icp monitoring

1. ICP waveforms & monitoring
Dr Sashanka

2. Physiology
Waveforms
Monitoring

3. Physiology

5. Vintracranial vault=Vbrain+Vblood +Vcsf

8. “compliance reflects the ability
of the intracranial system to
compensate for increases in
volume without subsequent
increases in ICP. When
compliance is decreased, even
small increases in intracranial
volume result in large increases
in ICP.”

9. Normal ICP
It is difficult to establish a universal “normal
value” for ICP as it depends on age, body posture
and clinical conditions.
The upper limit of normal ICP – 15 mm Hg
(5 – 10 mm Hg)
Physiologic increase – Coughing, sneezing – 30-50
mm Hg

10. ICP waveforms

11. ICP monitoring waveforms
Flow of 3 upstrokes in one wave.
P1 = (Percussion wave) represents arterial pulsation
P2 = (Tidal wave) represents intracranial compliance
P3 = (Dicrotic wave) represents venous pulsation
In normal ICP waveform P1 should have highest
upstroke, P2 in between and P3 should show lowest
upstroke.
On eyeballing the monitor, if P2 is higher than P1 - it
indicates intracranial hypertension.

13. Related to
Cardiac cycle : within individual waves
Respiratory cycle : between consecutive waves

15. ICP waveform – pulsatile
Baseline is referred to as ICP
Magnitude of baseline, amplitude & periodicity of
pulsatile components
Earliest sign of ↑ ICP – Changes in pulsatile
components

16. Flat
EVD clogged / kinked
Patient expired

17. ↑⁄↓ amplitude
Increasing CSF volume
(or decreased)
If a large volume of CSF
is drained off, the
waveform will decrease
in amplitude.
Missing bone flap

18. Prominent P1 wave
The systolic BP is too
high

19. Diminished P1 wave
If the systolic BP is too
low, P1 decreases and
eventually disappears,
leaving only P2.
P2 and P3 are not
changed by this.

20. Prominent P2 wave
The mass lesion is
increasing in volume
The intracranial
compliance has
decreased
An inspiratory breath
hold (as ICP will also
rise)

21. Diminished P2 and P3 waves
Hyperventilation

22. Rounded ICP waveform
ICP critically high

23. Lundberg waves
Nils Lundberg

25. Lundberg A wave

26. Lundberg A waves
Increases of ICP sustained for several minutes and
then return spontaneously to baseline, which is
slightly higher than the preceding one.
Results from ↑ cerebrovascular volume due to
vasodilatation (Lundberg)
Results from normal compensatory response to
decreases in CPP. Hence give vasopressors.
(Rosner) – But may enhance lesion size & edema

27. 4 phases:
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

29. Lundberg B wave

30. Lundberg B waves
Short elevations of modest nature (10 – 20 mm Hg)
0.5 – 2 Hz
Relate to vasodilatation secondary to respiratory
fluctuations in PaCO2
Seen in ventilated patients (?)
Secondary to intracranial vasomotor waves, causing
variations in CBF
Reflects ↑ ICP in a qualitative manner

31. Lundberg C waves

32. Lundberg C wave

33. Lundberg C waves
More rapid sinusoidal fluctuation (0.1 Hz)
Corresponds to Traube-Hering-Meyer fluctuations
in arterial pressure brought about by oscillations
in baroreceptor and chemoreceptor reflex control
systems
Sometimes seen in normal ICP waveform
High amplitude – pre-terminal, seen on top of A
waves

34. ICP monitoring

35. Why look at ICP waveform analysis?
“…provides information about intracranial
dynamics that can help identify individuals who have
decreased adaptive capacity and are at risk for
increases in ICP and decreases in CPP, which may
contribute to secondary brain injury and have a
negative impact on neurologic outcome.”
C.J Kirkness et. al; J Neurosci Nurs. 2000 Oct; 32(5):271-7.

36. The main indications for ICP monitoring are:
Glasgow Coma Scale (GCS ) < 8
Posturing (extension, flexion)
Bilateral or unilateral pupil dilation (except with Epidural
Hematomas)
CT Scan results showing edema and/or mid-line shift
Physical assessment /neurological assessment findings which
indicate a need for monitoring

37. Contraindications:
Awake patient
Coagulopathy

38. Methods of ICP
measurement
Technology
external strain gauge
catheter tip (internal)
strain gauge
fibre-optic
Location
Ventricular (EVD/IVC)
Intraparenchymal
Subarachnoid
Subdural/Extradural
External Fontanelle

39. External Ventricular Drain
EVD connected to external strain gauge is the
gold standard for measuring ICP
Tip in foramen of Monro
Extensive history, low cost, reliability, therapeutic
Success rate of cannulation – 82%

41. Malposition: 4 – 20%
Did not have significant clinical sequelae
Occlusion : By brain matter / blood clots
Flush EVD
Hemorrhage : 0 – 15% (1.1%)
Most asymptomatic
Intervention in 0.5%

42. Infection : 0 – 22% (8.8%)
Risk factors : IVH, SAH, craniotomy, CSF leakage, systemic
infection, depressed skull #
Duration of catheterization & irrigation of catheter
Venue of insertion – No difference
Extended tunneling
Sandalcioglu - <5 vs >5 cm – 83% vs 17%
Leung – No difference
Prophylactic catheter exchange : No difference

43. Prophylactic antibiotics:
Periprocedural vs none – No difference
Periprocedural vs entire duration – No difference
Guidelines for the Management of Severe Traumatic
Brain Injury – No antibiotic prophylaxis
Antibiotic impregnated catheter:
Rifampin + Minocycline (Zabramski) – 9.4 to 1.3%
Cost

44. When to pull the EVD out?
CT evidence of resolution of cerebral oedema,
and
Improvement of ICP (consistently under 20-25)
Or if the EVD is infected.

45. Fibreoptic ICP monitor
Catheter tip measures the amount of light reflected off a
pressure sensitive diaphragm
Intraparenchymal Camino ICP monitor
Ease of insertion – Right frontal
Also in the region with pathology
Can be inserted in severely compressed ventricles or those with
midline shift
Low risk of hemorrhage and infection
Zero drift: Recalibration cannot be performed
2 mm Hg (first 24 hrs); 1 mm Hg (first 5 days) – Manufacturer
0.5 – 3.2 mm Hg drift - Actual

47. Miniature Strain Gauge
Codman MicroSensor ICP Transducer
Microchip pressure sensor at the tip of a flexible nylon cable that produces
different electricity based on pressure
Intraventricular (Correlation coefficient 0.97 with EVD, Drift 0.2 mm Hg)
Intraparenchymal (Less accurate)
Subdural space (Not enough studies)

48. Spiegelberg Parenchymal Transducer
Air pouch at the tip that is maintained at constant volume
Pressure transducer located in ICP monitor
Recalibration can be made easily
Good correlation with ICP measured by ventriculostomy

50. Compliance Monitor
Experimental stage
Change in volume per unit change in pressure
Spielberg compliance monitor injects small amount of air into the air balloon
pouch and measures the pressure response to this change in volume
Inverse relationship between compliance and ICP

51. Noninvasive ICP monitoring
CT, clinical examination, monitoring pressure in epidural space
Optic Nerve Sheath Diameter (ONSD)
Measured by ultrasound
Critical value is different in different studies
Venous Opening Pressure (VOP)
Measured by venous ophthalmodynamometry
Requires dilatation of pupil
Performed intermittently – Only screening purpose
Cochlear fluid pressure, Flow velocity in intracranial arteries, Delay in VEPs

52. Pediatric ICP monitoring
ICP monitoring only as an option for treating patients with severe traumatic
brain injury
(GCS < 8)
Similar complication rates as in adults

53. BRAIN HERNIATION SYNDROME

56. BRAIN HERNIATION
• most common types
– Subfalcine herniation
– descending transtentorial herniation
• Others
– Posterior fossa herniations
• ascending transtentorial herniation
• tonsillar herniation
– Transalar herniation
• Rare but important types
– transdural/transcranial herniations
– brain displacements across the sphenoid
wing

57. SUBFALCINE
HERNIATION

58. Subfalcine herniation
• most common
• supratentorial mass in one hemicranium
• affected hemisphere pushes across the midline
under the inferior "free" margin of the falx,
extending into the contralateral hemicranium

60. Subfalcine herniation: imaging
Axial and coronal images show that
•cingulate gyrus
•anterior cerebral artery (ACA)
•internal cerebral vein (ICV)
are pushed from one side to the other under the
falx cerebri.
The ipsilateral ventricle appears compressed
and displaced across the midline

62. Complications
• unilateral obstructive hydrocephalus
– foramen of Monro occlusion
• Periventricular hypodensity with "blurred"
margins of the lateral ventricle
– Fluid accumulates in the periventricular white
matter

63. Complications
• When severe, the herniating ACA can be
pinned against the inferior "free" margin of
the falx cerebri
🡪 secondary infarction of the cingulate gyrus

65. TRANSTENTORIAL
HERNIATION

66. Transtentorial herniations
descending
herniations
ascending herniations

67. Descending transtentorial
herniations• the second most common
• a hemispheric mass
• initially produces subfalcine herniation
• As the mass effect increases,
the uncus of the temporal lobe is pushed medially
begins to encroach on the suprasellar cistern
hippocampus follows
hippocampus effaces the ipsilateral quadrigeminal
cistern
both the uncus and hippocampus herniate inferiorly
through the tentorial incisura

68. "Dysautonomia, Multisystem Atrophy and Parkinson's." Dysautonomia, Multisystem
Atrophy and Parkinson's. N.p., n.d. Web. 18 Nov. 2014

70. Descending transtentorial
herniation
• Unilateral
• Bilateral ;"central“
– Severe

71. unilateral DTH: imaging
early
uncus is displaced medially
Ipsilateral aspect of the suprasellar cistern
effaced
Ipsilateral prepontine + cerebellopontine angle
cistern enlarged

73. Descending transtentorial
herniation
As DTH increases
hippocampus also herniates
medially
quadrigeminal cistern
compression midbrain pushed
toward the opposite side of the incisura

74. Descending transtentorial
herniation
severe cases
entire suprasellar and quadrigeminal cisterns
are effaced.
The temporal horn can even be displaced almost
into the midline

76. bilateral DTH
both hemispheres become swollen
the whole central brain is flattened against the
skull base
All the basal cisterns are obliterated
hypothalamus and optic chiasm are crushed
against the sella turcica

79. Complete bilateral DTH
both temporal lobes herniate medially into the
tentorial hiatus
midbrain and pons displaced inferiorly through
the tentorial incisura
The angle between the midbrain and pons
is progressively reduced from 90° to almost 0°

81. Complications
• CN III (oculomotor) nerve compression
– CN III palsy
• PCA occlusion as it passes back up over the
medial edge of the tentorium
– secondary PCA (occipital) infarct

84. Kernohan notch
• As the herniating temporal lobe pushes the
midbrain toward the opposite side of the
incisura
– contralateral cerebral peduncle is forced
against the hard edge of the tentorium
• Pressure ischemia 🡪 ipsilateral hemiplegia
– the "false localizing" sign

88. Duret hemorrhage
"Top-down" mass effect displaces the midbrain
inferiorly
closes the midbrain-pontine angle
Perforating arteries from basilar artery
are compressed and buckled

89. hypothalamic and basal
ganglia infarcts
complete bilateral DTH
perforating arteries from the
circle of Willis compression against the
central skull base
hypothalamic and basal ganglia
infarcts

93. POSTERIOR FOSSA
MASS: TONSILLAR
HERNIATION
ASCENDING

95. Tonsillar herniation
• The cerebellar tonsils are displaced inferiorly
and become impacted into the foramen
magnum.
• congenital (e.g., Chiari 1 malformation)
– mismatch between size and content of the posterior
fossa
• Acquired
– an expanding posterior fossa mass pushing the tonsils
downward—more common
– intracranial hypotension: abnormally low intraspinal
CSF pressure
• tonsils are pulled downward

96. Tonsillar herniation: imaging
• Diagnosing tonsillar herniation on NECT scans
may be problematic.
Cisterna magna obliteration

98. Tonsillar herniation: imaging
• MR: much more easily diagnosed
• In the sagittal plane
– the tonsillar folia become vertically oriented
– the inferior aspect of the tonsils becomes
pointed
– Tonsils > 5 mm (or 7 mm in children) below the
foramen magnum are generally abnormal
• especially if they are peg-like or pointed (rather than
rounded)

99. Tonsillar herniation: imaging
• In the axial plane, T2 scans show that the
tonsils are impacted into the foramen
magnum
– obliterating CSF in the cisterna magna
– displacing the medulla anteriorly

101. Complications
•obstructive hydrocephalus
•tonsillar necrosis

102. ASCENDING TRANSTENTORIAL HERNIATION

104. Ascending transtentorial herniation
•caused by any expanding posterior fossa mass
–Neoplasms > trauma

106. Complications
•Acute intraventricular obstructive
hydrocephalus
–caused by compression of the cerebral aqueduct

109. OTHER LESS COMMON HERNIATION:
TRANSALAR
TRANSDURAL
TRANSCRANIAL HERNIATIONS

110. Transalar Herniation
•brain herniates across the greater sphenoid wing
(GSW) or "ala"
•ascending > descending

111. Ascending transalar herniation
•caused by a large middle cranial fossa mass
•An intratemporal or large extraaxial mass
Temporal lobe + sylvian fissure + MCA
up and over the greater sphenoid wing

117. References
•Osborn, Anne G. "Secondary Effects and
Sequellae of CNS Trauma."Osborn's Brain:
Imaging, Pathology, and Anatomy. Salt Lake City,
UT: Amirsys Pub., 2013. N. pag. Print.
•Osborn, Anne G. "Cerebral Vasculature: Normal
Anatomy and Pathology."Diagnostic
Neuroradiology. St. Louis: Mosby, 1994. N. pag.
Print.