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 in diagnostic

imaging technology allow more accurate diagnoses in individuals with

1

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.

PATIENT’s PROFILE

CASE NUMBER:054435

NAME OF PATIENT: Nilcar Domingo

ADDRESS: Laslasong, Sta. Maria, Ilocos Sur

2

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

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

3

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 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).

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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

DATE JANUARY 22-24 HOME VISIT

(February 25,2005)

P

Conscious and coherent.

Nilcar is 6 years old and not yet studying.

There is no family background of obstructive hydrocephalus in their family.

The patient is very shy to express feelings.

The fourth stage of Erickson’s theory on G&D, which is Industry versus Inferiority, is altered as evidenced by, the child was not able to enhance his skills and was not

Nilcar showed psychosocial improvements like: he is now engaging social interactions with other children.

He was discharged last January 27,2006.

He started to regain his confidence.

He wanted to go to school already.

No more irritable maybe because he is now in their home.

He is now more active than before.

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able to socialize with other children.

Patient is irritable at times.

E

Experienced urinary incontinence and sometimes-urinary retention.

May only evacuate stool 3X a week due 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 formed).

He can control his urination already.

Returned to normal evacuation of formed stools with yellow color.

A/R

Can perform ADL up to the minimum level of functioning. E.g. combing the hair.

Experienced body weakness, headache and dizziness.

Had a disturbed sleep wake cycle due to headache.

Negative for edema.

Unable to play his toys because dizziness etc..

Showed independence in performing ADL but still there is a need to support him.

No more body weakness and dizziness felt by the patient.

He is playing with his playmates.

S

The patient has a decreased skin turgor e.g. dry skin

No known history of allergy to foods and medicines.

Skin color is pale. A dry lip was also

noted. Pink palpebral

conjunctiva was also observed.

The patient is

The skin turgor and appearance has improved.

He is not pale already.

He is experiencing seizure anymore.

Generally, the patient improved.

6

positive for seizure activity therefore there is a high risk for injury.

O

Negative for chest retractions.

With O2 inhalation connected via a nasal cannula level at 2LPM.

Experienced coughing at times (productive).

Respiratory rate of 40 cycles per minute was noted (not consistent)PR: 150 bpmT: 37.4-37.8oC.

Prefers semi-fowlers position.

Still experiencing productive cough.

DOB is negative.PR- 140 bpmT- 37RR- 30 cpm

N

Signs of dehydration were noted.

The patient’s appetite was decreased.

Experienced nausea, vomiting.

The patient has a decreased appetite.

With an IVF of D5 0.3 NaCl regulated at 30 gtts/minute.

DAT diet is maintained.

Regained his appetite.

He is not experiencing nausea and vomiting.

7

DIAGNOSTIC PROCEDURES

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

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The CSF should be clear and colorless

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

9

B. ACTUAL

NAME AND PURPOSE

OF PROCEDURE

ACTUAL VALUES NORMAL VALUES NURSING

IMPLICATIONS

NURSING

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 GLUTAMIC OXALOACETIC TRANSAMINASE

150.4 units Up to 25 units An increase in ALT

maybe used to

monitor the course of

hepatitis and other

liver disorder.

Explain the purpose

of the test to the

client or to the

watcher.

Instruct the watcher

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SGPT/SERUM GLUTAMIC PYRUVIC TRANSAMINASE

2.CEREBROSPINAL FLUID ANALYSIS (CSF ANALYSIS)01-10-2006 Usually specimens

122.3 units Up to 30 units

An increase in ALT

maybe due to the

effects of treatments

that maybe toxic to

the liver.

Elevated SGPT levels

due to the

destruction of liver

cells secondary to

toxic effects of drugs.

to monitor signs of

drug toxicity. (e.g.

blood dyscrasias,

dermatological

symptoms, drug

allergy,

hypersensitivity and

stomatitis.

Monitor results of the

test as indicated.

Interpret result and

inform the client’s

relatives.

Refer to the

physician concerning

the results of the

test.

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are obtained for cell count, culture, glucose and protein testing.

CSF COLOR/APPEARANCE

CELL COUNT:

WBC

RBC

Slightly

xanthochromatic

41 cells/mm3

Rare

Clear and colorless

0-5 cells/mm3

None

A deviation in color of

the CSF from clear to

xanthochromatic

indicates an

abnormality like

lesion in the choroids

plexus or blockage of

the flow of CSF.

Higher than the

normal value which

indicates bacterial

meningitis/encephalit

is

Explain the

significance of the

procedure to the

watcher or to the

patient.

Emphasize on

medication

compliance to

prevent further

infection like

meningitis.

Refer results to the

physician.

Proper positioning of

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GLUCOSE

TOTAL PROTEIN

3.URINALYSIS12-30-2005

To have a clinical information about the kidney functions and

1.18 mmol/L

173 mg/ L

2.75 – 4.4 mmol/L

150- 450 mg/ L

Traces of RBC in the

CSF indicate cerebral

contusion, laceration

or subarachnoid

hemorrhage.

Decrease amount of

glucose in the CSF is

an implication that

there is acute

meningitis or

subarachnoid

hemorrhage.

Normal

the patient after

lumbar puncture.

Patient is positioned

prone for 2 hours,

then flat on bed for 6

more hours, then

keeping patient flat

overnight.

If headache occurs

after LP, instruct

client to rest,

analgesic agents and

hydration may do.

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helps diagnose other diseases.

COLOR

PH

ALBUMIN

SPECIFIC GRAVITY

PUS CELLS

RBC

Yellow

5.0

negative

1.030

1-2

Negative

Amber/straw

4-6

negative

1.010-1.025

1-2

Negative

Signifies pyuria or

due to the

medications taken by

the client.

Normal

Normal

Signifies

concentrated urine

due to urinary

retention.

Normal

Explain the purpose

of the procedure and

talk to the level of

understanding to the

client.

Refer results to the

physician.

Obtain a good urine

specimen. It should

be midstream urine.

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4.CHEST X- RAY (01-11-2006)

To evaluate Respiratory status and to determine if the heart if there is cardiomegaly.

5.COMPUTERIZED AXIAL TOMOGRAPHY (01-05-2006)

Fine streaky

infiltrates seen in the

inner lung fields.

Hilar nodularities

seen

The heart is not

enlarged

Diaphragm and sulci

are intact

Bony thorax is

unremarkable

The lungs should be

clear.

There should be no

nodularities seen

Diaphragm and the

sulci should be intact.

There should be no

cardiomegaly.

CT scanning should

Normal

Primary pulmonary

tuberculosis is

considered.

Explain the

procedure to the

watcher or to the

client.

Check for baseline

vital signs as

ordered.

Provide information

regarding the

appearance of the

machine.

15

CT scanning is non invasive and painless and has a high degree of sensitivity for detecting lesions.

Multiple plain and

contrast enhanced

axial slices of the

head demonstrates

dilatation of the

lateral and 3rd

ventricles but normal

sized 4th ventricle.

No tumor, AV

malformations,

abscess or

dysthrophic

calcification seen.

No shift of the

septum pellucidum

noted

No fluid levels noted

within the paranasal

sinuses.

reveal no dilatation

of the ventricles, no

lesions or abscess

and there should be

no signs of IICP.

Results showed that

Obstructive

hydrocephalus

probably secondary

to ductal stenosis.

Explain that the

procedure is painless.

Explain the purpose

of the procedure to

the nearest kin.

Instruct client to lie

quietly throughout

the procedure.

Review of relaxation

techniques maybe

helpful for

claustrophobic

patients.

Sedation can be used

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The posterior fossa

structures are intact.

No neurologic signs

of increased

intraventricular

pressure

Intact orbits, skull

bone and calvarium.

if agitation,

restlessness or

confusion will

interfere with a

successful study.

NPO for 4 hours prior

to the procedure

should be instructed

to the client.

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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.

The Cerebellum overlies the pons and medulla, extending beneath

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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

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

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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 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

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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

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;

22

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

CAUSESObstruction of CSF flow

Congenital malformationSecondary to injury

Infection*Ductal stenosis*

Increases risk to the development of Obstructive Hydrocephalus

Blockage between the ventricular andSubarachnoid spaces

23

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

Gradual thinning of the brain substance

SIGNS AND SYMPTOMS

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

Signs and symptoms

Vomiting*Full

fontanellePapilledemaDecreased

pulse*Anorexia*

Convulsion*Drowsiness*Intellectual

DX Procedures

Radiologic studies*

CSF analysis*

Blood chemistry*CT scan*

MRIVentriculograp

24

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.

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

25

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 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.

26

NURSING CARE PLAN

CUESS & O

CEPHALOCAUD

AL

NURSING

DIAGNOSIS

NANDA APPROVED

ANALYSIS NURSING

OBJECTIVES

(SMART)

NURSING

INTERVENTION

S

RATIONALE EVALUATION

S>”Nasakit kanu

ti ulo na ken

maulaw ulaw

suna nga

tumakder idi

damu na nga

marikna toy sakit

na adding” as

verbalized by the

mother.

O> Pain rating

scale using the

P> Acute pain risk for

E> related to increase

IICP, tissue and nerve

trauma.

S> as evidenced by

changes in sleep

patterns.

> Dizziness

> Headache (on and

off)

Pain is considered an unpleasant sensory perception and emotional experience associated with actual or potential tissue damage. Acute pain lasts for a relatively short period of time and remits as the pathology resolves. Pain could be

01-22-06

Within the shift with proper medical and nursing management, the patient will verbalize decrease pain from 4 to at least 1 using the Wong baker Faces scale 0-5, 5 being the highest.

INDEPENDENT:

Monitor vital signs.

Document location and intensity of pain (0-5) and investigate changes in pain characteristics

Vital signs are general indicators of circulatory status and adequacy of perfusion.

Aids in evaluating need for and effectiveness of interventions. Changes may indicate

01-22-06

Level of attainment: goal partially met

AEB: Pain experienced by the patient is reduced from severe to mild.

27

Wong baker

faces rating scale

reveals that the

level of pain is

grade 4(It hurts a

whole lot more).

> The patient

looks weak.

> Dizzy

> On and Off

headache

attributed to IICP because as the pressure increases in the cranial vault, there is no other way to release the pressure; as a result there is compression of nerves and the brain itself (Medical Surgical Nursing 6th ed.)

.

Proper positioning (semi-fowlers).

Avoid coughing or straining.

COLLABORATIVE:

Administer medications

developing complications.

With this kind of position, pressure will be lessened because it prevents the congestion of blood in the head region.

Coughing or straining will further increase ICP.

Analgesics relieve pain by blocking the pain impulses at

28

P> Injury risk for

E> r/t muscle

weakness, dizziness

and convulsion or

seizure.

S> as evidenced by

(not applicable,

presence of signs and

CausesPresence of

health threatsDizzinessSeizure

Body is lacking of energy to sustain

body’s needs

01-22-2006 Within my shift, the mother will be able to acquire knowledge regarding the consequences of falling and injury with proper health teachings.

as ordered e.g. analgesics and antibiotics.

Refer to the physician regarding the pain experienced by the client for further diagnosis.

INDEPENDENT:

Provide safe environment or room for the client

Advise the

the pain receptor sites.

By referring to the physician, he may order an appropriate diagnostic procedure to determine the cause of the pain.

Safe room environment helps eliminate the risk for injury.

Bedside rails may help prevent the

01-22-2006

Level of attainment: Goal met.

AEB: The mother understands the health teachings regarding the

29

symptoms establishes

an actual diagnosis.Body weakness

Risk for falling

Possible consequences

like injury(med surge Nsg.6th ed)

mother to raise the bedside rails during seizure

Observe signs of seizure disorders

COLLABORATIVE:

Administer anti-convulsive drugs.

patient from falling from the bed.

Assessing the time and correct symptoms of seizure may help in the diagnosis of what kind of seizure disorder that the client had.

Anti convulsive drugs stabilizes nerve membranes throughout the CNS to decrease excitability and hyper excitability to

risk of injury to the patient.

30

S>Agsarwa

sarwa pay isuna

nga kanayon

added by the

mother.

O> The patient

appears very

weak.

P> Imbalanced

nutrition less than

body requirements

E> related to nausea,

vomiting and

anorexia.

S> As evidenced by

weight loss, weakness

and dizziness

> Nausea

Imbalance nutrition refers to a relative or absolute deficiency or excess of one or more essential nutrients

Body can’t sustain normal

function

Deficiencies arise

01-24-2006 Within 2 days, Nilcar will show improvement in nutrition as evidenced by nausea and vomiting free state and increase consumption of at least half of the served foods.

Consult the pharmacist with regards to site, time and delivery of drugs that might have action adversely contraindicated to the patient.

INDEPENDENT:

Instruct the relatives to give plain crackers to the client.

Encourage the client to drink

stimulation.

The pharmacist together with the physician knows the correct formulations of drugs and their actions.

Crackers will alleviate nausea and vomiting.

This may help to replace fluids and electrolyte deficiencies due to vomiting

01-26-2006

Level of Attainment: Goal partially met.

AEB: The patient still experiencing N/V at times and the appetite is moderately improved as

31

> He has a dry

skin and has a

decreased skin

turgor.

> The clients

weight is 17kgs.

Signs and symptoms of imbalanced

nutrition Weight loss Growth

retardation Mental

retardation (Medical Surgical Nursing 6th ed.)

fluids with electrolytes such as Gatorade and other nutritionally enriched drinks or shakes unless contraindicated

Encourage small frequent feeding.

Promote oral care.

Small frequent feeding may help to decrease gastric motility because a full stomach excites to digest the contents thus less hyper motility.

The taste in the mouth is unpleasant; therefore oral care is needed to instruct to

evidenced by one fourth of the served food is consumed.

32

COLLABORATIVE:

Administer intravenous fluids as ordered.

Administer anti- emetics

lessen the unpleasant taste.

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

Anti-emetic drugs works by reducing the hyperactivity

33

P> Fluid volume

deficit

E> related to

inadequate intake of

food and fluids,

vomiting and diuretic

use.

S> as evidenced by

dry skin and mucous

membrane

> Decreased skin

turgor.

Fluid volume deficit is characterized by a decrease in extra cellular fluid including circulating blood volume due to loss of G.I. fluids, polyuria, sweating due to fever and exercise and third space losses.(Med & Surge Nursing 6th ed).

01-24-2006 Within 2 days, Nilcar will be free from vomiting and the skin turgor will improved and the intake and output will normalized.

as ordered if vomiting and nausea persist.

Work with other health care provider as a group. e.g. forwarding lab request and orders.

INDEPENDENT:

Monitor vital signs.

Encourage patient to increase fluid intake unless contraindicate

of the vomiting reflex.

Inorder to come up with the best possible care to the patient.

Vital signs reflects changes within the body

By increasing fluid intake, the lost water and electrolytes will be replenished.

01-26-2006

Level of attainment: goal partially met.

AEB: Patient is still experiencing nausea and vomiting and the skin turgor is moderately improved. Level of hydration also improved.

34

S> “Manipud idi

naospital isuna

ket managbut

buteng met

> Weakness

P> Fear/anxiety

E> R/T changes in

health status,

possibility of surgical

procedures and

Anxiety is emotional illness characterized by fear, autonomic neuron system symptoms and avoidance behavior (ABC’s of Psychiatric

01-24-2006

Within the shift, the patient will be able to demonstrate appropriate range of feelings and lessened fear or the anxiety will be

d

Monitor I & O

Administer IV fluids as ordered

COLLABORATIVE:

Monitor electrolyte level specifically Sodium

INDEPENDENT:

Sustained diuresis could cause patients total fluid volume to become depleted.

Replaces fluid and electrolyte losses to prevent electrolyte imbalances.

As fluid pulled from extracellular spaces, sodium may follow the shift causing hyponatremia.

01-24-2006

Level of attainment: Goal partially met.

AEB: The patient still manifest fear

35

isunan, no kuma

adda umasideg

kenyana nga

saan na nga am-

ammu ket

agkumot suna ti

ules” as

verbalized by the

mother.

O> Fear

> Anxiety

> Prefers to be

alone.

embarrassment.

S> as evidenced by

fear of non-specific

consequences.

P> Knowledge deficit regarding condition, treatment, self-care and discharge needs.E> R/T unfamiliarity

Nursing, Ray A. Gapuz).

Knowledge deficit is a condition in which the client or the nearest kin don’t have enough knowledge about

reduced to a manageable level

01-24-2006 Within the shift, the nearest kin will be able to understand the disease process

Establish trusting relationship to the patient.

Explain to the client whatever procedure will be done and demonstrate first with a doll.

COLLABORATIVE:

Informing the physician about the fear/anxiety experienced

Demonstrates concern and willingness to help the client. Encourages discussion of sensitive subjects.

Helps patient understand purpose of what is being done and reduces concerns associated with the unknown.

This could help the physician to decide whether he will refer the patient to a specialist in

although it is reduced to almost manageable level.

01-24-2006

Level of attainment: Goal met

AEB: the mother

36

with the disease/condition.S> As evidenced by inaccurate follow through of instructions or asking questions regarding the disease.

the disease. This is evidenced by lack of skill in performing proper hygiene and or taking inappropriate medications or not participating in treatment regimen. (Medical Surgical Nursing, 6th ed.)

and will participate in the treatment regimen.

by the patient.

INDEPENDENT:

Review disease process, patient or parents expectation.

Explain all procedures done to the patient.

Explain the importance of treatment regimen.

COLLABORATIVE:

psychiatry.

Provides knowledge base from which patient can make informed therapy choices.

Inorder for them to be informed and have knowledge with the procedure.

For the faster recovery of the patient.

The physician has a wider

acquired sufficient knowledge on the disease process and participates on the care of the patient.

37

Refer to the physician so that the physician will explain the disease process.

knowledge about the disease in terms of management and the disease itself.

38

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).

40

DRUG STUDY

NAME OF DRUG

ORFERED DOSE

MECHANISM OF ACTION

INDICATION CONTRAINDICATION

SIDE EFFECTS AND ADVERSE

EFFECTS

NURSING RESPONSIBILITIES

Isonicotinic acid hydrozide

Isoniazide (INH)

Pyrazinamide

200 mg/5 ml 5.5 OD PO

250 mg/5 ml 9 ml OD PO

Unknown. Appears to inhibit cell wall biosynthesis by interfering lipid and DNA synthesis. Bactericidal.

Unknown. Bactericidal

Actively growing tubercle bacilli.

Adjunct treatment of tuberculosis (Primary complex).

Contraindicated to patients with acute hepatic disease or isoniazid liver damage.

Contraindicated to patients hypersensitive to drug and in those with hepatic disease.

Seizures, optic neuritis, hepatitis, hemolytic anemia, jaundice.

Anorexia, nausea, vomiting, dysuria, hyperuricemia, rash urticaria, pruritus.

Always give isoniazid with other antituberculotics to prevent development of resistant organisms.

Explain the action of the drug to the watcher.

Instruct client or the watcher to take drug exactly as prescribed.

Tell the watcher that the drug may change the color of the urine, feces or sputum or saliva.

Explain the action of the drug.

41

Rifampicin

Phenobarbital Sodium

Phenobarbital

Mannitol

200 mg / 5 ml 5.5 ml OD PO

30 mg ½ tab. BID PO

40 ml every 8

Bactericidal

A barbiturate that probably depresses monosynaptic and polysynaptic transmission in the CNS and increases the threshold for seizure activity in motor reflex.

An osmotic

Pulmonary tuberculosis (Primary complex)

All forms of epilepsy/febrile seizures.

Reduction of

Contraindicated in patients hypersensitive to the drug.

Contraindicated to patients hypersensitive to barbiturates and in those with history of manifest or latent porphyria.

Headache, fatigue, drowsiness, dizziness, anorexia, nausea, vomiting, wheezing, discoloration of body fluids.

Drowsiness, lethargy, hypotension, nausea, vomiting, apnea, rashes.

Instruct the watcher or the patient to report photophobia.

Use cautiously in patients with liver disease.

Give 1 hour before or 2 hours after meals for optimal absorption.

Don’t stop drug abruptly because seizure may worsen.

Explain to the client and the watcher about the mechanism of action of the drug.

42

Diazepam

Ampicillin

hours IV

3.2 mg IVF

800 mg IV every 6 hours ANST (-).

diuretic that increases the osmotic pressure of glomerular filtrate inhibiting tubular reabsorption of water and electrolytes.

Unknown. A benzodiazepine that probably potetiaurstes the effects of GABA.Depresses CNS at the limbic system and sub cortical levels of the brain and suppresses the spread of seizure activity.

An aminopenicillin

intraocular or intracranial pressure.

Adjunct in seizure disorder.Status epilepticus.

Bacterial meningitis or septicemia.

Contraindicated to patients hypersensitive to drug and in those with anuria, severe dehydration and metabolic edema.

Contraindicated in patients hypersensitive to drug.

Seizures, dizziness, hypotension, heart failure, tachycardia, blurred vision, dry mouth, nausea and vomiting.

Drowsiness, hypotension, blurred vision, diarrhea, nausea, vomiting, headache, fatigue, rash, urine retention.

Monitor vital signs including fluid intake and output. Instruct client that he may feel thirsty.

Instruct the watcher to report adverse reactions and discomfort at IV site. Instruct also the client.

Warn patient to avoid activities that require alertness.

Warn patient not to abruptly stop drug because withdrawal symptoms may occur.

43

that inhibits cell wall synthesis during microorganism multiplication.

Contraindicated to patients hypersensitive to drugs or other prenicillins.

Lethargy, hallucinations, seizures, dizziness, nausea, vomiting, gastritis, anemia, agitation, confusion,stomatitis.

Explain the action of the drug to the patient and to the watcher.

Before giving drug, wait for the result of the skin test.

Give drug 1-2 hours before or 2-3 hours after meals.

PATIENT DISCHARGE INSTRUCTION SHEET

NAME OF PATIENT: NILCAR DOMINGOADDRESS: LASLASONG, STA. MARIA, ILOCOS SURAGE: 6 YEARS OLDCIVIL STATUS: SINGLENAME OF INSTITUTION: GABRIELA SILANG GENERAL HOSPITALWARD: PEDIATRIC WARDADMITTING DIAGNOSIS: BACTERIAL MENINGITIS, PTB, TYPHOID FEVER, AND UTIFINAL DIAGNOSIS: NON-COMMUNICATING HYDROCEPHALUS SECONDARY TO BACTERIAL MENINGITIS STAGE II

44

A. DIET

Name of Diet: Diet as ToleratedDescription: 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

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

DRUG

DOSAGE AND

THIS IS FOR

TIME FREQUENCY DURATION SIDE

EFFECTS

WHAT TO

DO

MEDICATIONS AND

FOODS TO BE

AVOIDED

Phenobarbital

30 mg ½ tab PO Adjunct

8 am – 6 pm

Twice a day (BID)

6 days Drowsiness, lethargy,

Warn parents

Chloramphenicol, MAO inhibitors,

45

Rifampicin

Isoniazid

therapy for febrile seizure

200 mg/5ml 3ml PO Anti

tuberculotic drug.

200 mg/5 ml 3ml PO Antituberculoti

c drug

8 am

8 am

Once a day

Once a day

2 months

2 months

bradycardia, hypotension, nausea, vomiting, respiratory depression.

Headache, drowsiness, generalized numbness, anorexia, nausea, vomiting, acute renal failure, hyperuricemia,

Peripheral neuropathy, memory impairment, optic neuritis, nausea, vomiting, hyperglycemia.

not to stop drug abruptly.

Explain the action of the drug.

Give 1 hour before or 2 hours after meals for optimal absorption

Instruct the parents to give meds as prescribed

Advise the mother to give the

Corticosteroids, digoxin, TCA’s

No food is contraindicated.

Avoid acetaminophen, analgesics, anticonvulsants, beta blockers,chloramphenicol, diazepam, narcotics.

No food is contraindicated.

Contraindicated with antacids, laxatives, meperidine, anticonvulsants, phenytoin, disulfiram.

Foods containing Tyramine

46

Pyrazinamide

Streptomycin

250 mg/5ml 6.5 ml PO Anti

tuberculotic drug

500 mg PO Anti biotic

8 am

8 am

Once a day

Once a day

2 months

2 months

Malaise, anorexia, nausea, vomiting, dysuria, hyperuricemia, rashes and urticaria

Vomiting, nausea, vertigo, ototoxicity, leukopenia,

drug 1 hour before or 2 hours after meals.

Tell the mother or the patient to report adverse reactions.

Use cautiously in patients with DM.

Obtain specimen for culture and

None

Acyclovir, cephalosporins and other amonoglycosides.

47

apnea, anaphylaxis

sensitivity test before giving the first dose.

Watch out for signs and symptoms of superinfection.

C. ACTIVITIES AND REHABILITATION

ALLOWED NOT ALLOWED MODIFIED

Enough rest and sleep. Performing personal hygiene up to the

optimum level of functioning. Consuming nutritious foods and

adequate diet. Involving in social interactions with

other children

Strenuous activities Walking Performing active range of motion

exercises.

D. SPECIAL CARE INSTRUCTIONS

D.1. PROCEDURES AND TREATMENT

48

PROCEDURES AND TREATMENT

TIME FREQUENCY DURATION

Continuing the prescribed home medications.e.g. PZA, INH, Rif, and streptomycin

Increase fluid intake

8 am Once a day

At least 6-8 glasses a day

2 months

lifetime

D.2. SYMPTOMS TO REPORT TO THE PHYSICIAN IMMEDIATELY

1. Body weakness2. Seizure3. Vertigo4. Nausea and vomiting5. Productive cough

E. FOLLOW UP CARE

REPORTED TO (INSTITUTION)

DATE PHYSICIAN REMARKS

Gabriela Silang General Hospital, OPD

February 10, 2006 Dr. Jean T. Mahor Continue medications as prescribed.

Increase fluid intake Socialize with other

49

children.

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

____________________________________DATE AND TIME

50

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.

BIBLIOGRAPHY

BOOKS:

52

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

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