Anesthesia For Neurosurgery Barash 37 Flashcards
Basal Ganglia is made of
1-Caudate Nucleus 2-Substantia Nigeria 3-Red Nucleus 4-Globus Pallidus 5- Putamen
Dysfunction if Extrapyramidal System lead to
Parkinson’s
Essential Tremors
Ataxia
Supratentorium contains
1) Paired Cerebral Hemispheres
2) Diencephalon : Thalamus and Hypothalamus
What makes the extrapyramidal system
Basal Ganglia
Cerebellum
Auditory and Vestibular system
Where the diencephalon located
Cephalad to the midbrain
Thalamus role
Sensory and motor Relay station
Connect the cortex and the rest of the nervous system functionally and physically
Hypothalamus located where? It’s function ? It is connected to ?
Below the thalamus
Autonomic and Endocrine function
Connected to the pituitary glad via the Infundibulum
Limbic play a role in (3)
1) Cognitve
2) Memory
3) Emotional
The limbic system components are :
Amygdala
Hippocampus
Some regions of the Cortex : Insular region example
Part of the hypothalamus
Brain stem has nuclei for CN 3 and 12 . true or False ?
True
Brain receives 70 % blood from and 30 % from
70% from Two internal carotid arteries .
30% from vertebral arteries posteriorly forming the basilar artery , subsequently converge to for circle of willin
Common carotid emerges from the
Aortic arch and divides at the level of the thyroid cartilage in the internal and the external carotid arteries
The internal carotid artery traverse the ____through the ____and subsequently travels through the _____and into the _____
The skull though foreman lace rum
The cavernous sinus and into the carotid groove .
Bil vertebral arteries originate from the_____and converge to form the ____at the _____junction
From the Subclavian arteries
Form the basilar artery
At the pontmedullary junction
Basilar reached midbrain and divides into the
Posterior cerebral arteries and anastomoses with the PCOMs = completes the circle of Willis .
Less than ___% of people demonstrate a complete circle of Willis
50 %
All the sinus Darin into the
Sigmoid sinus and thereafter the internal jugular veins
CSF is produced mostly by choroid Plexus of lateral and third ventricle. True or False ?
True
Average volume of CSF in an adult is
150 ml ( approx)
CSF is created at a rate of ___ and moves from
15- 20 ml .hr
Moves from the ventricles via the aqueduct of sylvius to the fourth ventricle .
CSF flow
Choroid plexus of third and lateral ventricle(aqueduct of Sylvius )»_space;4th ventricle» ( Foramen of Magendie and lateral foramina of Lushka)»_space;Subarachnoid space of the cranium .
Primary sinus where CSF gets reabsorbed
Superior Sagittal Sinus via arachnoid villi and granulations
Some CSF traverses the Foramen Magnum , enters the subarachnoid space of the spinal column . This movement is important how?
Acute and chronic compensation in elevated ICP
How vertebraes
33 vertebrae 7 C 12 T 5L 9 fused sacral (5) And coccygeal (4)
Dorsal Columns containing tracts responsible for :
Proprioception, light touch
Central gray Matter *
Lateral Spinothalamic Tract responsible for
Pain and temperature
Central gray matter *
The outer white mater contains the ______Tract
lateral Corticospinal
Lateral gray column contain the cell bodies of the ______neurons that enter the _____chain , running on either side of the vertebral bodies , arising from
Preganglionic
Sympathetic chain
Arsing from T1 to L2/L3
Spinal cord ends
L1 or L2 in adults
Conus medullaris and film terminale
Spinal cord receives blood from :
1 anterior spinal
2 posterior spinal arteries
The anterior spinal artery originates from
6 - 8 major radicular arteries derived from the aorta.
The largest of the radicular arteries in the anterior spinal artery is the
Artery of Adamkiewicz
Occurs at T11/T12 but supplies T8 to conus medullaris terminus
Artery of Adamkiewicz is responsible for supplying blood to the _______of the spinal cord
Anterior 2/3 of the spinal cord
The posterior Spinal arteries supply the ______and ______and feeds ______of the spinal cord
Dorsal horn and the white matter
Posterior 1/3 of the spinal cord.
Brain is ___% of total body weight and ___% of O2 consumption and ____% of total body glucose consumption
2% Total Body weight
20% O2 consumption
25% total glucose consumption
brain glucose consumption
5mg/100g/min
CMRO2 normal is
3 - 3.8 ml/100g/min
Normal CBF
50ml/100g/min or 750 ml/min .therefore the brain receives 15% of the cardiac output
Irreversible Brain injury will occur how long after lack of O2 supply ?
4 to 5 minutes of global ischemia
CBF is regulated by …
Flow- metabolism coupling
CPP is the
≠ between MAP and ICO or CVP depends on which is bigger
CBF itself equal to
CPP/CVR
Cerebral auto regulation remain intact between MAP of ___ and it function by ___
*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)
In health brains the LLA may be as high as MAP of
80 mmHg
Altering CVR is accompanied by ( 2 things )
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
Above the Upper Limit and Lower to the LLA CBF is
Pressure dependant
Below the LLA what occurs?
Max cerebral vasodilation and Ischemia
Above the autoregulation upper limit , what occurs ?
Max vasoconstriction
Increased perfusion pressure»_space; disrupted BBB» Cerebral edema or cerebral hemorrhage.
Chronic HTN, autoregulatory curve is shifted
Right
Anesthetics do what to your autoregulation ?
Anesthetics, especially the potent ones have a dose dependent DECREASE in autoregulation
What physiologic parameters play important role in regulating CBF ? Which is most important ?
A)MAP
B)PaCO2 : most important **
CBF is linear to PaCO2 ( but the PaCO2 must be between 20 and 80 mmHg )
C) Temp
Hypoventilation does what to the CBF ?
Increase Remember CO2 ( vasodilates you )
What does hyperventilation to your CBF ?
Decrease
Remember low CO2= vasoconstriction
A change in PaCO2 of ___mmHG correlates with changes in ___of _____
PaCO2 change of 1 mmHg = same change in CBF of 1- 2 ml/100g/min
What happens is PaCO2 is lower than 20 mmHG
Max cerebral vasoconstriction»_space; Tissue hypoxia»_space;> reflex vasodilation.
That’s why you start hyperventilating when your ICP is acutely elevated. But that reflex vasodilation can cause ischemia.
The effects of hyperventilation on CBF and ICP only sustainable for how long ?
only 6 hours .
BC Phof CSF will renormalize
When does PaO2 have effect on CBF ?
Marked hypoxia aka PaO2 < 50 mmHg
CBF increases dramatically!
When can PaO2 cause vasoconstriction
When > 350 mmHg Slight vasoconstriction ( to protect itself from O2 toxicity ( O2 free radical formation )
How does Temp affect CBF ?
6- 7% DECREASE in CBF per 1 º C DECREASE in core temp .
Regional CBF is governed by
Humoral and Neurogenic factors
Catecholamines and mediators involved in regional cerebral vasoconstriction are
A1 agonists
Ionic Ca+
Endothelium
Thromboxane A2
Catecholamines and mediators involved in regional cerebral vasodilation are
B2 agonist
Nitric Oxide
Adenosine
PGs
Neurogenic influence over local CBF regulation :
Ach
Dopamine
Serotonin
Substance P
What the effects of Anesthetics on CBF ? ( not autoregulation)
Profound effect !!!
IV anesthetic effects on CBF
Propofol, Etomidate, Benzodiazepines, Thiopental DECREASE CBF bc»_space; decrease in CRMO2»_space; flow-metabolism coupling .
* Autoregulation and PaCO2 remain intact with those !
Ketamine effects on CBF, CMRO2 , Autoregulation, PaCO2 ( 2)
1) Increases CBF and CMRO2
2) Little effect in autoregulation and PaCO2
Volatile anesthesic effects on CBF and autoregulation .
1) Potent volatiles Sevo, ISO and Des = DIRECT cerebral vasodilators ! but»_space; decrease CRMO2»_space; flow-metabolism coupling»_space; offset CBF = none to min. Increase in CBF at lower dose , but at high doses»_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 .
N2O effects on CBF
Direct cerebral vasodilator +
Minimal effect on CRMO2 +
Variable effect on cerebral autoregulation capacity
Propofol + N2O = preserved autoregulation
Sevo+ N2)= impaired autoregulation
Spinal Cord Perfusion Pressure SCPP=
MAP- SSSP ( Spinal subarachnoid Space pressure )
Volume of brain
1400 ml
volume of CSF in cranium
150 ml
CBV ( cerebral volume )
150 ml
Monroe Kellie Doctrine
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
CBV decrease how ?
Reflex arterial vasoconstriction + increase venous Efflux from brain and venous sinuses .
Care of elevated ICP patients
1) Avoid Hypoventilation
2) Maintain CPP
3) Reduce intracranial volume : Mannitol, CSF 4)diversion, Cerebral vasoconstricting anesthetics ????
5) Consider decompression craniectomy
Normal ICP is
7 - 15 mmHg ( 5-15 mmHg PP)
Poor neurological outcome is from ICP above
20 - 25 mmHg
High ICP does what to CBF ?
Decrease
Intracranial elastance curve
Visualizing the ICP -Volume relationship
Cerebral elastance formula
E= dP/dV
Lumbardrain, extraventricular drain.
“Flat of the curve “( intracranial elastance curve means :
Elastance is low
In normal brain , changes in volume compensated for easily by CSF and CBV
Elbow of the curve ( intracranial elastance curve )means :
Elastance increases
Small increase in volume = rapid rise in ICP
Most common cause of elevated ICP is
**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
Why dexamethasion only can treat vasogenic edema ?
BC it upregulates the proteins responsible for the integrity of the tight junctions
How can increase CBV increase ICP ?
Increase arterial inflow plus decreased venous efflux = rise in ICP
What can increase arterial inflow ?
Vasodilators
Hypercapnia
Severe hypoxemia/ Acidosis
What can cause decreased Venous efflux ? Thus increasing ICP
Jugular vein obstruction
Elevated pressure within the airways
Clinical symptoms of elevated Intracranial Hypertension.
Headache
N/V
Papilledema
As ICP continues to increase you will see what ?
Cushing Triad
1 HTN
2 Bradycardia
3 Irregular respiration
Signs of herniation
Depends on structures herniating Pupillary Dilation Oculomotor weakness Absent light reflex Cardiorespirations
CT results of elevated ICP
Effacement of Sulci
Compression of ventricles
Midline shift
Even possible ventriculomegaly
In acute phase of spinal cord injury , what are the s/s ?
Flaccid paralysis and hypotension
Flaccid paralysis and Hypotension are seen in which phase of spinal injury ?
Acute
Spastic , Pain and risk for autonomic hyperreflexia are seen in which phase spinal cord injury ?
Chronic
Both chronic and acute spinal injury may have what s/s ?
Loss of sensory, motor, autonomic function below the level of injury.
Most important monitor of CNS function is
Neuro exam of an an awake and responsive patient.
BAEP and VEPs are less commonly used. True or False ?
True
Amplitude is measured in ____ for SSEP and BAEP and measured in _____for MEPs
Microvolts
Millivots
Latency is measured in ___ refers to the _____
Milliseconds
Refers to The delay in peak signal following stimulation and reflects transit time along the neural pathway.
SSEP elicited from ____and is measured at the level of ______
A peripheral nerve
Subcortex : upper cervical spine , inion and cortex : scalp.
SSEP stimuli travel through
Posterior Column/ Medial Lemnicus pathway in the CNS
SSEP is useful for monitoring integrity of
Peripheral Nerves Dorsal Column Brainstem Subcortex ( upper cervical spine, inion) Sensory cortex of the brain
SSEP stimuli are recorded in the contralateral side scalp because
Sensory tracts crosses at the brainstem before getting through the thalamus and up the sensory Cortex
SSEP are used during
Spine Surgery
Neurovascular brain surgery : cerebral aneurysm clipping.
Significant changes in SSEP means
Decrease amplitude by 50%
Increase Latency by 50%
MEPs are produced at the level of the
Cortex by direct stimulation of the cerebral cortex or by
Indirect stimulation of the scalp
Lower extremity SSEP which artery ?
ACA
Upper extremity SSEP which artery ?
MCA
MEPs for assessing what ?
Motor cortex and anterolateral spinal cord ( containing the corticospinal tracts )
MEPs how is stimulation produced ?
Indirect electrical stimulation of motor cortex via scalp electrodes»_space;pulses travel caudad» depolarization of upper motor neurons in spinal cord» accumulating in the ventral horn»_space; alpha motor neurons»_space;motor endplates» muscle movement
Muscles relaxant effects on SSEP vs MEPs
SSEP muscle relaxants helpful to remove artifacts by the EMG activity
MEP muscle relaxants inhibit measurement of muscle response
Change Latency of MEPs less worrisome change than in SSEPs
True
EMG sensitive to what type of injury ?
Mechanical and Thermal
Does not monitor ischemia ,
Is EMG sensitive to muscle relaxant ?
Yes !
What are BAEPs used for ?
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
VEPs and anesthetics ?
Exquisitely sensitive to almost any anesthetic regimen , diff to obtain and interpret the signals = they are not used often
Potent volatile and N2O causes what to SSEPs
Greatest inhibition»_space; Decreased amplitude , increase latency
IV anesthetics , limited effect on SSEPS unless?
What about opioids ?
Very high doses
Opioids Salem unless a bolus = decrease amplitude.
N2O affects amplitude or latency more ?
Amplitude
Etomidate and Ketamine effects on SSEP
Increases amplitude!!! Even are used to enhance SSEP
Scalp MEPs are sensitive to
Anesthesia
Potent volatile greatly inhibitory
But can still use Mac of 0.5
TIVA for MEPs is the usual . True or False ?
True
BAEPS are ____ regardless of anesthetic regimen being used . Deep anesthesia may cause _____ but ______will cause some increase in interweave latencies
Robust !
Small increase in latency
Cold irrigation of fluid at the brainstem
Most sensitive neuromonitoring modality to anesthesia ?
Very
Inhalation w/ or w/o N2O > TIVA
Use opioids TIVA, muscle relaxant and BIS
TCD measures
Blood Flow Velocity
Decrease arterial diameter does what to blood flow velocity ?
Decrease
Normal ICP
7 to 15 mmHg
Monitoring begins when ICP > 20 mmHg
What ICP values means severe life threatening Intracranial hypertension?
ICP > 40mmHg
The presence of characteristic Lindbergh waves provides
State of brain
How many Lindbergh waves ? What are they ?
(3 ) A, B, C waves
A waves are
(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.
B waves are
(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)
C waves are
Small oscillation , 4 to 8 times a minute ,
ICO is Normal
Reflects systemic changes in vasomotor tone, with LITTLE pathologic significance
Most commonly use ICP monitoring device
Ventriculostomy or
External Ventricular Drain aka EVD ( transducer is zeroed at the auditory meatus )
Connected to lateral ventricle
What is the gold standard ICP monitoring ?
Ventriculostomy or EVD placed int the lateral ventricle
A ventriculostomy can
Monitor ICP
Drain CSF
Deliver drugs ( i.e ABX, thrombolytic)
EVDs have great risk for
Infection,
CSF sepsis
What is SjVO2 ? What tool measures it ?
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
SjVO2 less than 55%=
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%
Other measures of cerebral metabolism are brain tissue oxygen monitor and microdialysis catheter ?
True
Brain tissue o2 monitor measure what ?
Partial pressure of O2 ( PbtO2) in a portion of brain interstitium , directly or indirectly , via Clark-type electrode
What is normal PbtO2 ?
25 to 48 mmHg
Reflects balance between O2 supply vs demand in the region around the electrode
What affects PbtO2?
FIO2 PaO2 CO Hemoglobin concentration Local O2 extraction CBF
In pathologic brain state , PbtO2 less than … are considered significant
PbtO2< 20 mmHg
What does SjVO2 80 - 85 % mean?
Low O2 extraction or high O2 delivery
When do we monitor brain tissue Oxygen ?
TBI and SAH
Glutamate level means ____and glycerol level means____ measured by cerebral microdialysis
Glutamate = ischemic neuronal stress Glycerol= cell membrane degradation
Cerebral Oximerty is
Transcutaneous measurement of REGIONAL cerebral blood oxygenation ( rSO2) over the frontal cortices bilaterally.
Cerebral oximetry reflect arterial or venous blood ?
Both
Bc Oxygenation is given as a %tage of maximum hemoglobin saturation. Oxymoglobin and deoxymoglobin
Significant hypoxia in cerebral oximetry is when
A decreased of at least 20 % from baseline
Cerebral Oximetry relies on pulsatile flow , True or False ?
False ! Pulse oximetry relies on pulsatile flow not cerebral oximetry
When you have low cerebral oximetry what factors can prevent long term injury
Increasing the systemic BP
increasing the CO
Increasing the FIO2
increasing the PaCO2 : fix the vasoconstriction
RBC transfusion= increase O2 carrying capacity
Brain is susceptible to rapid ischemic injury because?
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
Focal ischemia vs global ischemia
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 ,
Saving the Penumbra
Increase CPP and reduce brain edema
Repercussion injury of the brain
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
Hypothermia and cerebral protection
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
27 ºC is
Profound hypothermia used in cold- cardiopulmonary bypass
12 to 18 ºC is
Deep hypothermia used in circulatory arrest
Cerebral hyperthermia is good or bad
Detrimental !
Ischemia tripled 1ºC in animals
Must be avoided in cerebral ischemia
Satins upregulate
Nitric oxide synthase.
How are volatiles cerebral protectors (5) ?
1) Reduce ischemia-induced glutamate release
2) Increase antiapoptotic mediators
3) Activate ATP- dependent K channel
4) Reduce excitotoxic stressors
5) Increase CBF
What is the only subtstrate that can be aerobically metabolized by the brain under normal conditions ?
Glucose
Is glucose stored in the CNS ?
No
When no sugar bc of limited cerebral circulation»_space; no ATP»_space; energy requirement not supplied»_space; cellular injury quickly ensues .
Cerebral glucose consumption normal value is _____and it parallels what ?
5mg/100g/min
Cerebral Glucose Consumption parallels CRMO2
Hypoxemia or hypoglycemia , which is more detrimental to brain ?
Roughly EQUALLY detrimental
Define hyperglycemia ___ and what effect on neuro outcome .
BG> 180mg/dL
Worsen neuro outcome
By worsening cerebral acidosis in an anaerobic setting (bc the glucose converts to lactic acid !)
Temporary clipping of cerebral vessel what anesthetic you give ?
Propofol 1- 2 mg/kg followed by 150 mcg.kg.min to induce “Burst suppression” prior to the planned ischemia
Deep hypothermia in what cardiac and neuro sx to protect nervous system?
Aortic arch repair or giant basilar aneurysm clipping - 12ºC to 18 ºC
Prior to throracoabdominal aortic aneurysm repair what can be done for neuro protection?
Placement of a lumbar CSF drain»_space;to lower the CSF and maintain spinal cord perfusion when radicular arteries from the aorta are at surgical risk
Preop of patient with Intracranial mass lesions what is the most important thing to ascertain ?
Ascertain presence or extent of Intracranial Hypertension , this should be assumed until proven otherwise .
get this info from H&P, CT , MRI, ICP measurements.
What do patients with elevated ICP complain of ?
Headache Dizziness Visual or gait disturbances N/V Seizures
What do patients with elevated ICP show on physical exams?
Altered LOC Confusion Papilledema Loss of strength or sensation Cranial nerve dysfunction
Radiology studies quantify degree of ICP showing
Slit ventricles or
Shift of midline brain > 5 mm = advanced pathology
What lab may accompany elevated ICP ?
Electrolyte disturbances due to pituitary pathology SIADH
Or due to diuretics , steroids, anticonvulsants
Premedication with Benzo and opioids even in small doses can lead to what ?
Elevated ICP bc they depress respirations»_space; elevated PaCO2» ICH
What meds to continue preop with these patients with elevated ICP?
Corticosteroids ( i.e Dexamethasone ) and anticonvulsants
Preop for Spine surgery , especially acute focus on
Airway exam
Hemodynamics
Level of injury
The degree of injury : complete vs non complete
Induction of GA and airway mngmt in elevated ICP , unsecured aneurysm , cervical spinal cord injury focus on
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
What does SUX do to ICP ?
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
During intubation of pt with high ICP
Rapid rise in arterial BP will worsen ICP esp when autoregulation fails , or pt w. Unsecured aneurysm
Maintenance of GA in intracranial sx with high ICP what is paramount until the dura mater is opened?
ICP control
Once Mayfield fixation and head positioned safely give
Mannitol 0.5 1.5 mg/kg if you need to control the ICP
Give dexamethasone 10 mg
Sometimes give anticonvulsant prophylactic
High ICP, volatile MAC is limited to ___if used at all
0.5 MAC
Instead give IV anesthetic i.e.propofol w/ or w/o opioids short acting i.e. remifentanil or Alfentanil
> 0.5 MAC may interfere with SSEP and MEPs true or false ?
True
Why is N2O avoided in elevated ICP cases ?
Mild vasodilating effect
Potential intradural air
Or can interfere with monitoring
MEP and EMG you can give muscle relaxants , what can you use instead ?
Remifentanil infusion 0.2 mcg/kg/min
Have you vasopressor on board to maintain the
CPP
When autoregulation is inhibited either bc of the disease or the anesthetic , what does CBF depends on
MAP
So that means avoid hypertension
Ventilation Management in neurosurgery , Intracranial sx , what is Tidal Volume and peak pressure goal ?
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
Why do you avoid PEEP in elevated ICP pts
( unless you need it for better oxygenation )
Bc : increase intrathoracic pressure»_space; impede cerebral venous drainage
What mode is used in neuro sx ?
PPV ( positive pressure ventilation) bc it allows direct control of PaCO2 !!!
Esp in sitting craniotomy where negative intrathoracic pressure»_space; VAE ( venous air embolism )
Primary goal of fluid management in neuro surgery is to
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
Can we give fluids with dextrose to those neuro patients ? Why ?
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
Moderate to severe hyponatremic state give
3% saline at rate of
50 to 100 ml/hr
Check serum Na+ q 1 hr
Central Pontine myelinosis can happen when …
Rapid rise in serum Na+ > 3-4 mEq/L/hr
AVOID that !!
Mannitol can cause short lived electrolyte imbalance which are ?
How can Mannitol impair cerebral perfusion ?
Hyponatremia
Hyperkalemia
By causing dehydration = impair cerebral perfusion
What can large amount of 0.9%NS cause ?
Hyperchloremic acidosis»_space; AKI due to renal tubular acidosis
Preop Coags must be corrected. True or False
True
Patients on anticoagulants = required to draw preop coag labs
Non urgent Neuro surgery patients should have platelet count of
100,00/mm3
Craniotomy with low bleeding risk a Type and Screen ( T&S) with neg Antibody ( ABS ) is enough
Neuro surgery with high risk bleeding are ____ what should be available ?
Aneurysm clipping
AVM resection
Tumor craniotomies that invade the cranial sinuses
RBC that are T&C should be available for intro op
For coagulopathy that happens bc of brain releasing tissue thromboplastin you may need available
FFP, PLTs, Cryo
Which Neuro surgery usually associated with more profound blood loss, volume shifts and need for transfusion
Comple Spine sx especially planned osteostomies or tumor
Multiple blood products should immediately available for these cases
Repeat CBC and Coags should be performed
Strict glycemic control in neuro sx is target of
90 to 180 mg/dL = improved outcome , it is no longer 80 to 100 mg/dL bc that target can lead to hypoglycemia.
If hyperglycemia in neuro sx give
Insulin IV bolus + infusion
If hypoglycemia give
50% Dextrose
20 to 50 mL
Keep monitoring sugar to titrate how much to give
Emergence from GA in Neurosx what 2 things do you watch ?
Hemodynamics and ventilatory parameters while ensuring prompt neuro exam
Postcraniotomy , what happens to BP often ?
HTN»_space; worse cerebral edema , increased surgical site bleed
Labetalol, Esmolol, nicardipine, clevidipine
Posterior Fossa Surgery , those pts w/ pre brainstem dysfunction , emergence is
Slow
Time to safe extubate prolonged
What to avoid on emergence in elevated ICP patients ?
Coughing ..
So give a low dose infusion of Remifentanil or/and intratracheal Lidocaine
How to prevent PONV in ICP patients ?
Dexamethasone prophylactic
What patients you do not give Dexamethasone to ?
1) dx of lymphoma = can cause tumor lysis of lymphoma»_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 .
MC metastatic tumors to the brain
Melanoma
Supratentorial lesions are MC tumors from support cells
Yes
After the mayfield pins are applied what response can you see ? How can you fix it ?
Same response as laryngoscopy . Give proprofol , opioids, or short acting BB such as Esmolol.
How do you decrease brain volume for optimal surgical exposure and minimize retractor-related edema ?
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
Be careful with what type of patient when giving mannitol and why ?
CHF , Pulm edema, Renal Failure
Bc the initial elevation in central volume can be detrimental to those patients prior to diuretic phase .
Choice of anesthetics depends heavily on
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 )
Normal GCS is 13 to 15 is extubted when ?
At end of case
Adequate analgesia while avoiding obtunded patient with what meds ?
Short acting opioids , remi/fentanyl, LA infiltration , IV Tylenol, Precedex
What is special about patient with infratentorial tumors and tumors of the posterior fossa ?
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
Posterior fossa tumor sx require what type of neuromonitoring ?
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
Acoustic neuroma, mestases , meningiomas and hemangioblastomas are tumors of the posterior fossa . True or False ?
True.
These tumors are close to the brainstem and cranial nerves
Sitting position = risk for ?
VAE
When VAE causes significant hemodynamic change it is because …
Air is entrained into the heart and pulmonary circulation»_space; impaired gas exchange»_space; intrapulmonary shunt»_space; hypoxemia and concomitant DECREASE in ETCO2 .
If air entrainment is severe»_space; arrhythmia, decreases CO , severe pulmonary hypertension , circulatory collapse
How do you monitor VAE ?
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
Prevent VAE by doing what ?( 3)
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 .
Treatment of VAE
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
Sellar mass patient have
Visual defects . Know that preop to ≠ if anesthetic is the cause .
SIADH is common with them bc the post pit is compresses»_space;Excess circulation ADH»_space; volume overload and hyponatremia
Pituitary surgery : acromegaly , what airway ?
Smaller size ETT
Awake fiberoptic or VL
Acromegaly and cardiac effects
Cardiac rhythm issues and HCM so careful with the cardiac depressant meds
ACTH tumors cause
Cushing syndrome ( high cortisol level)
TSH secreting adenomas please do what with them before surgery ?
Make sure they are euthyroid before sx unless vision is threatened
Hallmark of DI is
Polyuria w/ dilute urine output
Desmopressin and fluid replacement
Tx of SIADH
Restrict water
Treat underlying cause
Demeclocycline , a tetracycline abx that inhibits ADH in the renal tubules
What accident can happen with pituitary sx ?
Entry into the cavernous sinus or internal carotid
Cerebral aneurysm MC occur where ?
40% ACA
25% PCOM
25 MCA
Only 10% vertebrobasilar system
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
Small 10 mm
Large 10 to 24 mm
Giant > 24mm
Rupture risk at > 6 mm = treatment required
Ruptured aneurysm patient may also have …
Rebleeding Vasospam of cerebral artery Hydrocephalus Cardiac dysfunction Neurogenic pulm edema Seizures
Nimodipine is the only intervention that decreases risk of …
vasospasm
Statins via pleotrophic effect “may” also decrease vasospasm
Aneurysm surgery , you need to monitor BP very closely with ___ and prevent movement with ___
A- line , also for blood sample to repeat Coags since they get heparin periodically
Muscle relaxant
During Aneurysm surgery , extravasation of dye into the brain parenchyma means
Aneurysmal or feeding rupture : give protamine quick !
Hyperventilation
Mannitol
Burst suppression
Place EVD
Possibly get ready for an emergency craniotomy
AVMs are
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
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
Anesthetic plan
AVM sx , what kind of access is rec ?
CVC bc the greates risk is rebleeding
Why do we avoid hypotension in AVMs ?
Bc they get seizures or focal neuro deficits from the ischemic steal that hypotension causes
Are AVMs shunts ?
Yes, high flow -low resistance shunts . Bc of that , rapid rise in BP during DL will less likely rupture the AVMs
AVMs emergence , make sure what is available
Antihypertensive meds
Bc of NPPB Normal perfusion pressure breakthrough
NPPB is caused by
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
Prophylactic anticonvulsant is given to AVM patients bc
50% experience seizures post op
Carotid surgery.
Remove carotid plaque causing
symptomatic cerebral ischemia , indicated when plaque > 70 % in the ipsilateral ICA
Carotid endarterectomy better than carotid stenosis because _____but disadvantage is
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
What block is done for carotid endarterectomy?
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
Awake carotid endarterectomy requires laying flat for long time , who is not a candidate ?
COPD and CHF patients ?
If patient becomes confused during carotid endarterectomy what must CRNA do ?
Increase the systemic BP > 20% of preop values to assure adequate perfusion and oxygenation since ischemia has ensued.
Asleep carotid sx with
GA and monitoring of cerebral ischemia via EEG ( MC)
EEG shows ipsilateral slowing of oscillations as ischemia
SSEP and MEP may also be used
What is carotid Stump pressure ?
Pressure in the internal carotid artery distal to the cross-clamp
Reflects adequate collateral blood flow via circle of Willis
What is a desirable stump pressure?
> 50 mmHg
Hypoventilation and hypocapnia lead to steal phenomenon from watershed areas of cerebral perfusion.
Yes it does :)
What the heck is water shed
BP control in carotid sx , why?
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 .
Where is cross-clamping done in carotid sx ?
Above and below the plaque , usually at the level of carotid artery below the plaque and the ICA above the plaque
Once cross- clamping happens what do you do with the BP ?
Increase it to improve collateral flow on the contralateral, use a vasopressor .
Why is bradycardia and even hypotension possible during carotid sx ?
Bc the surgeon manipulates the carotid baroceptors, he can infiltrate the carotid sinus with lidocaine to prevent that response .
Why does HTN remain peristaltic even after restoring the carotid flow?
Bc the surgery denervated the carotid baroreceptors + cerebral vessels distal to the stenotic carotid have been maximally dilated»_space; autoregulation is impaired . So now you have HTN + cerebral vasomotor paralysis = great recipe for cerebral edema and cerebral hemorrhage!
POST op carotid sx neuro compromise is because of
Cerebral emboli or ICA thrombosis
Are you worried about airway post carotid sx ? And why or why not ?
Yes
Neck hematoma»_space;compromise airway»_space;may be hard to reintubate»_space; may first need to surgically explore the hematoma
Very common procedure for treatment of epilepsy is
Lobectomy with amygdalohippocampectomy
Antiepiletics can increase metabolism of
Muscle relaxants
Opioids
Dexmedetomidine
** need higher dosages
What meds can enhance epileptiform activity
Methohexital
Etomidate
Alfentanil (50mcg/kg)
What meds to avoid when electrocorticography ECoG planned ?
Benzo
Tp prevent awareness with very little effect adverse effect on ECoG, what meds ?
Scopolamine, N2O, high dose opioids
Or simply dexmetomidine .
Counsel the pt that awareness may happen
Hold propofol and potent volatiles to 0.5 MAC ____minutes prior to ECoG
30
Asleep-awake-asleep technique
Asleep with SGA or nasopharyngeal tube with propofol, remifentanil and dexmedetomidine
Awake : airway device removed so patient can tallk
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?
In a way that allow Acces to face constantly .
Padding and position before sedation *
How to treat seizures during craniotomy ?
Cold saline applied to brain surface by surgeon and small bolus of propofol 20 mg IV .
