Neuroanesthesia Flashcards
What is the normal cerebral blood flow?
50 ml/100 g/min
<20 ml/100 g/min - ischemic changes
<10 ml/100 g/min - neuronal death
How is cerebral blood flow regulated?
Cerebral autoregulation:
(1) blood pressure
(2) PaCO2
(1) ensures constant blood flow over a wide range of blood pressure ~60-160 mmHg: above or below, autoregulation is lost and CBF becomes solely dependent on MAP
(2) cerebral vasculature reacts from 20-80 mmHg: vasoconstriction - hypocarbia
vasodilation - hypercarbia
How does hypertension affect cerebral autoregulation?
Shifts to the right - requires higher pressure to maintain adequate perfusion
e.g. 100-180 mmHg
Over time, treated hypertension may revert back to the usual range
Describe CBF/CMRO2 relationship
Under normal conditions, the CMRO2 is directly related to CBF
Cerebral vasculature dilate or constrict to supply for the demand aka coupling
How does PaCO2 affect cerebral perfusion in normal and ischemic regions?
(1) hypercarbia - vasodilation
(2) hypocarbia - vasoconstriction
(1) normal tissues vasodilate more –> more blood shunted to non-ischemic area aka Steal Phenomenon
(2) normal tissues vasoconstrict more –> more blood shunted away from non-ischemic aka Reverse Steal or Robin Hood Phenomenon
Describe the use of hyperventilation in neuroanesthesia
(A) aims to rapidly decrease ICP and ‘relax’ the brain
ETCO2 25-30 mmHg ~PaCO2 30-35 mmHg
Short-term effect of 6-10hrs only, afterwards bicarbonate ions start to compensate
Prolonged hyperventilation –> respiratory alkalosis –> oxyhemoglobin curve shifts to the left –> decreased unloading of O2 –> further ischemia
(B) lowers seizure threshold
How to manage increased ICP?
– hyperventilation (most rapid)
– diuresis: mannitol, furosemide, hypertonic saline
– head elevation: at least 15 deg to facilitate drainage
– control BP: nicardipine
– if ventilated: use lower PEEP - higher intrathoracic pressure may block venous drain
What are the expected nociceptive stimuli in cranial surgery?
- laryngoscopy, intubation
- placement of pins
- scalp incision
- opening of skull up to dura
- High-dose opioid: e.g. fentanyl 5-10 ug/kg
- lidocaine 1.5 mg/kg to help blunt response to laryngoscopy/intubation
Basic principles in providing anesthesia during neurosurgery
- maintain cerebral perfusion
- manage ICP (keeping the brain relaxed during surgery)
- burst suppression if needed (propofol, thiopental): usually during temporary clipping
- monitor serum glucose, acid-base balance, temperature
- use short-acting agents (to facilitate early neurologic assessment)
- blunt response to nociceptive stimuli
- smooth emergence
- upright/sitting position: at-risk for VAE
Options for preinduction anxiolysis
- individualized
- dexmedetomidine > BZD
Dexmedetomidine - respiratory function is preserved, reduced interference with EP monitoring; can be continued as infusion intra-op
BZD - disinhibition, can delay awakening and interfere with postoperative assessment
Sudden drop in ETCO2, sudden hypotension in a craniotomy patient positioned upright
T/C VAE - air entrainment whenever operating field is higher than the right atrium
What is the most sensitive modality in detecting VAE?
- TEE - <0.25ml
- Doppler
- PA catheter, ETCO2
- Cardiac output, CVP, BP
What are the steps to do if VAE is suspected?
- alert surgeon
- stop further air entrainment: flood the field with saline, press neck veins to increase JVP
*Durant maneuver - left lateral decubitus - prevent expansion of entrained air - D/C N2O
- support CV function: inotropes, vasopressors, fluid
- aspirate air (if with RA catheter)
Complications associated with VAE
a) stroke or MI - especially if with patent foramen ovale
b) pulmonary hypertension - secondary to INC pulmonary vascular resistance
c) CV collapse
d) bronchoconstriction
Most common causes of nontraumatic SAH
Cerebral aneurysm, AVM
Complications associated with aneurysmal SAH
1) Rebleeding
- leading cause; will rebleed if untreated
- highest during 1st 24hr post-ictus
2) Vasospasm
- r/t breakdown of RBC byproducts released into the subarachnoid space
- highest 5-7days post-ictus
Optimal time for aneurysmal clipping
- within 72hr
Temporary clipping - tolerated for ~10-14mins
>30mins lead to ischemia
> use burst suppression
What agents are used to induce burst suppression?
barbiturate (thiopental), propofol, etomidate, isoflurane (2 MAC)
Perioperative management in aneurysmal SAH
Triple H: hypertension (~20-30 mmHg above baseline), hypervolemia (CVP ~8-10 mmHg), hemodilution (Hct ~27-30%)
- strict control of BP: nitroprusside/nitroglycerin, labetalol, nicardipine
- control of intravascular volume
- intra-op IABP and CVP monitoring
- burst suppression
- duration of temporary clipping
What Hunt-Hess grading do you expect changes in sensorium?
3 - confusion/lethargy starts, mild focal deficits
5 - comatose, posturing
1 - mild headache, no deficits
2 - nuchal rigidity, moderate to severe headache
Perioperative management in AVM
Strict BP control to avoid rupture - cautious use of deliberate hypotension
‘Autoregulation breakthrough’ - esp. with large AVM
- more blood flow to the previously poorly perfused area –> cerebral edema and/or hemorrhage
Perioperative concerns in posterior fossa tumor
- critical area because of proximity to the brainstem and cerebellum
- WOF vagal reflexes during dissection/manipulation (inform surgeon, glycopyrrolate or BB)
- be alert for Cushing reflex in sudden bradycardia
- position: sitting, prone
- post-resection ‘reperfusion’ –> swelling, increased ICP
Important in the preoperative evaluation of a patient for transsphenoidal pituitary resection
Hormonal evaluation and imaging
How to optimize the transsphenoidal surgical field?
Pushing the tumor inferiorly into the sella:
- controlled/permissive hypercapnia - PaCO2 40-45 mmHg
- lumbar drain (for larger tumors) - injecting isotonic saline or draining CSF
- injecting air into the subarachnoid
- elevating head
Postoperative concerns for transsphenoidal surgery
Diabetes insipidus - monitor fluids, serum Na
Bleeding –> increased ICP
Upon opening the dura, the surgeon complains of a tight brain. What to do next?
- transiently hyperventilate to a PaCO2 25-30 mmHg
- elevate head
- diuresis:
- mannitol (time with removal of bone)
- furosemide
- shift volatile to TIVA
- drain CSF in 10-20ml aliquots
- deliberate hypotension (last resort)
Fluid choices for neurosurgery
NSS - commonly used; WOF hyperchloremic acidosis (assoc. w/ AKI)
BSS - to minimize hyperchloremic acidosis e.g. plasma-lyte
Colloids may be used
Avoid dextrose-containing: once glucose is metabolized, becomes slightly hypotonic –> cerebral swelling
Type of traumatic brain injury that is a true neurosurgical emergency
Epidural hematoma - displaced temporal bone fracture –> middle meningeal artery –> rapidly expanding hematoma
- can experience lucid interval
Subdural hematoma - more insidious
Important consideration in a patient with traumatic brain injury?
Assume cervical injury: in-line stabilization during intubation
Perioperative management of TBI
- glucose 100-160 mg/dl (hyperglycemia is associated w/ worse prognosis)
- CPP: 60-70 mmHg (SBP > 100 mmHg)
- coagulopathy: treat INR > 1.4 and PC < 75,000
- fluids and electrolytes (esp. with diuresis, IVF resuscitation)
- hyperventilation is avoided in the 1st 24h (reserved if herniation is imminent)
- empiric steroid has no benefit
- seizure: levetiracetam
- postop ventilation: low TV, PaCO2 35-40 mmHg, PEEP <15 cm H2O, PaO2 >60 mmHg
- avoid hyperthermia (infectious vs central fever)
- neurogenic PE (secondary to SNS stimulation after injury)
What % is considered severe stenosis?
> 70% - candidate for CEA or stenting
What is the significance of stump pressure?
Stump pressure - taken after clamping CCA & ECA
- to assess adequacy of collateral flow and/or need for shunt
- >40-50 mmHg is adequate
Anesthesia used in CEA:
a) GA - IV or IH
b) RA - deep or cervical plexus block (C2-C4 levels) - preferred for continuous neurologic assessment
BP goals in CEA:
- high-normal intra-op
> permissive hypertension (~10-20% above) to increase collateral flow during clamping
> deliberate hypertension (~30-40% above) until ischemic symptoms resolve - low-normal after clamping (relief of stenosis)
Why is low-normal BP preferred post-CEA?
- decreases stress on suture
- decreases risk of reperfusion
- decreases myocardial workload
Postop concerns in CEA
Airway obstruction:
- secondary to expanding hematoma
Reperfusion Injury:
- usually 1-5 days postop
- associated with poorly controlled BP after unclamping
Loss of chemoreceptor function:
- up to 10 months postop
- do not respond well to hypoxia and increased resting PaCO2 ~6 mmHg
Possible problems during preoperative embolization
Done within 48hr of open repair to minimize intra-op blood loss
1) hemorrhagic
- sudden increase in MAP
- protamine to reverse heparin (1mg per 100u)
- anti-hypertensive
- mannitol
2) thrombotic
- increase BP to increase collateral blood flow
- maintain normocarbia
- tissue plasminogen activator, GP IIb/IIIa inhibitor
BP goal post-embolization
permissive hypotension (~15-20 mmHg above) for 24hr - to prevent cerebral edema & hemorrhage
~20-30% above MAP - to prevent vasospasm
