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HYDROCEPHALUS

BY:
MURNIWATI BINTI ZAKARIA
LEARNING OUTCOMES
AT THE END OF THIS TOPIC , THE
STUDENT WILL BE ABLE TO :

1.Define what is hydrocephalus

2. Explain cause and risk factors for


hydrocephalus.

3. Explain the pathophysiology for hydrocephalus.


4.State symptoms for hydrocephalus.

5.Explain classification for hydrocephalus.

6.Explain laboratory and diagnostic test for


hydrocephalus.

7.Explain treatment for hydrocephalus.

8. Explain nursing management for patient with


hydrocephalus.

9.Explain nursing care plan for patient with


hydrocephalus.
DEFINITION
 Condition caused by an imbalance in the
production and absorption of CSF in the
ventricular system.

 When production exceeds absorption


,CSF accumulates ,usually under pressure
,producing dilation of the ventricles.
 Greek words “hydro” meaning water , and
“cephalus” meaning head .

 Sometime known as “water in the brain”

People with hydrocephalus :


- abnormal accumulation of CSF in the ventricles
,or cavities ,of the brain.
- this condition may increased intracranial
pressure inside the skull and progressive
enlargement of the head.,convulsion ,and
mental disability.
 hydrocephalus does not cause any
intellectual disability if treated properly.
CAUSE AND RISK FACTORS
 is usually the result of a brain infection or a malformation
in the fetus prior to birth.

 Although the baby's head may not appear abnormally


large at birth, it expands rapidly from month to month.

 If untreated, the baby usually dies by the end of the


second year.

 If the blockage of CSF is only partial, the child may live


for a number of years or may even live a normal life
span.
ETIOLOGY
Congenital hydrocephalus result from defects,
such as Chairi malformations.
( abnormality of the lower part in the brain
( cerebellum ).

 Also associated with spina bifida.

 Acquired hydrocephalus results from space-


occupying lesions, hemorrhage, intracranial
infections or dormant development defects.
 Hydrocephalus can be caused by
impaired cerebrospinal fluid ( CSF ) flow,
re- absorption ,or excessive CSF
production.
 Common cause :
- CSF flow obstruction

- hindering the free passage of the CSF through


the ventricular system and sub-arachnoids
space.

( eg. stenosis of the cerebral aqueduct or


obstruction of the intervetricular foramina –
foramina of Monro
(the small opening (on both the right and left
sides) that connects the third ventricle in the
diencephalons with the lateral ventricle in the
cerebral hemisphere )
secondary to tumors ,hemorrhage
,infections or congenital malformations.

 Also cause by overproduction of CSF

( relative obstruction ) eg. *papilloma of


choriod plexus.
(*A benign epithelial tumor forming a
rounded mass)
SYMPTOMS
 Characteristic features of hydrocephalus in
children include :

 cephalomegaly
 a thin, transparent scalp
 a bulging forehead with prominent fontanell
 a downward gaze.
 Other clinical findings include:
 convulsions
 abnormal reflexes
 a slowed heartbeat and respiratory rate
 headache
 Vomiting
 Irritability
 Weakness
 problems with vision.
 Blindness and continuing mental
deterioration from brain atrophy can result
if treatment is not instituted.
CLASSIFICATION
A) COMMUNICATING

B) NON- COMMUNICATING
A.COMMUNICATING HYDROCEPHALUS:

 Also known as non-obstructive


hydrocephalus

 It is caused by impaired cerebrospinal


fluid reabsorption in the absence of any
CSF-flow obstruction.
 It has been theorized that this is due to
functional impairment of the arachnoids'
granulations, which are located along the
superior sagittal sinus and is the site of
cerebrospinal fluid reabsorption back into
the venous system.
 Various neurologic conditions may result
in communicating hydrocephalus,
including :
 subarachnoid/intraventricular hemorrhage,
 meningitis,
 Chiari malformation
 congenital absence of arachnoidal
granulations (Pacchioni’s granulations).
 Normal pressure hydrocephalus (NPH) :

- characterized by enlarged cerebral ventricles, with


only intermittently elevated cerebrospinal fluid
pressure.

- The diagnosis of NPH can be established only with


the help of continuous intraventricular pressure
recordings (over 24 hours or even longer.
- Dynamic compliance studies may be also
helpful. Altered compliance (elasticity) of the
ventricular walls, as well as increased
viscosity of the cerebrospinal fluid, may play
a role in the pathogenesis of normal
pressure hydrocephalus.
B.NON-COMMUNICATING

 Also known as obstructive hydrocephalus:

 cause 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.

 Since the skull bones have not yet firmly


joined together, bulging, firm anterior and
posterior fontanel's 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 bifida—often associated
with meningocele or myelomeningocele—
develop hydrocephalus.
ACQUIRED
 as a consequence of CNS infections,
meningitis, brain tumors, head trauma,
intracranial hemorrhage (subarachnoid or
intraparenchymal) and is usually
extremely painful.
PATHOPHYSIOLOGY
 The primary site of CSF formation is believed to
be the choroid plexusus of the lateral ventricles.

 CSF flows from the lateral ventricles through the


foramen of Monro to the third ventricle, then
through the aqueduct of Sylvius into the fourth
ventricle through the foramen of Luschka and
the midline foramen of Magendie into the
cisterna magna.

 From there it flows to the cerebral and cerebellar


subarachnoid spaces where it is absorped.
 Causes of Hydrocephalus are varied but
result in either impaired absorption of CSF
within the arachnoid space (formerly
referred to as communicating
hydrocephalus) or obstruction to the flow
of CSF through the ventricular system
(formerly referred as noncommunicating
hydrocephalus
 Most cases of obstruction are the result of
developmental malformations; other
causes include :

 neoplasm
 infection and trauma
 Obstruction to the normal flow
 can occur at any point in the CSF
pathway, which produces increased
pressure and dilation of the pathways
proximal to the site of obstruction.
 Impaired absorption can result from :
 meningitis
 prenatal maternal infections
 meningeal malignancy (secondary to
leukemia or lymphoma)
 an arachnoid cyst
 tuberculosis.
CLINICAL MANIFESTATIONS
 Abnormal rate of head growth
 Bulging fontanelle
 Tense anterior fontanelle (often bulging and
nonpulsatile)
 Dilated scalp veins
 Macewen’s sign (“cracked pot”)
 Frontal bossing
 Setting sun sign
 Sluggish and unequal pupils
 Irritability and lethargy with varying LOC
 Abnormal infantile reflexes
 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
 confusion.
LABORATORY AND DIAGNOSTIC
TEST
1 ) A prenatal diagnosis
- Level II ultrasonography of the fetus.

*** (Transuterine placement of


ventriculoamniotic shunts during late
pregnancy is still being developed as a
treatment modality).
2 ) CT scan
- postnatal.

3) MRI
- can be used if a complex lesion is
suspected.
TREATMENT
 Surgical correction is the only treatment
for hydrocephalus.

 consists of insertion of a
ventriculoperitoneal shunt
- which transports excess fluid from the
lateral ventricle into the peritoneal cavity.
 A less common procedure :
 insertion of a ventriculoatrial shunt

- which drains fluid from the brain's lateral


ventricle into the right atrium of the heart,
where the fluid makes its way into the
venous circulation.
- Periodic lengthening of the shunt is
necessary to accommodate growth in
children.

- A clogged malfunctioning shunt will have


to be replaced.
 Complications of surgery include:

 shunt infection
 septicemia (after ventriculoatrial shunt)
 adhesions and paralytic ileus
 shunt migration
 Peritonitis
 intestinal perforation (with peritoneal
shunt).
 Shunt placement
NURSING MANAGEMENT
 Teach the family about the management required for
the disorder

 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)

The major complications of shunts are infections


and malfunction
Other complications include subdural hematoma
caused by :

a too rapid reduction of CSF


 Peritonitis
 abdominal abscess
 perforation of organs
 Fistulas
 hernias and ileus.

A third ventriculostomy is a new non-shunting


procedure used to treat children with
hydrocephalus.
 Provide preoperative nursing care

 Assess head circumference, fontanelles,


cranial sutures, and LOC; check also for
irritability, altered feeding habits and a high-
pitched cry.

 Firmly support the head and neck when


holding the child.
 Provide skin care for the head to prevent
breakdown.

 Give small, frequent feedings to decrease the


risk of vomiting.

 Encourage parental-newborn bonding.


 Provide Postoperative nursing care (nursing
interventions are the same as those for
increased ICP)

 Assess for signs of increased ICP and check


the following; head circumference (daily),
anterior fontanelle for size and fullness and
behavior.

 Administer prescribed medications which may


include antibiotics to prevent infection and
analgesics for pain.
 Provide shunt care
 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.

 Prevent infection (usually from


Staphylococcus epidermis or
Staphylococcus aureus)
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
 Teach home care

 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.
 Explain how to recognize signs and
symptoms of increased ICP. Subtle signs
include changes in school performance,
intermittent headache, and mild behavior
changes.

 Arrange for the child to have frequent


developmental screenings and routine
medical checkups.
NURSING CARE PLAN

LETS DISCUSS IT
TOGETHER….
NURSING DIAGNOSIS &
INTERVENTIONS
Nursing Diagnosis
1. Ineffective cerebral tissue perfusion
related to decreased arterial or
venous blood flow.

Nursing Intervention
1.Monitor temperature. Administer
tepid sponge bath in presence of
fever.
2.Monitor intake and output. Weight as
indicated. Note skin turgor, status
and mucous membrane.

3.Maintain head or neck in medline or


neutral position, support with small
pillows or small towel rolls. Avoid
placing head on large pillow.
4.Provides rest period between care of
activities and limit durations of
procedures.

5.Decrease extraneous stimuli and


provide comfort measures such as
back massage , quiet environment
and gentle touch.
6. Help patient avoid or limit coughing,
crying ,vomiting and straining at
stool. Reposition the patient slowly.

7.Elevate the head of bed gradually


15-30 degree as tolerated or
indicated.

8.Collaborative : administer diuretic as


indicated. Administer supplemental
oxygen as indicated.
RATIONALE
1.Check temperature because fever can
reflex damage to hypothalamus. Increased
metabolic needs and oxygen consumption
occur ( especially with fever and shivering)
which can further increased ICP.

2. Monitor intake and output – useful


indicators of body water which is an
integral part of tissue perfusion.
3. Maintain head in neutral
position : turning bed to one site
compresses the jugular veins and
inhibits cerebral venous drainage
that may cause increased ICP.

4.Provides rest period between


cares and activities : Continual
activity can increased ICP by
producing a cumulative stimulant
effects.
5.Decrease extraneous and
provide comfort : provides calming
effects , reduces adverse
psychological response and promotes
rest.

6.Help patient avoid or limit


coughing ,crying ect. : these
activities increased intrathoracic and
intra- abdominal pressure.
7. Elevate the head or bed to 15-
30 degrees : Promotes venous
drainage from head ,reducing
cerebral congestion and edema and
increased ICP.
THANK YOU

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