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Mar: Sem 7 - Adv. Principles C > Neurosurgical Anesthesia > Flashcards

Neurosurgical Anesthesia Flashcards

1
Q

What is the mean CSF volume?

A

150 mL

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2
Q

Where does the CSF pool?

A
  • Cisterns
  • Area where arachnoid membrane and pia mater are further apart
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3
Q

The region where CSF is produced

A
  • Choroid Plexus
  • Highly organize tissue that lines all the ventricles
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4
Q

What cells excrete CSF?

A

Ependymal Cells

Mostly dependent on transport of sodium ions

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5
Q

What structures absorb CSF?

A

Arachnoid Villi

Have one-way valves to prevent backflow

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6
Q

Describe the Pathway of CSF

A
  • Formation of CSF in choroid plexus of lateral ventricles, excreted by ependymal cells.
  • CSF will travel into the third ventricle through the Foramen of Monro (Intraventricular Foramen)
  • CSF will travel along the Aqueduct of Sylvius into the fourth ventricle
  • CSF will travel through foramen of Luschka and Foramen Magendie
  • CSF will enter the Cisterna Magna (Cerebellomedullary Cistern)
  • CSF will go through the subarachnoid space surrounding the cerebrum and be absorbed into the arachnoid villi
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7
Q

Where does the absorption of the CSF into the bloodstream take place?

A

In the Superior Sagittal Sinus through the structures called Arachnoid Villi.

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8
Q

What is the Monro-Kellie Doctrine

A
  • The total volume of the brain, cerebrospinal fluid (CSF), and blood in the cranium is constant.
  • If one of these components increases in volume, the other two must decrease by the same amount
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9
Q

A term that can be used to refer to CSF build up/obstruction

A

Idiopathic Intracranial HTN (Pseudotumor Cerebri)

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10
Q

Idiopathic Intracranial HTN (Pseudotumor Cerebri) is most common in which patient population?

A

Common in obese women of reproductive age

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11
Q

The range for normal ICP

A
  • 7-15 mmHg
  • 10 mmHg when supine
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12
Q

What is considered pathological/ critical ICP?

A
  • > 20 mmHg
  • Brain herniation is possible when ICP is elevated
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13
Q

What is the gold standard for measuring ICP?

A

Intraventricular Monitor

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14
Q

What is normal Cranial Perfusion Pressure (CPP)?

A

60-80 mmHg

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15
Q

What is the critical ischemia CPP threshold?

A

30-40 mmHg

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16
Q

When will the autoregulation of CPP be disrupted?

A

Pathological states

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17
Q

Management of CPP during intracranial pathology

A

ICP management

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18
Q

Management of CPP during Hemodynamic instability/shock

A

MAP management

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19
Q

Causes of increase in ICP

A
  • Increase Cerebral Blood Flow
  • Tumor
  • Intracranial hematoma
  • Blood in CSF (SAH)
  • Infection (meningitis/ encephalitis)
  • Aquaductal stenosis
  • Idiopathic
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20
Q

Components of Cushing’s Triad

A
  • Bradycardia
  • Widen Pulse Pressure
  • Irregular Respirations
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21
Q

What type of position will decrease ICP?

A
  • Elevate head of bed
  • Improves venous drainage
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22
Q

PaCO2 of ________ mmHg quickly reduces ICP

A

30-35 mmHg

Achieved through hyperventilation, effects can last between 6-12 hours

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23
Q

What are ways to physically drain CSF?

A
  • Ventriculostomy
  • Lumbar drain
  • VP shunt
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24
Q

Drugs used to decrease ICP

A
  • Hyperosmotic Drug (Mannitol) 0.5-1 g/kg
  • Anticonvulsants (seizures increase CMRO2, give Keppra)
  • Loop Diuretic
  • Corticosteroids (best given 48 hours before surgery)
  • Anesthetics
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25
Q

What can be the negative effect of giving corticosteroids during a craniotomy?

A
  • Corticosteroids may increase blood glucose
  • Hyperglycemia can decrease elasticity of blood vessels → cerebral ischemia
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26
Q
A
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27
Q

Mild hyperventilation has a parallel reduction in __________

A

Cerebral Blood Volume

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28
Q

What are some concerns with hyperventilation to decrease ICP?

A
  • Potential ischemia in some areas
  • CBF and ICP lowering effect won’t be sustained long term (6-12 hours)
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29
Q

Management of Arterial BP for Neurosurgery

A
  • Maintain CPP between normal-high normal
  • Suggest MAP within 10-20% of average awake BP
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30
Q

Mannitol is usually given in incremental doses (12.5 gm) to limit ____________.

A

Rapid Hyperosmolarity

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31
Q

Neurons and glia rapidly swell d/t increase osmolarity (rebound effect). What drug can be given to inhibit the chloride channel and slow down the rebound effect?

A

Furosemide

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32
Q

What is the MOA of Keppra?

A
  • Binds to a synaptic vesicle protein 2A
  • SV2A mediates calcium-dependent neurotransmitter release
  • Binding of Keppra to SV2A inhibits rate of vesicle release

Dose: 500 mg over 15 minutes

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33
Q

Surgical Positioning & Associated Complications with neuro surgery

A
  • High risk of nerve damage and embolic complications!
  • Sequential compression stockings
  • Promote venous drainage; avoid contralateral jugular vein compression
  • Prevent brachial plexus injury
  • Avoid ischemic optic neuropathy (ION) in prone position
  • Low BP, low Hct, long surgery, large volume admin
  • Avoid vena cava compression
  • Airway: be aware that tongue will swell in prone position; secure tube WELL
  • Venous air embolism risk (when open head is above heart)
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34
Q

What is the IVF of choice for Neurosurgery?

A

Normal Saline (308 mOsm/L)

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35
Q

Effects of Hypothermia on the brain

A
  • Reduces electrophysical activity in the brain
  • May provide brain protection
  • Not advocated in neurosurgery (increase dysrhythmias and coagulopathy)
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36
Q

Glucose management during Neurosurgery

A
  • Increased plasma glucose aggravates cerebral ischemia in TBI
  • Low glucose can cause seizures/ brain dysfunction
  • Recommendations: 150-200 mg/dL
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37
Q
A
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38
Q

What is a Subdural Bolt?

A

A pressure transducer placed in subdural space or brain parenchyma

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39
Q

What is a Ventriculostomy?

A
  • Catheter placed into the ventricle which allows for monitoring and CSF drainage
  • Best way to measure ICP and control CSF drainage
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40
Q

What is a Lumbar Subarachnoid Catheter?

A

Catheter that allows CSF drainage by gravity but may be inaccurate for central CSF pressure if blockage occurs

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41
Q

What does a Cerebral Oximetry measure?

A
  • Measures regional blood hemoglobin oxygenation saturation (rScO2)
  • Measures balance between flow and metabolism
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42
Q

How does a Cerebral Oximetry work?

A
  • Uses near-infrared spectroscopy; similar to pulse ox
  • Sensor emits 2 alternating lights which pass through skin, skull, dura, and CSF to blood of cerebral cortex
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43
Q

Patient population that Cerebral Oximetry may be useful

A
  • Pt at risk of stroke
  • Cardiac surgery
  • Vascular surgery
  • Procedure that put a single hemisphere at risk
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44
Q

Normal Cerebral Oximetry range

A

70% +/- 20-30%

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45
Q

What is used to measure spontaneous brain activity?

A

Electroencephalogram (EEG)

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46
Q

What measures signals that result from specific stimuli?

A

Evoked Potentials

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47
Q

What is Somatosensory Evoked Potential?

A
  • Signal generated in response to applied sensory input
  • Cutaneous electrical stimulation of a peripheral sensory nerve
  • Signals are received in the cerebral sensory cortex and requires an intact pathway (dorsal column of spinal cord)
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48
Q

What is Motor Evoked Potential (MEP)?

A
  • Provides info about descending motor pathway
  • Cortex to the neuromuscular junction
  • Stimulus applied transcranial over motor cortex
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49
Q

Anesthesia Considerations for MEP’s

A
  • Very sensitive to anesthetics (more so than SSEP)
  • May cause patient movement/monitor derangement
  • May cause patient injury (bite tongue!)
  • Soft bite blocks required & documented
  • Latency unreliable; 50% decrease in amplitude = significant
  • No NMBD
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50
Q

If a patient is running SSEP/MEP what should the MAC be on the volatile anesthetic?

A
  • 1/2 Mac of Gas with a propofol/narcotic drip
  • Or just go full TIVA
  • SSEP/MEP are unaffected by opioids
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51
Q

Classification of Cerebrovascular Accident/Stroke

A
  • 20% are hemorrhagic (SAH, ICH)
  • 80% are embolic/ ischemic
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52
Q

Hemorrhagic strokes are how many more times likely to cause death than embolic stories?

A

4x

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53
Q

How are strokes diagnosed?

A
  • Clinical symptoms
  • CT Scan
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54
Q

Common stroke symptoms

A
  • “Worst headache of my life”/Thunderclap headache (SAH)
  • Visual disturbances
  • Nuchal rigidity
  • Change in LOC
  • Can also see ST-segment depression/T wave inversion related to catecholamine release
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55
Q

How does an embolic stroke occur?

A
  • Usually caused by embolism that develops elsewhere and travels to brain
  • Blocks blood flow
  • Ischemia results
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56
Q

What is the most common comorbidity for embolic stroke

A

Cardiovascular Disease (Afib, Cardiomyopathy, Recent MI, Cardiac Sx, Valvular disease)

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57
Q

How does an embolic stroke occur from Cardiomyopathy?

A

Dilated LV (floppy heart) is typically capable making an emboli → Blocking large cerebral vessels or carotid arteries

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58
Q

How does an undiagnosed PFO (Patent Foramen Ovale) lead to an embolic stroke?

A

Embolism formed in the vein can pass from venous to the arterial circulation

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59
Q

What is the goal when treating an embolic stroke?

A

Restore blood flow as quickly as possible

60
Q

Treatment for an embolic stroke

A
  • tPA: Tissue Plasminogen Activator (Alteplase)
  • Endovascular Thrombectomy (IR)
  • TCAR (Trans-Carotid Artery Revascularization)
  • Carotid endarterectomy (if carotid blockage or high risk for carotid blockage)
61
Q

How does tPA work?
What is the window of time to use tPA for an embolic stroke?

A
  • Catalyzes conversion of plasminogen to plasmin
  • Breaks down blood clots
  • Only effective if administered within ~2 hours of symptoms
62
Q

What is a Subarachnoid Hemorrhage (SAH)

A
  • Accumulation of blood between arachnoid space and pia mater
  • Requires immediate attention
63
Q

Symptoms of a SAH

A
  • Characteristic “thunderclap headache”
  • N/V
  • Vision disturbances
  • Cranial nerve deficits can occur
  • Meningitis-like symptoms if blood spreads down and irritates spinal nerves
  • Coma
64
Q

What is an Intracerebral Hemorrhage (ICH)

A

Bleeding in the parenchyma

65
Q

What are the common causes of an ICH?

A
  • HTN
  • Arteriovenous malformation
  • Aneurysm rupture/leak
  • Trauma
  • Coagulopathy
66
Q

Treatment for Hemorrhagic Stroke

A
  • Find and stop source of bleeding
  • Craniotomy (clipping or removal of AVM)
  • IR Coiling
  • Burr hole (usually for SDH)
67
Q

Craniotomy: Aneurysm Clipping Procedure

A
  • Open skull (bone flap) & dura
  • Retract brain tissue
  • Isolate aneurysm from circulation
  • Clip is placed across the base/neck of the aneurysm
  • Clips are permanent
  • During surgery, temporary clips may be placed to control bleeding
68
Q

Endovascular: Aneurysm Coiling IR Procedure

A
  • Vascular access obtained at groin site
  • Small catheter inserted into the aneurysm
  • Aneurysm filled with soft wire coils to prevent blood from flowing into it
  • May be balloon-assisted, stent-assisted, or use of flow diverters
69
Q

Considerations to take into account with Clipping vs Coliling

A
  • Clipping is more invasive, but lower re-treatment rate.
  • Not all patients can tolerate clipping (elderly, unstable)
  • Not all aneurysms can be coiled (size, shape, patient)
  • Coiling requires blood thinning therapy afterward
  • Coiling is relatively new (Fewer studies on outcomes/rebleeds)
70
Q

Anesthesia for Stroke: Induction Considerations

A
  • Must have tight control of blood pressure/MAP
  • Pre-induction arterial line
  • Gentle/slow induction (Esmolol, Intubate DEEP)
  • Rebleeding at induction is often fatal
71
Q

Anesthesia for Stroke: Maintenance Considerations

A
  • Approx 7% rupture rate intra-op toward late stages of dissection
  • Maintain appropriate anesthetic depth
  • NO MOVING
  • Burst suppression if required
  • Maintain CPP
  • Mild hyperventilation
  • Communication with surgeon
  • May need emergent induced hypotension: have prepped and ready… (ex: adenosine)
72
Q

Anesthesia for Stroke: Emergence Considerations

A
  • Free of coughing, straining, and arterial hypertension
  • Consider using lidocaine, esmolol, labetalol
  • Good amounts of narcotic/timing of narcotic gtt cessation
  • Time emergence with dressing, not final suture
  • Neuro check
73
Q

What is thought to be the cause of cerebral vasospasm?

A

Breakdown products of Hbg and NO

74
Q

How is vasospasm treated?

A
  • Treat with calcium channel blockers
  • Nimodipine/verapamil/nicardipine
75
Q

How is Cerebral Vasospasm prevented?

A
  • Triple H Therapy
  • Hypertension (20-30mmHg above baseline) Use Phenylephrine or dopamine gtt
  • Hypervolemia (really euvolemia)
  • Hemodilution (Hct low ~30)
76
Q

What medication can improve endothelial function and decrease oxidative stress and inflammation?

A

Statins

77
Q

What is the function of magnesium?

A

Inhibits calcium-channel smooth muscle contraction and mitigate cerebral vasospasm

78
Q

MOA of Cilostazol

A
  • Phosphodiasterase inhibitor
  • Antiplatelet
  • Vasodilator
79
Q

What is Stereotactic Neurosurgery?

A
  • Use of MRI/CT imaging and a highly specialized 3-D coordinate system to target precise areas deep within the brain
  • Typically used to guide biopsy of tumor, DBS, Focal seizure/lesion ablation
80
Q

Deep Brain Stimulators are typically use to treat what type of movement disorder?

A
  • Parkinson’s
  • Essential Tremor
  • Dystonia
  • Tourette
81
Q

What region of the brain does the DBS usually target?

A

Subthalamic Region

82
Q

Describe the stage 1 procedure of a DBS

A

1st Stage – Placement of electrodes under lighter sedation with stereotactic techniques, will wake patient up for intra-operative testing

83
Q

Describe the stage 2 procedure of a DBS

A

2nd Stage – GETA, ~1 week later, tunneling of leads from brain to generator (implanted under skin on chest)

84
Q

Anesthesia Consideration for Stage 1 DBS

A
  • A rigid head frame is applied w/ local anesthesia
  • Pt to MRI
  • Patient returned to OR; prepped, draped
  • MAC anesthesia provided
  • Burr holes established for placement of electrodes in subthalamic nucleus
  • Target tissue is stimulated with patient feedback
  • Leads are sutured in place and burr holes closed
  • Avoid BZD (interference)
  • Avoid Remi (may suppress Parkinsonian tremor)
  • Use propofol/ precedex
  • Have precordial doppler (risk of VAE)
85
Q

Anesthesia Consideration for Stage 2 DBS

A
  • Electrodes are accessed and connected to 1 or 2 generators placed below the clavicle
  • General anesthesia (Intubated)
  • Balanced anesthesia
  • Extubated on table
86
Q

What drugs may be given during a focal seizure ablation to induce seizure activity?

A
  • Ketamine
  • Methohexital
  • Etomidate
  • Alfentanil
  • Meperidine
87
Q

What drug needs to be avoided for a Stereotactic Ablation?

A

BZD (can suppress seizure activity)

88
Q

Anesthesia: Stereotactic Neurosurgery Considerations

A
  • Ensure absence of coagulopathy
  • Frame or other equipment may be in your way airway
  • No/limited neck extension
  • Glidescope/back-up options
  • SBP <150mmHg (decreased risk for bleeding)
  • Cardene gtt
  • If on levodopa, morning dose will be held
  • Muscle rigidity; potentially difficult IV start
  • Patient anxiety
  • Education, coaching, appropriate choice of sedation (nothing long-acting)
89
Q

Anesthesia Consideration for Awake Craniotomy

A
  • Patient is awake/alert for most of surgery
  • Scalp block placed for incision
  • Sedation/pain medication as appropriate
  • The brain itself does not feel pain!
  • Surgery on “sensitive areas” that control vision, speech, movement
  • Surgeon will want patient to talk/perform tasks to guide surgery & ensure no damage
90
Q

What kind of hematoma is largely associated with skull fractures?

A

Epidural Hematoma

91
Q

What vessel is torn in an Epidural Hematoma?

A
  • Tear in the middle meningeal artery.
  • Associated with LOC, life-threathening.
92
Q

What vessel is torn in a Subdural Hematoma?

A
  • Tear of the saggital vein
  • Slow bleed, can be acute or chronic
  • Sometimes found incidentally in elderly
93
Q

What is a surgical treatment for a SDH?

A

Burr Hole Surgery

94
Q

What is a Burr Hole?

A
  • Small holes surgically drilled into skull to drain blood and relieve pressure on brain
  • Emergent procedure. Frequently an “add on” case/weekends/nights
    Common for subdural bleeds
95
Q

Anesthesia Considerations for Burr Hole Surgery.

A
  • Not as invasive as a craniotomy
  • Still want an a-line and 2 IV’s
  • GETA
  • Can be a “plain vanilla” case
  • No evokes/no need for anything “fancy” with your anesthetic choice
  • Get in, drain blood, get out
96
Q

Anesthesia Considerations for Neuro Trauma

A
  • Intubate if GCS 8 or less
  • Full stomach
  • Cervical spine stability
  • Uncertain airway
  • Uncertain volume status
  • Increased ICP
  • Combative patient
  • Hypoxemic
  • Minimal 18G, 2 PIV
  • RSI
  • A-line
  • Keep paralyzed during surgery
  • Measures to decrease ICP
  • Extubate or keep intubated, ICU
97
Q

What is hydrocephalus?

A
  • Abnormal build of CSF in the ventricles
  • Ventricles wide → Pressure on Brain structures
98
Q

What can cause Hydrocephalus with a Normal ICP

A

Impaired CSF absorption from a previous insult

  • Trauma
  • SAH
  • Tumor
  • Infection
  • Idiopathic
99
Q

What triad is usually presented in hydrocephalus with a normal ICP?

A
  • Dementia
  • Gait changes
  • Urinary incontinence

Usually developed over weeks to months

100
Q

How is Hydrocephalus with Normal ICP diagnosed?

A
  • LP: normal or low CSF pressure
  • CT/MRI: enlarged ventricles
101
Q

What can cause Hydrocephalus with an elevated ICP?

A
  • Imbalance between production and absorption
  • Often congenital
  • Structural abnormalities (Chiari malformation, Tumors)
102
Q

Common symptoms of hydrocephalus with elevated ICP:

A
  • N/V
  • Altered LOC
  • Papilledema (swelling eyes)
  • Bradycardia
  • Hypertension
  • Breathing pattern change
103
Q

How is Hydrocephalus with Elevated ICP diagnosed?

A
  • LP: high pressure
  • CT: enlarged ventricles, more pronounced
104
Q

What is Chiari Malformation?

A
  • Brain tissue bulging into the spinal canal
  • The cerebellum pretty much pushes through the opening in the skull.
105
Q

What is communicating hydrocephalus?

A
  • CSF can exit the ventricles but can’t be effectively absorbed by the arachnoid villi.
  • Normal pressure hydrocephalus is a form of communicating hydrocephalus

Can be caused from meningitis or other infections

106
Q

What is non-communicating (obstructive) hydrocephalus?

A
  • CSF can’t escape from the ventricular system
  • Some tumors can cause obstruction
107
Q

What is the most common cause of non-communicating (obstructive) hydrocephalus?

A
  • Aqueductal stenosis
  • Narrowing of the Aqueduct of Sylvius between the 3rd and 4th ventricles
108
Q

What is a ventriculoperitoneal shunt (VP Shunt)?

A
  • Surgical method to treat hydrocephalus
  • Tube that connects brain ventricles to abdomen
  • Drain CSF
109
Q

What is the most common complication of a VP shunt?

A
  • Blockage
  • Infection
  • May do “revision” surgery
110
Q

Anesthesia Considerations for a VP Shunt

A
  • Usually supine with head turned to the side
  • Mild hyperventilation/control of CO2 & other techniques to decrease ICP
  • A general surgeon will obtain peritoneal access (usually laparoscopic)
  • Tunneling of catheter = very stimulating!
  • Need profound skeletal muscle relaxation
  • Need OG Tube to decompress stomach to avoid gastrostomy!
111
Q

What is a primary tumor?

A

Tumor that arises from the brain and its coverings

112
Q

Describe a meningioma

A
  • Usually benign brain tumor; arising from coverings of brain
  • Commonly near the sagittal sinus, VAE more likely during repair
113
Q

What are the different types of primary tumors?

A
  • Meningioma
  • Gliomas
  • Glioblastoma
114
Q

Describe a glioma

A
  • Non-aggressive primary brain tumor.
  • Surgical resection successful
  • Astrocytes, ependymal cells, oligodendrocytes are affected
115
Q

Describe a glioblastoma

A
  • Most aggressive and most common brain tumor
  • Micro invasion, grows quickly
  • Life expectancy weeks/months
116
Q

Intracranial Tumors Symptoms and Treatment

A
  • Commonly present with headache, seizures, or new neurologic deficits
  • Treatment may consist of surgical resection, chemotherapy, and/or radiation
117
Q

What are Pituitary Tumors

A
  • Tumor that arise from cells of the anterior pituitary gland
  • Almost always benign
  • May occur with tumors of parathyroid and pancreatic islet cells (Multiple Endocrine Neoplasia-Type I)
  • Surgically curative
118
Q

What are the two types of Pituitary Tumors?

A
  • Microadenomas (functional): hormone-secreting; symptoms related to hormone
  • Macroadenomas (non-functional): non-hormone secreting; symptoms relate to mass itself
119
Q

What hormones will be associated with functional pituitary tumors?

A
  • Prolactin (lactation, infertility, breast tissue development)
  • ACTH (adrenal hyperplasia)
  • Growth Hormone (acromegaly)
120
Q

What is the method of choice for resection of pituitary tumors?

A

Transsphenoidal Hypophysectomy

121
Q

Describe a Transsphenoidal Hypophysectomy procedure

A
  • Performed nasally to avoid complications associated with craniotomies
  • Otolaryngologist reaches sphenoid sinus.
  • Neurosurgeon excises tumor
    CSF leaks controlled with fat or muscle graft
  • Otolaryngologist performs a sella floor reconstructed with bone; sphenoid sinus closed.
122
Q

Transsphenoidal Hypophysectomy Anesthesia Considerations

A
  • Acromegaly: large tongue, long neck, redundant airway tissue
  • Consider fiberoptic intubation if difficult airway
  • Oral Rae tube, Secure tube well!
  • Standard induction and maintenance drugs
  • CV issues, Arterial line
  • Deliberate oropharyngeal/gastric suction prior to extubation
  • No nasal cannula or nasal airway postop
  • Complications: VAE, carotid injury, optic nerve injury
123
Q

Complications of Transsphenoidal Hypophysectomy

A
  • VAE
  • Carotid injury
  • Optic nerve injury
124
Q

What is an Acoustic Neuroma?

A

A noncancerous tumor that grows on the vestibulocochlear nerve (CN VIII), which connects the inner ear to the brain.

125
Q

When can a patient have bilateral acoustic neuroma

A

If they have neurofibromatosis

126
Q

Symptoms involved with acoustic neuromas

A
  • Hearing loss
  • Tinnitus
  • Disequilibrium
127
Q

Treatment of Acoustic Neuromas

A
  • Surgical resection common with auditory evoked potentials
  • Prognosis is very good; recurrence is common
128
Q

Where do most metastatic brain tumors originate from?

A
  • Lungs
  • Breast
  • Most likely diagnosed when more than one lesion is present
129
Q

Why will metastatic brain tumor resection have a high likelihood of bleeding during a resection?

A
  • Due to abnormal angiogenesis around the tumor
  • Have blood available
130
Q

Anesthesia Considerations for Craniotomy: Pre-op

A
  • Evaluate for increase ICP
  • Caution with preoperative sedatives (Hypoventilation, ↑ PaCO2 → cerebral vasodilation)
  • Assess potential for blood loss
  • Preoperative steroids for 24-48 hours
131
Q

Anesthesia Considerations for Craniotomy: Induction

A
  • 2 Large Bore IV’s
  • For sitting posterior fossa crani, the central line should have a right heart catheter!
  • Arterial line pre-induction (usually)
  • Need a rapid, reliable induction without increasing ICP
  • Stable BP during induction
  • Adequate depth before laryngoscopy
  • Adequate depth for pinning (propofol or remi bolus)
  • Protect eyes! Secure tube!
  • Nondepolarizing muscle relaxants as indicated (Can’t use with evokes… communicate with surgeon & evokes technician)
  • May be okay to induce with NDMR and let them wear off
  • Place soft bite blocks with evokes
132
Q

Anesthesia Considerations for Craniotomy: Maintenance

A
  • Combination of drugs with evokes (½ MAC, Narcotic or sedation drip)
  • Propofol bolus if burst suppression is required (aneurysm clipping)
  • Nitrous oxide is controversial d/t potential for venous air embolism
  • No spontaneous movements!!!
  • Remi works well to keep people still…
  • Maintain euvolemia (PRBC)
  • Retraction of dura over parietal lobe area can induce the trigeminal cardiac reflex (hypotension, bradycardia) → notify surgeon
  • Traction on dura can also cause brain irritation/seizures
133
Q

Anesthesia Considerations for Craniotomy: Emergence

A
  • Surgeon will likely want to see patient follow simple commands (squeeze hand, wiggle feet) before extubation
  • Will likely wake up and extubate but… depends on pre-op LOC & course of surgery
  • Figure out how you want to handle HOB away
  • Collaborate with surgeon
134
Q

How does a VAE occur?

A

Air enters venous circulation and travels to right ventricle and pulmonary circulation.

VAE can occur with the following: Not just neurosurgery…central venous catheter insertion/removal, CT injector, hemodialysis, penetrating chest injuries, lung biopsy, cardiovascular surgery, angioplasty, arthroscopy, laparoscopic procedures, and hysteroscopy, ENT surgeries, among many others…

135
Q

What will cause the highest risk of VAE?

A
  • High risk when the head is positioned above the heart
  • Sitting Crani/beach chair
136
Q

Complications when an air embolism is lodged in the pulmonary artery

A
  • Right heart failure
  • Bronchoconstriction
137
Q

Complications with an air embolism is passed through to the left side of the heart.

A
  • Cerebral embolism
  • Coronary artery embolism
138
Q

VAE Cardiac s/s

A
  • A mill-wheel murmur (loud and machinery-like) Can be heart w/doppler
  • HEMODYNAMIC INSTABILITY/Sudden drop in CO2
  • Tachy or bradyarrhythmias
  • Myocardial ischemia
139
Q

VAE Pulmonary s/s

A
  • Rales, wheezing
  • Cyanosis
  • Tachypnea
  • Apnea
140
Q

VAE CNS s/s

A
  • Altered mental status
  • Seizures
  • Coma
  • Transient focal neurological deficits
141
Q

What device is needed to help detect a VAE in high-risk surgeries?

A

Precordial Doppler

142
Q

Intraoperative VAE Management

A
  • Discontinue N2O if using (you probably shouldn’t be…)
  • Operative site flooded
  • Aspiration of right heart
  • All sitting posterior fossa procedures must have right heart catheter
  • Pure oxygen administered
  • Supportive treatment
143
Q

Where is ADH synthesized?

Where is ADH transported after it is synthesized?

A
  • Synthesized in supraoptic nuclei of the hypothalamus
  • Transported down supra-optic hypophyseal tract to the posterior pituitary
144
Q

What syndrome can occur if the posterior pituitary is damaged during a transsphenoidal tumor excision?

A
  • Diabetes Inspidus
  • Usually occurs 12-48 hours postop
145
Q

How is DI diagnosed?

A
  • Polyuria
  • Rising Serum Osmolality
  • Hypo-osmolar urine
146
Q

Treatment for DI

A
  • ½ normal saline
  • Hourly maintenance fluid + two-thirds previous hour’s urine output
  • Desmopressin if U/O > 350-400 ml/hr
147
Q

Sx of Increase ICP

A
  • Headache
  • N/V
  • Blurred vision
  • Somnolence
  • Papilledema
  • Midline shift on CT
  • Hydrocephaly
  • Edema
  • Cushing’s Triad

Mar: Sem 7 - Adv. Principles C (11 decks)

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