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 spaceoccupying 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
A
too rapid reduction of CSF Peritonitis abdominal abscess perforation of organs Fistulas hernias and ileus.
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 highpitched cry. Firmly support the head and neck
holding the child.
when
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 1530 degrees : Promotes venous drainage from head ,reducing cerebral congestion and edema and increased ICP.
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