LR ??? if need large amount = cerebral edema

194
Q

Can we give fluids with dextrose to those neuro patients ? Why ?

A

No.

1) Bc hyperglycemia = detrimental to Cerebral metabolism ( parallel increase in CRMO2) + worsen neuro outcome by worsening lactic acidocis in an anaerobic ( ischemic tissue is anaerobic ) bc sugar becomes lactic acid in aneorobic environment.
2) Bc Glucose get quickly metabolized and is not osmotically active , leaving free water = worsen brain edema

195
Q

Moderate to severe hyponatremic state give

A

3% saline at rate of
50 to 100 ml/hr
Check serum Na+ q 1 hr

196
Q

Central Pontine myelinosis can happen when …

A

Rapid rise in serum Na+ > 3-4 mEq/L/hr

AVOID that !!

197
Q

Mannitol can cause short lived electrolyte imbalance which are ?
How can Mannitol impair cerebral perfusion ?

A

Hyponatremia
Hyperkalemia

By causing dehydration = impair cerebral perfusion

198
Q

What can large amount of 0.9%NS cause ?

A

Hyperchloremic acidosis&raquo_space; AKI due to renal tubular acidosis

199
Q

Preop Coags must be corrected. True or False

A

True

Patients on anticoagulants = required to draw preop coag labs

200
Q

Non urgent Neuro surgery patients should have platelet count of

A

100,00/mm3

Craniotomy with low bleeding risk a Type and Screen ( T&S) with neg Antibody ( ABS ) is enough

201
Q

Neuro surgery with high risk bleeding are ____ what should be available ?

A

Aneurysm clipping
AVM resection
Tumor craniotomies that invade the cranial sinuses

RBC that are T&C should be available for intro op

202
Q

For coagulopathy that happens bc of brain releasing tissue thromboplastin you may need available

A

FFP, PLTs, Cryo

203
Q

Which Neuro surgery usually associated with more profound blood loss, volume shifts and need for transfusion

A

Comple Spine sx especially planned osteostomies or tumor

Multiple blood products should immediately available for these cases
Repeat CBC and Coags should be performed

204
Q

Strict glycemic control in neuro sx is target of

A

90 to 180 mg/dL = improved outcome , it is no longer 80 to 100 mg/dL bc that target can lead to hypoglycemia.

205
Q

If hyperglycemia in neuro sx give

A

Insulin IV bolus + infusion

206
Q

If hypoglycemia give

A

50% Dextrose
20 to 50 mL
Keep monitoring sugar to titrate how much to give

207
Q

Emergence from GA in Neurosx what 2 things do you watch ?

A

Hemodynamics and ventilatory parameters while ensuring prompt neuro exam

208
Q

Postcraniotomy , what happens to BP often ?

A

HTN&raquo_space; worse cerebral edema , increased surgical site bleed

Labetalol, Esmolol, nicardipine, clevidipine

209
Q

Posterior Fossa Surgery , those pts w/ pre brainstem dysfunction , emergence is

A

Slow

Time to safe extubate prolonged

210
Q

What to avoid on emergence in elevated ICP patients ?

A

Coughing ..

So give a low dose infusion of Remifentanil or/and intratracheal Lidocaine

211
Q

How to prevent PONV in ICP patients ?

A

Dexamethasone prophylactic

212
Q

What patients you do not give Dexamethasone to ?

A

1) dx of lymphoma = can cause tumor lysis of lymphoma&raquo_space; can’t diagnosis ( at least delay giving it until after diagnosis .
2) avoid in pituitary sx because it suppresses the hypothalamic -pituitary- adrenal axis + can increase false positive post op hypopituitarism .

213
Q

MC metastatic tumors to the brain

A

Melanoma

214
Q

Supratentorial lesions are MC tumors from support cells

A

Yes

215
Q

After the mayfield pins are applied what response can you see ? How can you fix it ?

A

Same response as laryngoscopy . Give proprofol , opioids, or short acting BB such as Esmolol.

216
Q

How do you decrease brain volume for optimal surgical exposure and minimize retractor-related edema ?

A

Mild hyperventilation
Mannitol 0.5 to 1.5 mg/kg ( or as bolus for full effect )
Or hypertonic 3% saline at 50 to 100 ml /hr w/ na+ surveillance

217
Q

Be careful with what type of patient when giving mannitol and why ?

A

CHF , Pulm edema, Renal Failure

Bc the initial elevation in central volume can be detrimental to those patients prior to diuretic phase .

218
Q

Choice of anesthetics depends heavily on

A

1) Avoiding increase in ICP ( at least until the dura mater is open ) ,
2) maintain the CPP,
3) what neuromonitoring is being used
4) And ensuring RAPID emergence

Short acting , tritrable drugs preferred : propofol, remifentanil, Sevo, Des and maybe N2O ( unless contraindicated )

219
Q

Normal GCS is 13 to 15 is extubted when ?

A

At end of case

220
Q

Adequate analgesia while avoiding obtunded patient with what meds ?

A

Short acting opioids , remi/fentanyl, LA infiltration , IV Tylenol, Precedex

221
Q

What is special about patient with infratentorial tumors and tumors of the posterior fossa ?

A

Bc of how close they are to the brainstem = more hemodynamic problems intra op and post + changes in respiratory control and arousal level

They often stay intimidated bc of altered LOC and delayed emergence

222
Q

Posterior fossa tumor sx require what type of neuromonitoring ?

A

Specific CN monitoring i.e. BAERs or EMG of cranial nerves .
Because they are close to the brainstem and CN they can cause : altered respiratory patterns, Cardiac dysrhythmia , CN dysfunction

223
Q

Acoustic neuroma, mestases , meningiomas and hemangioblastomas are tumors of the posterior fossa . True or False ?

A

True.

These tumors are close to the brainstem and cranial nerves

224
Q

Sitting position = risk for ?

A

VAE

225
Q

When VAE causes significant hemodynamic change it is because …

A

Air is entrained into the heart and pulmonary circulation&raquo_space; impaired gas exchange&raquo_space; intrapulmonary shunt&raquo_space; hypoxemia and concomitant DECREASE in ETCO2 .
If air entrainment is severe&raquo_space; arrhythmia, decreases CO , severe pulmonary hypertension , circulatory collapse

226
Q

How do you monitor VAE ?

A

Precordial Doppler US , detects presence of air, qualitative aspect of air

TEE , more sensitive, can detect quantity of air but can’t use continuously bc the probe will stop working as it gets hotter

227
Q

Prevent VAE by doing what ?( 3)

A

1) Decrease height difference between operative site and the heart as much as possible.
2) Euvolemia
3) And surgeon using bone wax to close visible open Dural venous sinuses or larger veins .

228
Q

Treatment of VAE

A

1)Notify the surgeon to flood the surgical files
2)Give 100% O2
3)Aspirate air through multi orifice CVC positioned at the junction of the SVC and the right atrium
4) Support hemodynamic : vasopressors, fluids, inotropes, adjust OR table so head is at level of the heart <> that’s for severe VAE bc it will disrupt the surgical field
PEEP does not actually help, only in theory
If you are using N2O stop it immediately, it will increase air bubble

229
Q

Sellar mass patient have

A

Visual defects . Know that preop to ≠ if anesthetic is the cause .
SIADH is common with them bc the post pit is compresses&raquo_space;Excess circulation ADH&raquo_space; volume overload and hyponatremia

230
Q

Pituitary surgery : acromegaly , what airway ?

A

Smaller size ETT

Awake fiberoptic or VL

231
Q

Acromegaly and cardiac effects

A

Cardiac rhythm issues and HCM so careful with the cardiac depressant meds

232
Q

ACTH tumors cause

A

Cushing syndrome ( high cortisol level)

233
Q

TSH secreting adenomas please do what with them before surgery ?

A

Make sure they are euthyroid before sx unless vision is threatened

234
Q

Hallmark of DI is

A

Polyuria w/ dilute urine output

Desmopressin and fluid replacement

235
Q

Tx of SIADH

A

Restrict water
Treat underlying cause
Demeclocycline , a tetracycline abx that inhibits ADH in the renal tubules

236
Q

What accident can happen with pituitary sx ?

A

Entry into the cavernous sinus or internal carotid

237
Q

Cerebral aneurysm MC occur where ?

A

40% ACA
25% PCOM
25 MCA
Only 10% vertebrobasilar system

238
Q

Small aneurysm are les than ___mm diameter
Large are ___to ___ mm diameter
Giant aneurysm are more than ____mm diameter.
Rupture risk increase when aneurysm is > ____6 mm , generally requiring treatment

A

Small 10 mm
Large 10 to 24 mm
Giant > 24mm
Rupture risk at > 6 mm = treatment required

239
Q

Ruptured aneurysm patient may also have …

A
Rebleeding 
Vasospam of cerebral artery 
Hydrocephalus 
Cardiac dysfunction 
Neurogenic pulm edema 
Seizures
240
Q

Nimodipine is the only intervention that decreases risk of …

A

vasospasm

Statins via pleotrophic effect “may” also decrease vasospasm

241
Q

Aneurysm surgery , you need to monitor BP very closely with ___ and prevent movement with ___

A

A- line , also for blood sample to repeat Coags since they get heparin periodically
Muscle relaxant

242
Q

During Aneurysm surgery , extravasation of dye into the brain parenchyma means

A

Aneurysmal or feeding rupture : give protamine quick !
Hyperventilation
Mannitol
Burst suppression
Place EVD
Possibly get ready for an emergency craniotomy

243
Q

AVMs are

A

Plexus of arteries and areterialized veins that form a nidus which may lead to cerebral hemorrhage, headache , seizures, or signs of ischemia due to “steal effect “

70 % are supatentorial

244
Q

7% of cerebral AVMs include a flow-related cerebral aneurysm as well, make sure to look for this information and account for it in your

A

Anesthetic plan

245
Q

AVM sx , what kind of access is rec ?

A

CVC bc the greates risk is rebleeding

246
Q

Why do we avoid hypotension in AVMs ?

A

Bc they get seizures or focal neuro deficits from the ischemic steal that hypotension causes

247
Q

Are AVMs shunts ?

A

Yes, high flow -low resistance shunts . Bc of that , rapid rise in BP during DL will less likely rupture the AVMs

248
Q

AVMs emergence , make sure what is available

A

Antihypertensive meds

Bc of NPPB Normal perfusion pressure breakthrough

249
Q

NPPB is caused by

A

Autoregulation inhibited in normal brain vessels as they are maximally dilated as a result of long standing steal by the AVM. After the AVM is resected, those vasoparalyzed vessels don’t know how to constrict =» cerebral hyperemia, cerebral edema, headache, risk for post op bleeding

250
Q

Prophylactic anticonvulsant is given to AVM patients bc

A

50% experience seizures post op

251
Q

Carotid surgery.

A

Remove carotid plaque causing

symptomatic cerebral ischemia , indicated when plaque > 70 % in the ipsilateral ICA

252
Q

Carotid endarterectomy better than carotid stenosis because _____but disadvantage is

A

Less post op stroke, and restenosis but disadvantage: need GA or regional , cardiac event , CN injury

carotid stenosis : very minimum sedation , less CN injury but higher stroke and restenosis post op

253
Q

What block is done for carotid endarterectomy?

A

Superficial and sometimes Deep cervical plexus block to provide anesthesia to dermatomes C2- C4

Low remi or propofol may be given bc it’s important the patient to responds to commands on the contralateral side

254
Q

Awake carotid endarterectomy requires laying flat for long time , who is not a candidate ?

A

COPD and CHF patients ?

255
Q

If patient becomes confused during carotid endarterectomy what must CRNA do ?

A

Increase the systemic BP > 20% of preop values to assure adequate perfusion and oxygenation since ischemia has ensued.

256
Q

Asleep carotid sx with

A

GA and monitoring of cerebral ischemia via EEG ( MC)
EEG shows ipsilateral slowing of oscillations as ischemia

SSEP and MEP may also be used

257
Q

What is carotid Stump pressure ?

A

Pressure in the internal carotid artery distal to the cross-clamp
Reflects adequate collateral blood flow via circle of Willis

258
Q

What is a desirable stump pressure?

A

> 50 mmHg

259
Q

Hypoventilation and hypocapnia lead to steal phenomenon from watershed areas of cerebral perfusion.

A

Yes it does :)

What the heck is water shed

260
Q

BP control in carotid sx , why?

A

While morbidly of this surgery is caused by neuro complications, mortality is caused by cardiac complications.

They have chronic HTN pre op & other CV diseases & other comorbidities ,so keep their BP at baseline prior to cross clamping .

261
Q

Where is cross-clamping done in carotid sx ?

A

Above and below the plaque , usually at the level of carotid artery below the plaque and the ICA above the plaque

262
Q

Once cross- clamping happens what do you do with the BP ?

A

Increase it to improve collateral flow on the contralateral, use a vasopressor .

263
Q

Why is bradycardia and even hypotension possible during carotid sx ?

A

Bc the surgeon manipulates the carotid baroceptors, he can infiltrate the carotid sinus with lidocaine to prevent that response .

264
Q

Why does HTN remain peristaltic even after restoring the carotid flow?

A

Bc the surgery denervated the carotid baroreceptors + cerebral vessels distal to the stenotic carotid have been maximally dilated&raquo_space; autoregulation is impaired . So now you have HTN + cerebral vasomotor paralysis = great recipe for cerebral edema and cerebral hemorrhage!

265
Q

POST op carotid sx neuro compromise is because of

A

Cerebral emboli or ICA thrombosis

266
Q

Are you worried about airway post carotid sx ? And why or why not ?

A

Yes

Neck hematoma&raquo_space;compromise airway&raquo_space;may be hard to reintubate&raquo_space; may first need to surgically explore the hematoma

267
Q

Very common procedure for treatment of epilepsy is

A

Lobectomy with amygdalohippocampectomy

268
Q

Antiepiletics can increase metabolism of

A

Muscle relaxants
Opioids
Dexmedetomidine
** need higher dosages

269
Q

What meds can enhance epileptiform activity

A

Methohexital
Etomidate
Alfentanil (50mcg/kg)

270
Q

What meds to avoid when electrocorticography ECoG planned ?

A

Benzo

271
Q

Tp prevent awareness with very little effect adverse effect on ECoG, what meds ?

A

Scopolamine, N2O, high dose opioids
Or simply dexmetomidine .
Counsel the pt that awareness may happen

272
Q

Hold propofol and potent volatiles to 0.5 MAC ____minutes prior to ECoG

A

30

273
Q

Asleep-awake-asleep technique

A

Asleep with SGA or nasopharyngeal tube with propofol, remifentanil and dexmedetomidine
Awake : airway device removed so patient can tallk

274
Q

Awake craniotomy .Airway is critical bc apnea may require intubation, but your patient is in the mayfield head holder fixed . So how do you put the drape?

A

In a way that allow Acces to face constantly .

Padding and position before sedation *

275
Q

How to treat seizures during craniotomy ?

A

Cold saline applied to brain surface by surgeon and small bolus of propofol 20 mg IV .