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Supervised By: Prof Dr.WALID S. MAANI
Presented by : Rami R. Abusaleh

 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
2
Anatomy
3
Blood
Choroid
Plexus
lateral
ventricles
foramen of
Monro
Third
ventricle
Aqueduct
of Sylvius
fourth
ventricle
foramen of
Magendie
subarachnoid
space
Granulation
Of Pachioni

CSF Circulation
4

Histology
5
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
6
Monro-Kellie doctrine
THE VOLUME PRESSURE
RELATIOSHIP
7

 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
8
Normal ICP

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

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.
10
COMPENSATORY
MECHANISMS

 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
11

Pathology
12
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
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
 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

Herniation:

16
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
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

Cushing’s Triad

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:
19

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
20
Herniation CP

Herniation of
intracerebral contents
21

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
 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


ICP Monitoring
25
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
26
1) Subdural
2) Subarachnoid
3) Interparenchymal
4) Intraventricular
5) Lumber puncture
Invasive Systems ICP
Monitoring
27
ICP MONITORING
Video
28

•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

•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

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.
31

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

34
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.

 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
35

 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.
36
Intracranial Pressure Monitoring,
Experience in Jordan
University Hospital

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 .
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
 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
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

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).

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.

 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
43
BRAIN OEDEMA

44
BRAIN OEDEMA

Thank You
45

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Increased intracranial pressure

  • 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 2 Anatomy
  • 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 6 Monro-Kellie doctrine
  • 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 8 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. 10 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 11
  • 12.  Pathology 12 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
  • 16.  16 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
  • 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: 19
  • 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 20 Herniation CP
  • 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 25 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
  • 26. 26 1) Subdural 2) Subarachnoid 3) Interparenchymal 4) Intraventricular 5) Lumber puncture Invasive Systems ICP Monitoring
  • 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. 31
  • 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.  34 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 35
  • 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. 36 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 43 BRAIN OEDEMA