Elevated Intracranial Pressure

Physiology and Pathophysiology

fixed intracranial volume - 80% brain, 10% blood, 10% CSF
limited compliance of the intracranial compartment beyond a small increase in volume (large increases in pressure for small increases in volume)
CSF is produced in the choroid plexus at a rate of ~20 mL/hr, and passes through the ventricular system, through the arachnoid space, and is reabsorbed by the arachnoid granulations near the apex of the skull

Hydrocephaly

communicating hydrocephaly
- due to imbalance of CSF production and reabsorption, leading to an elevation of pressure throughout the ventricular system and subarachnoid space
- due to:
  - inadequate removal of CSF by the arachnoid granulations (meningitis, SAH, carcinomatosis, CSVT)
  - excessive CSF production (choroid plexus papilloma)
- imaging findings:
  - symmetrical expansion of all ventricles
  - effacement of cerebral sulci and cisternal compression
- treatment: remove CSF anywhere (lumbar drain, intraventricular drain)
noncommunicating/obstructive hydrocephaly
- due to an obstruction in the flow of CSF, leading to localized upstream hydrocephaly
- causes:
  - obstruction due to IVH or inflammation
  - mass lesion
- imaging findings:
  - generation of pressure differentials leads to tissue shifts, herniation
  - acute obstructive hydrocephalus can lead to periventricular interstitial edema
- management:
  - removal of CSF from upstream of the obstruction (?EVD from lateral ventricle)
  - removal of CSF from downstream could precipitate herniation by increasing pressure gradients

Brain Edema

vasogenic edema is due to disruption of the blood-brain barrier, with capillary leak
- tends to involve the white matter
- diagnostics:
  - CT scan - hypoattenuation
  - MRI - hyperintensity on T2/FLAIR without diffusion restriction, contrast enhancement
  - LP - elevated CSF protein
- causes:
  - tumours
  - infection
  - inflammation
  - traumatic tissue damage, hemorrhage
  - cerebral venous thrombosis
  - PRES
- management:
  - many causes are responsive to steroids (e.g. edema due to tumours, infection, inflammation)
  - osmotherapy efficacy may be limited by BBB disruption
cytotoxic edema is due to neuronal injury and neuron swelling
- imaging: affects both grey and white matter
  - CT: hypoattentuation, ?loss of grey/white junction
  - MRI: diffusion restriction with hyperintensity on DWI
- causes:
  - focal ischemic stroke
  - global hypoxic-ischemic brain injury
  - acute liver failure
  - prolonged seizures
- management: not responsive to steroid
interstitial edema (hydrostatic edema)
- secondary to obstructive hydrocephalus
- imaging will show hydrocephalus with periventricular edema
- management: treat hydrocephalus
osmotic cerebral edema
- due to the presence of an osmotic gradient which favours entry of water into the brain
- causes
  - acute hyponatremia
  - dialysis disequilibrium syndrome
  - rebound edema from hyperosmolar therapy

Causes of ICP Elevation

Intracranial mass lesion
1. Tumour
2. Hematoma
3. Abscess or subdural empyema
Cerebral edema
1. Focal edema
  1. Large ischemic stroke
  2. Perihematomal edema
2. Global edema
  1. TBI with DAI
  2. Anoxic brain injury
  3. Hyperammonemia
  4. Hyponatremia
  5. Hypercapnia
  6. Hyperthermia
  7. Encephalitis
  8. PRES
  9. Post-carotid endarterectomy hyperperfusion syndrome
Communicating hydrocephalus
1. Meningitis
2. Leptomeningeal carcinomatosis
3. SAH
4. Superior sagittal sinus thrombosis
Obstructive hydrocephalus
1. Any flow-limiting lesion (extraventricular, intraventricular)
Venous outflow issues
1. Cerebral venous sinus thrombosis (CSVT)
2. Jugular vein compression or thrombosis
3. External neck compression
4. SVC syndrome
5. Severe systemic venous congestion
6. Thoracic or intra-abdominal compartment syndrome

Clinical Manifestations

diffuse elevation of ICP:
- headache (worsened by coughing, sneezing, lying down, exertion)
- vomiting (+/- nausea, projectile, and refractory to medical therapy)
- altered LOC
- visual alterations (vision loss, flashing lights, diplopia)
- abducens nerve (CN VI) palsy with lateral gaze palsy
- Cushing's triad (hypertension, bradycardia, irregular respirations) which is a late manifestation of severe brain injury -- but isolated hypertension may be seen early
Herniation Syndromes (secondary to focal elevation of ICP)

Diagnosis of Elevated ICP

Neuroimaging

CT scan performance depends on the cause of ICP elevation. For focal anatomic lesions, it is excellent and can easily detect tissue shifts. For causes of elevated ICP with anatomically normal brains (diffuse processes), the CT scan may be falsely normal. In these cases, consider MRI.

Warning

Normal CT imaging doesn't rule out elevated ICP.

Opening Pressure Measurement

For patients who are lying in a supine position, the opening pressure of the lumbar puncture is a validated measurement of intracranial pressure. Multiply the opening pressure (in cm H2O) by 0.7 to get the mm Hg value.

When is LP safe? In the presence of focal pathology, lumbar puncture may be dangerous. This is particularly true in the case of noncommunicating hydrocephalus or mass lesions with threatened downward herniation. In the absence of a mass lesion or CSF obstruction, lumbar puncture is a safe strategy to measure intracranial pressure. This may be both diagnostic and therapeutic, since removal of CSF via lumbar puncture will be beneficial among patients with communicating hydrocephalus.

Consider LP in suspected causes of meningitis, pseudotumour cerebri in which CT rules out focal lesions at risk of herniation.

Continuous ICP Monitoring

general indications:
- known or likely to have elevated ICP
- poor neurological examination
- favourable prognosis + aggressive care goals
- certain disease state (TBI) as opposed to others (ischemic stroke)
- no high quality evidence that ICP monitoring and treatment is beneficial
disease-specific indications
- TBI: with GCS <= 8 and CT evidence of hematoma, contusion, swelling, herniation, or compressed basal cisterns
- SAH: EVD generally indicated for patients for acute hydrocephalus
techniques
- external ventricular drain (EVD)
  - burr hole to penetrate the skull, and blind catheter advancement into the lateral ventricle using landmarks. Bedside procedure.
  - allows for continuous pressure transduction, CSF sampling, therapeutic drainage
  - the most accurate but most invasive form of ICP monitoring
  - complications: 10% develop ventriculitis, there can be some trauma from the blind insertion through brain tissue
- Intraparenchymal monitor
  - less invasive, lower infeciton rate
  - cannot sample CSF for diagnostic or therapeutic purposes
  - localized pressure may not reflect general ICP
  - measurements tend to drift, and re-calibration is not possible

Pressure Interpretation

ICP

Normal ICP is 5-15 mmHg (8-20 cm H2O). 1 cm of water equals 0.74 mm of mercury (Hg).
Sustained (>10-15 minutes) levels >20-22 mmHg are an indication for ICP targeted therapy ("ICP crisis")
- Transient elevations should not trigger intervention
- important to take into context other factors:
  - absolute value
  - ICP waveform
  - cerebral perfusion pressure
  - clinical context

ICP Waveform Analysis

Three waves (P1, 2, 3). Normally P1 > P2 > P3 in descending pattern (see below).
- P1 percussion wave - reflections off choroid plexus
- P2 tidal wave - brain compliance
- P3 dicrotic wave - aortic valve closure
As ICP elevates, brain compliance is compromised and P2 becomes higher than P1 and can eventually fuse together into P1-2
Abnormal ICP waveforms can precede absolute ICP elevations.

PLateau waves

defined as "pathological A waves": transient, periodic severe elevations in ICP (up to 50-100 mm Hg) usually lasting for 5-30 minutes.
- they can occur spontaneously, or can be precipitated by coughing, pain, changes in position
- often accompanied by clinical deterioration and symptoms
  - pupillary dilatation
  - reduced consciousness
  - ataxia, posturing
  - headaches, nausea, vomiting
  - visual loss
due to a spiral of ICP elevation, reduced CPP, cerebral vasodilation:
can be mistaken for other phenomena
- seizures
- orthostatic hypotension
generally self-resolve, but episodes >30 minutes can lead to irreversible damage due to impaired perfusion
can be terminated by interventions that cause cerebral vasoconstriction (hyperventilation, vasopressors that induce hypertension)

Cerebral Perfusion Pressure

$$ CPP = (MAP - ICP) $$ - The CPP is the driving pressure for bloodflow through the brain. A normal CPP is 50-90 mm Hg, and should be maintained above >60 mmHg. - Cerebral autoregulation will maintain a stable cerebral blood flow across a wide range of CPP values (e.g., ~50-140 mm). However, an injured brain may lose autoregulatory capacity leading to increased blood flow in response to elevated CPP. - possible that obtaining an adequate CPP is is more important that a normal ICP. Ideally maintain CPP >60 mm Hg - vasopressors w/ arterial MAP monitoring (arterial catheter needs to be calibrate to level of tragus) - For patients with ICP elevation whose precise ICP is unknown, it may be reasonable to target a higher Bp than normal (e.g., target MAP >75-80 mm).

Treatment of Elevated ICP

Treat the underlying disorder

resect the tumour
manage metabolic disorders
VP shunt for patients with refractory hydrocephalus
?steroids for vasogenic edema

Basic Measures (for all neuro-crit patients)

avoid excess intrathoracic pressure by providing adequate sedation and analgesia, avoid coughing and ventilatory asynchrony; avoid excessively elevated airway pressures/PEEP
avoid compression of the jugular veins by keeping the head in neutral position, avoid a C-collar, and avoid IJV CVCs if possible (i.e. first line subclavian or femoral placement)
target normocapnia
- decreasing PaCO2 causes vasoconstriction of cerebral arteries leading to decreased ICP but also reduced blood flow. Therefore, hyperventilation (PaCO2 25-30 mmHg) should only be used as a short-term bridge to immediate NSx intervention, otherwise it can lead to cerebral hypoperfusion, secondary ischemic injury, and worsening cerebral edema in the long term
- monitor CO2 levels closely with a combination of ETCO2 and blood gases
- for most patients, a reasonable target is a low-normal PaCO2 of 35-40 mmHg
target normonatremia. Target a normal sodium level, and avoid any large and rapid decreases in Na. Avoid hypotonic fluid infusions.
target normothermia. Fevers increase cerebral metabolic demands and need for arterial perfusion. Consider routine Tylenol, external cooling devices, etc.
elevate HOB?? -- does reduce ICP, but also arterial cerebral perfusion. One study found this reduced CPP and increased plateau waves. Do not exceed 45 degrees HOB elevation.

Osmotherapy

unclear indications: consider for worsening despite conservative best practices with normonatremia.
Agents: Undiluted (1 mEq/mL) sodium bicarbonate which is the same tonicity as 6% saline (2-3 ampules as emergency therapy), 3% hypertonic saline bolus, 23.4% saline, hypertonic sodium acetate
Clinical end-points
- Keep sodium < 155 mEq/L
- Avoid NAGMA and/or hyperchloremia (>110-115 mEq/L)
- Avoid increases in sodium by more than 6-8 mEq/day to avoid ODS
- Avoid volume overload (may have to use diuretics as well)
May have to taper off hypersomolar therapy as everything that goes up must come down. Increasing the patient's sodium may cause a transient improvement in ICP, but eventually the sodium will need to be lowered back to normal. Unfortunately, the brain tissue will rapidly adapt to being hypernatremic, so lowering the sodium back to normal carries a risk of rebound ICP elevation.
- do this if the sodium has been elevated for more than 1-2 days

Mannitol

nephrotoxic, and induces a diuresis. Requires close serum osmolality monitoring
can cause rebound ICP elevation as mannitol crosses the BBB and can cause vasogenic edema
less effective than HTS and causes more AKI, and potentially more mortality than HTS
HTS is recommended in guidelines over mannitol for TBI or ICH

Mannitol

Overall, do not use mannitol routinely. Strongly consider 3% hypertonic saline over this if possible (also in accordance with guidelines).

Sedation

Consider a deeper sedation approach to avoid coughing, ventilatory dyssynchrony. Avoid suctioning if possible. Add PRN opioids. Temporary paralysis with refractory coughing or dyssynchrony.
Use propofol as it reduces brain metabolic activity and is easily titratable

Seizure

If the patient is worsening, rule out NCSE (consider EEG).
consider seizure prophylaxis in certain contexts (specific brain injuries)

Neurosurgical Intervention

Hydrocephalus --> EVD
Refractory elevated ICP can be treated with decompressive craniectomy. Evidence is best for younger patients with large strokes involving the middle cerebral artery (i.e. malignant MCA syndrome)