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INCREASED INTRACRANIAL PRESSURE

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 OUTLINE
● Intracranial pressure
○ Normal values
○ Monro-Kellie Doctrine hypothesis
○ Autoregulation
○ Cushing reflex
● Intracranial hypertension
○ Signs , symptoms, physical examination , ICP monitoring
○ Causes of intracranial hypertension
○ Complication -> brain herniation
● Management of increased ICP
○ Nonpharmacolodic therapy
○ Pharmacologic therapy
○ Surgical intervention
● Staircase and algorithm for management of increased ICP
 Introduction

https://www.mdpi.com/fluids/fluids-04-00196/article_deploy/html/images/fluids-04-00196-g001-550.jpg
 Intracranial pressure
Intracranial volume is composed of cerebrospinal fluid (CSF), blood, brain, and pathologic
items such as tumors or blood clots, and this volume must be constant for a given individual:

In the steady state, intracranial pressure (ICP) is mainly dependent on CSF volume and
cerebral blood volume.

● CSF volume is highly dependent on the dural venous sinus pressure

● Cerebral blood volume is dependent on cardiac parameters and cerebral autoregulation

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 69 Physiology of the Cerebrospinal Fluid and Intracranial Pressure , page 472 e1
 Normal values

● The upper limit of normal ICP in adults and older children is given as 15 to 20 mm Hg.
● “Normal” values for ICP depend on age, body posture, and clinical conditions.
○ In the supine position, ICP in healthy adults is reported as 7 to 15 mm Hg.
○ In the vertical position, it may become negative (as low as –15 mm Hg).
○ Transient physiologic changes resulting from coughing or sneezing often produce
pressures exceeding 30 to 50 mm Hg, but ICP returns rapidly to baseline levels.

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 69 Physiology of the Cerebrospinal Fluid and Intracranial Pressure , page 472 e2
 Monro-Kellie Doctrine

The Monroe-Kellie doctrine is critical to understanding

cerebral fluid homeostasis, pathophysiology, and patient
management in edematous states.
This doctrine defines the cranial vault (calvaria) as a
fixed-volume structure. Within the fixed volume of the skull,
the sum of the volume is derived from brain parenchyma
(1250– 1500 mL volume), cerebrospinal fluid (125–150
mL), and blood (125–150 mL). Per the Monroe-Kellie
doctrine, increases in any of the three components results
in a corresponding decrease in the other components

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 69 Physiology of the Cerebrospinal Fluid and Intracranial Pressure , page 472 e1
 Monro-Kellie Doctrine
Under edematous conditions, increases of intraparenchymal fluid
(edema) expand the brain tissue volume that necessarily leads to
the reduction in cerebral blood and cerebrospinal fluid volume.
Consequently, relative increases in brain volume due to cerebral
edema can cause reduced blood volume (flow) and significant
secondary injury from ischemia or brain herniation.

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 69 Physiology of the Cerebrospinal Fluid and Intracranial Pressure , page 472 e1
 Monro-Kellie Doctrine

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 69 Physiology of the Cerebrospinal Fluid and Intracranial Pressure , page 472 e1
 Cerebral autoregulation
Cerebral perfusion pressure (CPP) depends on mean systemic arterial pressure (MAP) and ICP
by the following relationship:

Normally, CBF is constant over a wide range of blood pressures (i.e., blood pressure autoregulation of CBF) via
actions mainly within the cerebral arterioles. Cerebral arterioles are maximally dilated at lower blood pressures
and maximally constricted at higher pressures so that CBF does not vary during normal fluctuations

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 69 Physiology of the Cerebrospinal Fluid and Intracranial Pressure , page 472 e1
 Autoregulation

● CPP > 150 mmHg (Hyperemic state). ->

blood vessel become “leaky” (breakdown BBB )
-> cerebral edema

● CPP < 50 mmHg (Reactive vasodilation) ->

hypoperfusion, ischemia

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , CHAPTER 388 Invasive Physiologic Monitoring for Traumatic Brain Injury 3032
 Cushing reflex
The Cushing reflex (vasopressor response, Cushing reaction, Cushing effect, and Cushing phenomenon)
is a physiological nervous system response to acute elevations of intracranial pressure (ICP),
resulting in Cushing’s triad of widened pulse pressure (increasing systolic, decreasing diastolic), bradycardia,
and irregular respirations

1st stage : BP ↑ HR↑

(sympathetic activation ; MAP > ICP ; remain brain perfusion)
2nd stage : BP ↑ HR ↓
(increased BP -> +baroreceptors in the aortic arch
-> + parasympathetic activation -> bradycardia)
Later stages : BP ↑HR ↓↑ irregularity in breathing
(shallow breaths with occasional periods of apnea ; compression
of the brainstem by increased ICP-> distortion of the respiratory centers)
(agonal breathing ; herniation of the brain begins,
-> respiratory and cardiac arrest)

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 69 Physiology of the Cerebrospinal Fluid and Intracranial Pressure , page 472 e1
 Signs and symptoms
Increased ICP without localizing sign

Cushing’s triad
Sign of brain herniation
Bulging fontanelle
https://www.ncbi.nlm.nih.gov/books/NBK482119/
Signs and symptoms

Increased ICP with localizing sign

Cerebral cortex
- Frontal
- Temporal
- Parietal
- Occipital
Subcortical

https://www.ncbi.nlm.nih.gov/books/NBK482119/
 Physical examination
- Neurological exam
- A funduscopic exam : papilledema which is a tell-tale sign of raised ICP as the cerebrospinal
fluid is in continuity with the fluid around the optic nerve.

https://www.ncbi.nlm.nih.gov/books/NBK482119/ , Nakprn physio Facebook, ,

 ICP monitoring
- Neurological exam
- Funduscopic exam
- Imaging (CT, MRI of brain) :
- cerebral edema (low density and loss of gray/white matter differentiation, on an
unenhanced image)
- signs of raised ICP such as enlarged ventricles, herniation, or mass effect from
causes such as tumors, abscesses, and hematomas, among others
- Measurement of Opening Pressure with a Lumbar Puncture
- External Ventricular Drain (EVD)
- Optic Nerve Sheath Diameter (ONSD)
- Transcranial Doppler (TCD) ultrasonography
- Tympanic membrane displacement (TMD)
- Invasive ICP Monitoring ; Intraventricular catheters, Intra-parenchymal catheters

https://www.ncbi.nlm.nih.gov/books/NBK482119/
 Etiology

Physiologic cause Pathologic cause

- Coughing based on the intracerebral components
- Sneezing causing elevated pressures:
- Valsava - Increase in brain volume
- Generalized swelling of the brain
- Stress
or cerebral edema from a variety
- Blood pressure change
of causes such as trauma,
- Emotion response ischemia, hyperammonemia,
- Body positioning uremic encephalopathy, and
hyponatremia

https://www.ncbi.nlm.nih.gov/books/NBK482119/
 Etiology
Pathologic cause
Mass Increase in CSF Decreased Increase in Blood Other Causes
Reabsorption of CSF Volume

● Hematoma ● Choroid ● Obstructive ● Increased ● Idiopathic or

● Tumor plexus tumor hydrocephalus cerebral blood benign intracranial
● Abscess ● Decreased ● Meningeal flow during hypertension
● Infarct Reabsorption inflammation or hypercarbia, ● Skull deformities
of CSF granulomas aneurysms such as
● Venous stasis craniosynostosis
from Venous ● Hypervitaminosis
sinus A, tetracycline use
thromboses
● Elevated central
venous
pressures, e.g.,
heart failure
https://www.ncbi.nlm.nih.gov/books/NBK482119/
 Complication of Increased ICP
The clinical implication of the change in volume of the component :
a decrease in cerebral blood flow or herniation of the brain.

Major herniation syndromes

1. Cingulate/Subfalcine herniation
2. Uncal/Transtentorial herniation
3. Central herniation
4. Cerebellar tonsillar herniation

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 375 Neuropathology of Traumatic Brain Injury, page 2912 e1
 1. Cingulate/Subfalcine herniation
Pathophysiology :
If one hemisphere is forced under the falx, the cingulate lobe is the first portion of that
hemisphere to be displaced -> confused and drowsy ,anterior cerebral artery is also
displaced beneath the falx -> infarction within this vessel’s territory
-> contralateral lower extremity weakness and urinary incontinence

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 375 Neuropathology of Traumatic Brain Injury, page 2912 e1
 1. Cingulate/Subfalcine herniation (cont)
Radiographic features:
● CT : midline shift of the septum pellucidum
in severe herniation -> displaced tissue compress the corpus callosum ,
contralateral cingulate gyrus and ipsilateral lateral ventricle, foramen of Monro -> dilation
of the contralateral lateral ventricle.
Complications
- Contralateral
hydrocephalus
- Ipsilateral ACA territory
infarction
- Focal necrosis of the
cingulate gyrus

https://radiopaedia.org/articles/subfalcine-herniation
 2. Uncal/Transtentorial herniation
Pathophysiology : The medial portion of the temporal lobe, the uncus, is the
first portion of the hemisphere to be displaced -> compressing the
ipsilateral CN III, midbrain and the PCA
● Compress ipsilateral CN III -> ipsilateral pupillary dilation. (loss of
parasym) and paresis of all EOM except the LR (CN VI) and the SO (CN
IV) -> Down-and-out position , Ptosis
● Uncal herniation against midbrain at ipsilateral cerebral peduncle
(corticospinal tract in crus cerebrii) -> contralateral hemiparesis
● Midbrain is shifted away -> contralateral cerebral peduncle being
driven into the unyielding tentorium ->
ipsilateral hemiparesis (Kernohan’s phenomenon)
● Compression of reticular formation -> decreased level of
consciousness
● Compression of one or both PCA -> occipital lobe infarction.
-> visual field disturbances (contralateral homonymous hemianopia)

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 375 Neuropathology of Traumatic Brain Injury, page 2912 e1
 2. Uncal/Transtentorial herniation (cont)
Radiographic features : Uncal herniation can be suggested on CT, however, MRI is the gold standard
● Unilateral descending tentorial herniation : medial displacement of the uncus, mass effect and
obliteration of the suprasellar cistern (ipsilateral), widening of cerebellopontine angle (ipsilateral),
midbrain hemorrhage on the same side, inferomedial displacement of posterior communicating and
posterior cerebral arteries

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 375 Neuropathology of Traumatic Brain Injury, page 2912 e1
 3. Central herniation

Pathophysiology :
If both hemispheres herniate transtentorially, descent of the diencephalon, midbrain, and pons
● Pressure on dorsal aspect (pretectum,superior colliculi)-> paralysis of upward eye gaze-> Sunset eyes
● Progressive central herniation (rostral to caudal progression)-> brainstem dysfunction -> oculomotor
palsy(Pupil dilate and fixed), progressive alteration of consciousness ,decerebrate or decorticate posturing,
rigidity or paralysis, abnormal respiratory pattern, coma, and eventually death

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 375 Neuropathology of Traumatic Brain Injury, page 2912 e3
 3. Central herniation (cont)

https://radiopaedia.org/articles/central-herniation?lang=us#image_list_item_23046545
 4. Tonsillar herniation
Pathophysiology :
● brainstem and cerebellum herniate through the foramen magnum into the cervical spinal canal
-> neck stiffness and head tilt
● The cerebellar tonsils and medulla are forced together at this opening with lethal compression of vital
medullary centers -> depression of concious level -> respiratory irregularities-> respiratory arrest

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 375 Neuropathology of Traumatic Brain Injury, page 2912 e3
 4. Tonsillar herniation
Radiographic features :
● Visualization of tonsils extending
below the foramen magnum
● anterior brainstem displacement
● loss of CSF surrounding
Complication
● obstructive supratentorial hydrocephalus
(compress 4th ventricle)
● Compression of the posterior inferior
cerebellar artery by the herniated tonsils
can lead to cerebellar infarcts
● Duret hemorrhage

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , Chapter 375 Neuropathology of Traumatic Brain Injury, page 2912 e3
 Herniation

https://pubs.rsna.org/doi/full/10.1148/rg.2019190018#fig12
 Management of increased ICP
The goals of ICP management ; Treatment should be initiated if ICP greater than 22 mmHg
sustained for 5 mins
1. Maintain adequate brain oxygen delivery
2. To avoid further injury
3. Ultimately to prevent herniation.

Management principles : Assessment and management of the A*BC

1. Maintenance of cerebral perfusion pressure by raising MAP
2. Treatment of the underlying cause *
3. Lowering of ICP

Treatments
● Nonpharmacologic therapy
● Pharmacologic therapy
● Surgical intervention
https://www.ncbi.nlm.nih.gov/books/NBK482119/ , CCSAP 2022 Book 1
 Management of increased ICP

Youmans and Winn Neurological Surgery, 4 - Volume Set, 8th Edition , CHAPTER 69Physiology of the Cerebrospinal Fluid and Intracranial Pressure pg 472.e9
 1. Nonpharmacologic therapy
● Head position and cervical collars
○ semi-recumbent position of up to 30 degrees : minimize venous outflow resistance
and promote displacement of CSF from the intracranial compartment to the spinal
compartment
○ Keep the neck midline to facilitate venous drainage from the head
○ In TBI, cervical collars should be used until a spinal cord injury is ruled ou
● Hyperventilation to induce hypocapnia ; reduce ICP immediately, but the effect may be
transient. In severe TBI cases, sustained extreme hyperventilation (PaCO 2 less than 30
mm Hg) for 5 days ; brain tissue oxygen monitoring to sustain a near normal range
(35–40 mm Hg)
● Surgical considerations ; for EVD, mass evacuation, DHC
● Body temperature ; Maintaining normothermia (less than 99.5°F [37.5°C])
○ Fever - 1st line treatment ; scheduled acetaminophen and external cooling blankets
○ failure of tier 0, 1, and 2 therapies -> mild-to-moderate hypothermia

https://www.ncbi.nlm.nih.gov/books/NBK482119/ , CCSAP 2022 Book 1

 Management algorithms for body temperature & shivering

CCSAP 2022 Book 1, Treatment of elevated ICP , https://www.accp.com/docs/bookstore/ccsap/cc2022b1_sample.pdf

 1. Nonpharmacologic therapy (cont)
● Blood pressure (BP) – CPP optimization ; Brain Trauma Foundation (BTF) guidelines maintain
SBP ≥ 100 mmHg for patients 50 to 69 years old
or SBP≥ 110 mmHg for patients 15 to 49 or > 70 years old
maintain CPP target 60–70 mmHg
● Glycemic control : normal BG levels between 80 and 110 mg/dL ; decreased morbidity and
mortality, decreased hospitalization and cost-effectiveness
○ hyperglycemia in critically ill patients - achieve BG values absolutely < 180 mg/dL

https://www.ncbi.nlm.nih.gov/books/NBK482119/ , CCSAP 2022 Book 1, Treatment of elevated ICP , https://www.accp.com/docs/bookstore/ccsap/cc2022b1_sample.p

 2. Pharmacologic therapy
● Diuretics; Acetazolamide ;inhibits carbonic anhydrase–mediated CSF production
● Osmotherapy
○ Hypertonic saline solutions ; sodium chloride, sodium acetate, and sodium
bicarbonate ; 3% to 23.4%
○ Mannitol
● Sedation and analgesia ; for agitation ; 1st line sedative- Propofol, analgesic - Fentanyl
● Neuromuscular blockers ; reserved as a tier 2 strategy to treat IICP caused by
posturing, ventilator dyssynchrony, or increases in thoracic or abdominal pressures.
; cisatracurium or vecuronium as a muscle relaxant
● Pentobarbital ; for patients with refractory intracranial hypertension
● Steroids ; for primary and metastastic brain tumors, to decrease vasogenic cerebral edema ;
intravenous dexamethasone, 4 mg every 6 hours
● Seizure prophylaxis ; Phenytoin is recommended to decrease the incidence of early PTS
(within 7 days of injury)
https://www.ncbi.nlm.nih.gov/books/NBK482119/ , CCSAP 2022 Book 1, Treatment of elevated ICP , https://www.accp.com/docs/bookstore/ccsap/cc2022b1_sample.p
 2. Pharmacologic therapy (cont)
● Osmotherapy (cont)
○ Mannitol ; mannitol 20% solution for injection
■ MOA : osmotic effects, plasma expansion and cerebral microcirculation
■ Dose : bolus of 0.25 g/kg to 1 g/kg body weight; long-term reduction of ICP is needed,
0.25 to 0.5 g/kg can be repeated every 2 to 6 hours
■ >> keep Serum Osm 300 to 320 mOsm
■ Contraindication : SBP < 90 mmHg, children, Renal disease
■ S/E : AKI, electrolyte imbalance (hypo/hyperNa/K), rebound intracranial hypertension
○ Hypertonic saline solutions ; sodium chloride, sodium acetate, and sodium bicarbonate ;
3% to 23.4%
■ MOA : osmotic effects, plasma expansion and cerebral microcirculation , immunologic
and antioxidants properties
■ Herniating -> 30 mL of 23.4% HTS central intravenous bolus over 5–10 minutes
■ S/E : Osmotic demyelination Syndrome, coagulopathy, electrolyte imbalance( HyperCl,
hypoHCO)
https://www.ncbi.nlm.nih.gov/books/NBK482119/ , CCSAP 2022 Book 1, Treatment of elevated ICP ,
 3. Surgical intervention
● Surgical resection : responsible for severe or refractory intracranial hypertension
● Cerebrospinal fluid drainage
○ temporary external drainage (ventriculostomy) : both measuring and controlling ICP
○ temporary internal drainage (ventriculosubgaleal shunt [VSGS])
○ permanent internal drainage (ventriculoperitoneal/atrial/pleural shunt or third ventriculostomy)
● Decompressive craniectomy : The benefit of decompressive craniectomy in other pathologic conditions,
such as middle cerebral infarction

https://www.ncbi.nlm.nih.gov/books/NBK482119/ ,
The Seattle International Severe Traumatic Injury Consensus Conference (SIBICC)
 Diagram of diagnosis and treatment of
intracranial hypertension

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2452989/
 Staircase therapeutic approach of intracranial hypertension

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7241587/