2b. Intracranial Pressure & Spinal Cord Blood Supply Flashcards
normal ICP
5-15 mm Hg in adults
intracranial HTN
sustained increase in ICP above 20-25 mm Hg
causes of intracranial HTN (4)
- obstructed CSF absorption
- brain edema
- expanding mass
- elevated CBF
one of the first signs of increasing ICP is?
nausea and vomiting
other s/s of inc ICP
- changes in LOC
- headache
- seizures
- eyes: impaired movement, papilledema, pupillary changes
- changes in speech
- posturing
- changes in VS
cushing’s triad
- increased SBP
- decreased HR
- irregular respiratory pattern
gold standard for ICP monitoring
intraventricular catheter- ventriculostomy
complication of ICP monitoring
infection
patients that need ICP monitoring
TBI
GCS <9
abnormal CT scan
Normal CT with two of the following:
- > 40 years old
- Uni or bilat posturing
- SBP<90 mm Hg
3 components of ICP waveform
- heart pulse waves
- respiratory waves
- slow vasogenic waves
true or false: steroids are contraindicated in TBI
true
arterial blood delivered to spinal cord va:
75% anterior spinal artery
25% posterior spinal arteries
major source of blood to the lower 2/3 of the spinal cord is via the…
artery of adamkiewicz
interruption of blood flow through the artery of adamkiewicz can l/t…
paraplegia
what comprises cranial volume?
blood
brain
CSF
ICP may be decreased by reduction of any of the following…
CBF
CSF
cerebral edema
cerebral mass
how does PaCO2 affect CBF?
hyperventilation decreases PaCO2 which causes vasoconstriction, this decreases CBF and therefore ICP
PaCO2 30-35 causes…
vasoconstriction of cerebral vessels
PaCO2 < 30 …
danger zone
risk of cerebral ischemia
(b/c O2 offloading is reduced)
Rx that reduce CMRO2
Propofol, Thiopental
what happens when BP surpasses upper limit of autoregulation?
cerebral edema
ways to promote CBF reduction via venous drainage
HOB 30º
head and neck midline to avoid JV compression
Keep PEEP at physiologic levels
position to avoid to promote venous drainage
Trendelenburg
to promote CBF reduction, what agents to avoid?
strong vasodilating agents: NTG, SNP
PaO2 below what increases CBF?
50
what is used for chronic treatment of CSF reduction?
VP or ventriculoatrial shunt
Rx to reduce CSF and treat idiopathic intracranial hypertension
Acetazolamide & furosemide
mainstays of cerebral edema treatment (3):
- diuretics (loop + osmotic)
- corticosteroids
- hypertonic saline (not common)
*be mindful of hypovolemia
why are corticosteroids contraindicated in TBI?
cause elevated serum glucose, which can produce poor outcomes when cerebral ischemia is present
what are ways to reduce cerebral mass?
- surgical debulking of cerebral tumors
- mass reduced when cellular water is reduced with osmotic diuretics
intracranial aneursym
focal protrusion arising from weakened arterial walls at major bifurcations of the arteries at the base of the brain
how are aneurysms most commonly treated
endovascular coiling (>50%) or microsurgical clip ligation
what is the most common cause of SAH
aneurysm rupture into the subarachnoid space
explain T = P x r
T = circumferential wall tension
P = transmural pressure
r = mean vessel radius
increased blood pressure > increased tension stress > progressive vessel dilatation + weakening of vessel wall > enlargement of aneurysm
which law defines enlargement of aneurysms until rupture?
Law of Laplace: wall tension is proportional to vessel radius
when does aneurysm rupture occur?
when mechanical stress on wall exceeds strength of wall tissue
what scale is used for prognostic clinical outcome for SAH?
Hunt-Hess Grading System
Hunt-Hess score 0
unruptured, asymptomatic aneurysm
Hunt-Hess score 1
ruptured aneurysm
minimal headache
no neurologic deficits
Hunt-Hess score 2
moderate to severe headache
no deficit other than cranial nerve palsy
Hunt-Hess score 3
drowsiness, confusion
mild focal motor deficit
Hunt-Hess score 4
stupor, significant hemiparesis
early decerebration
Hunt-Hess score 5
deep coma
decerebrate rigidity
what Hunt-Hess scores require intubation?
4 and 5
s/s SAH
worst HA of my life
LOC (50%)
nausea and vomiting
fever
photophobia
morbidity from SAH results from…
vasospasm!!!
rebleeding
obstructive hydrocephalus (if bleeding blocks outflow of CSF)
leading cause of morbidity and mortality following SAH
vasospasm
may lead to cerebral infarct
amount of bleeding in SAH is directly proportional to…
incidence of vasospasm
vasospasm occurs how many days after SAH?
4-9
why is it important to maintain CPP during vasospasm?
ischemic areas depend on pressure to receive blood flow
triple H therapy for vasospasm
Hypertensive (higher CPP; use pressors)
Hypervolemic (crystalloids, colloids)
Hemodilution (Hct 27-32%; blood less viscous)
what can be used for daily monitoring of vasospasm?
transcranial doppler
Rx for vasospasm
nimodipine
how does nimodipine treat cerebral vasospasm compared to other CCBs?
Nimodipine primarily targets L-type calcium channels in cerebral arteries, which are associated with vasospasm after subarachnoid hemorrhage (SAH).
Unlike other calcium channel blockers, nimodipine has a more selective effect on cerebral vessels, making it suitable for preventing and treating cerebral vasospasm.
what is the gold standard for detection of intracranial aneurysms?
digital subtraction angiography
23% of patients with intracranial aneurysm have…
neurogenic pulmonary edema
EKG changes with intracranial aneurysm
PVCs
T wave inversion
ST depression
induction for craniotomy for intracranial aneurysm
- goal = smooth induction
- decrease CBF by inducing cerebral vasoconstriction
- pressors (CPP) i.e. phenylephrine during and after induction
- pts may benefit from moderate hyperventilation during induction
anesthetic maintenance for craniotomy for intracranial aneurysm
Iso or Sevo 0.5 MAC (if EP monitoring)
Avoid N2O
Propofol gtt (↓ CMRO2)
other maintenance for craniotomy for intracranial aneurysm
BP control (aline preop)
Substantial HTN = rebleeding, rupture, permanent neuro deficits or death
Substantial hypoTN = cerebral ischemia and infarct
emergence for craniotomy for intracranial aneurysm:
Hunt-Hess I-III
extubate
titrate BBlockers and vasodilators
emergence for craniotomy for intracranial aneurysm:
Hunt-Hess IV-V
remain intubated + sedated postop
avoid coughing
HOB elevated 30º on transport
Intra-op Concerns for AVM intubation
fiberoptic awake
(if arrives with stereotactic frame)
Intra-op Concerns for AVM: complication
VAE
place central line
Intra-op Concerns for AVM: msc
Aline
mild hypothermia
brain relaxation
strategies for brain relaxation
↓ PaCO2 (dec cerebral vascular volume)
mannitol/furosemide (monitor K+ and Na+)
mild hypothermia at what ºC can ↓ CMRO2 and to ↓ susceptibility to ischemia?
Mild hypothermia (33–34°C)
(CMRO2 decreases ~30% @ 33°C)
effective and safe induction agents for AVM
Barbiturates, propofol, and etomidate
methods to blunt stimulation of laryngoscopy & Mayfield placement
+Deepen with VAA
+Esmolol
+Lido
+Short acting opioids
+Dexmedetomidine
NMBs for AVM induction
non-depolarizing agents, avoid sux
emergence for AVM
close regulation of BP = key
suppress cough = lidocaine IV
HOB elevated 20-30º
treat increases in BP for AVM
B-blockers or vasodilators
monitors for tumor craniotomy when sitting or beach chair position and why?
precordial doppler,
CVP monitoring, or
TEE on standby
d/t risk of VAE
induction for tumor craniotomy
DEEP anesthesia
complete skeletal muscle paralysis to avoid ↑ICP
anesthesia maintenance for tumor craniotomy
maintain CPP
maintain euvolemia and eucapnia (consider mannitol)
consider mild hyperventilation
HOB 20-30 degrees
may require CSF drain
tumor craniotomy emergence
goal = rapid awakening
avoid bucking, coughing (lidocaine)
treat BP w/ BBs and vasodilators
what MAP may a surgeon require to test hemostasis after tumor is resected during craniotomy?
transient increase to 90-100 mm Hg
awake craniotomy indications
epilepsy
tumors involving motor or speech (eloquent cortex)
patients with full understanding only
induction for awake crani
LMA
Mayfield headrest
cranium removal
patient positioning
awake crani premapping
mannitol slow infusion
Precedex
scalp block
aline
foley
preop management for ventricular shunt
assess for cushing’s triad
HA w/ ICP > 15 mm Hg
no preop med required
goals for ventricular shunt
normocarbia and normovolemia
how does hyperventilation and hypocarbia affect ventricular shunt maintenance
makes cannulation of vessel difficult
maintain PeCO2 35-40 mm Hg
how does seizure activity during GA manifest?
abrupt changes in HR and BP
increased CO2 production
termination of seizures
propofol, barbiturates, benzos
other: surgeon may apply cold saline to brain surface
