INCREASED
INTRACRANIAL PRESSURE
Dr.Muhammad Yusuf,SpS FINS
INCREASED ICP
Outline
Anatomy of the intracranial vault
Physiology: CBF and CPP
Pathophysiology
Monitoring
Treatment
The Intracranial Cavity
The contents of the intracranial
cavity
1: The brain about 1400 ml.
2: The blood 75-100 ml.
3: The CSF 75-100 ml.
All these three compartments are essentially
non compressible, and any change in the
volume of the brain, causes a reciprocal change
in the volume of one or both of the other two
compartments. This is called the Monro-Kellie
doctrine.
CSF
Obstruction to the flow of CSF at any point,
results in dilatation of the venticular system
proximal to the obstruction with profound
effect on intracranial pressure.
Intracranial Vault
Bony structure
Brain & interstitial fluid 80%
Blood (CBV) 10%
CSF 10%
Monroe- Kellie Doctrine
Because of a rigid skull, the
intracranial contents cannot
expand significantly……
Intracranial vault
Brain
Blood
CSF
Cerebral Blood Flow
Amount of blood in transit through brain
Certain CBF for given pressure gradients and given
metabolic state
CBF is not altered by compartment size
Since vasculature resides in rigid skull, it is possible
to increase CBV and ICP and have decreased CBF
Cerebral Blood Flow
Blood supply matches metabolic needs
Regulated:
- Mechanically – metabolic by-products
which alter blood vessel caliber
- By sensitivity to CO2 and O2
- By adenosine and oxygenases
- Perfusion pressure
Kaplan, NM, Lancet 1994; 344:1335.
Cerebral Perfusion Pressure
CBF= inflow - outflow
CPP more sophisticated measure due to the
inclusion of a third pressure CSF
pressure
Cerebral Perfusion Pressure
CPP = inflow – outflow
CPP = P carotid – P intracranial
or
P carotid – P jugular
CPP = MAP - ICP
Autoregulation
CBF is regulated over a wide range of MAP
Range of 60-150 mmHg
Regulated by the tone of small arteries and
arterioles and by Blood Brain Barrier (BBB)
PATHOPHYSIOLOGY
Primary injury
- parenchymal injury
Secondary injury
- reaction of neural tissue to primary injury
edema
cell death
Pathophysiology
Cerebral Edema
increase in brain volume
increase in Na+ and H2O
Classification of Cerebral Edema
Interstitial
Vasogenic
Cytotoxic
Interstitial Edema
Increased CSF hydrostatic pressures
Altered absorption of CSF
Increased edema of periventricular white
matter due to CSF movement across
ventricles.
Prototype
- obstructive hydrocephalus
Vasogenic Edema
Increased permeability of brain capillary
endothelial cells to macromolecules.
Neurons are not primarily injured
Vasogenic Edema
Vasogenic Edema
Tumor
Abscess
Hemorrhage
Contusion
Infarction
Meningitis
Lead encephalopathy
Cytotoxic Edema
Cellular swelling due to cell injury
- neuronal, glial, and endothelial
Failure of ATPase dependant Na exchange
Edema is a reflection of cell death rather than
a contributing factor
Cytotoxic Edema
Cytotoxic Edema
HIE
Re-perfusion injury
Osmotic disequilibrium
Symptoms of Increased ICP
Headache
Bulging fontanels
Papilledema
Altered mental status
Neurological deficit
- common is 3rd nerve palsy
- dilated pupil(s)
Increased ICP
Try to prevent
Primary injury
-parenchymal damage
Secondary injury
- reaction of neural tissue to injury
edema
cell death
Factors That Worsen Secondary
Injury
↓ BP
↓ PaO2
↑ PaCO2
INCREASED ICP
Monitoring
Non-Invasive Invasive
Assess perfusion Intubation
A-line
BP measurement CVP
Jugular venous bulb
Pulse Oximetry ABG’S, LYTES, OSM
ICP device
INCREASED ICP
General Care
HOB elevated 30° ↑ venous drainage
Head midline ↑ venous drainage
No jugular catheters prevent venous obstruction
Normothermia avoid ↑ metabolism
↓ Pleural pressures (zero peep) ↑ venous
drainage
INCREASED ICP
Sedation
Prevents ↑ BP ↑ ICP
Maintenance of artificial airway
Prevents agitation
INCREASED ICP
Glucocorticoids
Useful in peritumoral and intratumoral
edema
Improves tumor glucose utilization, decreasing
necrosis and edema formation.
Phospholipase A2 activity is blocked , less
arachidonic acid is formed and PG, TXns, and LTs
thus less endothelial permeability.
Inhibits inflammatory cell lysozyme thus decreasing
inflammatory cells.
Indications for ICP monitoring
GCS ≤ 8
Cisterns compressed or absent
Midline shift > 5mm
Post surgical removal of intracranial
hematoma
Less severe brain injury in a setting that
requires deep sedation or anesthesia
ICP Monitoring Devices
Location Product
Ventricular catheter with drainage
Parenchymal Codman, Camino
Subarachnoid Bolt system
Subdural Codman, Camino
Epidural
Purpose of ICP Monitoring
Prevention of Herniation…
What to do with the information?
Goal: Adequate oxygen delivery to
maintain the metabolic needs of the
brain.
Intracranial pressure < 20.
Cerebral perfusion pressure 50-70.
Manipulation of ICP
Brain
Mannitol
- dehydrates the brain, not the patient
- monitor osmolality
Hypertonic saline
Manipulation of ICP
Blood
Decrease cerebral metabolic demands
- sedation, analgesia, barbiturates
- avoid hyperthermia
- avoid seizures
Hyperventilation
- decreases blood flow to the brain
- only acutely for impending Herniation.
Mannitol
Manipulation of ICP
CSF
External drainage
- therapeutic as well as diagnostic
- technical issues
- infectious issues
Manipulation of CPP
CPP = MAP- ICP
Maintain adequate intravascular
volume
CVP
replace losses – urine, CSF, Blood
Increase MAP
Effects of increased ICP
D :Internal Brain herniation: resulting in strangulation, compression of
vital structures and blood vessels.
1. Cingulate herniation: compress the internal cerebral vein and the anterior
cerebral artery.
2. Central transtentorial herniation:
* Compression of the 3rd. nerve -------------> Dilated pupils .
* Compression of the post. cerebral art. ----> Hemianopia. Total blindness.
* Compression or ischemia of the brain stem.-> Decerebration. Coma.
* Distortion of the brain stem --------------> Hemorrhages.
3. Uncal herniation. compression of the mid-brain, 3rd nerve and the post.
cerebral art.
4. Tonsilar herniation: Occurs when the cerebellar tonsils,
herniate through the foramen magnum, resulting in compression of
medulla, Decerebration, coma, cardiovascular and respiratory
abnormalities (apnea).
Brain
herniation
1.Cingulate herniation
2.Central transtentorial
herniation
3.Uncal herniation
4.Tonsilar herniation
Medical Treatment of
raised intra cranial pressure.
1. Sedation, and positioning:
2. Hypertonic solutions:
* Manitol: 0.5- 1gm/ Kg body wt. over 30 min. bolus injection.
* Furosemide: is effective in reducing brain edema, and reducing CSF
production. 40-120 mg daily.
* Glycerol: can be given orally as well as I.V. 0.5-2 gm/ Kg. every 4 hrs.
3. Steroids: Dexamethasone 4mg four times a day.
4. Hyperventilation:
5. Hyperbaric oxygen: (rarely used).
6. Hypothermia:
7. Induced barbiturate coma: Has been used to reduce intracranial pressure in
head injuries, and to increase brain tolerance to focal ischemia in aneurysm
surgery , strokes and SAH.
Herniation Syndromes
Critically important herniation syndromes:
Uncal Herniation:
- occurs when a lateral expanding mass lesions
pushes the uncus and hippocampal gyrus over the
lateral edge of the tentorium
- Unilateral dilated pupil progresses to brain
stem dysfunction
Herniation Syndromes
Central Herniation
- downward displacement of the hemispheres
and basal nuclei inferior displacement of midbrain
& surroundings thru tentorial notch
- initially affects diencephalon then progresses
into midbrain and pons.
a) Subfalcial (cingulate) herniation ;
b) uncal herniation ; c) downward
(central, transtentorial) herniation ;
d) external herniation ; e) tonsillar
herniation.
Types a, b, & e are usually caused
by focal, ipsilateral space
occupying lesions, ie., tumor or
axial or extra-axial hemorrhage.
Cushing Reflex
Bradycardia
Hypertension
Altered respiratory status
OFTEN A VERY LATE CLINICAL FINDING!
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