Head injury ICP

Normal ICP

Normal values

The normal range of ICP varies with age.
Values for paediatrics are not well established.

Age group	Normal range (mm Hg)
Adults and older childrenᵃ	<10 to 15
Young children	3 to 7
For term infantsᵇ	1.5 to 6

ᵃthe age of transition from “young” to “older” child is not precisely defined
ᵇmay be subatmospheric in newborns

Raised intracranial pressure

The Monro- Kellie hypothesis

Under normal conditions the total volume of the intracranial cavity remains constant and is formed from three main components:

Blood (CBV, both arterial and venous),
Fluid (CSF)
Cerebral parenchyma.

An increase in one compartment normally results in compensation in another through translocation of CSF and venous blood to maintain constant ICP.

When compensatory mechanisms are exhausted, an exponential increase in ICP occurs.
Patients with ICP below 22 mmHg (BTF guidelines) have significantly better outcomes.
Raised intracranial pressure (>22mmHg) can induce ischaemia and hypoxia by reducing CPP (MAP– ICP);

As CBF is directly proportional to CPP, the presence of hypotension, elevated ICP, and hypoxia can severely limit cerebral supply after TBI.

Oedema is common after TBI and can be attributed to three distinct mechanisms:

Vasogenic

Breakdown of BBB endothelium → intravascular flow of protein-rich exudate into the brain interstitium → increasing extracellular volume without cell swelling.

Cytotoxic

Increases in intracellular volume without BBB disruption
Ion influxes + increased membrane permeability of neural cells → cellular swelling (cytotoxic oedema)
Cytotoxic oedema is the most common brain oedema and results in decreased interstitial volume.

Osmotic

Necrotic tissue is hyperosmolar, causing osmotic- gradient driven fluid accumulation in the cell.

Intracranial pressure (ICP)

Cerebral perfusion pressure (CPP) and cerebral autoregulation

ICP is integral to the determination of a patient’s autoregulatory status.

Cerebral autoregulation is the process by which arterioles in the cerebral vasculature dilate or constrict in order to maintain a constant nutrient supply to the brain
Pressure autoregulation—which maintains a constant flow of blood to the brain despite changing systemic blood pressures—is a subtype of autoregulation

After TBI, pressure autoregulation can be disrupted making the brain pressure passive.

The status of autoregulation changes the approach to patient care in important ways.

A patient with deficient pressure autoregulation will do better with a lower CPP target (typically 60 mmHg, as long as perfusion needs are met), since higher values can elevate ICP [18].
Conversely, patients with intact pressure autoregulation will do better with a higher CPP target (typically 70 mmHg)

Different methods of assessing pressure autoregulation have been proposed, such as the pressure reactivity index (PRx) which is a running correlation coefficient between ICP and MAP values. There is, however, no consensus on the accuracy, reproducibility or clinical validity of any such method at present
An extension of autoregulatory principles has led to the notion of CPPopt (the CPP at which the PRx is most negative)

Experimental: phase II COGiTATE study evaluated feasibility and safety of targeting CPPopt, calculated over a preceding 4 h period
Experimental approaches are exploring the possibility that individualized ICP thresholds could be the ICP value at which PRx is consistently higher than + 0.20

Compliance

The amount the ICP increases related to a fixed increase in intracranial volume
Another metric that can be derived when ICP values are known.
Patients with poor compliance have less reserve and likely require tighter ICP control.
There are ongoing efforts to make compliance measurements available at the bedside given the value of these measurements in clinical care
Analysis of the ICP waveform has long been known to reflect compliance, albeit with imprecision eg

RAP index,

A correlation coefficient between mean ICP and the ICP pulse amplitude (defined as the difference between the highest and lowest ICP measured during one cardiac cycle
Has shown promise for informing compensatory reserve and intracranial compliance

Morphological Clustering Analysis of ICP Pulse (MOCAIP)

Another computationally intense method being explored for similar purposes
MOCAIP involves the analysis and measurement of various morphological characteristics of the ICP waveform

Cerebrovascular autoregulation is the process by which the brain’s arterioles alter their caliber to maintain a constant nutrient supply in relation to change in systemic blood pressure, blood viscosity, the concentration of nutrients and metabolites as well as other variables. Pressure autoregulation is the autoregulatory mechanism with highest familiarity and is depicted here in the Lassen curve. Between the upper and lower limits of pressure autoregulation cerebral blood flow remains relatively constant despite changes in systemic blood pressure because of changes in arteriole diameter. This mechanism can be lost as a result of brain injury and the brain becomes pressure passive as a result. It is now felt important for clinicians caring for severe TBI patients to be familiar with autoregulatory principles, to be able to measure the status of pressure autoregulation and to incorporate this knowledge into the care plan. Adapted from Budohoski et al., 2013.

Engorgement of the brain from autoregulatory mechanisms seems to underlie plateau waves.

The vasodilatory and vasoconstriction cascades reflect broad autoregulatory processes which can influence the diameter of the cerebral vasculature and thus the cerebral blood volume and intracranial pressure despite injury to the brain. These cascades were described by Rosner based on clinical observations. These cascades are clinically relevant as they demonstrate a means by which ICP can be reduced by increasing nutrient delivery to the brain. Adapted from Rosner et al., 1995.

When cerebrovascular autoregulation is active, ICP elevations are tolerated for a longer duration

Rosner’s vasodilatory and vasoconstriction cascades.

Secondary brain injury

Following the initial trauma is attributable in part to cerebral ischemia;

The critical parameter for brain function and survival is adequate cerebral blood flow (CBF) to meet CMRO2 demands

CBF is difficult to quantitate

Can only be measured continuously at the bedside with specialized equipment and difficulty.
CBF depends on cerebral perfusion pressure (CPP), which is related to ICP (which is more easily measured)

Cerebral perfusion pressure (CPP) = Mean arterial pressure (MAP) - Intracranial pressure (ICP)

Note: the actual pressure of interest is the mean carotid pressure (MCP) which may be approximated as the MAP with the transducer zeroed ≈ at the level of the foramen of Monro.
As ICP rises, CPP is reduced at any given MAP. Normal adult CPP is >50mm Hg.
Cerebral autoregulation

A mechanism whereby over a wide range, large changes in systemic BP produce only small changes in CBF.
Due to autoregulation, CPP would have to drop below 40 in a normal brain before CBF would be impaired.
In the head injured patient

Older recommendations were to maintain CPP≥ 70mm Hg due to increased cerebral vascular resistance.
However, recent evidence suggests that elevated ICP (≥20mm Hg) may be more detrimental than changes in CPP (as long as CPP is >60mm Hg)

Higher levels of CPP were not protective against significant ICP elevations).

ICP

Upper limit of normal ICP: 15mmHg, physiological inc. due to coughing, sneezing to 30-50mmHg

Things important to know with ICP

Munro kellie doctrine

Vintracranial vault = Vbrain + Vblood + Vcsf

Studies have shown ICP >25mmHg for TBI patients increases mortality significantly

However studies have not shown a value of ICP that predicts good eGOS in patients with raised ICP

Intracranial pressure volume compensation
Autoregulation of cerebral blood flow

Maintenance of constant cerebral blood flow with varying systemic blood pressures

CPP=MAP-ICP

ICP changes fast with BP
A decrease in CPP results in an increase of both blood pressure and ICP pulsatility → correlation between spontaneous waves of blood pressure (BP) and ICP depends on the autoregulatory reserve (pressure reactivity index (PRx)):

When CPP decreases below auto regulatory reserve → there is less blood in cerebral vessels → the wall tension of cerebral vessels drops → inc. transmission of arterial pulse wave into the intracranial contents
When mass lesion is present → raised ICP → blood and CSF exits the intracranial compartments → reduction in brain compliance → inc. transmission of arterial pulse wave into the intracranial contents

Pressure reactivity index (PRx):

Correlation coefficient between changes in BP and ICP
PRx increases from relatively low values (no association) to values approaching 1.0 (strong positive association)
The PRx provides a practical means of assessing the degree of autoregulation and is useful in elucidating the contribution of the cerebrovasculature to mechanisms causing ICP rise.
PRx has also been shown to be a useful marker for determining optimum treatment goals, such as for CPP
PRx should be negative correlation with ICP: normal if + is then abnormal

As there is greater correlation between ICP and MAP wave, there is dec. in CPP (FV), which is shown in the PRx

A: patient is dying

B: patient is recovering

Autoregulatory reserve: difference between the CPP at a given moment and the lower limit of autoregulation.

Lower limit of autoregulation is within the range of 50 to 7 mm Hg,
The autoregulatory reserve for a CPP of 90 mm Hg would be 20 to 40 mm Hg.

ICP principles

The following are approximations to help simplify understanding ICP:

Normal intracranial constituents (and approximate volumes):

Brain parenchyma (which also contains extracellular fluid): 1400ml
Cerebral blood volume (CBV): 150ml
Cerebrospinal fluid (CSF): 150ml

These volumes are contained in an inelastic, completely closed container (the skull)
The pressure is distributed evenly throughout the intracranial cavity

In reality, pressure gradients exist

The modified Monro-Kellie doctrine:

The sum of the intracranial volumes (CBV, brain, CSF, and other constituents (e.g. tumor, hematoma…)) is constant

An increase in any one of these must be offset by an equal decrease in another.

The mechanism:

There is a pressure equilibrium in the skull.
If the pressure from one intracranial constituent increases

As when that component increases in volume → it causes the pressure inside the skull (ICP) to increase.

When this increased ICP exceeds the pressure required to force one of the other constituents out through the foramen magnum (FM) (the only true effective opening in the intact skull) that other component will decrease in size via that route until a new equilibrium is established.
The craniospinal axis can buffer small increases in volume with no change or only a slight increase in ICP.
If the expansion continues, then the new equilibrium will be at a higher ICP.
The result:

CSF displacement

Initially at pressures slightly above normal
If there is no obstruction to CSF flow (obstructive hydrocephalus)
CSF can be displaced from the ventricles and subarachnoid spaces and exit the intracranial compartment via the FM

Venous blood

Subsequent increases in ICP
Can also be displaced through the jugular foramina via the IJVs

Arterial blood

Further increases in ICP
Arterial blood is displaced and CPP decreases, eventually producing diffuse cerebral ischemia.
At pressures equal to mean arterial pressure, arterial blood will be unable to enter the skull through the FM, producing complete cessation of blood flow to the brain, with resultant massive infarction

Increased brain edema, or an expanding mass (e.g. hematoma) can cause cerebral herniation

Although brain tissue cannot actually exit the skull

Intracranial hypertension (IC-HTN)

Traumatic IC-HTN may be due to any of the following (alone or in various combinations):

Cerebral edema
Hyperemia:

Inc blood to brain
The normal response to head injury.

Possibly due to vasomotor paralysis (loss of cerebral autoregulation).

May be more significant than oedema in raising ICP

Traumatically induced masses

Epidural hematoma
Subdural hematoma
Intraparenchymal hemorrhage (hemorrhagic contusion)
Foreign body (e.g. bullet)
Depressed skull fracture

Hydrocephalus due to obstruction of CSF absorption or circulation
Hypoventilation → hypercarbia → vasodilatation
Systemic hypertension (HTN)
Venous sinus thrombosis
Agitation or posturing → Increased muscle tone and Valsalva maneuver → increased intrathoracic pressure → increased jugular venous pressure → reduced venous outflow from head
Sustained posttraumatic seizures (status epilepticus)

A secondary increase in ICP

Sometimes observed 3–10 days following the trauma,
Associated with a worse prognosis.
Possible causes include:

Delayed hematoma formation

Delayed epidural hematoma
Delayed acute subdural hematoma
Delayed traumatic intracerebral hemorrhage (or hemorrhagic contusions) with perilesional edema:

Usually in older patients, may cause sudden deterioration.
May become severe enough to require evacuation (p.926)

Cerebral vasospasm
Severe adult respiratory distress syndrome (ARDS) with hypoventilation
Delayed edema formation: more common in paediatric patients
Hyponatremia

Clinical presentation

Cushing’s triad

The classic clinical presentation of IC-HTN (regardless of cause) is Cushing’s triad

Hypertension
Bradycardia

Due to stimulation of vagus nerve
Can occur independently of hypertension.

Respiratory irregularity

Full triad is only seen in ≈ 33% of cases of IC-HTN.

Patients with significant ICP elevation due to trauma, brain masses (tumor), or hydrocephalus (but paradoxically not with pseudotumor cerebri) will usually be obtunded.

Cushing response is defined as HTN and bradycardia that arise as a result either of generalized CNS ischemia or of local ischemia due to pressure on the brainstem.

Other features

Triad:

Headache
Vomiting:

Vomiting without any associated nausea is especially suggestive of intracranial disease

Papilledema

Papilledema is a reliable and objective measure of raised ICP, with good specificity.

Varying degrees of cranial nerve palsies may arise as a result of pressure on brainstem nuclei (esp CN6).
Abnormal respiration: Depending on the anatomic location of lesion.

Cheyne-Stokes respiration:

Damage to the diencephalic region,

Sustained hyperventilation:

Dysfunction of the midbrain and upper pons.

Slow respiration:

Midpontine lesions

Ataxic respiration:

Pontomedullary lesions
Greater medullary involvement
Complete irregularity of breathing, with irregular pauses and increasing periods of apnea

Rapid shallow breathing:

Upper medullary lesions

CT scan and elevated ICP

CT findings may be correlated with a risk of IC-HTN

No combination of CT findings has been shown to allow accurate estimates of actual ICP.

60% of patients with closed head injury and an abnormal CT will have IC-HTN.

“Abnormal” CT:

Hematomas (EDH, SDH or ICH)
Contusions
Compression of basal cisterns
Swelling
Herniation

Only 13% of patients with a normal CT scan will have IC-HTN.

However, patients with a normal CT AND

2 or more risk factors identified

60% risk of IC-HTN

Only 1 or none are present

4% risk of IC-HTN

Risk factors for IC-HTN with a normal CT

Age >40 yrs
SBP <90 mm Hg
Decerebrate or decorticate posturing on motor exam (unilateral or bilateral)

Types of ICP waveforms

Normal waveforms

The normal ICP waveform (as occurs with normal blood pressure and in the absence of IC-HTN)

Rarely seen since ICP is usually monitored only when it is elevated.

The origin of the variations seen in the normal tracing is somewhat in dispute.

One explanation describes these two types of waveforms

Formed by two waves

Vascular pulse

P1 = Percussion wave

Arterial pulsation

P2 = Tidal wave

Intracranial compliance

P3 = Dicrotic wave

Venous pulsation

ICP (PULSE)

Possibly act as measure of elastance (ΔP / ΔV)

Useful measure of cerebrovascular reactivity (PRx)

Respiratory pulse

Expiratory: inc. intrathoracic pressure → inc Central venous pressure → dec. CSF drainage → Inc ICP → inc wave
Inspiratory: Dec. intrathoracic pressure → dec Central venous pressure → inc. CSF drainage → dec ICP → dec wave

Reversed in mechanically ventilated patients,

Opposite to that in the lumbar subarachnoid space, which follows the pressure in the inferior vena cava

Changes to normal waveform

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Flat:

Evd clogged/kinked

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Dec/Inc amplitude

⬆️ or ⬇️ CSF volume

If large amount of CSF is drained the waveform will ⬇️ in amplitude

Missing bone flap

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Prominent P1 wave

Systolic BP too high

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Diminishing P1 wave

Systolic BP too low P1 dec. and eventually disappears leaving only P2

P2 and P3 are not changed by this

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Prominent P2 wave

The mass lesion is ⬆️ in volume

The intracranial compliance has ⬇️

An inspiratory breath hold (as ICP will also rise)

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Diminished P2 and P3 wave

Hyperventilation

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Rounded ICP waveform

ICP critically high

Intracranial HTN increases P2 and P3 waves

Pathological waveforms

As ICP rises + cerebral compliance decreases → the venous components disappear + the arterial pulses become more pronounced.

In right atrial cardiac insufficiency, the CVP rises and the ICP waveform takes on a more “venous” or rounded appearance and the venous “A” wave begins to predominate.

A number of “pressure waves” that are more or less pathologic have been described. Currently, this classification is not considered to be of great clinical utility, with more emphasis being placed on recognizing and successfully treating elevations of ICP.

Lundberg ICP waves

Lundberg type	Criteria	Pathophysiology
A wave	Mean wave ICP >50 mmHg lasting 5–20 min before returning to elevated baseline	Low CPP results in vasodilatation (raised CBV and ICP) and ischemia (Cushing response to restore CPP). Suggests ICP exceeding limits of cerebral compliance, and ongoing ischemia.
B wave	Mean wave ICP 20–50 mmHg lasting 30 s to 3 min	Seen in sleep; respiratory changes and variations in CBF. Suggests qualitative rise in ICP and that A waves may form.
C wave	Mean wave ICP <20 mmHg occurring every 10 s	ICP transmission of cyclic Traube–Hering–Meyer variation in SBP due to oscillations in baroreceptor and chemoreceptor control. Sometimes seen in normal ICP waveform

Lundberg pressure waves — A, B, and C, and are independent of respiratory or cardiovascular waveforms.

Lundberg A waves

AKA plateau waves

Plateau waves will rarely be seen because they are usually aborted at the onset by instituting treatments

Amplitude

≥ 50mm Hg

5– 20 minutes.

Usually accompanied by a simultaneous increase in MAP (it is debated whether the latter is cause or effect)

Increases in ICP that are sustained for several minutes and then return spontaneously to a new baseline, which is usually slightly higher than the preceding one

Due to increase in CBV due to vasodilation. (an exaggerated attempt to maintain CBF )

These plateau waves are a normal compensatory response to decreases in CPP and that therefore effective management involves the use of vasopressors. Has 4 phases

Drift phase → Plateau phase → Ischaemic response phase → resolution phase

Pathological state → inc. ICP → A decline in CPP → which triggers a vasodilation → Vasodilation increases ICP to the plateau level (Plateau phase) → Inc. in ICP → dec. in CPP → (cycle continues until vasodilatory capacity is exhausted) → until CPP is restored and the plateau phase can be terminated VIA:

Treatment for the raised ICP is started OR
Cushing response forms:

Cerebral ischemia forms → triggers brainstem vasomotor centers to mount a Cushing response (ischemic response phase) → restores CPP in the resolution phase

Lundberg B waves

AKA pressure pulses

Amplitude of

10–20mm Hg is lower than A waves.
< 50mmHg

Variation with types of periodic breathing. Last 30 secs–2 mins

0.5 to 2/min

Due to: intracranial vasomotor waves from

Physiological cyclical oscillations of cardiac output from respiratory cycling

Low amplitude (<3mmHg)
Inspiration → dec intrathoracic pressure → dilates the thoracic vena cava → acutely decreases atrial filling → Cardiac output falls → reduced CBF → intracranial vasodilatation (myogenic autoregulation) → CBV increase → ICP rise
Expiration → same as above but reverse → As cardiac output and CBF increase the cycle reverses with vasoconstriction reducing CBV and ICP
Thus CBF is maintained about a mean with small oscillations and corresponding changes in ICP.

Tissue metabolism regulating cerebral blood flow.

Accumulation of metabolic products at a tissue level → vasodilatation → inc CBF → CBV and ICP increase.
As the metabolic load is washed out vasoconstriction occurs, CBF, CBV and hence ICP falls.

Will become pathological in the presence of reduced intracranial compliance

The amplitude of the ICP oscillations can be increased

Lundberg C waves

AKA Traube-Hering waves

Frequency of 4–8/min.

Low amplitude: 20mmHg

May sometimes be seen in the normal ICP waveform.

High amplitude C-waves may be pre-terminal, and may sometimes be seen on top of plateau waves

Mean wave <20mmHg

Entire wave increased every 10 secs

ICP transmission of cyclic variation in SBP

Seen in healthy people where their clinical use is not certain yet