MASSIVE INTRACRANIAL

FLUID COLLECTION
-hydrocephalus-

BY: Aiza Qen S. De Monteverde

OBJECTIVES:
To define Hydrocephalus, its types,
causes, diagnostics and treatment
Points on how to assess
hydrocephalus
Awareness of signs and symptoms of
vp shunt malfunction
Points on medical and surgical
management of hydrocephalus and
nursing interventions
DESCRIPTION:
-Is an imbalance of CSF absorption
or production caused by
malformation, tumors, hemorrhage,
infection or trauma.
-results in head enlargement and
increased ICP.
FUNCTIONS OF CSF
buffers the brain to protect it from normal
movements of the head
cushions the spinal and brain from jolts.
it helps maintain normal chemical balance
it assists in the maintenance of the blood-
brain barrier.
Protects brain from chemical intrusion from
the rest of the body.
 NORMAL CSF FLOW

• Once formed, (in the choroid plexus) CSF circulates throughout the
ventricular system, exits the foramen of Magendie and Luschka circulates
through the subarachnoid space of the spinal cord and brain, and is then
absorbed.

(Normal production of CSF in adults: 500 ml per day and in a child 25 ml per
day.)
The term hydrocephalus is derived from the Greek, hydor (water) and kephale
(head). Hydrocephalus is an accumulation of cerebrospinal fluid (CSF) in the
ventricles, which results in dilatation of the ventricles. As fluid volume increases,
pressure increases within the intracranial vault.
TYPES:
COMMUNICATING:
Hydrocephalus occurs as
a result of impaired
absorption within the
subarachnoid space.
Interference of the
cerebrospinal fluid within
the ventricular system
does not occur. CSF is
blocked after it exits from
the ventricles
NONCOMMUNICATING:
Obstruction of
cerebrospinal flow within
the ventricular system
occurs. "obstructive"
hydrocephalus - occurs
when the flow of CSF is
blocked along one or more
of the narrow pathways
connecting the ventricles.
Congenital hydrocephalus Acquired hydrocephalus

The cranial bones fuse by the

end of the third year of life. For This condition is acquired as a
head enlargement to occur, consequence of CNS-infections,
hydrocephalus must occur meningitis, brain tumors,
before then. The causes are head trauma,
usually genetic but can also be intracranial hemorrhage
acquired and usually occur (subarachnoid or
within the first few months of intraparenchymal) and is usually
life, which include 1) extremely painful for the patient.
intraventricular matrix
hemorrhages in premature
infants, 2) infections, 3) type II
Arnold-Chiari malformation, 4)
aqueduct atresia and stenosis,
and 5) Dandy-Walker
malformation.
Under surface of the cerebellum. Sagittal section of the cerebellum, near the
(Tonsil visible at center right.) junction of the vermis with the hemisphere.
(Tonsil visible at bottom center.)

Arnold-Chiari malformation is a congenital anomaly of

the brain in which the cerebellar tonsils are elongated
and pushed down through the opening of the base of the
skull (see foramen magnum), blocking the flow of
cerebrospinal fluid (CSF).
 All of the black in the middle is water and the brain matter is the rim of white
along the outside of the skull.
Dandy-Walker syndrome (DWS), or Dandy-Walker complex, is a congenital
brain malformation involving the cerebellum and the fluid filled spaces around it.
The Dandy-Walker complex is a genetically sporadic disorder that occurs one in
every 25,000 live births, mostly in females.
Causes of hydrocephalus
Hydrocephalus develops when there is impedance to CSF flow or
absorption.

Rarely hydrocephalus will occur due to the overproduction of CSF, as in choroid plexus
papilloma.

Congenital anomalies, including aqueductal stenosis, Chiari I and II malformation, and Dandy-
Walker malformation. (Most common causes of hydrocephalus during the neonatal and early
infancy period.)

Acquired hydrocephalus problems in infancy are most commonly secondary to intraventricular

hemorrhage due to prematurity (Greenberg, 2001).

Infections in utero also are a factor in some cases of neonatal hydrocephalus, and are caused
by viruses or bacteria.(Guinea pigs, rabbits, and cats are known to be vectors for viruses that
can cause asymptomatic infection in pregnant women. However, the virus crosses the placenta
to cause potentially catastrophic neurologic problems in the developing fetus (Wright et al.,
1997). Therefore, pregnant women should be counseled to avoid exposure to these animals.

Masses such as tumors, vascular malformations or cysts, and hematoma secondary to trauma.

Infectious processes such as meningitis can impede reabsorption of CSF at the level of the
arachnoid villi resulting in hydrocephalus (Greenberg, 2001).
DIAGNOSIS:

-Ultrasonography

-CT Scan

-MRI (MRI cine is a new investigation used to evaluate

hydrocephalus. Its value is not established yet.)
 Medical Care:
Medical treatment is used to delay surgical intervention. It may be
tried in premature infants with post hemorrhagic hydrocephalus (in
the absence of acute hydrocephalus). Normal CSF absorption
may resume spontaneously during this interim period.
Medical treatment is not effective in long-term treatment of chronic
hydrocephalus. It may induce metabolic consequences and thus
should be used only as a temporizing measure.
Medications affect CSF dynamics by the following mechanisms:
Decreasing CSF secretion by the choroid plexus -
Acetazolamide and furosemide
Increasing CSF reabsorption - Isosorbide (effectiveness is
questionable)
Decadron may be administered to decrease edema
secondary to increased ICP.
Acetazolamide (ACZ) and furosemide (FUR) treat posthemorrhagic hydrocephalus in

neonates. Both are diuretics that also appear to decrease secretion of CSF at the level

of the choroid plexus. ACZ can be used alone or in conjunction with FUR. The

combination enhances efficacy of ACZ in decreasing CSF secretion of the choroid

plexus. If ACZ is used alone, it appears to lower risk of nephrocalcinosis significantly.

Medication as treatment for hydrocephalus is controversial. It should be used only as a

temporary measure for posthemorrhagic hydrocephalus in neonates.

Drug Category: Carbonic anhydrase inhibitors -- These agents inhibit an enzyme found

in many tissues of the body that catalyzes a reversible reaction in which carbon dioxide

becomes hydrated and carbonic acid dehydrated. These changes may result in a

decrease in CSF production by the choroid plexus.

ASSESSMENT:
1. INFANT:  Failure of upward gaze: This is due to
Increased head circumference. > 98th pressure on the tectal plate through the
percentile of age suprapineal recess.
Thin, widely separated bones of the head  Macewen sign: A "cracked pot" sound
that produce a cracked spot sound is noted on percussion of the head.
(Macewen’s sign) on percussion.  Unsteady gait: This is related to
Anterior fontanel tense, bulging, and non spasticity in the lower extremities.
pulsating.  Large head: Sutures are closed, but
Dilated scalp veins chronic increased ICP will lead to
Frontal bossing progressive abnormal head growth.
 Unilateral or bilateral sixth nerve palsy
Sun setting eyes is secondary to increased ICP.
2. CHILD:
Behavior changes such as irritability and
lethargy.
Headache on awakening
Nausea and vomiting
Ataxia LATE SIGNS: a high and shrill cry and seizure
Nystagmus activities
Papilledema: if the raised ICP is not treated,
this can lead to optic atrophy and vision
loss.
 NURSING MEDICAL
INTERVENTIONS:
Monitor vital signs
Assess for any progression of head circumference.
Monitor any change or increase in the head
circumference, change in feeding patterns etc (as
written on the previous slide)
Administer medications as prescribed
Utilize aseptic and or clean technique in any
procedure to prevent infection
Assess nutritional status of patient
Provide comfort and safety
Provide emotional support to patient and family
 Acetazolamide (Diamox) -- Noncompetitive reversible inhibitor of enzyme
Drug Name carbonic anhydrase, which catalyzes the reaction between water and carbon
dioxide, resulting in protons and carbonate. This contributes to decreasing CSF
secretion by choroid plexus.
Pediatric Dose 25 mg/kg/d PO tid; not to exceed 100 mg/kg/d
Documented hypersensitivity; hepatic insufficiency, hyponatremia, hypokalemia,
Contraindicatio
hyperchloremic acidosis, severe renal insufficiency, nephrocalcinosis, adrenal
ns
gland failure

Alkalizes urine and may decrease excretion of amphetamines, procainamide,

quinidine, flecainide, anticholinergics, and mecamylamine; may increase
excretion and lower plasma levels of salicylate, phenobarbital, and lithium; can
Interactions
increase cyclosporine levels and decrease primidone levels; concurrent
salicylates may increase accumulation and toxicity, including CNS depression
and metabolic acidosis

Pregnancy C - Safety for use during pregnancy has not been established.

Can cause hyperglycemia in diabetics; concurrent digoxin can increase

susceptibility to ACZ-induced hypokalemia; in patients taking other diuretics,
ACZ can aggravate hypokalemia; can aggravate preexisting acidosis, which can
Precautions be prevented by initiating prophylactic electrolyte replacement; this may consist
of sodium citrate starting at 8 mEq/kg/d titrated, keeping serum bicarbonate
levels >18 mEq/L and sodium and potassium within reference ranges
Obtain baseline CBC prior to initiating therapy; recheck regularly during therapy
 Drug Category: Loop diuretics -- These agents increase excretion of water by
interfering with the chloride-binding cotransport system, which results from inhibition of
reabsorption of sodium and chloride in the ascending loop of Henle and distal renal
tubule.
Furosemide (Lasix) -- Mechanisms proposed for lowering ICP
include lowering cerebral sodium uptake, affecting water transport
Drug Name into astroglial cells by inhibiting cellular membrane cation-chloride
pump, and decreasing CSF production by inhibiting carbonic
anhydrase. Used as adjunctive therapy with ACZ in temporary
treatment of posthemorrhagic hydrocephalus in neonates.
Pediatric Dose 1 mg/kg/d IV
Documented hypersensitivity to drug or sulfonylureas, hepatic
Contraindications coma, anuria, severe electrolyte depletion, concurrent ethacrynic
acid (may cause ototoxicity), or lithium (may cause lithium toxicity)
May increase ototoxic potential of aminoglycoside antibiotics; may
Interactions increase salicylate toxicity if given with salicylate; may decrease
arterial response to norepinephrine
Pregnancy C - Safety for use during pregnancy has not been established.
Excessive use can cause dehydration and circulatory collapse; can
cause electrolyte imbalance as hypokalemia, hyponatremia,
Precautions hypochloremic alkalosis, hypomagnesemia, and hypocalcemia;
therefore, monitor serum electrolytes; may increase blood glucose
in patients with diabetes; may cause photosensitivity
Drug Category: Corticosteroids-are a class of steroid hormones that are produced in the adrenal cortex.
Corticosteroids are involved in a wide range of physiologic systems such as stress response,
immune response and regulation of inflammation, carbohydrate metabolism, protein catabolism, blood
electrolyte levels, and behavior.
Decadron is an steroid and it comes in Intravenous as well as oral tablets. Intravenous
form is used for immediate action and result and tablets are used to maintain the effect
Drug Name
of Decadron
The range of initial doses is 0.02 to 0.3 mg/kg/day in three or four divided doses (0.6
Pediatric Dose
to 9 mg/m2bsa/day).

Systemic fungal infections (see WARNINGS, Fungal infections).

Contraindications DECADRON tablets are contraindicated in patients who are hypersensitive to any components of this
product.

This drug should not be used with the following medications because very serious interactions may
occur: live vaccines, mifepristone. Before using this medication, tell your doctor or pharmacist of all
Interactions
prescription and nonprescription/herbal products you may use, especially of: aminoglutethimide, large
doses of aspirin and aspirin-like drugs
Do not have immunizations, vaccinations, or skin tests unless specifically directed by your doctor. Live
vaccines may cause serious problems (e.g., infection) if given while you are using this medication.
Avoid contact with people who have recently received oral polio vaccine or flu vaccine inhaled through
the nose.
This medication may mask signs of infection or put you at greater risk of developing very serious
infections. Report to your doctor any injuries or signs of infection (e.g., persistent sore
throat/cough/fever, pain during urination, muscle aches) that occur while using this medication or
within 12 months after stopping it.
Before using this medicine, consult your doctor or pharmacist if you have: current fungal infections.
Precautions
Caution is advised when using this drug for a long time in children. This medication may temporarily
slow down a child's rate of growth, but it will probably not affect final adult height. Monitor your child's
height periodically.
A preservative (benzyl alcohol) that may be found in some dexamethasone products, which are not
preservative-free, can infrequently cause serious (sometimes fatal) problems if given in large amounts
(more than 100 milligrams per kilogram daily) to an infant during the first months of life. The risk is
also greater with low-birth-weight infants. Symptoms include sudden gasping, low blood pressure, or a
very slow heartbeat. If you notice any of these symptoms in your newborn, report them to the doctor
immediately. If possible, use the preservative-free form of this drug when treating newborns.
SURGICAL INTERVENTIONS:
1.The goal of surgical treatment is to prevent
further CSF accumulation by bypasing the
blockage and draining the fluid from the ventricles
to a location to where it maybe absorbed.
2. In ventriculoperitoneal shunt, the CSF drains
into the peritoneal cavity from the lateral ventricle.
3. In an atrioventricular shunt, CSF drains into the
right atrium of the heart from the lateral ventricle,
bypassing the obstruction (used in older children
and in children with pathological conditions of the
abdomen.)
NURSING INTERVENTIONS
POST OPERATIVELY:
Monitor vital signs and neurological signs.
Position the client on the un-operated side to prevent pressure on
the shunt bulb.
Keep the child flat as prescribed to avoid rapid reduction of
intracranial fluid.
Observe for increased ICP; if increased ICP occurs, elevate the
head of the bed to 15 to 30 degrees to enhance gravity flow
through the shunt.
Monitor for signs of infection and assess dressing for drainage.
Measure head circumference.
Monitor intake and output.
Provide comfort measures; administer medications as prescribed,
which may include diuretics, antibiotics, or anticonvulsants.
Instruct parents on how to recognize shunt infection or malfunction.
In a toddler, headache and a lack of appetite are the earliest
common signs of shunt malfunction.
COMPLICATIONS:
Related to progression of hydrocephalus
Visual changes
Occlusion of posterior cerebral arteries secondary to downward transtentorial herniation
Chronic papilledema injuring the optic disc
Dilatation of the third ventricle with compression of optic chiasm
Cognitive dysfunction
Incontinence
Gait changes
Related to medical treatment
Electrolyte imbalance
Metabolic acidosis
Related to surgical treatment
Signs and symptoms of increased ICP can be a consequence of undershunting or shunt obstruction or
disconnection.
Subdural hematoma or hygroma is secondary to overshunting. Headache and focal neurological signs
are common.
Treat seizures with antiepileptic drugs.
Shunt infection occasionally can be asymptomatic. In neonates it manifests as alteration of feeding,
irritability, vomiting, fever, lethargy, somnolence, and a bulging fontanelle. Older children and adults
present with headache, fever, vomiting, and meningismus. With VP shunts, abdominal pain may occur.
Shunts can act as a conduit for extraneural metastases of certain tumors (eg, medulloblastoma).
Hardware erosion through the skin occurs in premature infants with enlarged heads and thin skin who
lie on 1 side of the head.
VP shunt complications include peritonitis, inguinal hernia, perforation of abdominal organs, intestinal
obstruction, volvulus, and CSF ascites.
VA shunt complications include septicemia, shunt embolus, endocarditis, and pulmonary hypertension.
Lumboperitoneal shunt complications include radiculopathy and arachnoiditis.
Symptoms of Shunt
Malfunction/Hydrocephalus
A shunt infection can also cause the shunt not to
work properly and cause CSF to backup, leading to
enlarged ventricles. Signs and symptoms of shunt
infection also relate to signs of shunt malfunction. In
addition, other signs and symptoms related to shunt
infection include:
Fever.
Redness, tenderness, skin breakdown, or fluid
collection noted at the shunt on the scalp or
anywhere along the shunt tract.
Drainage at the incisional areas related to the shunt.
Abdominal pain, tenderness, or refusing to eat or
drink
 INFANTS TODDLERS

 Enlargement of the  Head enlargement

baby’s head  Vomitting
 Fontanel is full and  Headache
tense when the infant
 A loss of previous
is upright and quiet
abilities (sensory of
 Vomitting, Irritability,
motor function)
Sleepiness, downward
 Seizures
deviation of the eyes
 Seizures  Lack of apetite
OLDER CHILDREN

Vomiting
Vision problems
Irritability and or tiredness
Loss of coordination and balance
Difficulty in waking up or staying
awake
Seizures
Decline in school performance
For the most part, shunts function well. However,
there are complications that can occur. A
blockage or obstruction of the shunt is the most
common complication of the system. Obstruction
may occur at any point along the path of the
shunt. The opening at the ventricular end may
become plugged with brain, choroid plexus
tissue, or blood. The peritoneal end may also
become blocked by scar tissue. An obstructed
shunt causes an increased volume of CSF in the
ventricular system of the brain. This can lead to
the same symptoms as those listed below for
hydrocephalus. The shunt can be repaired
(shunt revision) in surgery lasting about 1 – 2
hours.
Reference

Medical Surgical
textbooks: Bruners
and Sudarths,
Saunders
Internet
Nurse Avenue
Medscape