icp

1. Presented To: Presented By:
Mrs. Vinay Kumari Amandeep Kaur
Associate Professor Msc. (N) 2nd year
MMCON 1915703

2.  The skull is a rigid structure.
 It contains:
 Brain
 Blood
 Cerebro spinal fluid (CSF)
 Any increase of theses contents and/or the addition
of any mass will lead to increase in the pressure
(the Monroe-Kellie doctrine).

3.  Brain 1300-1750 mls
 Tissue 300-400 mls.
 Intra-cellular fluid 900-1000 mls.
 Extra-cellular fluid 100-150 mls
 Blood 100-150 mls.
 CSF 100-150 mls.

4.  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.

5.  CEREBROSPINAL FLUID
 Secreted at the rate of 500 mls per day
 Secreted by the choroid plexus in the lateral ventricles
 Flows through the ventricular system
 Exits to the subarachnoid space through the foramina of
Magendie and Luschka
 Absorbed into the venous system via the arachnoid
granulations
 Any obstruction to the flow will lead to
HYDROCEPHALUS and increased pressure.

6.  BRAIN OEDEMA
 An excess of brain water may occur:
 Around lesions within the brain:
 Tumor
 Abscess
 In relation to traumatic damage
 In relation to ischemic brain insult
 Leads to increase in the pressure.
 Types of edema:
 Vasogenic (extra cellular): tumors
 Cytotoxic (intra cellular): metabolic states
 Interstitial (extra cellular): increased IVP

7. Pressure
Flow = ----------------
Resistance
Cerebral Perfusion Pressure
(systemic pressure – intracranial pressure)
Cerebral Blood Flow = --------------------------------------
Cerebral Vascular Resistance

8.  Brain 80 – 85 %
 CSF 8 – 12 %
 Cerebral blood volume 5 – 8 %
 Total Intra cranial volume 1500 ± 100ml

9.  Autoregulation of cerebral blood flow
 Regulation of CSF
 Regulation with help of metabolic changes

10.  Pathologic States that increase the volume of
one component necessitate decrease in the
volume of another to maintain normal Intra-
Cranial Pressure.
 Brain
 CSF
 Cerebral blood volume

11.  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

12.  Awake patient
 Coagulopathy

13.  Intracranial pressure (ICP) is the pressure
inside the skull and thus in the brain tissue and
cerebrospinal fluid (CSF)
 Normal range 5 – 15 mm Hg

14.  Normally 0-140 mm CSF (0-10 mm Hg)
 There are normal regular waves due to pulse and
respiration
 With increased pressure “pressure waves” appear
 With continued rise of ICP the PP falls
 When PP falls CBF is reduced
 Electrical cortical activity fails if CBF is 20ml/100gm/min
 When intracranial pressure reaches mean arterial pressure
circulation to the brain stops.

17.  Internal herniation:- Temporal lobe is pushed
down though Tentorium in cisura
 External herniation:- Cerebellar tonsills/
peduncle herniate through foramen magnum →
Compressing over IV ventricle → ↓CPP →
Death == “CONING”

18.  Effective pressure that allows the perfusion of
blood through the brain
 CPP = MAP – ICP
 Mean arterial pressure (MAP) = DP+ (SP-DP)
 DP + PP/3 3
 (ICP  CVP)
 CPP  MAP – CVP

19.  Normal CBF 45 – 50 ml / 100 gm / min
 Range 20 ml / kg / min to 70 ml / kg / min
 CBF Highest Frontal region
 CBF Medium Parietal region
 CBF Lowest Temporal area

20.  Cerebral Autoregulation
 Normal range MAP 50 – 150 mm Hg
 If Head injured ~~ Failure of autoregulation
 CBF = < 20ml / kg /min.
 Adverse effect on ICP

21.  Increased ICP is defined as a sustained
elevation in pressure above 20mm of Hg
 ICP <15 mm of Hg – Intracranial hypertension
• Acute
• Chronic
Levels ICP in mmHg
Normal
Mild
Moderate
Severe
Very Severe
5 – 15
16 - 20
21 - 30
31 - 40
41 & Above

22.  During slow increase in volume in a continuous mode,
the ICP rises to a plateau level at which the increase
level of CSF absorption keeps pace with the increase in
volume.
 Intermittent expansion causes only a transient rise in
ICP at first. When sufficient CSF has been absorbed to
accommodate the volume the ICP returns to normal.

23.  Expansion to a critical volume does however cause
persistent rise in ICP which thereafter increases
logarithmically with increasing volume ( volume -
pressure relationship).
 THE VOLUME PRESSURE RELATIOSHIP

24.  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). This is accompanied by dilatation
of small pial arteries and some slowing of venous flow
which is followed by pulsatile venous flow.

25.  CPP α CBF
 CPP α 1/ICP
 ↑ICP → ↓CBF, ↓Blood volume, ↑CO2

26.  Cerebral Oedema
 Vasogenic
 Cytotoxic oedema
 Hypoxemia
 Hyponatremia/ Water Intoxication
 Post-Cardiac Arrest
 Inflammatory—Meningitis/Encephalitis
 Interstitial oedema
 Intra Cranial Space Occupying Lesions
 Enlarged ventricular system
 Pneumocephalus
 Increase in C.B.F.
 Impaired cerebral venous drainage

27. Neonates/Infants
 Secondary cerebral oedema to peri-natal
hypoxia or trauma
 Congenital hydrocephalus
Older Infants/Toddlers/Children
 Meningitis
 Brain tumors (Infra tentorial)
 Pseudo tumor cerebrii
 Trauma
 Reye’s syndrome

28.  Thorough clinical assessment
 “WARNING SIGNS”:
Confusion, agitation, restlessness,
aggressiveness
Personality changes
Glasgow Coma Score (GCS)

29. Findings Score
1) Eye opening
Spontaneous
To voice
To Pain
None
4
3
2
1
2) Best verbal response
Oriented
Confused speech
Inappropriate words
Incomprehensible sounds
None
5
4
3
2
1
3)Best motor response
Obeys Commands
Localizes pain
Withdraws
Abnormal flexion
Extension
None
6
5
4
3
2
1
Prognostic value as per GCS
Score Percentage
GCS 3/ less
GCS 3 – 5
GCS 6 – 8
100
60 – 84
36 – 46

33. Meaning : The monitoring of intracranial pressure is
used in treating severe traumatic brain injury patients.
This process is called intracranial pressure monitoring.
All current clinical available measurement methods are
invasive and use various transducer systems.
 Ventricular system
 Sub-arachnoid space
 Epidural space
 Brain parenchyma

34.  Intraventricular catheter
 Subarachnoid screw
or bolt
 Epidural sensor

35. 1. External Ventricular Drainage (EVD). Invasive
monitoring using the EVD technique, where a catheter
is placed into one of the ventricles through a burr hole,
is considered the gold of ICP monitoring. In addition to
measuring ICP, this technique can also be used for
drainage of CSF and administering of medicine intra-
thecally, for example, antibiotic administration in cases
of ventriculitis, possibly resulting from EVD
placement itself.

38. 2. Micro-transducer ICP Monitoring Devices.
This group of invasive ICP monitoring devices can
be divided into fiber optic devices, strain gauge
devices, and pneumatic sensors.

40.  The idea of a noninvasive method of measuring
ICP is captivating, as complications seen in
relation to the invasive methods of ICP measuring,
that is, hemorrhage and infection, are avoidable.
Different techniues have been proposed.
1. Transcranial Doppler Ultrasonography (TCD).
The TCD technique applies ultrasound to initially
measure the blood flow velocity in the middle
cerebral artery. The difference between systolic
and diastolic flow velocity, divided by the mean
flow velocity, is called the pulsatility index (PI).

41. 2. Tympanic Membrane Displacement (TMD). The
technique takes advantage of the communication of the
CSF and the perilymph via the perilymphatic duct.
Stimulation of the stapedial reflex causes a movement
of the tympanic membrane, which is shown to correlate
to ICP.
3. Fundoscopy and Papilledema. Papilledema, or optic
disc swelling, due to raised ICP can be visualized by
fundoscopy and graded by the Fris´en Scale into 5
categories depending on signs of disturbed axoplasmic
transport.

42.  Fundo-scopy and Papilledema

44.  A, B, & C waves
 Factors influencing waves
Systolic blood pressure
Alterations in respiration
Deteriorating neurological status
 Components of waves
P1 (upward spike)
P2 (tidal wave)
P3 (small notch)

47. A waves
 Plateau waves
 Most life threatening
 Seen in 5-20 min intervals
 Increased I.C.P.
 CPP compromised
 Amplitude 50 – 60 mm of Hg

51. B waves
 Saw toothed appearance
 Occur every 30 – 60 sec
 Amplitude 25 – 50 mm of Hg
 Indicates Unstable ICP& unconsciousness
 Stimulation ↑ amplitude

53. C waves
 Lowest amplitude
 Occur in 4 – 8 min intervals
 Never get elevated >20 – 25 mm of Hg
 Clinical significance unknown

57.  Infection
 intracranial hemorrhage or haematoma
 CSF Leakage
 Mechanical failure or blockage
 Over drainage of CSF

58. The Patient with Increased Intracranial Pressure

59. ASSESSMENT
 History
 Present Illness
 Obtain Subjective Data
 Neurologic examination
 Mental Status
 LOC
 Cranial Nerve Function
 Cerebral Function (balance and coordination)
 Reflexes
 Motor and Sensory Function
 Abnormal Respiratory Pattern

60. NURSING DIAGNOSIS
 Ineffective airway clearance related to diminished
protective reflexes
 Ineffective breathing patterns related to neurologic
dysfunction
 Ineffective cerebral tissue perfusion related to the
effects of increased ICP
 Deficient fluid volume related to fluid restriction
 Risk for infection related to ICP monitoring system

61. PLANNING AND GOALS
 Maintenance of patent airway
 Normalization of respiration
 Adequate cerebral tissue perfusion through
reduction in ICP
 Restoration of fluid balance
 Absence of infection
 Absence of complication

62. NURSING INTERVENTION
 Maintaining patent airway and adequate
ventilation
 Monitor vital signs
 Maintain fluid balance
 Position client with head of the bed elevated 30 to
45 degrees and neck in neutral position
 Maintain a quiet environment
 Avoid use of restraints
 Prevent straining at stool
 Prevent excessive cough and vomiting
 Prevent complication of immobility
 Preventing infection
 Administer medication as ordered

63. EVALUATION
 Maintained patent airway
 Attains optimal breathing pattern
 Attains desired fluid balance
 Infection prevented
 Complications prevented

64.  I.C.P. is an important parameter
 Physiology
 Pathology related to increased ICP
 Monitoring of ICP
 Interaction between ICP and anaesthetic agents
 Anaesthesiologist as Peri-operative Physician

65.  B.Mokri, “TheMonro-Kellie hypothesis: applications
in CSF volume depletion,” Neurology, vol. 56, no. 12,
pp. 1746–1748, 2001.
 A. Monro, Observations on Structure and Functions of
the Nervous System, Creech and Johnson, Edinbourg,
UK, 1783.
 G. Kellie, “Appearances observed in the dissection of
two individuals; death from cold and congestion of the
brain,” Transactions of the Medico-Chirurgical Society
of Edinburgh, vol. 1, article 84, 1824.
 F.Magendie, “Recherches anatomique et physiologique
sur le liquide c´ephalo-rachidien ou c´erebro-spinal,”
Paris, France,1842.