This document discusses intracranial pressure (ICP) and factors that influence it such as cerebral blood flow. It defines normal ICP and describes how ICP can be measured. Increased ICP is discussed including potential causes such as cerebral edema and mass lesions. Clinical manifestations of increased ICP are outlined including changes in vital signs, ocular signs, decreased motor function, and headache. Diagnostic studies and collaborative therapies to manage increased ICP are also summarized.

1. Dr. Dipali Dumbre
Ph.D Nursing
Medical Surgical Department
SCON

2.  Intracranial pressure. is the hydrostatic force measured
in the brain CSF compartment.
 Normal ICP is the total pressure exerted by the three
components within the skull: brain tissue, blood, and CSF.

3.  Skull has three essential components:
- Brain tissue = 78%
- Blood = 12%
- Cerebrospinal fluid (CSF) = 10%
 Any increase in any of these tissues causes
increased ICP

5. Measuring ICP
 ICP can be measured in the ventricles, subarachnoid
space, subdural space, epidural space, or brain
parenchymal tissue using a pressure transducer.
 Normal intracranial ICP ranges from 0 to 15 mm Hg.
 A sustained pressure above the upper limit is considered
abnormal.

6. Cerebral Blood Flow
 “Cerebral blood flow (CBF) is the amount of blood in
milliliters passing through 100 g of brain tissue in 1
minute”.
 The global CBF is approximately 50 ml/min per 100 g of
brain tissue.
 There is a difference in flow between the white and gray
matter of the brain.
 The white matter has a slower blood flow, approximately
25 ml/min per 100 g, and the gray matter has a faster
blood flow, approximately 75 ml/min per 100 g.

7.  Grey Matter:
 Grey matter (or gray matter) is a major component of
the central nervous system, consisting of
 Neuronal cell bodies,
 Neuropil(dendrites and axons )
 Synapses
 Capillaries.

8.  Grey matter is distinguished from white matter in that it
contains numerous cell bodies and relatively few
myelinated axons, while white matter contains relatively
few cell bodies and is composed chiefly of long-range
myelinated axon tracts.
 The colour difference arises mainly from the whiteness of
myelin.
 grey matter actually has a very light grey color with
yellowish or pinkish color, which come
from capillary blood vessels and neuronal cell bodies

9.  Synapse is a structure that permits a neuron(or nerve cell)
to pass an electrical or chemical signal to another neuron.
 Axons are also known as nerve fibers. The function of the
axon is to transmit information to different neurons,
muscles and glands.

10.  White matter is made of the nerve fibres
 White matter refers to areas of the central nervous
system (CNS) that are mainly made up of myelinated axon
 White matter is named for its relatively light appearance
resulting from the lipid content of myelin.

11.  White matter appears to be almost white.
 White matter consists mostly of myelinated axons
 Myelin is a lipid tissue (a fat) with capillaries
 It helps to keep the electrical in the nerve fibre.
 This is important for fast and accurate sending of
signals.
 In the brain white matter is surrounded by grey
matter .
 White matter is used to connect different areas of grey
matter.

13. Autoregulation of Cerebral Blood Flow
 The brain has the ability to regulate its own blood flow in
response to its metabolic needs despite wide fluctuations
in systemic arterial pressure.
 Autoregulation is the automatic adjustment in the
diameter of the cerebral blood vessels by the brain to
maintain a constant blood flow during changes in arterial
blood pressure (BP).
 The purpose of autoregulation is to ensure a consistent
CBF to provide for the metabolic needs of brain tissue and
to maintain cerebral perfusion pressure within normal
limits.

14.  The lower limit of systemic arterial pressure at which
autoregulation is effective in a normotensive person is a
mean arterial pressure (MAP) of 50 mm Hg.
 Below this, CBF decreases, and symptoms of cerebral
ischemia, such as syncope(Loss of consciousness and
blurred vision, occur.
 The upper limit of systemic arterial pressure at which
autoregulation is effective is a MAP of 150 mm Hg.

15.  The cerebral perfusion pressure (CPP) is the pressure
needed to ensure blood flow to the brain.
 CPP is equal to the MAP minus the ICP (CPP=MAP−ICP)
Example: Systemic blood pressure = 122/84
 MAP = 97
 ICP = 12 mm Hg
 CPP = 85 mm Hg
 Normal CPP is 70 to 100 mm Hg. CPP >50 mm Hg is
associated with ischemia and neuronal death.
 A CPP below 30 mm Hg results in ischemia and is
incompatible with life.
 Normally, autoregulation maintains an adequate CBF and
perfusion pressure primarily by adjusting the diameter of
cerebral blood vessels and metabolic factors that impact
ICP.

16. INCREASED
INTRACRANIAL
PRESSURE

17. Causes
 Cerebral edema:
 Vasogenic cerebral edema:
 Vasogenic edema occurs due to a breakdown of
the tight endothelial junctions that make up the blood–
brain barrier.
 This allows intravascular proteins and fluid to penetrate
into the parenchymal extracellular space.
 Once plasma constituents cross the barrier, the edema
spreads; this may be quite rapid and extensive.
 As water enters white matter, it moves extracellularly
along fiber tracts and can also affect the gray matter.

19.  Cytotoxic cerebral edema:
• In cytotoxic edema, the blood–brain barrier remains
intact but a disruption in cellular metabolism impairs
functioning of the sodium and potassium pump in
the glial cell membrane, leading to cellular retention
of sodium and water.
• Swollen astrocytes(Star Shaped Glial cell) occur in gray
and white matter.
• It can occur in early ischemia, encephalopathy,
early stroke or hypoxia, cardiac arrest.

22.  Interstitial cerebral edema:
 Interstitial edema occurs in obstructive hydrocephalus due
to a rupture of the CSF–brain barrier.
 This results in flow of CSF, causing CSF to penetrate the
brain and spread to the extracellular spaces and the white
matter.
 Interstitial cerebral edema differs from vasogenic edema as
CSF contains almost no protein.

23. 2.Mass Lesions
 Brain abscess
 Brain tumor (primary or metastatic)
 Hematoma (intracerebral, subdural, epidural)
 Hemorrhage (intracerebral, cerebellar, brainstem)
3. Head Injuries
 Contusion
 Hemorrhage
 Posttraumatic brain swelling
4.Brain Surgery&Cerebral Infections
 Meningitis
 Encephalitis

24. Mechanism of increased ICP

25. Clinical Manifestation
 Change in Level of Consciousness:
The level of consciousness (LOC) is the sensitive and
reliable indicator of the patient's neurologic status.
Changes in LOC are a result of impaired CBF, which
deprives the cells of the cerebral cortex and the reticular
activating system (RAS) of oxygen.
 The RAS is located in the brainstem, with neural
connections to many parts of the nervous system.
An intact RAS can maintain a state of wakefulness even in
the absence of a functioning cerebral cortex.
Interruptions of impulses from the RAS or alterations in
functioning of the cerebral hemispheres can cause
unconsciousness (abnormal state of complete or partial
unawareness of self or environment).

26.  Changes in Vital Signs:
Changes in vital signs are caused by increasing pressure on
the thalamus, hypothalamus, pons, and medulla.
Manifestations such as Cushing's triad may be present but
often do not appear until ICP has been increased for some
time or is suddenly markedly increased (e.g., head
trauma).
A change in body temperature may also be noted because
of increased ICP impacting the hypothalamus.
“Cushing's triad”:
Cushing's triad is a clinical triad variably defined as
having Irregular respirations , Bradycardia and Systolic
hypertension (Widening Pulse Pressure)

27. 3.Ocular Signs :
 Compression of cranial nerve (CN) III, the oculomotor nerve,
results in dilation of the pupil on the same side as or ipsilateral
to the mass lesion, sluggish or no response to light, inability to
move the eye upward, and ptosis of the eyelid.
 These signs can be the result of a shifting of the brain from the
midline, compressing the trunk of CN III and paralyzing the
muscles controlling pupillary size and shape.
 In this situation, a fixed, unilaterally dilated pupil is considered
a neurologic emergency that indicates herniation of the brain.
 Papilledema, an edematous optic disc seen on retinal
examination, is also noted and is a nonspecific sign associated
with persistent increases in ICP.

28. 5.Decrease in Motor Function.
 As the ICP continues to rise, the patient manifests changes in
motor ability.
 A contralateral (opposite side of the mass lesion) hemiparesis
or hemiplegia may develop, depending on the location of the
source of the increased ICP.
 If painful stimuli are used to elicit a motor response, the
patient may localize to the stimuli or withdraw from it.
 Noxious stimuli may also elicit decorticate (flexor) or
decerebrate (extensor) posturing.
 Decorticate(Felxion) posture consists of internal rotation and
adduction of the arms with flexion of the elbows, wrists, and
fingers as a result of interruption of voluntary motor tracts in
the cerebral cortex.
 Decerebrate (Extension) posture may indicate more serious
damage and results from disruption of motor fibers in the
midbrain and brainstem. In this position, the arms are stiffly
extended, adducted, and hyperpronated.

29. 6.Headache.
 Although the brain itself is insensitive to pain,
compression of other intracranial structures, such as the
walls of arteries and veins and the cranial nerves, can
produce headache.
7.Vomiting.
 Vomiting, usually not preceded by nausea, is often a
nonspecific sign of increased ICP.
 This is called unexpected vomiting and is related to
pressure changes in the cranium.
 Projectile vomiting may also be seen and is related to
increased ICP.

30. Diagnostic Studies
 History and physical examination
 Vital signs, neurologic assessments, ICP measurements
 Skull, chest, and spinal x-ray studies
 CT scan, MRI, PET, EEG, angiography
 Transcranial Doppler studies
 ECG
 Laboratory studies, including CBC, coagulation profile,
electrolytes, serum creatinine, ABGs, ammonia level,
general drug and toxicology screen, CSF analysis for
protein, cells.

31. Collaborative Therapy
 Elevation of head of bed to 30 degrees with head in a neutral
position
 Intubation and mechanical ventilation
 ICP monitoring
 Cerebral oxygenation monitoring
 Maintenance of PaO2 at 100 mm Hg or greater
 Maintenance of fluid balance and assessment of osmolality
 Maintenance of systolic arterial pressure between 100 and
160 mm Hg
 Maintenance of CPP >60 mm Hg
 Reduction of cerebral metabolism (e.g., high-dose
barbiturates)

32.  Drug therapy
• Osmotic diuretic (mannitol):
Mannitol (Osmitrol) (25%) is an osmotic diuretic and is
given intravenously.
Mannitol acts to decrease the ICP in two ways:
 Plasma expansion : There is an immediate plasma-
expanding effect that reduces the hematocrit and blood
viscosity, thereby increasing CBF and cerebral oxygen
delivery.


33. Osmotic effect: vascular osmotic gradient is created by
mannitol. Thus fluid moves from the tissues into the
blood vessels. Therefore the ICP is reduced by a decrease
in the total brain fluid content.
“ Fluid and electrolyte status must be monitored when
osmotic diuretics are used.”
• Antiseizure drugs (e.g., phenytoin):
 Barbiturates produce a decrease in cerebral metabolism
and a subsequent decrease in ICP.
 A secondary effect is a reduction in cerebral edema and
production of a more uniform blood supply to the brain

34. • Corticosteroids (dexamethasone [Decadron]) (for brain
tumors, bacterial meningitis):
They act by stabilizing the cell membrane and by
inhibiting the synthesis of prostaglandins thus preventing
the formation of proinflammatory mediators.
 Corticosteroids are also thought to improve neuronal
function by improving CBF and restoring autoregulation.
• Histamine (H2)-receptor antagonist or proton pump
inhibitor to prevent GI ulcers and bleeding

35. Measurement of ICP
Indications for ICP Monitoring.
 ICP monitoring is used to guide clinical care when the
patient is at risk for or has elevations in ICP.
 It may be used in patients with a variety of neurologic
insults, including hemorrhage, stroke, tumor, infection, or
traumatic brain injury.
 ICP should be monitored in patients admitted with a
Glasgow Coma Scale (GCS) score of 8 or less and an
abnormal CT scan or MRI (hematomas, contusion,
edema,)

36. Methods of Measuring ICP
 The “gold standard” for monitoring ICP is the
ventriculostomy, in which a specialized catheter is
inserted into the right lateral ventricle.

37. Normal ICP Waveforms

38. P1
 Percussion wave
 Represents arterial pulsations; normally the highest of the
three waveforms.
P2
 Rebound wave or tidal wave
 Reflects intracranial compliance or relative brain volume.
When P2 is higher than P1, intracranial compliance is
compromised.
P3
 Dicrotic wave
 Follows dicrotic notch; represents venous pulsations;
normally the lowest waveform.