Increase Intracranial Pressure: Case Report
Increase Intracranial Pressure: Case Report
Increase Intracranial Pressure: Case Report
S.Y 2010-2011
CASE REPORT
INCREASE INTRACRANIAL
PRESSURE
Submitted by:
Alexander E. Salvio
Submitted to:
Mr. Mhelmarl C. DAvid
Intracranial pressure
Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain
tissue and cerebrospinal fluid (CSF). The body has various mechanisms by which it
keeps the ICP stable, with CSF pressures varying by about 1 mmHg in normal adults
through shifts in production and absorption of CSF. CSF pressure has been shown
to be influenced by abrupt changes in intrathoracic pressure during coughing
(intraabdominal pressure), valsalva (Queckenstedt's maneuver), and communication
with the vasculature (venous and arterial systems). ICP is measured in millimeters
of mercury (mmHg) and, at rest, is normally 7–15 mmHg for a supine adult, and
becomes negative (averaging −10 mmHg) in the vertical position. Changes in ICP are
attributed to volume changes in one or more of the constituents contained in the
cranium.
Intracranial hypertension, commonly abbreviated IH, is elevation of the pressure
in the cranium. ICP is normally 0–10 mm Hg; at 20–25 mm Hg, the upper limit of
normal, treatment to reduce ICP is needed.
The Monro-Kellie hypothesis
The pressure-volume relationship between ICP, volume of CSF, blood, and brain
tissue, and cerebral perfusion pressure (CPP) is known as the Monro-Kellie doctrine
or the Monro-Kellie hypothesis.
The Monro-Kellie hypothesis states that the cranial compartment is
incompressible, and the volume inside the cranium is a fixed volume. The cranium
and its constituents (blood, CSF, and brain tissue) create a state of volume
equilibrium, such that any increase in volume of one of the cranial constituents
must be compensated by a decrease in volume of another.
The principal buffers for increased volumes include both CSF and, to a lesser
extent, blood volume. These buffers respond to increases in volume of the
remaining intracranial constituents. For example, an increase in lesion volume (e.g.
epidural hematoma) will be compensated by the downward displacement of CSF and
venous blood. These compensatory mechanisms are able to maintain a normal ICP
for any change in volume less than approximately 100–120 mL
Pathophysiology
The cranium and the vertebral canal, along with the relatively inelastic dura, form a
rigid container, such that the increase in any of its contents; brain, blood, or CSF,
will tend to increase the ICP. In addition, any increase in one of the components
must be at the expense of the other two; this relationship is known as the Monro-
Kellie doctrine. Small increases in brain volume do not lead to immediate increase in
ICP because of the ability of the CSF to be displaced into the spinal canal, as well
as the slight ability to stretch the falx cerebri between the hemispheres and the
tentorium between the hemispheres and the cerebellum. However, once the ICP
has reached around 25 mmHg, small increases in brain volume can lead to marked
elevations in ICP; this is due to failure of intracranial compliance.
Traumatic brain injury is a devastating problem with both high subsequent
morbidity and high mortality. Injury to the brain occurs both at the time of the
initial trauma (the primary injury) and subsequently due to ongoing cerebral
ischemia (secondary injury). Cerebral edema, hypotension, and hypoxic conditions
are well recognized causes of this secondary injury. In the intensive care unit,
raised intracranial pressure (intracranial hypertension) is seen frequently after a
severe diffuse brain injury (one that occurs over a widespread area) and leads to
cerebral ischemia by compromising cerebral perfusion.
Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is
normally fairly constant due to autoregulation, but for abnormal mean arterial
pressure (MAP) or abnormal ICP the cerebral perfusion pressure is calculated by
subtracting the intracranial pressure from the mean arterial
pressure: CPP = MAP − ICP One of the main dangers of increased ICP is that it can
cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean
systemic pressure, cerebral perfusion falls. The body’s response to a fall in CPP is
to raise systemic blood pressure and dilate cerebral blood vessels. This results in
increased cerebral blood volume, which increases ICP, lowering CPP further and
causing a vicious cycle. This results in widespread reduction in cerebral flow and
perfusion, eventually leading to ischemia and brain infarction. Increased blood
pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.
Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. an
haematoma) can result in midline shift, a dangerous sequela in which the brain
moves toward one side as the result of massive swelling in a cerebral hemisphere.
Midline shift can compress the ventricles and lead to hydrocephalus. Prognosis is
much worse in patients with midline shift than in those without it. Another dire
consequence of increased ICP combined with a space-occupying process is brain
herniation (usually uncal or tonsilar). In uncal herniation, the uncus hippocampus
becomes compressed against the free edge of the tentorium cerebelli, frequently
leading to brainstem compression. If brainstem compression is involved, it may lead
to respiratory depression and is potentially fatal. This herniation is often referred
to as "coning".
Major causes of morbidity due to raised intracranial pressure are due to global
brain infarction as well as decreased respiratory drive due to brain herniation
Increased ICP
On the whole, the intraventricular monitor is the most preferred type of ICP
monitor. Its disadvantages are offset by the use of antibiotics to prevent
infection and constant monitoring for complications.
Signs and symptoms
In general, symptoms and signs that suggest a rise in ICP including headache,
vomiting without nausea, ocular palsies, altered level of consciousness, back pain
and papilledema. If papilledema is protracted, it may lead to visual disturbances,
optic atrophy, and eventually blindness.
In addition to the above, if mass effect is present with resulting displacement of
brain tissue, additional signs may include pupillary dilatation, abducens (CrN VI)
palsies, and the Cushing's triad. Cushing's triad involves an increased systolic blood
pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory
pattern. In children, a slow heart rate is especially suggestive of high ICP.
Irregular respirations occur when injury to parts of the brain interfere with the
respiratory drive. Cheyne-Stokes respiration, in which breathing is rapid for a
period and then absent for a period, occurs because of injury to the cerebral
hemispheres or diencephalon. Hyperventilation can occur when the brain stem or
tegmentum is damaged.
As a rule, patients with normal blood pressure retain normal alertness with ICP of
25–40 mmHg (unless tissue shifts at the same time). Only when ICP exceeds 40–
50 mmHg do CPP and cerebral perfusion decrease to a level that results in loss of
consciousness. Any further elevations will lead to brain infarction and brain death.
In infants and small children, the effects of ICP differ because their cranial
sutures have not closed. In infants, the fontanels, or soft spots on the head where
the skull bones have not yet fused, bulge when ICP gets too high.A swollen optic
nerve is a reliable sign that ICP is elevated.
Nursing Interventions:
– Achieve airway clearance
l Suction to maintain patent airway
l Hyperoxygenation for suctioning
l Nasal drainage may indicate dural tear; suctioning of nares
contraindicated
l Auscultate lung fields
l No close mouth coughing
– Attain normal respiratory pattern
– Attain fluid balance
l Monitor skin turgor, mucous membranes, serum and urine osmolality
l Monitor IVF carefully
l Observe for CHF and pulmonary edema if giving Mannitol
l Good oral hygiene, monitor VS, monitor I&O
– Attain normal urine and bowel elimination
l Test urine for specific gravity and glucose
l Indwelling catheter
l Monitor UOP every 2-4 hours; output of > 200 ml/hr over two
consecutive hours may = diabetes insipidus
l Monitor bowel sounds; abd. Distension
l Test stools for occult blood
l Avoid extreme hip flexion
l Avoid Valsalva maneuvers – ask client to exhale when being moved or
turned
l Avoid isometric exercises that increase SBP
l Preoxygenate and hyperventilate prior to suctioning
Diagnostic Examination:
Physical examination
o Blood pressure
o Temperature (if elevated must consider brain abscess or encephalitis)
o Examine for neck stiffness which may indicate subarachnoid
hemorrhage but may also indicate cerebral abscess or encephalitis
o Examine for papilledema which may suggest cerebral abscess, brain
hemorrhage or brain tumor
o Full neurological examination, including cranial nerve examination,
visual fields and visual acuity, pupils reaction to light, eye movements, sensation
and motor power of face and limbs
Radiological investigations
o Skull X-Ray, if history of head injury
o CT Scan of brain, if suspected brain tumor, subarachnoid hemorrhage,
brain abscess
o Radioisotope brain scan, may be indicated to localize specific brain
tumors and haematomas (blood clots)
o MRI scan of brain, may be necessary if need more discrimination of
brain masses
o Cerebral angiography, may be required to rule out arteriovenous
malformations and to define site or blood supply of a brain mass
o Chest X-Ray to look for lung cancer, if brain tumor is diagnosed (lung
cancer is the most common cause of brain cancer)
EEG - may show electrical abnormalities in the region of the brain mass (but
it may be normal). A cerebral abscess shows characteristic wave changes.
Note: Lumbar puncture - is Contra-indicated if suspect any mass lesion.
Medications:
Admnstration of osmotic diuretics (mannitol; glycerol) –removes water from the
areas of the brain with an intact blood brain barrier.
Furosemide (lasix),diuretic to reduce cerebral edema.
Carbonic anhydrase is a crucial enzyme needed in the production of cerebrospinal
fluid. When this enzyme is suppressed, production of CSF decreases, which also
lowers intracranial pressure.
The most common carbonic anhydrase inhibitor and the main drug used to treat
chronic IH is acetazolamide (Diamox). Methazolamide (Neptazane), a similar drug
from the same family as acetazolamide, can also be prescribed. Other drugs with
carbonic anhydrase inhibiting properties include furosemide (Lasix) and topiramate
(Topamax).
Acetazolamide was originally developed to treat glaucoma by reducing the
production of aqueous fluid within the eye, which lowers intraocular pressure.
Acetazolamide is a sulfonamide but its molecular structure differs from sulfa
drugs, which means that certain people who are allergic to sulfa antibiotics may
still be able to take acetazolamide. However, any treatment should first be
discussed with and supervised by your physician.
Daily dosages of acetazolamide can range from 1-4 grams depending on the
individual. In addition, potassium supplements may be necessary since most
carbonic anhydrase inhibitors are diuretics, as well. Many people notice tingling in
their face, hands and feet; a metallic taste when drinking carbonated beverages;
fatigue; and a lack of appetite when they first begin taking acetazolamide. These
initial side-effects tend to dissipate over time.
Carbonic anhydrase inhibitors can be difficult to tolerate long-term and for some
people, the drugs are just not effective. But since no drug has been specifically
developed to treat chronic IH, they are currently the only option.
Surgery
Optic Nerve Fenestration
When sight is at risk and drug therapy has been unsuccessful, an optic nerve
fenestration (also called an optic nerve sheath decompression) is usually
performed. The operation can be done on one optic nerve sheath (unilateral) or on
both optic nerve sheaths (bilateral).
During surgery, a small window-like opening is made in the sheath around the optic
nerve, which allows cerebrospinal fluid (CSF) to drain behind the eye and relieves
optic nerve swelling. This surgery is done primarily to save vision, rather than to
alleviate headaches.
Neurosurgical Shunts
Shunt operations are also performed when drug therapy has been unsuccessful.
Shunts may be used to control papilledema and prevent vision loss, as well as to
treat headaches that have been unresponsive to any medication. A neurosurgical
shunt is a surgically-implanted catheter that is used to drain CSF into another area
of the body such as the abdomen. A shunt lowers intracranial pressure by removing
CSF to another site, where it can be absorbed.
Most Common Types of Shunts
Lumboperitoneal shunt (LP shunt)
An LP shunt diverts CSF from the lumbar sub-arachnoid space (spine) to the
peritoneum (abdominal cavity).
Many shunts used today have programmable valves, which means that the valves
are externally adjustable. The advantage of a programmable valve is that after
surgery, a physician can adjust the valve’s rate of drainage non-invasively, with the
use of a magnetized device. Shunts with programmable valves can be affected by
magnets used to produce MRIs, and may need to be adjusted after the imaging is
completed.
Shunts have a checkered history with an initial 50% success rate and alternately, a
high revision rate of 50%. They are the most common pediatric neurosurgical
procedure and the second most common neurosurgical procedure for adults.
To make an informed decision, it is always best to discuss both the risks and
benefits of any treatment with your physician.
Causes
Causes of increased intracranial pressure can be classified by the mechanism in
which ICP is increased:
mass effect such as brain tumor, infarction with oedema, contusions,
subdural or epidural hematoma, or abscess all tend to deform the adjacent
brain.
generalized brain swelling can occur in ischemic-anoxia states, acute liver
failure, hypertensive encephalopathy, pseudotumor cerebri, hypercarbia, and
Reye hepatocerebral syndrome. These conditions tend to decrease the
cerebral perfusion pressure but with minimal tissue shifts.
increase in venous pressure can be due to venous sinus thrombosis, heart
failure, or obstruction of superior mediastinal or jugular veins.
obstruction to CSF flow and/or absorption can occur in hydrocephalus
(blockage in ventricles or subarachnoid space at base of brain, e.g., by
Arnold-Chiari malformation), extensive meningeal disease (e.g., infectious,
carcinomatous, granulomatous, or hemorrhagic), or obstruction in cerebral
convexities and superior sagittal sinus (decreased absorption).