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PRESENTER:Dr.NAVEEN KUMAR
MODERATOR:Dr.T.V.SHENOY
 Definition
 Pathophysiology of icp-
Compliance,autoregulation
 ICP waveforms
 Lundberg waves
 Indications and contraindications ICP
monitoring
 Methods of monitoring-non invasive and
Invasive monitoring systems
16-Feb-15ICP MONITORING/CNK 2
 The pressure or force exerted within the rigid
cranial vault by the intracranial contents
C.P.P=M.A.P-I.C.P
16-Feb-15ICP MONITORING/CNK 3
 ICP depends on age, body posture
HORIZONTAL SITTING
16-Feb-15ICP MONITORING/CNK 4
Coughing ,
valsalvas maneuver , sneezing,
isometric exercises,
Tracheal suctioning
raise the intracranial pressure - 30-50 mm Hg
16-Feb-15ICP MONITORING/CNK 5
16-Feb-15ICP MONITORING/CNK 6
 Cerebral auto regulation is a mechanism whereby
over wide range, large changes in systemic BP
produce only small changes in CBF.
 CPP would have to drop below 40 in a normal brain
before CBF would be impaired,
16-Feb-15ICP MONITORING/CNK 8
 Net increase in water content of both
intracellular & extracellular compartment of
cerebral tissue
 Classification :
 Vasogenic edema : neoplasms, hematomas,
abscesses
 Cytotoxic edema : hypoxia/ischemia
 Interstitial edema : obstructive
hydrocephalus—.
ICP MONITORING/CNK
 Initial injury:
◦ hypoperfusion & relative ischaemia
 24 - 48 hrs post trauma:
◦ Some areas remain hypoperfused and infarcted
◦ Other areas develop relative hyperemia despite no
 in cerebral metabolic demands (uncoupling)
◦ BBB injury results in cerebral edema
 48 - 72 hrs post trauma:
◦  CBF and  CBV  ICP
 At any time:
◦ Pain, agitation, seizures, pyrexia, BS abnormalities
  ICP
16-Feb-15 11
ICP MONITORING/CNK
Direct neuronal disruption Blood-brain barrier injury
Cytotoxic edema
Vasogenic edema
Ischaemia
Hyperemia
Intracranial hypertension
Haematoma
CSF volume
Increased cerebral
blood volume
16-Feb-15 12
 Compliance
reflects the ability
of the intracranial
system to
compensate for
increases in volume
without subsequent
increases in ICP.
16-Feb-15ICP MONITORING/CNK 13
ICP MONITORING/CNK
100
0
40
60
80
20
Volume
ICP mm Hg
ICP controlled due
to compensation
Small volume
marked ICP
16-Feb-15 14
 The shape of the CSF waveform is similar to
the arterial waveform .
 Brain tissue pressure and ICP changes with
each cardiac cycle and thus the ICP waveform
is a modified arterial pressure wave
16-Feb-15ICP MONITORING/CNK 15
P1 = Percussion wave
represents arterial
pulsation
P2 = Tidal wave
represents intracranial
compliance
P3 = Dicrotic wave
represents venous
pulsation
16-Feb-15ICP MONITORING/CNK 16
Prominent P1 wave Diminished P1 wave
16-Feb-15ICP MONITORING/CNK 17
Prominent P2 wave
Diminished P2 and P3
waves
16-Feb-15ICP MONITORING/CNK 18
Rounded ICP waveform Flat
16-Feb-15ICP MONITORING/CNK 19
Nils Lundberg
16-Feb-15ICP MONITORING/CNK 20
16-Feb-15ICP MONITORING/CNK 21
 comprise a steep rise in ICP from near
normal values to 50 mm Hg or more,
persisting for 5–20 minutes and then falling
sharply.
 These waves are always pathological and
indicate greatly reduced compliance.
 They are frequently accompanied by
neurological deterioration.
16-Feb-15ICP MONITORING/CNK 22
1. Drift phase : ↓ CPP → vasodilatation
2. Plateau phase : Vasodilatation → ↑ ICP
3. Ischemic response phase : ↓ CPP → Cerebral
ischemia → Brainstem vasomotor centres →
Cushing response
4. Resolution phase : Cushing response →
Restores CPP
16-Feb-15ICP MONITORING/CNK 24
 These rhythmic oscillations occur every 1–2
minutes.
 ICP rises in a crescendo manner to levels 20–
30 mm Hg higher than baseline and then falls
abruptly.
 These waves were associated with Cheyne-
Stokes respiration.
 Due to a vasomotor center instability
16-Feb-15ICP MONITORING/CNK 25
16-Feb-15ICP MONITORING/CNK 26
 oscillations occur with a frequency of 4–8 per
minute and are of smaller amplitude than B
waves.
 More rapid sinusoidal fluctuation (0.1 Hz)
synchronous with fluctuations in arterial
pressure brought about by oscillations in
baroreceptor and chemoreceptor reflex control
systems
 Seen in normal ICP waveform so limited
pathological significance.
16-Feb-15ICP MONITORING/CNK 27
16-Feb-15ICP MONITORING/CNK 28
◦ Glasgow Coma Scale (GCS ) < 8
◦ CT Scan results showing edema and/or
mid-line shift
◦ Physical assessment /neurological
assessment findings which indicate a need
for monitoring
16-Feb-15ICP MONITORING/CNK 29
Haemorrhage With associated
hydrocephalus
Decerebrate / Decorticate Posturing
Bilateral or unilateral pupil dilation
Brain tumours
Hypoxic brain swelling
Reye’s syndrome
16-Feb-15ICP MONITORING/CNK 30
 Anticoagulation therapy/bleeding disorders
 Scalp infection
 Brain abscess
16-Feb-15ICP MONITORING/CNK 31
 based on their accuracy, reliability and cost
as follows:
 Intraventricular devices – fluid-coupled
catheter with an external strain gauge
 Intraventricular devices – microstrain gauge
or fiberoptic
 Parenchymal pressure transducer devices
 Subdural devices
 Subarachnoid fluid-coupled devices
 Epidural devices
16-Feb-15ICP MONITORING/CNK 32
16-Feb-15ICP MONITORING/CNK 33
16-Feb-15ICP MONITORING/CNK 34
 Cannulated into of lateral ventricles
 The catheter is connected to a fluid-filled
system
 The transducer converts the measured
pressure to an electrical signal.
 the catheter to be zeroed with the transducer
positioned at the level of the center of the
brain (level of foramina of Monroe / tragus)

16-Feb-15ICP MONITORING/CNK 35
16-Feb-15ICP MONITORING/CNK 36
Advantages
 Most accurate
 Allows drainage of CSF as treatment or for
culture
 Inexpensive
 Can give intrathecal antibiotics
 Can re-zero in situ
16-Feb-15ICP MONITORING/CNK 37
16-Feb-15ICP MONITORING/CNK 38
Disadvantages
 Higher infection rate (less so with antibiotic
impregnated)
 Can block with air, blood and debris
 Haemorrhage
 Difficulty in accessing with ventricular
collapse
 CSF drainage can cause herniation
16-Feb-15ICP MONITORING/CNK 39
 Inserted through a support bolt or tunnelled
subcutaneous from burr
 Common site: non dominant frontal lobes
16-Feb-15ICP MONITORING/CNK 40
 Advantages:
Can use with collapsed ventricles
Not dependent on fluid coupling
Low infection rate
Disadvantages:
Cannot recalibrate in vivo(issue after 5d)
Cannot drain CSF
Local not global pressure measure
expensive
16-Feb-15ICP MONITORING/CNK 41
Subdural devices ,Subarachnoid fluid coupled
Devices ,Epidural devices
 Advantages :No parenchymal damage
 Disadvantages: Inaccurate, unreliable
16-Feb-15ICP MONITORING/CNK 42
 Fluid coupled
 External strain guage
 Catheter tip
 Fiber optic
16-Feb-15ICP MONITORING/CNK 43
 Based on an assumption that changes in ICP
affect the physical dimensions and/or
acoustic properties of the cranial vault or
intracranial structures .
 The common drawback of all these methods
is that they measure only relative changes of
ICP
16-Feb-15ICP MONITORING/CNK 44
 Ultrasound Time of the Flight Techniques
 Transcranial Doppler Ultrasonography
 Mechanical / Acoustic Methods
 Magnetic Resonance Imaging
 Electroencephalography
16-Feb-15ICP MONITORING/CNK 45
 Ultrasound Time of the Flight Techniques
 Transcranial Doppler Ultrasonography
 Mechanical / Acoustic Methods
 Magnetic Resonance Imaging
 Electroencephalography
16-Feb-15ICP MONITORING/CNK 46
 Ultrasound Time of the Flight Techniques
 Transcranial Doppler Ultrasonography
 Mechanical / Acoustic Methods
 Magnetic Resonance Imaging
 Electroencephalography
16-Feb-15ICP MONITORING/CNK 47
 Ultrasound Time of the Flight Techniques
 Transcranial Doppler Ultrasonography
 Mechanical / Acoustic Methods
 Magnetic Resonance Imaging
 Electroencephalography
16-Feb-15ICP MONITORING/CNK 48
 Ultrasound Time of the Flight Techniques
 Transcranial Doppler Ultrasonography
 Mechanical / Acoustic Methods
 Magnetic Resonance Imaging
 Electroencephalography
16-Feb-15ICP MONITORING/CNK 49
 Tympanic Membrane Displacement (TMD)
 Otoacoustic Emission (OAE)
 Ocular Measurements
Optic Nerve Sheath Diameter
Ophthalmodynamometry
 Manipulations on the Jugular Vein
16-Feb-15ICP MONITORING/CNK 50
 Tympanic Membrane Displacement (TMD)
 Otoacoustic Emission (OAE)
 Ocular Measurements
Optic Nerve Sheath Diameter
Ophthalmodynamometry
 Manipulations on the Jugular Vein
16-Feb-15ICP MONITORING/CNK 51
 Tympanic Membrane Displacement (TMD)
 Otoacoustic Emission (OAE)
 Ocular Measurements
Optic Nerve Sheath Diameter
Ophthalmodynamometry
 Manipulations on the Jugular Vein
16-Feb-15ICP MONITORING/CNK 52
 Tympanic Membrane Displacement (TMD)
 Otoacoustic Emission (OAE)
 Ocular Measurements
Optic Nerve Sheath Diameter
Ophthalmodynamometry
 Manipulations on the Jugular Vein
16-Feb-15ICP MONITORING/CNK 53
16-Feb-15ICP MONITORING/CNK 54
 Cottrell and young’s textbook of
neuroanaesthesia, 5th edition
 Miller’s anesthesia, 7th edition
 Paul G Barash clinical anaesthesia, 6th edition
16-Feb-15ICP MONITORING/CNK 55
THANK YOU
16-Feb-15ICP MONITORING/CNK 56

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Monitoring and treatment of increased intracranial pressure cnk

  • 2.  Definition  Pathophysiology of icp- Compliance,autoregulation  ICP waveforms  Lundberg waves  Indications and contraindications ICP monitoring  Methods of monitoring-non invasive and Invasive monitoring systems 16-Feb-15ICP MONITORING/CNK 2
  • 3.  The pressure or force exerted within the rigid cranial vault by the intracranial contents C.P.P=M.A.P-I.C.P 16-Feb-15ICP MONITORING/CNK 3
  • 4.  ICP depends on age, body posture HORIZONTAL SITTING 16-Feb-15ICP MONITORING/CNK 4
  • 5. Coughing , valsalvas maneuver , sneezing, isometric exercises, Tracheal suctioning raise the intracranial pressure - 30-50 mm Hg 16-Feb-15ICP MONITORING/CNK 5
  • 7.  Cerebral auto regulation is a mechanism whereby over wide range, large changes in systemic BP produce only small changes in CBF.  CPP would have to drop below 40 in a normal brain before CBF would be impaired,
  • 9.  Net increase in water content of both intracellular & extracellular compartment of cerebral tissue  Classification :  Vasogenic edema : neoplasms, hematomas, abscesses  Cytotoxic edema : hypoxia/ischemia  Interstitial edema : obstructive hydrocephalus—.
  • 10.
  • 11. ICP MONITORING/CNK  Initial injury: ◦ hypoperfusion & relative ischaemia  24 - 48 hrs post trauma: ◦ Some areas remain hypoperfused and infarcted ◦ Other areas develop relative hyperemia despite no  in cerebral metabolic demands (uncoupling) ◦ BBB injury results in cerebral edema  48 - 72 hrs post trauma: ◦  CBF and  CBV  ICP  At any time: ◦ Pain, agitation, seizures, pyrexia, BS abnormalities   ICP 16-Feb-15 11
  • 12. ICP MONITORING/CNK Direct neuronal disruption Blood-brain barrier injury Cytotoxic edema Vasogenic edema Ischaemia Hyperemia Intracranial hypertension Haematoma CSF volume Increased cerebral blood volume 16-Feb-15 12
  • 13.  Compliance reflects the ability of the intracranial system to compensate for increases in volume without subsequent increases in ICP. 16-Feb-15ICP MONITORING/CNK 13
  • 14. ICP MONITORING/CNK 100 0 40 60 80 20 Volume ICP mm Hg ICP controlled due to compensation Small volume marked ICP 16-Feb-15 14
  • 15.  The shape of the CSF waveform is similar to the arterial waveform .  Brain tissue pressure and ICP changes with each cardiac cycle and thus the ICP waveform is a modified arterial pressure wave 16-Feb-15ICP MONITORING/CNK 15
  • 16. P1 = Percussion wave represents arterial pulsation P2 = Tidal wave represents intracranial compliance P3 = Dicrotic wave represents venous pulsation 16-Feb-15ICP MONITORING/CNK 16
  • 17. Prominent P1 wave Diminished P1 wave 16-Feb-15ICP MONITORING/CNK 17
  • 18. Prominent P2 wave Diminished P2 and P3 waves 16-Feb-15ICP MONITORING/CNK 18
  • 19. Rounded ICP waveform Flat 16-Feb-15ICP MONITORING/CNK 19
  • 22.  comprise a steep rise in ICP from near normal values to 50 mm Hg or more, persisting for 5–20 minutes and then falling sharply.  These waves are always pathological and indicate greatly reduced compliance.  They are frequently accompanied by neurological deterioration. 16-Feb-15ICP MONITORING/CNK 22
  • 23. 1. Drift phase : ↓ CPP → vasodilatation 2. Plateau phase : Vasodilatation → ↑ ICP 3. Ischemic response phase : ↓ CPP → Cerebral ischemia → Brainstem vasomotor centres → Cushing response 4. Resolution phase : Cushing response → Restores CPP
  • 25.  These rhythmic oscillations occur every 1–2 minutes.  ICP rises in a crescendo manner to levels 20– 30 mm Hg higher than baseline and then falls abruptly.  These waves were associated with Cheyne- Stokes respiration.  Due to a vasomotor center instability 16-Feb-15ICP MONITORING/CNK 25
  • 27.  oscillations occur with a frequency of 4–8 per minute and are of smaller amplitude than B waves.  More rapid sinusoidal fluctuation (0.1 Hz) synchronous with fluctuations in arterial pressure brought about by oscillations in baroreceptor and chemoreceptor reflex control systems  Seen in normal ICP waveform so limited pathological significance. 16-Feb-15ICP MONITORING/CNK 27
  • 29. ◦ Glasgow Coma Scale (GCS ) < 8 ◦ CT Scan results showing edema and/or mid-line shift ◦ Physical assessment /neurological assessment findings which indicate a need for monitoring 16-Feb-15ICP MONITORING/CNK 29
  • 30. Haemorrhage With associated hydrocephalus Decerebrate / Decorticate Posturing Bilateral or unilateral pupil dilation Brain tumours Hypoxic brain swelling Reye’s syndrome 16-Feb-15ICP MONITORING/CNK 30
  • 31.  Anticoagulation therapy/bleeding disorders  Scalp infection  Brain abscess 16-Feb-15ICP MONITORING/CNK 31
  • 32.  based on their accuracy, reliability and cost as follows:  Intraventricular devices – fluid-coupled catheter with an external strain gauge  Intraventricular devices – microstrain gauge or fiberoptic  Parenchymal pressure transducer devices  Subdural devices  Subarachnoid fluid-coupled devices  Epidural devices 16-Feb-15ICP MONITORING/CNK 32
  • 35.  Cannulated into of lateral ventricles  The catheter is connected to a fluid-filled system  The transducer converts the measured pressure to an electrical signal.  the catheter to be zeroed with the transducer positioned at the level of the center of the brain (level of foramina of Monroe / tragus)  16-Feb-15ICP MONITORING/CNK 35
  • 37. Advantages  Most accurate  Allows drainage of CSF as treatment or for culture  Inexpensive  Can give intrathecal antibiotics  Can re-zero in situ 16-Feb-15ICP MONITORING/CNK 37
  • 39. Disadvantages  Higher infection rate (less so with antibiotic impregnated)  Can block with air, blood and debris  Haemorrhage  Difficulty in accessing with ventricular collapse  CSF drainage can cause herniation 16-Feb-15ICP MONITORING/CNK 39
  • 40.  Inserted through a support bolt or tunnelled subcutaneous from burr  Common site: non dominant frontal lobes 16-Feb-15ICP MONITORING/CNK 40
  • 41.  Advantages: Can use with collapsed ventricles Not dependent on fluid coupling Low infection rate Disadvantages: Cannot recalibrate in vivo(issue after 5d) Cannot drain CSF Local not global pressure measure expensive 16-Feb-15ICP MONITORING/CNK 41
  • 42. Subdural devices ,Subarachnoid fluid coupled Devices ,Epidural devices  Advantages :No parenchymal damage  Disadvantages: Inaccurate, unreliable 16-Feb-15ICP MONITORING/CNK 42
  • 43.  Fluid coupled  External strain guage  Catheter tip  Fiber optic 16-Feb-15ICP MONITORING/CNK 43
  • 44.  Based on an assumption that changes in ICP affect the physical dimensions and/or acoustic properties of the cranial vault or intracranial structures .  The common drawback of all these methods is that they measure only relative changes of ICP 16-Feb-15ICP MONITORING/CNK 44
  • 45.  Ultrasound Time of the Flight Techniques  Transcranial Doppler Ultrasonography  Mechanical / Acoustic Methods  Magnetic Resonance Imaging  Electroencephalography 16-Feb-15ICP MONITORING/CNK 45
  • 46.  Ultrasound Time of the Flight Techniques  Transcranial Doppler Ultrasonography  Mechanical / Acoustic Methods  Magnetic Resonance Imaging  Electroencephalography 16-Feb-15ICP MONITORING/CNK 46
  • 47.  Ultrasound Time of the Flight Techniques  Transcranial Doppler Ultrasonography  Mechanical / Acoustic Methods  Magnetic Resonance Imaging  Electroencephalography 16-Feb-15ICP MONITORING/CNK 47
  • 48.  Ultrasound Time of the Flight Techniques  Transcranial Doppler Ultrasonography  Mechanical / Acoustic Methods  Magnetic Resonance Imaging  Electroencephalography 16-Feb-15ICP MONITORING/CNK 48
  • 49.  Ultrasound Time of the Flight Techniques  Transcranial Doppler Ultrasonography  Mechanical / Acoustic Methods  Magnetic Resonance Imaging  Electroencephalography 16-Feb-15ICP MONITORING/CNK 49
  • 50.  Tympanic Membrane Displacement (TMD)  Otoacoustic Emission (OAE)  Ocular Measurements Optic Nerve Sheath Diameter Ophthalmodynamometry  Manipulations on the Jugular Vein 16-Feb-15ICP MONITORING/CNK 50
  • 51.  Tympanic Membrane Displacement (TMD)  Otoacoustic Emission (OAE)  Ocular Measurements Optic Nerve Sheath Diameter Ophthalmodynamometry  Manipulations on the Jugular Vein 16-Feb-15ICP MONITORING/CNK 51
  • 52.  Tympanic Membrane Displacement (TMD)  Otoacoustic Emission (OAE)  Ocular Measurements Optic Nerve Sheath Diameter Ophthalmodynamometry  Manipulations on the Jugular Vein 16-Feb-15ICP MONITORING/CNK 52
  • 53.  Tympanic Membrane Displacement (TMD)  Otoacoustic Emission (OAE)  Ocular Measurements Optic Nerve Sheath Diameter Ophthalmodynamometry  Manipulations on the Jugular Vein 16-Feb-15ICP MONITORING/CNK 53
  • 55.  Cottrell and young’s textbook of neuroanaesthesia, 5th edition  Miller’s anesthesia, 7th edition  Paul G Barash clinical anaesthesia, 6th edition 16-Feb-15ICP MONITORING/CNK 55

Editor's Notes

  1. CPP-Effective pressure that allows the perfusion of blood through the brain Brain 80 – 85 % CSF 8 – 12 % Cerebral blood volume 5 – 8 % Total Intra cranial volume 1500 ± 100ml
  2. Upward head elevation <=20 increased ICP
  3. Pathologic States that increase the volume of one component necessitate decrease in the volume of another to maintain normal Intra-Cranial Pressure
  4. Cerebral auto regulation is a mechanism whereby over wide range, large changes in systemic BP produce only small changes in CBF. CPP would have to drop below 40 in a normal brain before CBF would be impaired,
  5. Causes of ICP divided into vascular and non-vascular
  6. The normal ICP waveform contains three phases: P1 (percussion wave) from arterial pulsations P2 (rebound wave) reflects intracranial compliance P3 (dichrotic wave) represents venous pulsations
  7. The systolic BP is too high If the systolic BP is too low, P1 decreases and eventually disappears, leaving only P2. P2 and P3 are not changed by this.
  8. The intracranial compliance has decreased Hyperventilation
  9. ICP critically high EVD clogged / kinked Patient expired
  10. 4 phases Drift phase : ↓ CPP → vasodilatation Plateau phase : Vasodilatation → ↑ ICP Ischemic response phase : ↓ CPP → Cerebral ischemia → Brainstem vasomotor centres → Cushing response Resolution phase : Cushing response → Restores CPP
  11. Traube-Hering-Meyer
  12. Cannulated into of lateral ventricles The catheter is connected to a fluid-filled system The transducer converts the measured pressure to an electrical signal. the catheter to be zeroed with the transducer positioned at the level of the center of the brain (level of foramina of Monroe / tragus)
  13. Fiber optic-independent of head position drift 0.6mm hg Cathetor tip-low drift 0.1
  14. Dimensions of the cranium or its structures are determined  measures the transit time of an ultrasound wave and its (potentially multiple) echoes on their path through the cranium and calculates the corresponding distance(s) using known ultrasound propagation velocities in different tissues (e.g. bone, brain, or fluid)
  15. velocity of blood flow through the major intracranial vessels by emitting a high frequency (>2MHz) wave   ICP  can  be  estimated from  the  TCD  measurements  because  it  impedes  the blood  flow  and  consequently  decreases  the  velocity  of blood  flow.  indirectly by assessing the elasticity of the biological material in a defined part of the brain
  16. changes in ICP result in a small but measurable skull expansion which creates additional stress within the skull bones and modifies their mechanical properties.
  17. ICP is estimated from the latency of the second negative-going wave (N2) of the visual evoked potential,
  18. Transmission of intracranial pressure (ICP) to the perilymph of the cochlea may occur via the cochlear aqueduct and possibly other routes. Indirect measurement of perilymphatic pressure may be investigated by observing tympanic membrane (TM) displacement during stapedial reflex contraction. Inward displacement (negative peak pressure on audiogram) is suggestive of high, and outward of normal or low ICP . 
  19.  linear relationship between ICP and the sheath diameter measured with a trans-orbital ultrasound probe use of B-scan (or planar) ultrasound which provided longitudinal cross-section images of the optic nerve and its sheath  ONSD be used for identification of patients with intracranial hypertension that requires treatment (ICP>20mmHg, i.e. ONSD>5mmHg) rather than for a measurement of ICP.
  20. measurement of the retinal venous outflow pressure  applying external pressure on the sclera, while observing the retinal vessels through an ophthalmoscope. The pressure is gradually increased until the central retinal vein begins to pulsate,point when the applied external pressure nears the VOP and is approximately equal to ICP.
  21. occluding the jugular vein for a short period of time (~ 5 seconds) and measuring non-invasively, with a Hall sensor or an ultrasound transducer, the rate of change of blood flow in the jugular vein upstream of the occlusion.