The rigid cranial vault contains brain tissue (1,400 g), blood (75 ml), and CSF (75 ml) The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP. ICP is usually measured in the lateral ventricles; normal ICP is 10 to 20 mm hg. The Monro-kellie hypothesis states that because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others. Increased ICP is a syndrome that affects many patients with acute neurologic conditions. This is because pathologic conditions alter the relationship between intracranial volume and pressure. Although an elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, and toxic and viral encephalopathies.

1. NURSING MANAGEMENT
OF THE CLIENT WITH
INCREASED INTRACRANIAL
PRESSURE (ICP)
MR.ANILKUMAR B R , ASSISTANT PROFESSOR
MEDICAL - SURGICAL NURSING

2. OVERVEIW
•The rigid cranial vault contains brain tissue
(1,400 g), blood (75 ml), and CSF (75 ml)
•The volume and pressure of these three
components are usually in a state of
equilibrium and produce the ICP.
•ICP is usually measured in the lateral
ventricles; normal ICP is 10 to 20 mm hg.

3. THE RIGID CRANIAL VAULT

4. THE RIGID CRANIAL VAULT

5. THE MONRO-KELLIE HYPOTHESIS
•The Monro-kellie hypothesis states that
because of the limited space for expansion
within the skull, an increase in any one of
the components causes a change in the
volume of the others.

6. THE MONRO-KELLIE HYPOTHESIS

7. ETIOLOGY
• Increased ICP is a syndrome that affects many
patients with acute neurologic conditions.
• This is because pathologic conditions alter the
relationship between intracranial volume and
pressure.
• Although an elevated ICP is most commonly
associated with head injury, it also may be seen as a
secondary effect in other conditions, such as brain
tumors, subarachnoid hemorrhage, and toxic and viral
encephalopathies.

9. PATHOPHYSIOLOGY OF INCREASED ICP
Insulting or damaging to brain
Tissue edema
Increase Intra cranial pressure (
ICP)
Compression of ventricles of brain
Compression of blood vessels of
brain
Decreased cerebral blood flow
Decreased oxygen with death of

10. PATHOPHYSIOLOGY OF INCREASED ICP
Increase ICP with compression of brain stem
and respiratory center.
Accumulation of Co2
Vasodilation
Increase ICP resulting from increased blood
volume
DEATH

11. CLINICAL MANIFESTATIONS
• When ICP increases to the point at which the
brain’s ability to adjust has reached its limits,
neural function is impaired; this may be
manifested by clinical changes first in LOC
and later by abnormal respiratory and
vasomotor responses.

12. CLINICAL MANIFESTATIONS
• Any sudden change in the patient’s condition, such as
restlessness (without apparent cause), confusion, or
• Increasing drowsiness, has neurologic significance.
• As ICP increases, the patient becomes stuporous,
reacting only to loud auditory or painful stimuli.
• At this stage, serious impairment of brain circulation
is probably taking place, and immediate intervention
is required.

13. CLINICAL MANIFESTATIONS
• As neurologic function deteriorates further, the
patient becomes comatose and exhibits abnormal
motor responses in the form of decortication,
decerebration, or flaccidity.
• When the coma is profound, with the pupils dilated
and fixed and respirations impaired, death is usually
inevitable.

14. DECORTICATION, DECEREBRATION
POSTURE

15. OTHER CLINICAL MANIFESTATIONS
1. Changes in LOC
2. Changes in vital signs
3. Pupillary changes (due to increased pressure on the
optic and coulometer nerves
4. Headache is increasing in intensity and
aggravated by movements and straining.
5. Vomiting recurrent with little or nausea, esp. In
early morning.

16. 6. Papilledema from optic nerve compression.
7. Restlessness, headache, forced breathing
pattern, purposeless movements and
mental cloudiness.
8. Seizures activity: focal or generalized
9. Decreased brain stem function (CN deficits
such as loss of control reflexes and ability to
swallow.

17. ASSESSMENT AND DIAGNOSTIC FINDINGS
1.The diagnostic studies used to determine the
underlying
• Cause of increased ICP .
2. Cerebral angiography
3. Computed tomography (CT) scanning
4.Magnetic resonance imaging (MRI) or positron
emission tomography (PET).
5.Trans cranial Doppler studies provide information
about cerebral blood flow.

18. •Lumbar puncture is avoided in patients
with increased ICP because the sudden
release of pressure can cause the brain to
herniate.

19. COMPLICATIONS
1. Complications of increased ICP include
brain stem herniation
2. Diabetes insipidus syndrome
3. Inappropriate antidiuretic hormone (SIADH)
4. Brain stem herniation.

20. MEDICAL MANAGEMENT
• Increased ICP is a true emergency and must
be treated promptly.
• Invasive monitoring of ICP is an important
component of management, but immediate
management to relieve increased ICP involves
decreasing cerebral edema, lowering the volume
of CSF , or decreasing cerebral blood volume
while maintaining cerebral perfusion.

21. THESE GOALS ARE ACCOMPLISHED BY:
1. Administering osmotic diuretics and
corticosteroid.
2.Restricting fluids, draining csf.
3.Controlling fever maintaining systemic
blood pressure and oxygenation, and
reducing cellular metabolic demands.

22. MONITORING ICP
• The purposes of ICP monitoring are to identify
increased pressure early in its course (before
cerebral damage occurs), to quantify the
degree of elevation, to initiate appropriate
treatment, to provide access to CSF for
sampling and drainage, and to evaluate the
effectiveness of treatment.

23. MONITORING ICP
• An intraventricular catheter (ventriculostomy),
a subarachnoid bolt, an epidural or subdural
catheter, or a fiberoptic transducer-tipped
catheter placed in the subdural space or the
ventricle can be used to monitor ICP.

24. ICP MONITORING

25. ICP MONITORING

26. ICP MONITORING

27. DECREASING CEREBRAL EDEMA
•OSMOTIC DIURETICS (MANNITOL) May be
given to dehydrate the brain tissue and reduce
cerebral edema.
• They act by drawing water across intact
membranes, thereby reducing the volume of brain
and extracellular fluid.
• An indwelling urinary catheter is usually inserted
to monitor urinary output and to manage the
resulting diuresis.

28. OSMOTIC DIURETICS (MANNITOL

29. 1. Corticosteroids (e.g., Dexamethasone) help
reduce the edema surrounding brain tumors
when a brain tumor is the cause of increased
ICP.
2. Another method for decreasing cerebral
edema is fluid restriction .

30. MAINTAINING CEREBRAL PERFUSION
• The cardiac output may be manipulated to
provide adequate perfusion to the brain.
• Improvements in cardiac output are made using
fluid volume and inotropic agents such as
dobutamine hydrochloride.
• The effectiveness of the cardiac output is reflected
in the cerebral perfusion pressure, which is
maintained at greater than 70 mm hg.

31. DOBUTAMINE HYDROCHLORIDE.

32. REDUCING CSF AND INTRACRANIAL BLOOD VOLUME
• CSF Drainage Is Frequently Performed
Because The Removal Of CSF With A
Ventriculostomy Drain May Dramatically
Reduce ICP And Restore Cerebral Perfusion
Pressure. Caution Should Be Used In
Draining CSF Because Excessive Drainage
May Result In Collapse Of The Ventricles.

33. CONTROLLING FEVER
•Preventing a temperature elevation is critical
because fever increases cerebral metabolism
and the rate at which cerebral edema forms.
•Strategies to reduce temperature include
administration of antipyretic medications, as
prescribed, and use of a cooling blanket.

34. MAINTAINING OXYGENATION
•Arterial blood gases must be monitored to
ensure that systemic oxygenation
remains optimal.
•Hemoglobin saturation can also be
optimized to provide oxygen more efficiently
at the cellular level.

35. NURSING PROCESS: THE PATIENT WITH
INCREASED ICP
•The neurologic examination should be as
complete as the patient’s condition allows.
It includes an evaluation of mental status,
LOC, cranial nerve function, cerebellar
function (balance and
•Coordination), reflexes, and motor and
sensory function.

36. NURSING DIAGNOSIS
• Ineffective airway clearance related to diminished
protective reflexes (cough, gag)
• Ineffective breathing patterns related to neurologic
dysfunction (brain stem compression, structural
displacement)
• 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
(fiberoptic or intraventricular catheter)