Everything about Increased intracranial pressure Lecture Done by Rami R. Abualeh

1. 1
Supervised By: Prof Dr.WALID S. MAANI
Presented by : Rami R. Abusaleh

2. 
 Def: CSF is a clear, colorless body fluid found in the
brain and spine.
 Secretion  Absorption
 Any obstruction to the flow will lead to increase ICP
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Anatomy

3. 3
Blood
Choroid
Plexus
lateral
ventricles
foramen of
Monro
Third
ventricle
Aqueduct
of Sylvius
fourth
ventricle
foramen of
Magendie
subarachnoid
space
Granulation
Of Pachioni

4. 
CSF Circulation
4

5. 
Histology
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6. 1. Sum of the intracranial volumes of blood, brain, CSF, and other
components (for example, tumour, haematoma) is constant.
2. The skull is considered as an enclosed and inelastic container.
An increase in the volume of any one of the intracranial
contents must be offset by a decrease in one or more of the
others or be associated with a rise in ICP.
 3. Intracranial blood (especially in the venous compartment)
and CSF are the two components whose volume can adapt most
easily to accommodate an increase in the volume
of intracranial contents.2
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Monro-Kellie doctrine

7. THE VOLUME PRESSURE
RELATIOSHIP
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8. 
 Pressure Normally 0-140 mm CSF (0-10 mm Hg
 N.B: (Children 3-7 ,Term infants 1.5-6)
 There are normal regular waves due to pulse and
respiration
 With increased pressure “pressure waves” appear
 volume : Average intracranial volume = 1700 ml
1. Brain (80%) = 1400 ml
2. Blood (10%) = 150 ml
3. CSF (10%) = 150 ml
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Normal ICP

9. 
Cerebral Perfusion
Pressure
 CPP = MAP - ICP (Normal = 70 - 100 mm Hg)
 MAP = 1/3 Systolic + 2/3 Diastolic BP
CEREBRAL BLOOD FLOW (CBF)
Pressure
Flow = ----------------
Resistance
Cerebral Perfusion Pressure
(systemic pressure – intracranial pressure)
Cerebral Blood Flow = --------------------------------------
-
Cerebral Vascular Resistance

10. 
COMPENSATORY MECHANISMS FOR
EXPANDING MASSES:
 Immediate
 Decrease in CSF volume by movement of fluid to the lumbar
area.
 Decrease in the blood volume by squeezing blood out of sinuses
 Delayed
 Decrease in the extra-cellular fluid.
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COMPENSATORY
MECHANISMS

11. 
 WHEN COMPENSATORY MECHANISMS FAIL;
Pathology OCCURS:
 Brain Oedema
 Brain Herniation
 Ischemia if CPP (< 30-40 mm Hg)
 N.B: After head injury cerebral blood flow depends on SYSTOLIC BP
(Stress)
 N.B: The ICP finally rises to the level of arterial pressure which it self begins
to increase, accompanied by bradycardia or other disturbances of heart rhythm
(Cushing response).
COMPENSATORY
MECHANISMS FAIL
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12. 
Pathology
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Etiology of
intracranial
hypertension
Increased Volume
of Intracranial
Constituents.
Space Occupying
Lesions
Localised mass
lesions
Disturbance of
CSF circulation
Obstruction to
major venous
sinuses
Diffuse brain
oedema or
swelling
Idiopathic

13. 13
Localised
mass lesions
Traumatic
haematomas
Neoplasms
Abscess
Focal oedema secondary to
trauma, infarction, tumour
Disturbance of
CSF
circulation
Obstructive
hydrocephalus
Communicating
hydrocephalus
Obstruction to
major venous
sinuses
Depressed
fractures
overlying major
venous sinuses
Cerebral venous
thrombosis
Diffuse brain
oedema or
swelling
Encephalitis,
meningitis, diffuse
head injury,
subarachnoid
haemorrhage, Reye’s
syndrome, lead
encephalopathy, water
intoxication, near
drowning
Idiopathic
Benign
intracranial
hypertension

14.  There is no consistent relation between the severity of symptoms
and the degree of hypertension.
 A) Headache : (Traction on vessels + Compression on dura)
 characteristics:
1. Throbbing or bursting .
2. Worse in the morning
3. Exacerbated by any factors that further increase ICP (ex:
coughing, sneezing, or exertion)
4. Relived by vomiting & analgesia.
B)Visual Disturbance
C) Projectile vomiting
Clinical Presentation

15. 
Herniation:

16. 
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Herniation of
intracerebral contents
•Uncal: most frequently noted herniation
Results in ipsilateral pupil dilatation, decreased level of consciousness, changes in
respiratory patterns, respiratory arrest, and contralateral hemiplegia
•Subfalcine which results in affection of the ACA leading to contralateral leg weakness
Supratentorial herniation
•Results in loss of consciousness, small reactive pupils advancing to fixed/dilated
pupils, respiratory changes leading to respiratory arrest and decorticate posturing
advancing to flacidity
Central/Transtentorial herniation
•Tonsillar: As a result of a downward herniation the medula oblongata is compressed
and displaced causing respiratory and cardiac arrest
Infratentorial herniation

17. Early signs Late signs
A) Headache : : increasing
with projectile vomiting
A) Headache : increasing
with projectile vomiting
B) LOC: restlessness,
agitation, lethargy
B) LOC: difficult to arouse,
decreasing Glasgow Coma
Scale
C)Papilloedema:delayed or
sluggish reaction, unilateral
changes in size
C)Papilloedema: Loss of
vision if severe and
prolonged.
D) MOTOR: pronator drift,
weakened hand grasp
D) MOTOR: posturing,
flaccid muscles
E) MEMORY: mildly
impaired
E) VITAL SIGNS:
CUSHING’S TRIAD
F) SPEECH: slowed or
slurred
F) SPEECH: decreasing, or
with groans or moaning

18. 
Cushing’s Triad

19. 
1. HTN, high pulse pressure,
2. Cheynes-Stoke respiration,
3. Cushing’s response, in 1/3 of cases of tonsillar
herniation.
4. Hematoma.
 N.B: The most common anatomical locations affected by
herniation syndromes include subfalcine, central
transtentorial, uncal transtentorial, upward cerebellar,
cerebellar tonsillar/foramen magnum, and transcalvarial .
Signs of Herniation:
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20. 
Early:
 Headache, projectile vomiting and papilloedema.
Late:
 Change in the level of consciousness,
 Loss of motor and sensory functions, pupillary changes
(compression of Cranial Nerve III)
 Vital sign changes, bradycardia and irregular
respirations,
 Posturing: decorticate(flexion), decerebrate (extension)
or mixed (intermittent)
 Coma
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Herniation CP

21. 
Herniation of
intracerebral contents
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22. 
General Management
 Resuscitation : A.B.C, Head elevation
 IV:
 Fluid management.
 mannitol (Osmotic diuretics)
 Glucocorticoids
 Propofol
 Hypertonic saline bolus (may lower ICP)
 Treat the Cause (The best therapy for (ICH))
 Sedation : Keeping patients appropriately sedated can decrease ICP by reducing
metabolic demand,
 Bp control : maintain CPP >60 mmHg.
 Position : positioned to maximize venous outflow from the head

23.  INTRACRANIAL PRESSURE MONIRORING .
 Control Fever (as it increases brain )
 Antiepileptic therapy (if needed)
 Barbiturates : ( reduce brain metabolism and cerebral blood flow)
 Removal of CSF (ventriculostomy )
 Rapid aspiration of CSF should be avoided because it may lead to
obstruction of the catheter opening by brain tissue.
 Decompressive craniectomy
General Management

24. 

25. 
ICP Monitoring
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ICP Monitoring
Non-
invasive
systems
Tissue resonance
analysis (TRA),
Ocular
sonography
Transcranial
Doppler (TCD)
Intraocular
pressure
Tympanic
membrane
displacement
Invasive
systems
Subdural
Subarachnoid
Interparenchymal
Intraventricular
Lumber
puncture

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1) Subdural
2) Subarachnoid
3) Interparenchymal
4) Intraventricular
5) Lumber puncture
Invasive Systems ICP
Monitoring

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ICP MONITORING

28. Video
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29. 
•1)Simple, Spinal fluid doesn’t reflect the ICP if there is
no communication.
•2)May cause acute brain stem compression.
Lumber
puncture
•The "gold standard" of ICP monitoring catheters.
•placed into the ventricular system and affixed to a
drainage bag and pressure transducer with a three-way
stopcock.
•Advantages :
•accuracy, simplicity of measurement, and the unique
characteristic of allowing for treatment of some causes
of elevated ICP via drainage of CSF.
•Disadvantages: Infections
Intraventricular
Invasive Systems ICP
Monitoring

30. 
•consist of a thin cable with an electronic or fiberoptic transducer at
the tip.
•The most widely used device is the fiberoptic Camino system.
These monitors can be inserted directly into the brain parenchyma
via a small hole drilled in the skull.
•Advantages :
•Ease of placement.
•A lower risk of infection .
•Disadvantages:
•inability to drain CSF for diagnostic or therapeutic purposes.
•mechanical failure due to the complex design of these monitors.
Intraparenchymal :
•Epidural monitors contain optical transducers that rest against the
dura after passing through the skull.
•Inaccurate, as the dura damps the pressure transmitted to the
epidural space.
•They are of limited clinical utility.
•Used in the management of coagulopathic patients with hepatic
encephalopathy complicated by cerebral edema.
Epidural

31. 
Subarachnoid
•Subarachnoid bolts are fluid-coupled systems within a hollow screw that
can be placed through the skull adjacent to the dura. The dura is then
punctured, which allows the CSF to communicate with the fluid column
and transducer.
•The most commonly used subarachnoid monitor is the Richmond (or
Becker) bolt; other types include the Philly bolt, the Leeds screw, and the
Landy screw.
•Advantages:
•Low risk of infection and haemorrhage.
•Disadvantages:
•Often unreliable; therefore, they are rarely used.
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32. 
Non-invasive systems
• an ultrasound-based method, has shown some
promise.
Tissue resonance
analysis (TRA)
• can provide a noninvasive measure of optic
nerve sheath diameter, which has been found to
correlate with intracranial pressure.
Ocular sonography
• measures the velocity of blood flow in the
proximal cerebral circulation.
Transcranial
Doppler (TCD)
• can be assessed noninvasively using an
ultrasonic handheld optic tonometer.
Intraocular
pressure
• (measured using an impedance audiometer).
Tympanic
membrane
displacement

33. 33

34. 
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ICP monitoring
Indication
Bullock and colleagues:
There was sufficient class II and III evidence to support the following
recommendations (no class I) :
ICP monitoring is appropriate in patients with severe head injury (GCS 3-8 after
CPR) and an abnormal (CT) scan (haematomas, contusions, oedema or compressed
basal cisterns)
ICP monitoring is appropriate in patients with severe head injury and a normal CT
scan if ≥ 2 of the following features are noted on admission: age > 40 years,
unilateral or bilateral motor posturing, systolic blood pressure < 90 mm Hg
ICP monitoring is not routinely indicated in patients with mild or moderate head
injury; however, a clinician may choose to monitor ICP in certain conscious patients
with traumatic mass lesions.

35. 
 According to The Department of Neurosurgery, Faculty of
Medicine, Jordan University Hospital, Amman, Jordan.
 Objective: This retrospective study was done to evaluate the
Intracranial Pressure (ICP) monitoring and its effect on the
outcome of multi-trauma patients, including severe head
injury, in Jordan University, Hospital, as many studies were
published with controversies.
 This study was done by Prof Dr. Walid Maani, Dr.Awni
Musharbash, Dr. Qussai Saleh, Dr. Ahmed Tamimi & Dr.
Moh'd Abu-Elrub.
Intracranial Pressure Monitoring,
Experience in Jordan
University Hospital
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36. 
 Methods: A total of 67 patients were included in the study, and
in 42 patients ICP monitoring was used.
 Results: It was found that the mortality rate increases with the
higher readings in the ICP, reaching up to 100% in patients with
an ICP of 60mmHg and above. Although the mortality rate was
less in the ICP monitored patients (35.7%), compared to the
Non- ICP monitored patients (52%).
 Conclusion: The final outcome of severely head injured
patients is not truly known especially in multitrauma patients.
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Intracranial Pressure Monitoring,
Experience in Jordan
University Hospital

37. 
Role of CT
up to 1/3 of patients with initially normal scans developed CT scan
abnormalities within the first few days after closed head injury .

38. By Definition, the term ‘IIH’ describes patients with isolated raised (not
related to an intracranial disorder, a meningeal process or cerebral venous
thrombosi).
Typically affecting young obese women with menstrual irregularities or
taking OCPs, roduces a syndrome of increased intracranial pressure without
identifiable cause.
Pathophysiology:
 remain unclear but those proposed classically include :
1. increased brain water content.
2. excess CSF production.
3. reduced CSF absorption and increased cerebral venous pressure.
 Diagnosis : Modified Dandy criteria
Idiopathic intracranial
hypertension

39.  Signs and symptoms : of increased ICP .
1. No localising focal neurological signs except unilateral or bilateral sixth nerve
paresis.
2. CSF opening pressure ≥25 cm H2O* but without cytological or chemical
abnormalities.
3. Normal neuroimaging adequate to exclude cerebral venous thrombosis—that is,
MRI of the brain, often with additional sequences (CT or MR venography).
 TTT:
1. lumber puncture
2. weight loss
3. Medical treatment:
a) Carbonic anhydrase inhibitors, such as acetazolamide ,are the main medical
treatment classically prescribed for IIH. Acetazolamide decreases the
production of CSF in humans .
b) Topiramate particularly for the treatment of headaches.
c) Oral steroids
Idiopathic intracranial
hypertension

40. Surgery:
 is required in patients with a fulminant onset of disease or when other
treatments have failed to prevent progressive visual loss.
 In patients with papilloedema who have severe visual loss, but minimal or
no headache, optic nerve sheath fenestration (ONSF) is often advised, while
in those with visual loss, papilloedema and headache, a CSF diversion
procedure, such as ventriculo-peritoneal (VP) or lumbo-peritoneal (LP)
shunting, is preferred.
 Aggressive management with CSF shunting is usually required to prevent
catastrophic visual loss in those with acute and rapidly progressive visual
loss.
 These patients might benefit from a transient lumbar drain while awaiting a
more definite surgical procedure.
Idiopathic intracranial
hypertension

41. 
MRI findings in idiopathic intracranial hypertension.
Biousse V et al. J Neurol Neurosurg Psychiatry
2012;83:488-494©2012 by BMJ Publishing Group Ltd
Top: Posterior flattening of
the globes resulting in
shortening of the eyes and
hyperopic shift (arrows).
Dilation and tortuosity of
the optic nerve sheath
(arrowheads). Bottom left:
Empty sella (arrow)
Bottom right: Contrast-
enhanced magnetic
resonance venography
showing bilateral distal
transverse sinus stenosis
(arrows).

42. 
Resolution of bilateral transverse sinus stenosis after lumbo-peritoneal shunt in
a young obese woman with idiopathic intracranial hypertension.
Biousse V et al. J Neurol Neurosurg Psychiatry
2012;83:488-494
Resolution of
bilateral
transverse sinus
stenosis after
lumbo-peritoneal
shunt in a young
obese woman
with idiopathic
intracranial
hypertension.

43. 
 Increased ICP is defined as a sustained elevation in pressure
above 20mm of Hg
 An excess of brain water may occur:
1. Around lesions within the brain:
 Tumor
 Abscess
2. In relation to traumatic damage
3. In relation to ischemic brain insult
 Types of edema:
1. Vasogenic (extra cellular): tumors
2. Cytotoxic (intra cellular): metabolic states
3. Interstitial (extra cellular): increased IVP
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BRAIN OEDEMA

44. 
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BRAIN OEDEMA

45. 
Thank You
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