What is intracranial hypertension?

Intracranial hypertension is a medical condition characterized by increased pressure inside the cranial cavity. Causes may be idiopathic or secondary to conditions such as brain tumors, stroke, hydrocephalus, venous sinus thrombosis, or certain medications.

What is the normal range of intracranial pressure?

The normal range of intracranial pressure (ICP) in adults is generally considered to be between 5-15 mmHg. Values above this range may indicate intracranial hypertension, which necessitates further investigation and potentially urgent management.

What does cushing triad indicate?

This triad reflects the body's physiological response to severe intracranial hypertension, attempting to maintain cerebral perfusion pressure (CPP) in the face of elevated ICP. The presence of Cushing's triad is considered a neurosurgical emergency, as it suggests imminent brain herniation.

GENERAL THERAPY

Intracranial hypertension

David Goldemund M.D.
Updated on 13/03/2024, published on 04/12/2023

Definition

intracranial hypertension is defined as an increase in intracranial pressure (ICP) above the normal range (commonly used threshold is > 20 mmHg or 27 cm H₂O)
- the normal ICP range for adults in a horizontal position is ~ 7-15 mmHg; 1 mm Hg = 1.36 cm H₂O
IC hypertension occurs due to an increase in the volume of one or more of the main intracranial compartments (brain, CSF, blood vessels) due to the failure of the compensatory mechanism

Pathophysiology

the neurocranium forms a closed and rigid shell; normally, there are 3 incompressible environments in equilibrium (Monro-Kellie doctrine) :
- brain (80-90%)
- cerebrospinal fluid (5-10%)
- blood volume (5-10%)
normal intracranial pressure (ICP) is ~ 5−15 mm (increasing transiently with coughing, physical exertion, in Trendelenburg position) [Rangel-Castilo, 2008]
- ICP 16−20 mm Hg: mild hypertension
- ICP 21−40 mm Hg: moderate hypertension
- ICP 41−60 mm Hg: severe intracranial hypertension
- ICP > 60 mm Hg: critical hypertension
normal cerebral perfusion pressure (CPP) = 70-100 mmHg
- safe CPP is > 50 mmHg
- CPP 30- 50 mm Hg leads to reversible functional impairment
- CPP < 30mm Hg may result in irreversible changes
an increase in the volume of one compartment must be compensated by a decrease in the volume of other compartments (initial compensation)
after the exhaustion of compensatory mechanisms (critical volume), ICP starts to increase, followed by a decrease in cerebral blood flow (↓CPP)

CPP = MAP – (ICP + CVP)

MAP – Mean Arterial Pressure, CVP – Central Venous Pressure

2x DBP + SBP

MAP = ———————

Cerebrospinal fluid compartment

CSF is mainly produced by the choroid plexus in the brain’s ventricles, with an hourly production rate of ~ 10-25 mL
the total volume of CSF is ~ 90-150 mL
CSF circulates through the ventricles, over the surface of the brain and spinal cord, and through the subarachnoid space
it is absorbed into the bloodstream via Pacchioni granulations
- granulations are predominantly located along the superior sagittal sinus but can also be found in other dural sinuses
- CSF flows through these granulations into the dural venous sinuses, thereby maintaining CSF homeostasis
- permeability pressure of CSF is ~ 5mmHg
if the ICP rises, the CSF is resorbed faster, leading to a decrease in its volume (see below)

Vascular compartment

arterial portion – high-pressure system with active autoregulation
venous portion – low-pressure, capacitive system, relatively that is relatively passive
both parts can change their volume; the venous portion responds to an increase in ICP by reducing the volume of the compressible parts
autoregulation may be impaired in the affected area
- vasoparalysis (with vasodilatation) increases vascular volume and leads to the progression of vasogenic edema, thereby increasing ICP
- autoregulation is also impaired in advanced age or due to significant proximal arterial stenosis (where peripheral resistance increases and cerebrovascular reserve decreases)

→ cerebral perfusion regulation

Compliance

the cranial compartment is rigid with a fixed total volume of brain tissue, blood, and cerebrospinal fluid (CSF). According to the Monro-Kellie rule, any increase in one of these components must be compensated by a decrease in the others to maintain stable intracranial pressure (ICP)
compliance = capacity to accommodate changes in volume without a significant increase in ICP
- reduced compliance means that a smaller increase in intracranial volume can cause a significant rise in ICP
- factors affecting compliance
  - age (compliance decreases with age)
  - pathology (e.g., edema, hemorrhage)
  - physiological changes (e.g., arterial and venous pressure variations)
compliance curve = curve, where an initial increase in intracranial volume results in minimal changes in ICP due to compensatory mechanisms
once these mechanisms are exhausted, further volume increase leads to a sharp and rapid rise in ICP
a correlate of exhausted compliance is the presence of herniation signs on neuroimaging

Intracranial hypertension can occur due to an increase in the volume of any of the three components mentioned
Cerebrospinal fluid (CSF)	increased CSF production inflammatory irritation of the choroid plexus (choroiditis, epididymitis, leptomeningitis) posttraumatic plexus irritation decreased CSF resorption cerebral venous sinus thrombosis CVST) sclerosis of Pacchionian granulations meningitis brain edema altered CSF flow → all resulting in fluid accumulation and increased pressure
Blood	intravascular pathology (arterial/venous) impaired venous outflow sinus thrombosis compression or thrombosis of neck veins passive dilation of arteries due to loss of autoregulation) extravascular blood collection epidural, subdural, subarachnoid, intraventricular, and intracerebral bleeding
Brain tissue	edema cytotoxic vasogenic interstitial mass lesion (usually accompanied by edema) ischemia intracerebral hematoma tumor abscess contusions diffuse brain injury accompanied by edema hypoxia rapid changes in serum osmolarity hypoglycemia

Cerebral edema is classified into three main types based on the underlying pathophysiological mechanisms:
1. Extracellular
1.1 Vasogenic changes in capillary permeability lead to the transfer of osmotically active particles into the interstitium, serum proteins escaping from vessels drag water molecules along edema is movable, spreads in white matter, and follows the boundaries of grey and white matter causes a “finger-like” appearance on imaging typically present in: tumors (rapid tissue growth leads to the formation of new capillaries with defective walls) later phases of cerebral ischemia (from day 5) malignant hypertension posterior reversible encephalopathy syndrome (PRES) inflammatory processes 1.2 Hydrocephalic (interstitial) occurs due to increased CSF pressure and its movement through the ventricular wall (trans-ependymal movement) blood-brain barrier (BBB) is not disrupted accumulation of Na⁺ and water is present in the periventricular white matter
2. Intracellular (cytotoxic)
failure of the Na⁺/K⁺ pump → disruption of cell membrane permeability and intracellular retention of Na and water leads to increased intracellular volume and reduction of extracellular space edema is immobile and affects both grey and white matter typically seen in: acute ischemic stroke metabolic insults (water intoxication, severe hyponatremia) traumatic brain injury hypoxic injury

Intracranial hypertenseion due to extensive ischemia, cytotoxic edema and hemorrhagic transformation

Clinical presentation

headache
- typically, the earliest and most common symptom
- gradually progressing
- the pain increases with pressure on the jugular veins or during the Valsalva maneuver
- the supine position increases the pain, while the vertical position decreases it
nausea, vomiting
- “central” vomiting (sudden, projectile)
- classic vomiting accompanied by nausea
vertigo
- most commonly experienced as a feeling of imbalance; lesions in the posterior fossa may provoke rotational vertigo
blood pressure
- initially, BP rises as a regulatory mechanism to maintain cerebral perfusion pressure (CPP)
- with progressive intracranial hypertension, this mechanism fails, leading to a drop in BP
- secondary bradycardia (due to vagal irritation) may also occur

tachycardia
- sudden change from bradycardia to tachycardia may indicate vagal paralysis ⇒ Cushing’s triad
respiratory disorders
cranial nerve palsies
- particularly involving CN VI (abducens nerve), leading to double vision
- coma and unilateral non-reactive mydriasis are typical signs of uncal herniation
oliguria
- caused by diencephalon compression
papilledema
altered mental status
- from drowsiness to confusion; in severe cases, sopor or coma occur
brain herniation symptoms → syndrome of rostrocaudal deterioration
- progressive consciousness disorder
- progressive paresis, decerebrate or decorticate rigidity
- oculomotor disturbances
  - uncal herniation leads to ipsilateral mydriasis due to direct mesencephalon compression
  - contralateral mydriasis is caused by the shifting of the mesencephalon against the contralateral tentorium
- Cushing triad (hypertension + bradycardia + respiratory disturbances) indicates brainstem compression
  - the triad reflects the body’s physiological response to severe intracranial hypertension, attempting to maintain CPP; triad is considered a neurosurgical emergency

Diagnostic evaluation

Medical history and clinical evaluation

symptoms and signs are discussed above
neurological findings depend on the etiology of intracranial hypertension
careful monitoring of consciousness level is crucial (using GCS, Beneš-Drábek scale)
in patients with impaired consciousness, brainstem reflexes monitoring is essential to assess the development of rostrocaudal deterioration syndrome → see chapter Disorders of consciousness

Ophthalmologic examination

the head of the optic nerve (CN II) is swollen, with blurred borders
protrusion can be measured in diopters
arteries are narrowed, veins are widened and filled with stagnant blood
small punctate hemorrhages may be observed
in the initial phase of papilledema, vision is not impaired; prolonged congestion leads to optic atrophy with visual impairment

Neuroimaging

monitoring of parenchymal lesions (e.g., measurement of hematoma size, assessment of hemorrhagic transformation of contusion or ischemia, development of edema)
symptoms indicative of compliance exhaustion
- narrowing of the ventricular system (except for complications causing hydrocephalus)
- disappearance of subarachnoid spaces
- compression of the lateral ventricles
- compression of the basal cisterns
- midline structures shift (watch pineal calcification)
signs of non-communicating hydrocephalus include dilatation of the ventricles above the obstruction with transependymal fluid transfer (hypodense periventricular rim on CT, hyperintense areas on T2-weighted MRI)

Clinical and radiological aspects of brain herniation

Neurosonology

→ Neurosonology in intensive care

Intracranial pressure monitoring

allows verification and quantification of intracranial hypertension
IC pressure measurement:
- invasive using different types of sensors:
  - intraparenchymal (in parenchymal lesions)
  - intraventricular (used when CSF of blood drainage from the lateral ventricles is presumed)
  - subdural or epidural
- non-invasive (using transcranial Doppler)
indications unclear except for TBI
- essential in traumatic lesions with GCS < 8
- indication is less clear in ICH, although it’s probably useful in extensive intraventricular bleeding
- in acute hydrocephalus, external drainage is also a therapeutic procedure
the sensor should be used for a maximum of 5-7 days, after which the risk of infection increases and the accuracy of the measurement decreases
indications for full therapy of intracranial hypertension include persistent ICP above 15-20 mmHg or CPP < 50 mm Hg

Monitoring oxyhemoglobin (SjO₂) saturation in the jugular bulb

monitoring arteriovenous (A-V) difference in SjO₂ is a technique used to assess the balance between cerebral oxygen supply and demand; it provides insight into cerebral hemodynamics and metabolism.
a catheter is placed in the jugular bulb to measure venous O₂ saturation
by comparing SjO₂ with arterial oxygen saturation (SaO₂), clinicians can infer the brain’s oxygen utilization
- normal range 55-80% (difference 20-30%)
- a decrease in SjO₂ < 50% with normal arterial oxygen saturation indicates either ↓CBF (e.g., due to increased cerebrovascular resistance) or increased cerebral O₂ consumption (↑CMRO₂)
- an increase in SjO₂ > 85% (lower AV difference) indicates either hyperemia with ↑CBF or reduced cerebral metabolic demand (↓CMRO₂ in neuronal death)
it is necessary to take into account body temperature and the influence of medication during the evaluation
the technique reflects global cerebral oxygenation and may not accurately represent regional variations, especially in focal brain injuries
useful in traumatic brain injury; its efficacy in stroke is unknown