INTRODUCTION

Non-communicating or obstructive hydrocephalus secondary to

Bacterial Meningitis Stage II is the condition involved in this case study.

Nilcar Domingo, 6 years old from Barangay Laslasong, Santa Maria, Ilocos

Sur was my client. His case is initially diagnosed as Bacterial Meningitis, PTB,

Typhoid Fever, and Urinary Tract Infection. The final diagnosis of his

condition is Non-communicating or Obstructive Hydrocephalus Secondary to

Bacterial Meningitis Stage II.

Hydrocephalus in general, is the enlargement of the CSF

compartment. It is defined as an abnormal increase in CSF volume in any part

of all of the ventricular system. The two causes of hydrocephalus are

decreased absorption or overproduction of CSF. There are two types of

hydrocephalus: Communicating and Non-communicating Hydrocephalus.

The focus of this case study is purely on Non-communicating or

obstructive hydrocephalus.

Non-communicating hydrocephalus occurs when obstruction in the

ventricular system prevents the CSF from reaching the arachnoid villi. CSF

flow can be obstructed by congenital malformations, from tumors

encroaching on the ventricular system and by inflammation (meningitis) or

hemorrhage. The ependyma is particularly sensitive to viral infections.

Ependymitis is believed to the cause of congenital aqueductal stenosis.

In contrast to hydrocephalus that develop in utero or during infancy,

head enlargement does not occur in older children and increase in ICP

depend on whether the condition developed rapidly or slowly. Acute onset

hydrocephalus in older children usually is marked by symptoms of increased

ICP, including headache and vomiting followed by papilledema.

Incidence and prevalence data are difficult to establish as there is no

existing national registry or database of people with hydrocephalus and

closely associated disorders; however, hydrocephalus is believed to affect

approximately 1 in every 500 children. At present, most of these cases are

diagnosed prenatally, at the time of delivery, or in early childhood. Advances

1
in diagnostic imaging technology allow more accurate diagnoses in individuals

with atypical presentations, including adults with conditions such as normal

pressure hydrocephalus

OBJECTIVES OF THE STUDY

This case study on non-communicating or obstructive hydrocephalus

seeks to attain the following:

 Identify the risk factors of obstructive hydrocephalus.

 Acquire sufficient knowledge in the treatment of the condition.

 Be able to discuss the management of the condition.

 Be able to provide nursing care for an easy recovery of the patient.

 To device and implement a Nursing Care Plan appropriate to a non-

communicating hydrocephalus patient.

 Be able to trace the etiology, how the disease progresses, its clinical

manifestations and diagnostic procedures by establishing an

appropriate Pathophysiology of the disease which includes the

algorithm and its explanation.

2
 PATIENT’s PROFILE

CASE NUMBER:054435
NAME OF PATIENT: Nilcar Domingo

ADDRESS: Laslasong, Sta. Maria, Ilocos Sur

AGE: 6 years old

SEX: Male

CITIZENSHIP: Filipino

DATE OF BIRTH: January 16,1999

CATEGORY: Charity

DATE ADMITTED: December 24,2005

CHIEF COMPLAINTS: headache, nausea and vomiting, seizure, fever

ADMITTING DIAGNOSIS: Bacterial Meningitis, PTB, Typhoid Fever, and

UTI

ADMITTING PHYSICIAN: Dr. Maura Gonzales

ATTENDING PHYSICIAN: Dr. Jean T. Mahor

WARD: Pediatric Ward

FINAL DIAGNOSIS: Non-Communicating / Obstructive Hydrocephalus

Secondary to Bacterial Meningitis

DATE OF DISCHARGE: January 27, 2006

TIME: 2:30 PM

3
NURSING HISTORY OF PAST AND PRESENT ILLNESS

A. PRESENT ILLNESS

According to Nilcar’s mother Mrs.Marrissa Domingo, her son was

complaining of headache, fever, and seizure lasting for about 30 seconds

prior to hospital admission. December 21,2005, Nilcar’s condition became

more intense as evidenced by generalized seizure as verbalized by the

mother. They rushed Nilcar immediately at Sto. Nino Hospital in Sta.

Maria,Ilocos Sur.

In the hospital, he was admitted with an initial diagnosis of typhoid

fever, Urinary tract infection, pulmonary tuberculosis and Bacterial

Meningitis as revealed in his chart. He was then venoclyzed with D5 0.3 NaCl

solution. He was ordered with complete blood count (CBC) and the results

were normal. Urinalysis was also done to him revealing urinary tract

infection. Several diagnostic procedures like widal’s test was also performed

which revealed thypoid fever. He was started with ampicillin 400 mg TID

every 6 hours, Cotrimoxazole 40 mg/5 ml, 1 ½ teaspoonful every 12 hours,

mefenamic acid syrup 1 tsp. PRN for headache, paracetamol 120 mg/5 ml

every 4 hours for fever. All those informations were based on the client’s

chart and the client’s mother.

On the second day of hospitalization (same hospital) December 22,

2005, again a diagnostic procedure was ordered particularly Skull X-ray. The

result was normal. Headache and fever still persist. Ampicillin dosage was

increased to 500 mg every 6 hours. His condition improved and his parents

requested home against medical advise. Take home medications were

prescribe like chloramphenicol, cotrimoxazole and paracetamol.

December 22, 2005 at exactly 10:30 pm, Nilcar experienced

generalized spastic seizure but no fever was noted as verbalized by the

mother. They rushed him again at Sto. Nino Hospital. He was venoclyzed with

D5 0.3 NaCl 500 ml at 30 gtts/min. He was started with Ceftriaxone 600 mg

IV every 12 hours, Phenobarbital 1 tablet every 12 hours, Dexamethasone 1.5

4
mg IV every 8 hours and Diazepam 3 mg IV. He was also connected to O2

inhalation via nasal cannula due to difficulty of breathing.

Due to financial constraints, his parents requested for transfer to

Gabriela Silang General Hospital. So they transferred him.

December 24, 2005, Nilcar was admitted at Gabriela silang General

Hospital at around 10:15 in the morning. Same IVF was maintained and some

of his medications were also maintained. Included in the list of prescribed

drugs by his doctor were INH 200 mg/5 ml OD, PZA 250 mg/5 ml OD, RIF

200 mg/ 5 ml, 5.5ml OD, Phenobarbital 30 mg ½ tablet BID, Hexatidine oral

solution TID, Bactroban ointment, Pediasure 15-30 ml every 3 hours,

Diazepam 3.2 mg IVF and Ampicillin 800 mg IV every 6 hours ANST (-).

Several diagnostic procedures were also ordered like blood chemistry,

Skull/head scan, lumbar puncture or CSF analysis and widal’s test (Refer

results to the Dx procedures).

B. PAST ILLNESS

Nilcar’s mother verbalized that her son was very sickly during his

early childhood years. She added that Nilcar was diagnosed with primary

complex at age 3. Although headache was being experienced by Nilcar, it was

taken fore granted and was managed with plain analgesic 8paracetamol for

kids). Last November 2005,Nilcar complained to his mother about severe

headache and vomiting at times, but because of financial constraints, Nilcar

was not able to undergo a specific diagnostic procedure. Nilcar’s mother

admitted that she couldn’t give Nilcar a good nutrition because of the fact

that they belong family below poverty level. Nilcar’s mother also verbalized

that they don’t have a family history of the disease and believes that the

cause of her son’s sickness was purely environmental.

PEA/RSON ASSESSMENT

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DATE JANUARY 22-24 HOME VISIT

(February 25,2005)

 Conscious and  Nilcar showed

coherent. psychosocial
 Nilcar is 6 years old improvements like:
P and not yet studying. he is now engaging
 There is no family social interactions
background of with other children.
obstructive  He was discharged
hydrocephalus in last January
their family. 27,2006.
 The patient is very  He started to regain
shy to express his confidence.
feelings.  He wanted to go to
 The fourth stage of school already.
Erickson’s theory on  No more irritable
G&D, which is maybe because he is
Industry versus now in their home.
Inferiority, is  He is now more
altered as evidenced active than before.
by, the child was not
able to enhance his
skills and was not
able to socialize with
other children.
 Patient is irritable at
times.

 Experienced urinary  He can control his

incontinence and urination already.
E sometimes-urinary  Returned to normal
retention. evacuation of
 May only evacuate formed stools with
stool 3X a week due yellow color.
to anorexia, nausea
and vomiting.
 The color of his
urine is yellow.
 No diaphoresis was
noted.
 The consistency of
the stool is normal
(formed to semi

6
 formed).

 Can perform ADL up  Showed

to the minimum level independence in
of functioning. E.g. performing ADL but
A/R combing the hair. still there is a need
 Experienced body to support him.
weakness, headache  No more body
and dizziness. weakness and
 Had a disturbed dizziness felt by the
sleep wake cycle due patient.
to headache.  He is playing with his
 Negative for edema. playmates.
 Unable to play his
toys because
dizziness etc..

 The patient has a

 The skin turgor and
decreased skin
appearance has
turgor e.g. dry skin
improved.
 No known history of
 He is not pale
S allergy to foods and
already.
medicines.
 He is experiencing
 Skin color is pale.
seizure anymore.
 A dry lip was also
 Generally, the
noted.
patient improved.
 Pink palpebral
conjunctiva was also
observed.
 The patient is
positive for seizure
activity therefore
there is a high risk
for injury.

 Negative for chest

 Still experiencing
retractions.
productive cough.
 With O2 inhalation
 DOB is negative.
connected via a nasal
PR- 140 bpm
O cannula level at
T- 37
2LPM.
RR- 30 cpm
 Experienced
coughing at times
(productive).
 Respiratory rate of
40 cycles per minute

7
 was noted (not
consistent)
PR: 150 bpm
T: 37.4-37.8oC.
 Prefers semi-fowlers
position.

 Signs of dehydration  DAT diet is

were noted. maintained.
 The patient’s  Regained his
appetite was appetite.
N decreased.  He is not
 Experienced nausea, experiencing nausea
vomiting. and vomiting.
 The patient has a
decreased appetite.
 With an IVF of D5
0.3 NaCl regulated
at 30 gtts/minute.

DIAGNOSTIC PROCEDURES

8
A. THEORY

1. COMPUTED AXIAL TOMOGRAPHY OF THE BRAIN

 Makes use of a narrow X-ray beam to scan the head in

successive layers.

 The images provide cross sectional view of the brain with

distinguishing differences in tissue densities of the skull,

cortex, sub cortical structures and ventricles.

 Lessions in the brain are seen as variations in tissue density

differing from the surrounding normal brain tissue. An

abnormality of tissue indicates possible tumor masses, brain

infarction, displacement of ventricles and cortical atrophy.

2. VENTRICULOGRAPHY

 Clearly defines the site of blockage to the flow of

cerebrospinal fluid.

3.POSITRON EMISSION TOMOGRAPHY

 Permits the measurement of blood flow, tissue composition and

brain metabolism and thus indirectly evaluates brain function.

4. MAGNETIC RESONANCE IMAGING

 It has the potential for identifying a cerebral abnormality.

 It can provide information about the chemical changes within

cells.

5. LUMBAR PUNCTURE

 Carried out by inserting a needle into the lumbar subarachnoid

space to withdraw CSF.

 The test maybe performed to obtain CSF for examination, to

measure and reduce CSF pressure.

6. CEREBROSPINAL FLUID ANALYSIS

 The CSF should be clear and colorless

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 Pink, blood tinged or grossly bloody CSF may indicate a cerebral

contusion, laceration or subarachnoid hemorrhage.

 Specimens are obtained for chemical analysis, microbial

analysis, cell count and protein testing.

NORMAL RESULTS:

Albumin: 15-30 mg/dl

Wbc count: 0-5 cells/mm3

Chloride: 120-130mEq/L

Glucose: 50-75 mg/dL

Glutamine: 6-15 mg/dL

IgG : < 5 mg/dL

Lactic acid: 4.5-28.8mg/dL

Lactate dehydrogenase: 1/10 that of serum level

Protein: 15-45 mg/dL

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B. ACTUAL

NAME AND PURPOSE ACTUAL VALUES NORMAL VALUES NURSING NURSING

OF PROCEDURE IMPLICATIONS RESPONSIBILITIES

1. LIVER FUNCTION

TEST (01 – 10- 06)

Function is generally
measured in terms of
enzyme activity and serum
concentrations of
proteins, bilirubin,
ammonia, clotting factors
and lipids. However, the
nature and extent of
hepatic dysfunction
cannot be determined by
these tests alone.

 SGOT/SERUM 150.4 units Up to 25 units  An increase in ALT  Explain the purpose of

GLUTAMIC
maybe used to monitor the test to the client
OXALOACETIC

11
 TRANSAMINASE the course of hepatitis or to the watcher.

and other liver  Instruct the watcher

disorder. to monitor signs of

 An increase in ALT drug toxicity. (e.g.

maybe due to the blood dyscrasias,

effects of treatments dermatological

that maybe toxic to symptoms, drug allergy,

the liver. hypersensitivity and

stomatitis.

 Monitor results of the

test as indicated.

 Interpret result and

SGPT/SERUM
122.3 units Up to 30 units  Elevated SGPT levels inform the client’s
GLUTAMIC PYRUVIC
TRANSAMINASE due to the destruction relatives.

of liver cells secondary  Refer to the physician

to toxic effects of concerning the results

12
 drugs. of the test.

2.CEREBROSPINAL
FLUID ANALYSIS (CSF
ANALYSIS)
01-10-2006
 Usually specimens are
obtained for cell count,
culture, glucose and
protein testing.
 Explain the
CSF
Slightly xanthochromatic Clear and colorless  A deviation in color of significance of the
COLOR/APPEARANCE
the CSF from clear to procedure to the

xanthochromatic watcher or to the

indicates an patient.

abnormality like lesion  Emphasize on

in the choroids plexus medication compliance

or blockage of the flow to prevent further

of CSF. infection like

13
 meningitis.

CELL COUNT:  Refer results to the

41 cells/mm3 0-5 cells/mm3  Higher than the normal physician.

WBC
value which indicates  Proper positioning of

bacterial the patient after

Rare None
meningitis/encephalitis lumbar puncture.

Patient is positioned

RBC  Traces of RBC in the prone for 2 hours, then

CSF indicate cerebral flat on bed for 6 more

contusion, laceration or hours, then keeping

subarachnoid patient flat overnight.

1.18 mmol/L 2.75 – 4.4 mmol/L
hemorrhage.  If headache occurs

after LP, instruct

GLUCOSE  Decrease amount of client to rest, analgesic

glucose in the CSF is agents and hydration

an implication that may do.

14
 there is acute

meningitis or

173 mg/ L 150- 450 mg/ L subarachnoid

hemorrhage.

 Normal
TOTAL PROTEIN

3.URINALYSIS
12-30-2005
 Explain the purpose of

 To have a clinical the procedure and talk

information about the
to the level of
kidney functions and
helps diagnose other Yellow Amber/straw understanding to the
diseases.
client.

 Refer results to the

COLOR
 Signifies pyuria or due physician.

to the medications  Obtain a good urine

15
 5.0 4-6 taken by the client. specimen. It should be

midstream urine.

negative negative

 Normal
PH
1.030 1.010-1.025
ALBUMIN
 Normal

SPECIFIC GRAVITY
1-2 1-2  Signifies concentrated

urine due to urinary

Negative Negative retention.

PUS CELLS  Normal

RBC  Normal

16
  Fine streaky infiltrates  The lungs should be

seen in the inner lung clear.

4.CHEST X- RAY
(01-11-2006) fields.  Explain the procedure

 Hilar nodularities seen  There should be no  Primary pulmonary to the watcher or to

 To evaluate
Respiratory status and to  The heart is not nodularities seen tuberculosis is the client.
determine if the heart if
enlarged considered.  Check for baseline vital
there is cardiomegaly.
 Diaphragm and sulci  Diaphragm and the signs as ordered.

are intact sulci should be intact.  Provide information

 Bony thorax is regarding the

unremarkable  There should be no appearance of the

cardiomegaly. machine.

 Explain that the

procedure is painless.

17
5.COMPUTERIZED  Multiple plain and  CT scanning should
AXIAL TOMOGRAPHY
contrast enhanced reveal no dilatation of
(01-05-2006)
axial slices of the head the ventricles, no  Explain the purpose of
 CT scanning is non
demonstrates lesions or abscess and  Results showed that the procedure to the
invasive and painless
and has a high degree dilatation of the there should be no Obstructive nearest kin.
of sensitivity for
lateral and 3rd signs of IICP. hydrocephalus  Instruct client to lie
detecting lesions.
ventricles but normal probably secondary to quietly throughout the

sized 4th ventricle. ductal stenosis. procedure.

 No tumor, AV  Review of relaxation

malformations, abscess techniques maybe

or dysthrophic helpful for

calcification seen. claustrophobic

 No shift of the septum patients.

pellucidum noted  Sedation can be used if

 No fluid levels noted agitation, restlessness

within the paranasal or confusion will

sinuses. interfere with a

18
 The posterior fossa successful study.

structures are intact.  NPO for 4 hours prior

 No neurologic signs of to the procedure

increased should be instructed to

intraventricular the client.

pressure

 Intact orbits, skull

bone and calvarium.

19
ANATOMY AND PHYSIOLOGY OF THE ORGAN INVOLVED

Anatomy of the Central Nervous System

The brain can be subdivided into several distinct regions:

 The cerebral hemispheres form the largest part of the brain,

occupying the anterior and middle cranial fossae in the skull and

extending backwards over the tentorium cerebelli. They are made

up of the cerebral cortex, the basal ganglia, tracts of synaptic

connections, and the ventricles containing CSF.

 The Diencephalon (not shown above) includes the thalamus,

hyopthalamus, epithalamus and subthalamus, and forms the central

core of the brain. It is surrounded by the cerebral hemispheres.

 The Midbrain (not shown) is located at the junction of the middle

and posterior cranial fossae.

 The Pons sits in the anterior part of the posterior cranial fossa- the

fibres within the structure connect one cerebral hemisphere with

its opposite cerebellar hemisphere.

 The Medulla Oblongata is continuous with the spinal cord, and is

responsible for automatic control of the respiratory and

cardiovascular systems.

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 The Cerebellum overlies the pons and medulla, extending beneath the

tentorium cerebelli and occupying most of the posterior cranial fossa. It

is mainly concerned with motor functions that regulate muscle tone,

coordination, and posture.

Anatomical division of Central nervous system (CNS):

CNS: brain and spinal cord

Devoid of collagen except in vicinity of blood vessels and

meninges; contains no lymphocytes

blood-brain barrier: CNS capillaries impermeable to certain plasma

constituents especially larger molecules; absent in choroid plexus, pituitary

and pineal glands and vomiting center of hypothalamus

capillary endothelium: junctions btwn endothelial cells are sealed; little or

no pinocytosis in endothelium; luminal surface membranes contain enzymes

which destroy neurotoxic metabolites (neuroactive humoral substances)

astrocyte foot processes: maintain barrier

Gray (grey) matter: almost all neuron cell bodies and axons

neuropil: feltwork of axons and dendrites surrounding neurons and neuroglia;

esosinophilic; largely devoid of myelin

non-myelinated nerve fibers: when neurolemmocyte only

investment: small diameter axons (autonomic nervous system

and small pain fibres)

neuroglia: all neuroepithelial-derived non-neural cells of CNS

astrocytes: star-shaped with heavy metal impregnation; most

22
numerous glial cells in gray matter; highly branched packing cells;

form mass surrounding nerve cells processes and oligodendrocytes;

rounded, nuclei closely enmeshed in neuropil; mediate metabolic

exchange btwn neurons and blood; regulate composition of intercellular

environment in CNS

Glial fibrillary acidic protein (GFAP): unique intermediate filament;

demonstrated by immunoperoxidase method

fibrous astrocytes: astrocytes of white matter

with relatively straight cytoplasmic processes

protoplasmic astrocytes: astrocytes of gray matter with numerous

short highly branched cytoplasmic processes

glial limitans: relatively impermeable; foot processes invest

basement membrane CNS and innermost layer of meninges (pia

mater)

oligodendrocytes invest axons in myelin; form multiple myelin

internodes; contribute to ensheathment of as many as 50 individual

axons; small rounded condensed uclei; cytoplasm unstained by H&E;

tend to be aggregated around neuron cell bodies; most numerous glial

cell in white matter; analogous to satellite cells in ganglia; analogous

to neurolemmocytes in nerves

microglia (misnoma): monocyte-macrophage cells; invade CNS during

fetal period; small irregular nuclei; relatively little cytoplasm forms

fine, highly-branched processes; transform into large amoeboid

phagocytic cells

White matter (myelin): tracts of nerve fibers; substantial numbers

myelinated

myelinated nerve fibers: increased velocity of action potential; ÎMyelin

23
sheath formation begins in the CNS of the human embryo at about 4 months

gestational age with the formation of most sheaths at least commenced by

about the age of one year. From this time, successive layers continue to be

laid down with final myelin sheath thickness being achieved by the time of

physical maturity.â

Choroid plexus: arises from wall of four ventricles of brain; produces

cerebrospinal fluid (CSF); consists of mass of capillaries projecting into

ventricle; invested by modified ependymal cells separated from underlying

capillaries and suporting tissue by basement membrane; long bulbous

microvilli project from luminal surface ; continuous tight junctions (zonula

occludens) form blood-CSF barrier

Meninges

dura mater: thick; fibrous

arachnoid: nonvascular; spaces filled with cerebrospinal fluid (CSF)

pia mater: invests CNS

Pons: middle portion brain stem; btwn midbrain and medulla; two parts in

transverse section [basal pons & tegmental region]

basal pons (criss-crossed bundles of longitudinal and transverse fibers

btwn neuron cell bodies = pontine nuclei)

middle peduncles: of fibers from pontine nuclei that have passed in

transverse bundles across mid-line to enter cerebellum

Cerebellum: cortex of gray matter with central core of white matter

containing four pairs of nuclei; cortex in series deep convoluted folds =

folia; supported by branching medulla of white matter = arbor vitae

Cortex: three layers (= gray); white matter = medulla

24
molecular layer contains few neurons and lg number unmyelinated fibers;

stellate cells and basket cells

piriform (pear shaped) cells = Purkinge cells; fine axon extends downward

throug granular cell layer; extensively branching dendritic system arborizes

into outer molecular layer (demonstrated with heavy metal methods)

granular cell layer extremely cellular; non-myelinated axons pass outward to

molecular layer; bifurcate to run parallel to surface; synapse with dendrites

of piriform cells; plus  great stellate neurons = Golgi cell type II in

superficial part granular cell layer (more like deep part molecular layer)

Substantia nigra: lg mass gray matter extending throuout midbrain; divides

cerebral peduncles into dorsal and ventral parts; easily recognized by black

pigment (melanin in cytoplasm); extensive cnnections with cortex, spinal cord,

corpus striatum and reticular formation; functions in fine control of motor

function; multipolar neurons; contain dopamine (DOPA:

dihydroxyphenylalanine; precursor of dopamine and melanin)

neurotransmitter causing inhibitory effects on neurons of corpus striatum;

L-dopa, a dopamine precursor crosses blood-brain barrier.

PATHOPHYSIOLOGY OF THE DISEASE

A.ALGORITHM

25
 CAUSES
Obstruction of CSF flow
Congenital malformation
Secondary to injury
Infection*
Ductal stenosis*

Increases risk to the development of

Obstructive Hydrocephalus

Blockage between the ventricular and

Subarachnoid spaces

Due to congenital　　　　　　　*due to acquired

Defect following inflammation
In the periaqueductal region

Compression of the aqueduct by an extrinsic lesion posterior to the brain

Fluid distends the ventricles

Signs and
DX Procedures
symptoms

Radiologic
Vomiting*
Gradual thinning of the brain substance studies*
Full
fontanelle
CSF analysis*
Papilledema
Decreased
Blood
pulse* SIGNS AND SYMPTOMS chemistry*
Anorexia*
CT scan*
Convulsion*

* Note: inputs with asterisk were observed to the patient to the patient.

26
B. EXPLANATION

Non – communicating or obstructive hydrocephalus occurs when

obstruction in the ventricular system prevents the CSF from reaching the

arachnoid villi. CSF flow can be obstructed by congenital malformations,

from tumors encroaching on the ventricular system and by inflammation or

hemorrhage. Other causes include Ductal stenosis and bacterial meningitis.

The case of Nilcar that is obstructive hydrocephalus, the number one

etiology that they considered was bacterial meningitis. The bacterial

organisms replicate and undergo lysis in the CSF releasing endotoxins or cell

wall fragments. These substances initiate the release of inflammatory

mediators, which set the stage for a complete but coordinated sequence of

events by which neutrophils bind by the release of toxic oxygen products

(free radicals), permitting fluid to move across the capillary wall.

As a result of bacterial meningitis plus other causes, blockage occur

between the ventricular and subarachnoid spaces thus stenosis to the

aqueduct of sylvius may result. It is either a congenital defect or an

acquired defect following inflammation in the periaqueductal region,

compression of the aqueduct by an extrinsic lesion posterior to the brain

stem such as an aneurysm or with subdural Hematoma, atresia of the

foramina of luschka and magendie or the Arnold chiari malformation.

Fluid then distends the ventricles. There is a gradual thinning of the

brain substance, which is compressed between the distended ventricles and

the expanding skull.

Signs and symptoms occurs such as vomiting, separated sutures, full

fontanelles, papilledema, decreased pulse, anorexia, weight loss, convulsion,

drowsiness, intellectual dysfunction and IICP may develop.

Diagnostic findings such as Radiologic studies, CSF analysis, blood

chemistry and CT scan revealed Obstructive Hydrocephalus to Nilcar.

Other diagnostic procedures, which further reveal the presence of

Obstructive hydrocephalus, are PET scan, MRI, Ventriculography and other

diagnostic procedures.

27
MANAGEMENT

A. MEDICAL AND SURGICAL

On rare occasions, a spontaneous balance may occur between the

secretion of CSF and its absorption. If it does not, treatment is carried out

as early as possible to prevent damage to the brain.

The goal in management of children with hydrocephalus is to establish

equilibrium between the production and resorption of CSF.

Medical management consist in the use of acetazolamide (diamox), a

drug that reduces the production of cerebrospinal fluid. But since the cause

of the obstructive hydrocephalus in this case study is purely bacterial

meningitis, thus massive antibiotics was ordered (Ampicillin 800 mg IV q 6

hours ANST (-). If the child’s head growth in acute hydrocephalus is

increasing at or slightly above the normal rate after subarachnoid

hemorrhage or bacterial meningitis, repeated lumbar punctures maybe done

to maintain normal CSF pressure.

No medical treatment is available that can counteract the

accumulation of CSF in the brain. In cases in which a decision has been made

not to treat the hydrocephalus, medical treatment is exclusively palliative.

Theoretically, the treatment of choice for infants with progressive

hydrocephalus is surgery. Surgical management may consist of:

 Removal of obstruction

 Reduction in the amount of CSF produced through destruction of a

portion of the choroids or a third or fourth ventriculostomy.

 Shunting of CSF from the ventricle to another site in the normal

circulatory passageway of this fluid for the treatment of non-

communicating hydrocephalus caused by aqueductal stenosis

There was no surgical procedure done to my patient because the cause

is related to bacterial meningitis or acquired infection that can be

manageable by medical management alone.

Although several surgical procedures were recommended if the

disease may become worst particularly shunting. Ventricular shunt. The

28
shunt is an artificial device, made mostly of plastic (although some parts may

be metal), that includes a catheter inserted in the ventricle of the brain, a

one-way valve that allows the unidirectional flow of CSF out of the brain, and

a distal catheter that drains the CSF to an extra cranial location in the

body. The most preferred distal site remains the peritoneum, although, for

difficult cases with other coexisting abdominal problems, other options are

available, such as the right atrium, the gall bladder, the ureter, or the

bladder. In current practice, the overwhelming majority of shunts are

ventriculoperitoneal.

29
 NURSING CARE PLAN

CUES NURSING ANALYSIS NURSING NURSING RATIONALE EVALUATION

S & O
DIAGNOSIS OBJECTIVES INTERVENTIONS
CEPHALOCAUDAL
NANDA APPROVED (SMART)

S>”Nasakit kanu ti P> Acute pain risk for Pain is 01-22-06 INDEPENDENT: 01-22-06
considered an
ulo na ken maulaw E> related to increase Within the  Monitor vital  Vital signs are Level of
unpleasant sensory
shift with proper signs. general attainment: goal
ulaw suna nga IICP, tissue and nerve perception and
medical and indicators of partially met
emotional
tumakder idi damu trauma. nursing circulatory
experience
management, the status and AEB: Pain
na nga marikna toy S> as evidenced by associated with
patient will adequacy of experienced by
actual or potential
sakit na adding” as changes in sleep verbalize perfusion. the patient is
tissue damage.
decrease pain reduced from
verbalized by the patterns. Acute pain lasts
from 4 to at least  Document  Aids in severe to mild.
for a relatively
mother. > Dizziness 1 using the Wong location and evaluating need
short period of
baker Faces scale intensity of for and
O> Pain rating > Headache (on and time and remits as
0-5, 5 being the pain (0-5) and effectiveness
the pathology
scale using the off) highest. investigate of

30
Wong baker faces resolves. Pain could changes in pain interventions.
be attributed to characteristics. Changes may
rating scale
IICP because as indicate
reveals that the the pressure developing
increases in the complications.
level of pain is
cranial vault, there
grade 4(It hurts a is no other way to  Proper  With this kind
release the positioning of position,
whole lot more).
pressure; as a (semi-fowlers). pressure will
> The patient result there is be lessened
compression of because it
looks weak.
nerves and the prevents the
> Dizzy brain itself congestion of
(Medical Surgical blood in the
> On and Off
Nursing 6th ed.) head region.
headache
 Avoid coughing  Coughing or
or straining. straining will
further
increase ICP.

31
 COLLABORATIVE:

 Administer  Analgesics
medications as relieve pain by
ordered e.g. blocking the
analgesics and pain impulses
antibiotics. at the pain
receptor sites.
 Refer to the  By referring to
physician the physician,
regarding the he may order
pain an appropriate
experienced by diagnostic
the client for procedure to
further determine the
diagnosis. cause of the
pain.

32
P> Injury risk for 01-22-2006 INDEPENDENT: 01-22-2006
Causes Within my
E> r/t muscle weakness,
Presence of health shift, the mother  Provide safe  Safe room Level of
dizziness and convulsion threats will be able to environment or environment attainment: Goal
Dizziness acquire knowledge room for the helps eliminate met.
or seizure.
Seizure regarding the client the risk for
S> as evidenced by (not consequences of injury. AEB: The
Body is lacking of falling and injury  Advise the  Bedside rails mother
applicable, presence of
energy to sustain with proper mother to raise may help understands the
signs and symptoms body’s needs health teachings. the bedside prevent the health teachings
rails during patient from regarding the
establishes an actual
seizure falling from risk of injury to
diagnosis. Body weakness the bed. the patient.
 Observe signs  Assessing the
Risk for falling of seizure time and
disorders correct
Possible symptoms of
consequences like seizure may
injury help in the
(med surge Nsg.6th diagnosis of
ed) what kind of
seizure
disorder that
the client had.

33
 COLLABORATIVE:

 Administer  Anti convulsive

anti-convulsive drugs
drugs. stabilizes
nerve
membranes
throughout the
CNS to
decrease
excitability
and hyper
excitability to
stimulation.

 Consult the  The

pharmacist with pharmacist
regards to site, together with
time and the physician
delivery of knows the
drugs that correct
might have formulations of
action drugs and their
adversely actions.

34
 contraindicated
to the patient.

S>Agsarwa sarwa P> Imbalanced nutrition

01-24-2006 INDEPENDENT: 01-26-2006
pay isuna nga less than body Within 2 days,
Imbalance Nilcar will show  Instruct the  Crackers will Level of
kanayon added by requirements
nutrition refers to improvement in relatives to give alleviate Attainment:
the mother. E> related to nausea, a relative or nutrition as plain crackers nausea and Goal partially
absolute deficiency evidenced by to the client. vomiting. met.
vomiting and anorexia.
or excess of one or nausea and
O> The patient S> As evidenced by more essential vomiting free  Encourage the  This may help
nutrients state and client to drink to replace AEB: The
appears very weak. weight loss, weakness
increase fluids with fluids and patient still
> He has a dry and dizziness Body can’t sustain consumption of at electrolytes electrolyte experiencing
normal function least half of the such as deficiencies N/V at times
skin and has a > Nausea
served foods. Gatorade and due to vomiting and the appetite
decreased skin Deficiencies arise other is moderately
nutritionally improved as
turgor. Signs and enriched drinks evidenced by one
> The clients symptoms of or shakes fourth of the
imbalanced unless served food is
weight is 17kgs. nutrition contraindicated consumed.
 Weight loss
 Growth

35
 retardation  Encourage small  Small frequent
 Mental frequent feeding may
retardation feeding. help to
(Medical decrease
Surgical gastric motility
Nursing 6th ed.) because a full
stomach
excites to
digest the
contents thus
less hyper
motility.

 Promote oral  The taste in

care. the mouth is
unpleasant;
therefore oral
care is needed
to instruct to
lessen the
unpleasant
taste.

36
 COLLABORATIVE:

 Administer  IV fluids are

intravenous administered
fluids as to replace the
ordered. fluids and
electrolytes
that are lost
during vomiting
and this may
help to
hydrate the
patient.

 Administer  Anti-emetic
anti- emetics as drugs works by
ordered if reducing the
vomiting and hyperactivity
nausea persist. of the vomiting

37
 reflex.

 Work with  Inorder to

other health come up with
care provider the best
as a group. e.g. possible care
forwarding lab to the patient.
request and
orders.

P> Fluid volume deficit

01-24-2006 INDEPENDENT: 01-26-2006
E> related to
Fluid volume
inadequate intake of deficit is Within 2 days,  Monitor vital  Vital signs Level of
characterized by a Nilcar will be free signs. reflects attainment: goal
food and fluids,
decrease in extra from vomiting and changes within partially met.
vomiting and diuretic cellular fluid the skin turgor the body
including will improved and
use.
circulating blood the intake and  Encourage  By increasing AEB: Patient is
volume due to loss output will patient to fluid intake, still
of G.I. fluids, normalized. increase fluid the lost water experiencing
S> as evidenced by dry
polyuria, sweating intake unless and nausea and
skin and mucous due to fever and contraindicated electrolytes vomiting and the

38
membrane exercise and third will be skin turgor is
space losses.(Med replenished. moderately
> Decreased skin
& Surge Nursing improved. Level
turgor. 6th ed).  Monitor I & O  Sustained of hydration also
diuresis could improved.
> Weakness
cause patients
total fluid
volume to
become
depleted.

 Administer IV  Replaces fluid

fluids as and electrolyte
ordered losses to
prevent
electrolyte
imbalances.

COLLABORATIVE:

 Monitor  As fluid pulled

electrolyte from
level extracellular
specifically spaces, sodium
Sodium may follow the

39
 shift causing
hyponatremia.
S> “Manipud idi P> Fear/anxiety
01-24-2006 INDEPENDENT: 01-24-2006
naospital isuna ket E> R/T changes in Anxiety is
emotional illness Within the  Establish  Demonstrates Level of
managbut buteng health status,
characterized by shift, the patient trusting concern and attainment:
met isunan, no possibility of surgical fear, autonomic will be able to relationship to willingness to Goal partially
neuron system demonstrate the patient. help the client. met.
kuma adda procedures and
symptoms and appropriate range Encourages
umasideg kenyana embarrassment. avoidance behavior of feelings and discussion of
(ABC’s of lessened fear or sensitive AEB: The
nga saan na nga S> as evidenced by fear
Psychiatric the anxiety will subjects. patient still
am-ammu ket of non-specific Nursing, Ray A. be reduced to a manifest fear
Gapuz). manageable level  Explain to the  Helps patient although it is
agkumot suna ti consequences.
client whatever understand reduced to
ules” as verbalized procedure will purpose of almost
be done and what is being manageable
by the mother.
demonstrate done and level.
first with a reduces
doll. concerns
O> Fear
associated
> Anxiety with the
unknown.
> Prefers to be

alone. COLLABORATIVE:

40
  This could help
 Informing the the physician
physician about to decide
the whether he will
fear/anxiety refer the
experienced by patient to a
the patient. specialist in
psychiatry.

P> Knowledge deficit

01-24-2006 INDEPENDENT: 01-24-2006
regarding condition,
Knowledge deficit Within the
treatment, self-care
is a condition in shift, the nearest  Review disease  Provides Level of
and discharge needs.
which the client or kin will be able to process, patient knowledge base attainment:
E> R/T unfamiliarity
the nearest kin understand the or parents from which Goal met
with the
don’t have enough disease process expectation. patient can
disease/condition.
knowledge about and will make informed
S> As evidenced by
the disease. This is participate in the therapy AEB: the
inaccurate follow
evidenced by lack treatment choices. mother acquired
through of instructions
of skill in regimen. sufficient
or asking questions
performing proper  Explain all  Inorder for knowledge on
regarding the disease.
hygiene and or procedures them to be the disease
taking done to the informed and process and
inappropriate patient. have knowledge participates on
medications or not with the the care of the
participating in procedure. patient.

41
treatment regimen.
(Medical Surgical  Explain the  For the faster
Nursing, 6th ed.) importance of recovery of
treatment the patient.
regimen.

COLLABORATIVE:

 Refer to the  The physician

physician so has a wider
that the knowledge
physician will about the
explain the disease in
disease terms of
process. management
and the
disease itself.

42
PROMOTIVE AND PREVENTIVE MANAGEMENT

PROMOTIVE

 Patient and family education is a fundamental component of

rehabilitation and ample opportunity for learning about the disease

its causes and prevention and the rehabilitation process should be

provided.

 Assess the family’s ability to continue in the rehabilitation of the

patient like financial matters.

 Assessment of the patient’s adherence to medication regimen

 Evaluate the patient’s environment including home and play area

and social settings.

 Institute teachings regarding the importance of hygiene and

nutrition.

 Modify diet as needed.

PREVENTIVE

 Screenings are an ideal opportunity to lower risk by identifying

high-risk individuals or groups and educating the patient’s and the

community about recognition of obstructive hydrocephalus.

 Proper adherence to medication regimen prevents further

complications and eventually death.

 An early hospitalization reduces mortality and morbidity of this

kind disease.

 Preventing the spread of the causative agent of bacterial

meningitis such as hygiene and proper management of antibiotics

reduces such kind of complications (e.g. Obstructive

hydrocephalus).

44
 DRUG STUDY

NAME OF DRUG ORFERED MECHANISM OF INDICATION CONTRAINDICATIO SIDE EFFECTS NURSING

DOSE ACTION N AND ADVERSE RESPONSIBILITIES
EFFECTS

Isonicotinic acid 200 mg/5 Unknown. Appears Actively growing Contraindicated to Seizures, optic  Always give isoniazid
hydrozide ml 5.5 OD to inhibit cell wall tubercle bacilli. patients with acute neuritis, hepatitis, with other
Isoniazide (INH) PO biosynthesis by hepatic disease or hemolytic anemia, antituberculotics to
interfering lipid isoniazid liver damage. jaundice. prevent development
and DNA of resistant
synthesis. organisms.
Bactericidal.  Explain the action of
the drug to the
watcher.
 Instruct client or
the watcher to take
drug exactly as
prescribed.
Pyrazinamide 250 mg/5 Unknown. Adjunct Contraindicated to Anorexia, nausea,
ml 9 ml OD Bactericidal treatment of patients hypersensitive vomiting, dysuria,  Tell the watcher
PO tuberculosis to drug and in those hyperuricemia, rash that the drug may
(Primary with hepatic disease. urticaria, pruritus. change the color of
complex). the urine, feces or

45
 sputum or saliva.

 Explain the action of

the drug.

 Instruct the watcher

or the patient to
report photophobia.

Rifampicin 200 mg / 5 Bactericidal Pulmonary Contraindicated in Headache, fatigue,

 Use cautiously in
ml 5.5 ml tuberculosis patients hypersensitive drowsiness,
patients with liver
OD PO (Primary to the drug. dizziness, anorexia,
disease.
complex) nausea, vomiting,
 Give 1 hour before or
wheezing,
2 hours after meals
discoloration of
for optimal
body fluids.
absorption.

Phenobarbital 30 mg ½ A barbiturate All forms of Contraindicated to Drowsiness,  Don’t stop drug

Sodium tab. BID that probably epilepsy/febrile patients hypersensitive lethargy, abruptly because
Phenobarbital PO depresses seizures. to barbiturates and in hypotension, nausea, seizure may worsen.
monosynaptic and those with history of vomiting, apnea,  Explain to the client
polysynaptic manifest or latent rashes. and the watcher

46
 transmission in porphyria. about the mechanism
the CNS and of action of the
increases the drug.
threshold for
seizure activity in
motor reflex.

Mannitol 40 ml every An osmotic Reduction of Contraindicated to Seizures, dizziness,  Monitor vital signs
8 hours IV diuretic that intraocular or patients hypersensitive hypotension, heart including fluid intake
increases the intracranial to drug and in those failure, tachycardia, and output. Instruct
osmotic pressure pressure. with anuria, severe blurred vision, dry client that he may
of glomerular dehydration and mouth, nausea and feel thirsty.
filtrate inhibiting metabolic edema. vomiting.  Instruct the watcher
tubular to report adverse
reabsorption of reactions and
water and discomfort at IV
electrolytes. site. Instruct also
the client.

Diazepam 3.2 mg IVF Unknown. A Adjunct in Contraindicated in Drowsiness,  Warn patient to

benzodiazepine seizure disorder. patients hypersensitive hypotension, blurred avoid activities that
that probably Status to drug. vision, diarrhea, require alertness.
potetiaurstes the epilepticus. nausea, vomiting,
effects of headache, fatigue,  Warn patient not to

47
 GABA.Depresses rash, urine abruptly stop drug
CNS at the limbic retention. because withdrawal
system and sub symptoms may occur.
cortical levels of
the brain and
suppresses the
spread of seizure
activity.

Ampicillin 800 mg IV An aminopenicillin Bacterial Contraindicated to Lethargy,  Explain the action of

every 6 that inhibits cell meningitis or patients hypersensitive hallucinations, the drug to the
hours wall synthesis septicemia. to drugs or other seizures, dizziness, patient and to the
ANST (-). during prenicillins. nausea, vomiting, watcher.
microorganism gastritis, anemia,  Before giving drug,
multiplication. agitation, wait for the result
confusion,stomatitis of the skin test.
.  Give drug 1-2 hours
before or 2-3 hours
after meals.

48
 PATIENT DISCHARGE INSTRUCTION SHEET

NAME OF PATIENT: NILCAR DOMINGO

ADDRESS: LASLASONG, STA. MARIA, ILOCOS SUR
AGE: 6 YEARS OLD
CIVIL STATUS: SINGLE
NAME OF INSTITUTION: GABRIELA SILANG GENERAL HOSPITAL
WARD: PEDIATRIC WARD
ADMITTING DIAGNOSIS: BACTERIAL MENINGITIS, PTB, TYPHOID FEVER, AND UTI
FINAL DIAGNOSIS: NON-COMMUNICATING HYDROCEPHALUS SECONDARY TO BACTERIAL MENINGITIS STAGE II

A. DIET

Name of Diet: Diet as Tolerated

Description: This diet has no restrictions as long as the patient can tolerate it.
Purpose: The patient needs energy, electrolyte replacement and enough calories so this diet was instructed.

DIET WITHOUT RESTRICTION IN MODERATION FOODS TO BE AVOIDED

Diet as Tolerated  All nutritious foods  None  None

49
DIETARY INSTRUCTIONS:

1. The patient can eat all he wishes as long as he can tolerate those foods.

2. Increase fluid intake to at least 6-8 glasses a day.

3. High fiber, high calorie and high protein diet is preferred for faster recovery of the patient.

B. TAKE HOME MEDICATIONS

NAME OF DOSAGE AND TIME FREQUENCY DURATION SIDE EFFECTS WHAT TO DO MEDICATIONS AND

DRUG THIS IS FOR FOODS TO BE

AVOIDED

Phenobarbital 30 mg ½ tab PO 8 am – 6 Twice a day 6 days Drowsiness,  Warn  Chloramphenicol,

 Adjunct therapy pm (BID) lethargy, parents not MAO inhibitors,
for febrile bradycardia, to stop Corticosteroids,
seizure hypotension, drug digoxin, TCA’s
nausea, abruptly.  No food is
vomiting,  Explain the contraindicated.
respiratory action of
depression. the drug.

50
 200 mg/5ml 3ml PO
Rifampicin  Anti Once a day 2 months  Avoid acetaminophen,
tuberculotic 8 am Headache,  Give 1 hour analgesics,
drug. drowsiness, before or 2 anticonvulsants, beta
generalized hours after blockers,chlorampheni
numbness, meals for col, diazepam,
anorexia, optimal narcotics.
nausea, absorption  No food is
vomiting, acute contraindicated.
renal failure,
hyperuricemia,

Isoniazid 200 mg/5 ml 3ml 8 am Once a day 2 months Peripheral  Instruct  Contraindicated with
PO neuropathy, the parents antacids, laxatives,
 Antituberculotic memory to give meperidine,
drug impairment, meds as anticonvulsants,
optic neuritis, prescribed phenytoin, disulfiram.
nausea,
vomiting,  Advise the  Foods containing
hyperglycemia. mother to Tyramine
give the
drug 1 hour
before or 2
hours after

51
 meals.

 Tell the
mother or
the patient
to report
adverse
reactions.
Pyrazinamide 250 mg/5ml 6.5 ml 8 am Once a day 2 months Malaise,  Use  None
PO anorexia, cautiously
 Anti nausea, in patients
tuberculotic vomiting, with DM.
drug dysuria,
hyperuricemia,
rashes and
urticaria

Streptomycin 500 mg PO 8 am Once a day 2 months Vomiting,  Obtain  Acyclovir,

 Anti biotic nausea, vertigo, specimen cephalosporins and
ototoxicity, for culture other

52
 leukopenia, and amonoglycosides.
apnea, sensitivity
anaphylaxis test before
giving the
first dose.
 Watch out
for signs
and
symptoms
of
superinfecti
on.

C. ACTIVITIES AND REHABILITATION

ALLOWED NOT ALLOWED MODIFIED

 Enough rest and sleep.  Strenuous activities  Walking

 Performing personal hygiene up to the  Performing active range of motion
optimum level of functioning. exercises.
 Consuming nutritious foods and adequate
diet.
 Involving in social interactions with other

53
 children
D. SPECIAL CARE INSTRUCTIONS

D.1. PROCEDURES AND TREATMENT

PROCEDURES AND TIME FREQUENCY DURATION

TREATMENT

 Continuing the prescribed 8 am Once a day 2 months

home medications.
e.g. PZA, INH, Rif, and
streptomycin

 Increase fluid intake At least 6-8 glasses a day lifetime

D.2. SYMPTOMS TO REPORT TO THE PHYSICIAN IMMEDIATELY

1. Body weakness
2. Seizure
3. Vertigo
4. Nausea and vomiting
5. Productive cough

54
E. FOLLOW UP CARE

REPORTED TO DATE PHYSICIAN REMARKS

(INSTITUTION)

Gabriela Silang General Hospital, February 10, 2006 Dr. Jean T. Mahor  Continue medications as
OPD prescribed.
 Increase fluid intake
 Socialize with other children.

________________________________________ ________________________________________
SIGNATURE OF PARENT/S OVER PRINTED NAME SIGNATURE OF STUDENT OVER PRINTED NAME

____________________________________
DATE AND TIME

55
 SUMMARY AND COPY OF UPDATES

The term hydrocephalus is derived from the Greek words "hydro"

meaning water and "cephalus" meaning head. As its 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

surrounding the brain and spinal cord. The excessive accumulation of CSF

results in an abnormal dilation of the spaces in the brain called ventricles.

This dilation causes potentially harmful pressure on the tissues of the brain.

The ventricular system is made up of four ventricles connected by

narrow pathways. Normally, CSF flows through the ventricles, exits into

cisterns (closed spaces that serve as reservoirs) at the base of the brain,

bathes the surfaces of the brain and spinal cord, and then is absorbed into

the bloodstream.

CSF has three important life-sustaining functions: 1) to keep the brain

tissue buoyant, acting as a cushion or "shock absorber"; 2) to act as the

vehicle for delivering nutrients to the brain and removing waste; and 3) to

flow between the cranium and spine to compensate for changes in

intracranial blood volume (the amount of blood within the brain).

The balance between production and absorption of CSF is critically

important. Ideally, the fluid is almost completely absorbed into the

bloodstream as it circulates; however, there are circumstances which, when

present, will prevent or disturb the production or absorption of CSF, or

which will inhibit its normal flow. When this balance is disturbed,

hydrocephalus is the result.

56
 BIBLIOGRAPHY
BOOKS:

Doenges,Marilyn et.al., Nursing Care Plans: Guidelines for Individualizing

Patient Care, 4th edition, 2002.

Lippincott, Williams & Wilkins, Nursing Student Drug Handbook, 10th edition,

2009

Port, Carol Mattson et.al., Pathophysiology: Concepts of Altered Health

Status, 6th edition, 2002

Smeltzer, Suzane et.al, Brunner & Suddarth’s Textbook of Medical Surgical

Nursing, Volume 1 & 2, 10th edition, 2002

INTERNET:

www.yahoo.com

www.google.com

57
APPENDICES

58
DOCUMENTATIONS

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