ICL 10.4: Elevated ICP

Question 1

how many intracranial compartments are there?

Answer 1

6

anterior, middle and posterior fossa which each have a left and right side

the falx cerebri is what separates the cranial vault into left and right

Question 2

what are the only 3 things in the cranial vault?

Answer 2

1. blood
2. brain tissue
3. CSF

these all enter and exit the skull via the various foramen, arachnoid granulations, venous sinuses etc.

Question 3

what is the volume of the cranial vault and how much of it is brain, CSF and blood?

Answer 3

cranial volume = 1500 mL

brain = 1200 mL

CSF = 250

cerebral blood flow = 750 mL/min

none of these are static numbers! as BP changes, or CSF levels changes, the brain is adapting to maintain the fixed 1500 mL volume in the skull

Question 4

where does the cerebral blood flow of the brain come from?

Answer 4

the brain sees 20% of the total cardiac output which is a lot for just one small organ!

80% via the carotid arteries

20% via the vertebral arteries

Question 5

what is the cerebral perfusion pressure? what’s the formula to calculate it?

Answer 5

the pressure available to perfuse the brain

CPP = MAP - ICP

take the MAP, all the blood going to the brain, minus the pressure within the skull, ICP, and this is what you get!

so the CPP is like the MAP of the brain!

Question 6

why do we care about the cerebral perfusion pressure?

Answer 6

we care about CPP because it’s a surrogate for cerebral blood flow which is really important

the brain is very metabolically active and can’t store energy or use other substrates or perform anaerobic metabolism so a constant supply of glucose and oxygen are critical for it’s function

since we can’t monitor cerebral blood flow at bedside but we CAN monitor CPP at bedside, that’s why we care about CPP so it can tell us about the cerebral blood flow

Question 7

what is the significance of the cerebral metabolic rate for oxygen?

Answer 7

CMRO2 is the rate at which O2 is consumed in the brain by metabolic processes

it’s a key indicator of normal brain function because it means the oxygen and glucose are being supplied and toxins are being cleared `

Question 8

what is the Monro-Kellie doctrine?

Answer 8

“In a fixed skull, the total volume of brain, blood, and CSF is constant and if the volume of one constituent changes, there is a reciprocal change in one or both of the others.”

so it follows that elevated intracranial pressure occurs when this adaptation is impaired or overwhelmed

Question 9

what is intracranial pressure compensation?

Answer 9

in a normal state, your ICP is comprised of venous volume, arterial volume, brain and CSF

in a compensated state like when there is a mass in the skull, your ICP is still normal because you start to drain the CSF and venous volume

however, if the mass gets bigger and bigger you end up in a decompensated state where your ICP is elevated because your CSF and venous volume have been totally drained and the only thing left to get rid of are the arterial blood and brain tissue

Question 10

what’s the difference between acute vs. chronic ICP?

Answer 10

acutely elevated ICP occur when there’s an acutely expanding mass

if increased ICP happens over a slower period of time you can pretty high ICP without any symptoms

so time is a very important factor

Question 11

what is the normal cranial pressure gradient?

Answer 11

artery > vein > CSF > ICP

Question 12

what happens to the components of the cranial vault in a compensatory state?

Answer 12

the pressure gradient starts to shift!

first you you increase absorption or squeeze more CSF out of the brain to get CSF out in any way you can

then you start to squeeze blood out of the venous system through the internal jugular

if ICP is high enough you start to compress the smaller veins in the brain which starts to cause backup congestion because now you can’t get venous blood out since your veins are collapsing

once the ICP is crazy high, arteries will become compressed which will cause ischemia and infarction which causes more swelling and even higher ICPs

so this is a cyclic process that feeds into itself if it’s not interrupted

Question 13

what could cause increased ICP via the brain?

Answer 13

1. primary malignancy
2. metastatic lesion
3. cysts
4. abscesses
5. diffuse axonal injury

Question 14

what could cause increased ICP via the CSF?

Answer 14

1. increased CSF production
   ex. tumors that produce CSF = ependymoma, choroid plexus papilloma (rare)
2. decreased CSF absorption (most common)
   ex. subarachnoid hemorrhage, infection –> infection or blood can clog arachnoid granulations and prevent them from reabsorbing CSF; since we’re always making more CSF this would lead to increased ICP
3. obstruction of CSF flow
   ex. blood, infection, tumors, etc.

Question 15

what could cause increased ICP via the venous compartment?

Answer 15

1. deep venous thrombosis
   ex. jugular vein or cerebral sinus thrombosis
2. jugular compression
   ex. C-spine collar, neck surgery or hematoma
3. increased intrathoracic pressure
   ex. high positive end expiratory pressure like someone on high ventilator settings
4. increased abdominal pressure
   ex. IA compartment syndrome, constipation, bladder distention –> can inhibit venous drainage and effect the ICP!

this is why treating ICP is hard to do in isolation because it can be effected by so many other things in the body

Question 16

what could cause increased ICP via the arterial compartment?

Answer 16

1. cranial hemorrhage
   ex. intracerebral hemorrhage, subarachnoid hemorrhage, epidural hemorrhage
2. cerebral autoregulation

blood flow to the brain is regulated by constricting or dilating arteries and in this process the radius of the blood vessel is what determines the resistance to flow –> in the brain, this regulation is done by the small AND large arteries and the reason is because it’s super important to maintain cerebral blood flow by engaging all these arteries to make sure it’s really constant despite a wide range of cerebral pressure, metabolic factors and BP

Question 17

what is coupling? what is uncoupling?

Answer 17

the process of matching the blood flow to meet the metabolic supply and demand of the brain

when you have brain injury, there’s loss of the BBB mechanisms and the ionic gradients that maintain the neuron cell function which causes uncoupling and loss of autoregulation

once coupling is lost, managing ICP becomes very challenging

Question 18

what factors effect the autoregulation of the cerebral blood flow?

Answer 18

1. MAP
2. PaCO2
3. PaO2

slide 20 go look at it idk

Question 19

what are the 4 ways to monitor ICP?

Answer 19

1. ventricular
2. subarachnoid
3. intraparenchymal
4. epidural

gold standard is the ventricular monitor

Question 20

what is an extraventricular drain?

Answer 20

surgeon will insert the drain into the ventricle around the foramen of Monroe

this will monitor ICP and also drain CSF at the same tie

you have to level so that it reads out a proper ICP

so the nice thing about this drain is if you’re also monitoring BP along with the ICP, you can monitor the cerebral profusion pressure to make sure your therapies are optimizing the CPP based on what the MAP and ICP is:

CPP = MAP - ICP

Question 21

what are ICP waveforms?

Answer 21

P1 = percussion; arterial pulsation

P2 = tidal; brain compliance

P4 = dicrotic; venous pulsation

there are normal ranges of ICP but something more useful is the waveform! measuring ICP will give you a 3 peak waveform with P1, P2 and P3

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Question 22

what happens to the ICP waveforms as ICP increases?

Answer 22

a normal ICP waveform has P1 > P2 > P3 so the pressure of the artery is greater than the tissue in the brain which is greater than the venous pressure

as you start to develop higher pressures in the brain you lose the brain’s compliance so the P2 peak starts to get higher! so if you have someone with a quickly rising ICP who is trying to compensate, before you even reach high ICPs you will see the waveform start to change

so if there’s a good compensatory mechanism, the waveform is preserved but as the compensatory reserve runs out and you turn into a decompensated state, the waveform will start to change and P2 will become higher than P1

ICP thresholds are kind of fabricated; like usually ICP 20 or 25 is bad but with some people a level of 18 could be causing problems so that’s why it’s better to look at the waveform

Question 23

what are the 4 important ICP waveform patterns?

Answer 23

1. ICP waveform
2. Lundberg A wave
3. Lundberg B wave
4. Lundberg C wave

Question 24

what is an ICP waveform pattern?

Answer 24

if P2 elevates or exceeds the level of the P1 waveform, there is marked decrease in cerebral compliance

Question 25

what is a Lundberg A ICP waveform pattern?

Answer 25

this correlates to someone who is trying to intermittently vasodialate because the brain is so tight there’s no room for blood flow –> so it indicates low cerebral perfusion pressure! (CPP)

so on occasion the blood vessels will all just completely dilate to allow for a lot of blood flow to come in and try and profuse the brain which will cause a spike in ICP and it’ll be elevated for a period of time until the brain gets too overwhelmed by the increased ICP and the blood vessels will constrict again

so what you see is for a while your ICP is on the threshold of abnormal and you’re not getting enough blood flow which will cause the blood vessels to dilate and ICP to shoot up but it’s too high so then your blood vessels constrict and it drops again –> you see this pattern right before somebody is about to herniate!!!!!!**

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Question 26

what is a Lundberg B ICP waveform pattern?

Answer 26

a pattern of ICPs that are generated by the loss of vaso-motor control and vaso-motor center instability in the medulla

there’s sporadic higher levels of ICP that are random due to poor control of vessel radius

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Question 27

what is a Lundberg C ICP waveform pattern?

Answer 27

respiratory variation in the ICP just like there’s respiratory variation in heart rate

looks like oscillations

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Question 28

what are the symptoms of sudden increased ICP?

Answer 28

1. trancelike state
2. non-purposeful movement (can look like delirium or agitation which can get overlooked)
3. air hunger/suffocation
4. nystagmus, eye deviation, blurred vision
5. dysphagia

SO MANY SIGNS; it can manifest in a lot of ways so that’s why it’s so important to do neuro checks so it doesn’t get to the point where there’s overt brain herniation because that means there’s active brain damage

Question 29

what are the 7 types of brain herniation?

Answer 29

1. transcalvarial herniation
2. subfalcine herniation
3. diencephalic torsion/shift
4. uncal herniation
5. central downward trans-tectorial
6. downward cerebellar tonsil herniation
7. upward cerebellar/transtentorial herniation

Question 30

what does transtentorial herniation mean?

Answer 30

it’s a non-specific term!

it just means some part of the brain passes across the boundary of the tentorial notch

it can be seen with unilateral uncal transtentorial herniation, bilateral central transtentorial herniation, or upward transtentorial herniation

so transtentorial alone is not a specific enough term!

Question 31

what is a transcalvarial herniation?

Answer 31

a defect in the skull and the injured brain exits through that

there is no specific herniation syndrome for this, it will present with whatever region of the brain was effected from the injury

ex. gunshot with bullet exit wound

Question 32

what is a subfalcine herniation?

Answer 32

the cingulate gyrus and the corpus callosum pass under the falx cerebri

this can also cause a unilateral or bilateral ACA branch stroke because the ACA runs in the sinus at the falx cerebri!

Question 33

what are the symptoms of a subfalcine herniation?

Answer 33

1. leg weakness**
2. arm weakness or sensory apraxia (less common than leg problems)
3. abulia, akinetic mutism = severe amotivation
4. transcortical motor aphasia

Question 34

what is diencephalic torsion/shift?

Answer 34

when the thalamus and midbrain get torqued/pushed to the side

the problem with this is that the ascending arousal pathways travel through the central part of the brian and brainstem so torsion will destroy these fibers!

Question 35

how can you identify a diencephalic torsion/shift on a CT?

Answer 35

the measure of diencephalic torsion is measured at the level of the pineal gland which is easily identified on a CT scan because it’s calcified in most adults!

so looking at the shift of the pineal gland will correlate to the diencephalic torsion –> as the degree of pineal gland shift increases, there’s are increasing mental status changes and loss of consciousness

0-3 mm = alert, 3-5 mm = drowsy, 6-8 mm = stupor, 9-13 mm = coma

so if you’re looking at a CT scan and the degree of shift isn’t consistent with the level of consciousness, then that’s an indication that the diencephalic torsion isn’t the cause of the severe loss of consciousness and you should look for some other factor (like a metabolic condition)

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Question 36

what are the symptoms of a diencephalic torsion/shift?

Answer 36

1. sigh breaths; frequent sighing
2. Cheyne-Stokes respiratory pattern = slow ramping up of deeper and deeper breaths that are faster and faster that will plateau and wean away in a sinusoidal pattern that ends with apnea and then it starts over again
3. small sluggish pupils
4. EOM reflexes are still brisk
5. motor exam might be normal or Babinski sign
6. flaccid or posturing

Question 37

what is an uncal herniation?

Answer 37

Kernochan’s notch is what happens when the temporal lobe uncus sneaks over the tentorium

Question 38

what structures could an uncal herniation effect?

Answer 38

1. cerebral peduncle of the midbrain
2. CN 3
3. posterior cerebral artery
4. cerebral aqueduct has a periaqueductal gray around it which is where the arousal fibers travel

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Question 39

what are the symptoms of a uncal herniation?

Answer 39

think about the structures that are effected!! cerebral peduncles, CN 3, posterior cerebral artery, and periaqueductal grey

1. periaqueductal grey arousal fiber disruption = altered mental status
2. respiratory patterns: normal –> Cheyne-Stokes –> hyperventilation
3. CN 3 impairment = unilateral sluggish pupils –> dilated fixed –> midsized fix (once you lose both parasympathetic and sympathetic fibers)
4. cerebral peduncle impingement = contralateral weakness, rigidity, or flexor (decorticate posturing) from damage to corticospinal tract
5. posterior cerebral artery compression = vision loss –> homonymous hemianopsia if unilateral and Anton syndrome if bilateral

Question 40

what is Kernohan’s phenomenon?

Answer 40

it’s when there’s an uncal herniation and the uncus actually impinges on the contralateral cerebral peduncle which leads to false localizing signs because now you’re getting ipsilateral signs of weakness as the herniation which is super misleading

so if you’re asked where the lesion is with an uncal herniation, look at which side the CN 3 is impaired and the lesion will be on that side because Kernahan’s phenomenon can mess with which side the weakness is and make it not an accurate way to pinpoint where the lesion is

Question 41

what is a central herniation?

Answer 41

downward pressure on midbrain and pons

both temporal lobes can herniate through the tentorium

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Question 42

what are the symptoms of a central herniation?

Answer 42

1. compression of arousal pathways in both the midbrain and pons = altered mental status
2. respiratory patterns = hyperventilation –> fast/shallow pontine pattern–> ataxic/irregular
3. pupil changes: dilated fixed –> pinpoint fixed (pontine pupils) –> midsized fixed (complete brain death where parasympathetic and sympathetic fibers are gone)
4. eye movement changes
5. motor symptoms like bilateral/symmetric posturing: flexion (decorticate) –> extension (decerebrate) –> flaccid –> triple flexion

Question 43

what are the eye movement changes that you see with a central herniation and why do they happen?

Answer 43

1. dysconjugate gaze due to a unilateral or bilateral CN 6 stretch –> CN 6 exits the pons and goes up the clivus to enter the cavernous sinus so if everything is pushing down, CN 6 gets stretched since it’s stabilized by a ligament that won’t let it go down
2. up gaze restriction due to compression of the dorsal midbrain (Parinaud syndrome!)
3. loss of horizontal eye movements due to pontine compression (CN 6 innervates LR)

Question 44

what is the rostra-caudal pattern of deterioration during a central herniation progression?

Answer 44

1. distortion of brain stem where we’re compressing the pons and midbrain
2. arterial complications: PCA and SCA stroke, paramedian ischemia from basilar artery compression, Durret hemorrhages of the pons
3. venous complications: venous infarct (vein of Galen)
4. more edema from all the ischemia and compression which causes even more herniation and higher ICP –> once you get into this cycle it’s really hard to interrupt

Question 45

what is tonsillar herniation?

Answer 45

when the cerebellar tonsils herniate through the foramen magnum into the spinal cord

you’ve squished the medulla and the spinal cord!

this is the end stage of top-down herniation or you can get direct tonsillar herniation from cerebellar bleeds, etc.

Question 46

what are the symptoms of tonsillar herniation?

Answer 46

Cushing Triad!
1. hypertension

2. reflex bradycardia
3. acute apnea/irregular breathing

vasomotor center is in the lower part of the medulla in the reticular formation and when the medulla isn’t being professed because it’s being compressed by the tonsils, it has a massive sympathetic storm to try and profuse itself and it can cause BP in the 300s and eventually it will cause a reflex bradycardia from the carotid bodies

so this Cushing’s triad is pathopneumonic for tonsillar herniation

however, we don’t often see the full triad clinically because they’re often intubated so instead you’ll see they don’t breath over the ventilator; whatever the ventilator rate is set at the patient won’t breathe faster

Question 47

what is upward herniation?

Answer 47

this happens from infratentorial lesions directly in the brainstem or cerebellum that push up and down at the same time but the upward pushing is what causes the upward herniation

there is midbrain and diencephalon compression from upward compression

this also compresses the SCA and aqueduct obstruction

Question 48

what is a brain code?

Answer 48

acute brain herniation

at the end of this process herniation patients will either end up hemodynamically stable or that process will cause cardiac death

Question 49

how do we manage brain code?

Answer 49

ABCDs
1. secure the airway

2. control breathing
3. secure vascular access and hemodynamic monitoring
4. disability prevention
   - —————————-
5. STAT non-enhanced CT brain (3x)
6. CSF diversion if possible +/- emergent surgery
7. medical management

Question 50

why do we secure the airway when there’s a brain code?

Answer 50

if you see early signs of herniation you still want to do this because very quickly these people can lose their protective reflexes like cough and gag which protect them from aspirating

intubate with rapid sequence intubation

maintain in-line stabilizationUse glidescope/other devices designed not to avoid head tilt because you don’t know if they’ve had any spinal damage

give a paralytic to optimize first pass success when you’re intubating them

Question 51

what do you do when you’re trying to secure vascular access and hemodynamic monitoring during a brain code?

Answer 51

in any code, peripheral IV is great and IO is even better because it can allow you to give mannitol, vasopressors, etc. to help you manage elevated ICP in a quick manner instead of trying to get a central line which will take a lot longer

if you’re trying to give really high doses of NaCl though then you do need a central line

Question 52

what disability prevention precautions do you take during a brain code?**

Answer 52

1. optimize venous drainage
2. manipulate autoregulation
3. minimize cerebral edema development
4. maintain SBP 110-160 throughout

Question 53

how do you optimize venous drainage during a brain code to prevent disability?

Answer 53

1. HOB > 30 degrees helps gravity drain blood out of the brain

reverse Trendelenburg can be used for patients on bed rest even if they are on flat bed rest orders

2. loosen C-collar that could be compressing jugulars
3. manual in-line stabilization

Question 54

how do you manipulate autoregulation during a brain code to prevent disability?

Answer 54

you can by manipulate autoregulation by hyperventilating the patient by bagging them to get their CO2 down low enough to induce vasoconstriction – by narrowing blood vessels you will drop the cerebral blood flow which will drop the cerebral volume and drop the ICP

just make sure you don’t do this or too long or too aggressively because you will cause ischemia and stroke from loss of cerebral blood flow which will cause edema and increased ICP and totally counteract everything you’re trying to do

Question 55

how do you minimize cerebral edema development during a brain code to prevent disability?

Answer 55

hyperosmolar therapy!

you brain is over 75% water so by giving hypertonic saline or mannitol you can draw the water out and then that gets eliminated through the kidneys

this allows room for arterial blood flow and prevents strokes!

basically you’re dehydrating the brain

Question 56

how do you maintain SBP 110-160 during a brain code to prevent disability?

Answer 56

you want to maintain BP in a safe range so avoid hyper and hypo tension

use short acting medication for this via infusions; don’t do push doses!

you want to maintain BP because hypertension will cause increased ICP and hypotension will cause ischemia/infarction

Question 57

what is the teared approach for managing ICP?

Answer 57

1. ABCDs = HOB, targeting safe range of CO2, securing airway, managing pain etc.
2. deep sedation = this decreases metabolic demands of the brain so if you don’t have as much demands then you don’t need as much blood flow and you can get by with a lower blood volume in the skull which will reduce ICP –> the only bad thing is you’ll only be able to check neuro function via pupil response
3. hyperosmolar therapy = can be done in conjunction with deep sedation; will help decrease cerebral edema –> you should be careful though because you’re inducing possible heart failure, acute kidney injury, and arrhythmia which can cause toxin buildup
4. prolonged hyperventilation = only do this if absolutely necessary; will help with vasoconstriction to reduce blood flow in the skull –> place monitors to watch brain tissue oxygen and make sure the brain isn’t in a metabolic crisis
5. cerebral suppression = barbiturates or hypothermia to put them in a coma which decreases metabolic demand and oxygen consumption by almost 50% which decreases the amount of blood the person needs –> must be on continuous EEG monitoring and also must be careful about systemic effects of barbiturates and hypothermia
6. tilt tables = strap the patient in and tilt them almost vertically to increase venous drainage but this is VERY rarely used
7. laparotomy = if it’s a trauma patient who also has edematous bowel or increased abdominal pressure you can do a laparotomy to decrease intrabdominal pressure but this is also very rarely done