HYDROCEPHALUS

PREPARED BY:
AMOYEN, April
CABANELA, HazzelMae
DOMONDON, Daryll
GALAZO, Arvie Jay
GURTIZA, Ellen Grace
ZAMORA, Mary Rose

I.

DEFINITION

The term hydrocephalus is derived from the Greek words "hydro" meaning water
and "cephalus" meaning head. As the name implies, it is a condition in which the
primary characteristic is excessive accumulation of fluid in the brain. Although
hydrocephalus was once known as "water on the brain," the "water" is actually
cerebrospinal fluid (CSF)--a clear fluid that surrounds the brain and spinal cord. The
excessive accumulation of CSF results in an abnormal widening of spaces in the brain
called ventricles. This widening creates potentially harmful pressure on the tissues of
the brain.
People with hydrocephalus have abnormal accumulation of cerebrospinal fluid (CSF)
in the ventricles, or cavities, of the brain. This may cause increased intracranial
pressure inside the skull and progressive enlargement of the head, convulsion, and
mental disability.
Usually, hydrocephalus does not cause any intellectual disability if recognized and
properly treated. A massive degree of hydrocephalus rarely exists in typically functioning
people, though such a rarity may occur if onset is gradual rather than sudden.
Hydrocephalus occurs with a number of anomalies, such as NTDs.

Classification of Hydrocephalus:
Hydrocephalus can be caused by impaired cerebrospinal fluid (CSF) flow,
reabsorption, or excessive CSF production.

The most common cause of hydrocephalus is CSF flow obstruction, hindering the
free passage of cerebrospinal fluid through the ventricular system and
subarachnoid space (e.g., stenosis of the cerebral aqueduct or obstruction of the
interventricular foramina foramina of Monro secondary to tumors,
hemorrhages, infections or congenital malformations).

Hydrocephalus can also be caused by overproduction of cerebrospinal fluid

(relative obstruction) (e.g., papilloma of choroid plexus).

Based on its underlying mechanisms, hydrocephalus can be classified

into communicating, and non-communicating (obstructive). Both forms can be
either congenital, or acquired.
Communicating

 Communicating hydrocephalus, also known as non-obstructive hydrocephalus

It is caused by impaired cerebrospinal fluid resorption in the absence of
any CSF-flow obstruction.
It has been theorized that this is due to functional impairment of the
arachnoid granulations, which are located along the superior sagittal
sinus and is the site of cerebrospinal fluid resorption back into the venous
system.
Various neurologic conditions may result in communicating
hydrocephalus, including subarachnoid/intraventricular hemorrhage,
meningitis, Chiari malformation, and congenital absence of arachnoidal
granulations (Pacchionis granulations).

Normal

pressure

hydrocephalus (NPH)-

is

particular

form

of communicating hydrocephalus, characterized by enlarged cerebral

ventricles, with only intermittently elevated cerebrospinal fluid pressure.

Hydrocephalus ex vacuo- also refers to an enlargement of cerebral ventricles

and subarachnoid spaces, and is usually due to brain atrophy (as it occurs in
dementias), post-traumatic brain injuries and even in some psychiatric disorders,
such as schizophrenia.

Non-communicating
Non-communicating hydrocephalus, or obstructive hydrocephalus, is caused by a
CSF-flow obstruction (either due to external compression or intraventricular mass
lesions).

Foramen of Monro obstruction may lead to dilation of one or, if large enough
(e.g., in colloid cyst), both lateral ventricles.

The aqueduct of Sylvius, normally narrow to begin with, may be obstructed by

a number of genetically or acquired lesions (e.g., atresia, ependymitis,
hemorrhage, tumor) and lead to dilatation of both lateral ventricles as well as the
third ventricle.

Fourth ventricle obstruction will lead to dilatation of the aqueduct as well as the
lateral and third ventricles.

The foramina of Luschka and foramen of Magendie may be obstructed due to

congenital failure of opening (e.g., Dandy-Walker malformation).

The subarachnoid space surrounding the brainstem may also be obstructed

due to inflammatory or hemorrhagic fibrosing meningitis, leading to widespread
dilatation, including the fourth ventricle.

Congenital

The cranial bones fuse by the end of the third year of life. For head enlargement
to occur, hydrocephalus must occur before then. The causes are usually genetic
but can also be acquired and usually occur within the first few months of life,
which include 1) intraventricular matrix hemorrhages in premature infants, 2)
infections, 3) type II Arnold-Chiari malformation, 4) aqueduct atresia and
stenosis, and 5) Dandy-Walker malformation.

In newborns and toddlers with hydrocephalus, the head circumference is

enlarged rapidly and soon surpasses the 97th percentile. Since the skull bones
have not yet firmly joined together, bulging, firm anterior and posterior fontanelles
may be present even when the patient is in an upright position.

The infant exhibits fretfulness, poor feeding, and frequent vomiting. As the
hydrocephalus progresses, torpor sets in, and the infant shows lack of interest in
his surroundings. Later on, the upper eyelids become retracted and the eyes are
turned downwards (due to hydrocephalic pressure on the mesencephalic
tegmentum and paralysis of upward gaze). Movements become weak and the
arms may become tremulous. Papilledema is absent but there may be reduction
of vision. The head becomes so enlarged that the child may eventually be
bedridden.

About 80-90% of fetuses or newborn infants with spina bifidaoften associated

with meningocele or myelomeningoceledevelops hydrocephalus.

Acquired

This condition is acquired as a consequence of CNS infections, meningitis, brain

tumors,
head
trauma,
intracranial
hemorrhage
intraparenchymal) and is usually extremely painful.

II.

ETIOLOGY

(subarachnoid

or

Congenital hydrocephalus usually results from defects, such as Chairi

malformations. It is also associated with spina bifida.

Acquired hydrocephalus usually results from space-occupying

hemorrhage, intracranial infections or dormant development defects.

III.

lesions,

SIGNS AND SYMPTOMS

1. Abnormal rate of head growth

2. Bulging fontanelle
3. Tense anterior fontanelle (often bulging and nonpulsatile)
4. Dilated scalp veins
5. Macewens sign (cracked pot)
6. Frontal bossing
7. Setting sun sign
8. Sluggish and unequal pupils
9. Irritability and lethargy with varying LOC
10. Abnormal infantile reflexes
11. Possible cranial nerve damage

Manifestations in children include possible signs of increased ICP, which include

headache on awakening with improvement following emesis, papilledema, strabismus,
ataxia, irritability, lethargy, apathy and confusion.

IV.

RISK FACTORS

Birth defects

Brain tumors

Encephalitis

Head injury

Meningitis

Myelomeningocele

Spinal cord tumors

Spinal cord injury

V.

DIAGNOSIS

1. Level II ultrasonography of the fetus will allow a prenatal diagnosis. (Transuterine

placement of ventriculoamniotic shunts during late pregnancy is still being
developed as a treatment modality).
2. CT scan will diagnose most cases postnatally.
3. MRI can be used if a complex lesion is suspected.

VI.

MANAGEMENT

Nursing Management:
1. Teach the family about the management required for the disorder
a. Treatment is surgical by direct removal of an obstruction and insertion of shunt
to provide primary drainage of the CSF to an extracranial compartment,
usually peritoneum (ventriculoperitoneal shunt)
1. The major complications of shunts are infections and malfunction
2. Other complications include subdural hematoma caused by a too rapid
reduction of CSF, peritonitis, abdominal abscess, perforation of organs,
fistulas, hernias and ileus.
b. A third ventriculostomy is a new nonshunting procedure used to treat children
with hydrocephalus.
2. Provide preoperative nursing care
a. Assess head circumference, fontanelles, cranial sutures, and LOC; check also
for irritability, altered feeding habits and a high-pitched cry.
b. Firmly support the head and neck when holding the child.
c. Provide skin care for the head to prevent breakdown.
d. Give small, frequent feedings to decrease the risk of vomiting.
e. Encourage parental-newborn bonding.
3. Provide Postoperative nursing care (nursing interventions are the same as those for
increased ICP)
a. Assess for signs of increased ICP and check the following; head
circumference (daily), anterior fontanelle for size and fullness and behavior.
b. Administer prescribed medications which may include antibiotics to prevent
infection and analgesics for pain.
c. Provide shunt care
1. Monitor for shunt infection and malfunction which may be characterized
by rapid onset of vomiting, severe headache, irritability, lethargy, fever,
redness along the shunt tract, and fluid around the shunt valve.
2. Prevent infection (usually from Staphylococcus epidermis or
Staphylococcus aureus)

3. Monitor for shunt overdrainage (headache, dizziness and nausea).

Overdrainage may lead to slit ventricle syndrome whereby the ventricle
become accustomed to a very small or slitlike configuration, limiting the
buffering ability to increased ICP variations.
4. Teach home care
a. Encourage the child to participate in age-appropriate activities as tolerated.
Encourage the parents to provide as normal lifestyle as possible. Remind
both the child and parents that contact sports are prohibited.
b. Explain how to recognize signs and symptoms of increased ICP. Subtle signs
include changes in school performance, intermittent headache, and mild
behavior changes.
c. Arrange for the child to have frequent developmental screenings and routine
medical checkups.
Medication:

Mannitol

Hyperventilation

Loop Diuretics

Steroid

Acetazolamide

Barbiturate Coma