I.

INTRODUCTION

1. Description of the Disease

Hyperbilirubinemia (also known as

jaundice) is an increased level of serum

bilirubin in the blood. When red blood

cells break down, a substance called

bilirubin is formed. Newborn are not

easily able to get rid of the bilirubin and it

can build up in the blood and other tissues

and fluids of the baby's body.

Hyperbilirubinemia is one of the most common causes of jaundice in the neonate. A benign

self-limited condition, in most often is related to the developmental state of the neonate.

Historically, management guidelines were derived from studies on bilirubin toxicity in infants

with hemolytic disease. More recent recommendations support the use of less intensive therapy

in healthy term newborns with jaundice. Phototherapy should be instituted when the total serum

bilirubin level is at or above 15 mg per dL (257 mol per L) in infants 25 to 48 hours old, 18 mg

per dL (308 mol per L) in infants 49 to 72 hours old, and 20 mg per dL (342 mol per L) in infants

older than 72 hours. Few term newborns with hyperbilirubinemia have serious underlying

pathology. Jaundice is considered pathologic if it presents within the first 24 hours after birth, the

total serum bilirubin level rises by more than 5 mg per dL (86 mol per L) per day or is higher

than 17 mg per dL (290 mol per L), or an infant has signs and symptoms suggestive of serious

1
illness. The management goals are to exclude pathologic causes of hyperbilirubinemia and

initiate treatment to prevent bilirubin neurotoxicity.

Neonatal hyperbilirubinemia, defined as a total serum bilirubin level above 5 mg per dL (86

μmol per L), is a frequently encountered problem. Although up to 60 percent of term newborns

have clinical jaundice in the first week of life, few have significant underlying disease. However,

hyperbilirubinemia in the newborn period can be associated with severe illnesses such as

hemolytic disease, metabolic and endocrine disorders, anatomic abnormalities of the liver, and

infections.

Jaundice typically results from the deposition of unconjugated bilirubin pigment in the skin

and mucus membranes. Depending on the underlying etiology, this condition may present

throughout the neonatal period. Unconjugated hyperbilirubinemia, the primary focus of this

article, is the most common form of jaundice encountered by family physicians.

Depending on the cause of the hyperbilirubinemia, jaundice may appear at birth or at any

time afterward. The following are the most common symptoms of hyperbilirubinemia. However,

each baby may experience symptoms differently. Symptoms may include: yellow coloring of the

baby's skin (usually beginning on the face and moving down the body)poor feeding or lethargy

During pregnancy, the placenta excretes bilirubin. When the baby is born, the baby's liver

must take over this function. There are several causes of hyperbilirubinemia and jaundice which

include the following:

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 • PHYSIOLOGIC JAUNDICE

Physiologic jaundice occurs as a "normal" response to the baby's limited ability to excrete

bilirubin in the first days of life.

• BREAST MILK JAUNDICE

About 2 percent of breastfed babies develop jaundice after the first week. Some develop

breast milk jaundice in the first week due to low calorie intake or dehydration.

• JAUNDICE FROM HEMOLYSIS

Jaundice may occur with the breakdown of red blood cells due to hemolytic disease of

the newborn (Rh disease), having too many red blood cells, or bleeding.

• JAUNDICE RELATED TO INADEQUATE LIVER FUNCTION

Jaundice may be related to inadequate liver function due to infection or other factors.

About 60 percent of term newborns and 80 percent of premature babies develop jaundice.

Infants of diabetic mothers and of mothers with Rh disease are more likely to develop

hyperbilirubinemia and jaundice.

Infants without identified risk factors rarely have total serum bilirubin levels above 12 mg

per dL (205 μ mol per L). As the number of risk factors increases, the potential to develop

markedly elevated bilirubin levels also increases.

Common risk factors for hyperbilirubinemia include fetal-maternal blood group

incompatibility, prematurity. And a previously affected sibling, Cephalohematomas, bruising,

and trauma from instrumented delivery may increase the risk for serum bilirubin elevation.

3
Delayed meconium passage also increases the risk. Infants with risk factors should be monitored

closely during the first days to weeks of life.

Hyperbilirubinemia Global statistics

From July 2002 to June 2004, 367 cases of severe neonatal hyperbilirubinemia were

reported. Of these, 258 met the inclusion criteria for this study, for an estimated incidence of 1 in

2480 live births. There were 42 duplicate reports, 48 that did not fulfill the case definition and 19

(6.9% of cases that met the definition) that had incomplete data. The mean peak bilirubin level

reported was 471 µmol/L (standard deviation [SD] 76 µmol/L, range 156–841 µmol/L). The

baseline demographic characteristics of the study group are presented in Table 1. The mean

maternal age was 29.8 (SD 4.3) years, and 91 women (35.3%) were pregnant with their first

child. The most common maternal ethnicity reported was white (55.4%) followed by Asian

(24.3%), Aboriginal (7.6%), black (5.2%), Middle Eastern (4.0%), Latin American (2.8%) and

other (1.0%).

Reasons for Choosing the Case:

The group had chosen the Hyperbilirubinemia as the case to be studied. We agreed and

decide for this case because the patient is recently admitted at that time and the student nurses

could still have a better assessment and monitoring for a length of time. This is an advantage for

the group in facilitating and scrutinizing the cause of the problem which is less experienced by

pediatric patient. Eventually, it will give us a better understanding of the disease and know the

importance of being a competent student nurses as how we provide health teachings and perform

our independent nursing functions. May this study will also be a future reference that may help

other researchers/student nurses in doing/completing their requirements.

4
CURRENT TRENDS

1. Universal Screening Lowers Risk of Severe Jaundice in Infants

ScienceDaily (Sep. 30, 2009) — Screening all newborns for excessive bilirubin in the

blood can significantly decrease the incidence of severe jaundice which, in extreme cases, can

lead to seizures and brain damage, according to researchers at UCSF Children's Hospital and

Kaiser Permanente's Division of Research in Oakland, CA.

2. Don't Rely On Jaundiced Eye for Assessing Newborns, New Research Says

ScienceDaily (Apr. 1, 2009) — For hundreds of years, doctors, nurses and midwives

have visually examined newborn babies for the yellowish skin tones that signify jaundice,

judging that more extensive jaundice carried a greater risk of illness.

3. Prophylactic effect of clofibrate in low birth weight neonates’ hyperbilirubinemia

Study shows that clofibrate has a prophylactic effect to neonates with hyperbilirubinemia.

And that the duration of phototherapy in clofibrate group was lowered than the control group

according to studies.

2. Objectives

Learning Objectives: After a week of accomplishing this case study, the student nurses will be

able to:

Cognitive:

 Define Hyperbilirubinemia

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  Identify the modifiable and non-modifiable factors as well as the signs and symptoms of

the stated complication, treatment and preventions of hyperbilirubinemia.

 Grasp knowledge about the advancement of the complication, their effects and

manifestations

 Analyze and interpret laboratory results and relate them to the pathology of the diseases.

 Identify the treatment modalities available.

 Formulate nursing diagnoses related and significant to patient’s condition.

Affective:

 Empathize with the patient’s current condition.

 Provide comfort to the client as he copes up with her current situation.

Psychomotor:

 Demonstrate to the significant other the appropriate interventions to the patient.

 Assist the significant other on how to be acquainted with the patient’s actual condition.

 Provide health teachings to the support people that would help improve the patient’s

condition and administer medications as ordered and explain the need and purpose of the

treatment.

 Document pertinent data and information about the patient.

6
 II. NURSING HISTORY

1. Personal History

a. Demographic Data

Baby Supti is a week old infant; male, only child of Mr. and Mrs. Bakat who are

living in Batasan, Arayat Pampanga. He was born last 23 February 2010 in Emigdio C.

Cruz Memorial Hospital (ECCMH) and was delivered via normal spontaneous delivery.

Mrs. Baktong and Baby Supti stayed in the hospital for three (3) days until 26th of

February 2010 at 3 o’clock pm. But around 5 o’clock in the afternoon, she noticed that

Baby Supti’s entire body turned out to be yellowish and was immediately returned to

hospital and admitted on same date with the diagnosis of Hyperbilirubinemia secondary

to sepsis.

Informant: Mrs. Baktong, mother of the patient

b. Socioeconomic and Cultural Factors

b.1. Occupation and Mode of Expenditure

Mr. Bakti is the one who works in the family. He is a market vendor. He earns 3000

php/month. According to Mrs. Baktong, her husband’s income is not enough for them especially

at the present that they already have a child. Mrs. Baktong worked as a dressmaker in their

community who earns 2000php/ month prior to her conception. And since their family is already

7
growing Mr. Bakti need to work hard by rendering overtime to support the needs of his family.

Aside from sustaining their daily basic needs they also have to consider other monthly payables

such as water and electric bills. Mrs. Baktong emphasized that if they do not have any food to eat

they will just asked from the parents of Mr. Bakti,

b.2. Educational Attainment

Mr. Bakti is a high school graduate in Batasan High School. He did not continue his

studies because his parents do not have enough money to send him to school. The parents have

the notion that Mr. Bakti is not interested in going to school then because of peer pressure that

influences him to take for granted his study. Mrs. Baktong is also a high school graduate in

Batasan High School and was not able continue her studies as well due to financial constraints.

As an eldest child, she started working early to help her parents from work.

b.3. Religious Affiliation

Mr. and Mrs. Bakat is both Catholic. Their religion was started from the mother and

father of both sides. They also follow and practice some teachings of the Roman Catholic like

respecting the older ones and other more.

b.4. Cultural Factors affecting the Health of the Family

According to Mrs. Baktong, their family believes on ‘hilot’, ’tawas’ and herbal doctors.

This may affect the health condition of the family because they prefer to seek first the advice of

herbal doctors until his/her condition become worse. They tend to continue this kind of practice

because of financial crisis that they are experiencing now. The moment their condition becomes

worst and the herbal doctors could not cure their disease anymore that is the time they will send

him/her to the hospital for check up.

8
2. Family- Health Illness

a. Hereditary Diseases in the Family

According to Mrs. Baktong, the family does not have any hereditary disease. Any of both

sides of the family die because of old age and accident.

Lolo Tits Lola Peks Lolo Toy Lola Ting

LOL BRB Baktong Bakti LMAO BB

Baby Supti

- With hyperbilirubinemia

b. Existing diseases in the family

Mr. Bakti’s mother is still alive and in good health condition and his father died because

of old age. Mrs. Baktong’s father does not have any disease at present and her mother already

died because of old age also.

3. History of Present Illness

9
 a. Diseases or Ailments relevant to patient’s condition

Since Baby Supti is only 7 days old, her immune system is still not stable to fight for

diseases. According to Mrs. Baktong, when she gave birth to Baby Supti he has a normal brown

skin and without any yellowish discoloration on his body. That is why the physician advised

them to go home last 26 February 2010 at 3 o’clock in the afternoon.

b.Diseases not related to patient’s condition

Baby Supti does not have any other history of diseases which are not related to his condition

at present.

4. History of Present Illness

a. Chief Complaint

When Mrs. Baktong finally went home he noticed that Baby Supti was in good condition,

evident with a normal brown skin. After a few hours, she decided to bring back her son to

Emigdio C. Cruz Memorial Hospital last 26 February 2010 at 5:00 pm in the afternoon due to

yellow discoloration of his body.

b. Sequence of the Appearance of signs and symptoms

According to Mrs. Baktong they stayed in the hospital for three (3) days from February

23, at 3:00 in the afternoon of 26th of February the physician told Mrs. Baktong that they can go

home. Upon arriving in their home Baby Supti is just like any new born, he cries whenever he is

hungry and he sleep most of the time. At 4:00 pm in the afternoon Mrs. Baktong observed that

there is something wrong with the color of the skin of her baby and that she ignores what she

noticed. At 4:15 she noticed again that her baby is so restless and that he always cries, this time

she thought that her baby is only hungry and she breastfed him. The baby stops crying and sleep

10
again. Around 5:00 in the afternoon Mrs. Baktong noticed that her baby is already had a yellow

discoloration on his entire body. Mrs. Baktong calls for a help and they brought Baby Supti to

the hospital.

III. PHYSICAL ASSESSMENT (IPPA-CEPHALOCAUDAL APPROACH)

March 02, 2010

Vital signs

Temperature- 35.7°C

Respiratory Rate- 56bpm

Heart rate-118 bpm

Skin

 (+) Lanugo

 Skin color is pale yellow

 When pinched, skin goes back on its previous state after 1 sec.

 With birthmarks at the buttocks

Hair and scalp

 Black sticky hair

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  Has thin hair, not evenly distirbuted

 Absence of lesions and sores

 No dandruff

Nails

 Smooth nail contour and texture

 Capillary refill after 2 sec.

Head and neck

 Head is symmetrical to the body

 With a circumference of 35 cm.

 Upon palpation, anterior and posterior fontanel are soft

 With few visible veins at the frontal area

 No nodules or masses palpated

 Symmetric facial features and movements

Eyes

 Eyebrows are dark brown in color, symmetrical and parallel

 Eyelashes are dark brown, evenly distributed and turned outward

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  Eyelids are symmetrical in color, looseness with no palpable masses

 Icteric sclera

 Irish are black, round, symmetrical and proportional to the size of the eyes

Ears

 Ears of equal size and same appearance

 Firm cartilage

 Ears are mobile, not tender

 Recoils after it is folded

 No cerumen or drainage noted

Nose

 Symmetrical and straight

 Without sticky discharges

 With milia

 No tenderness palpated on the sinus area

Respiratory System

 Chest circumference is 32 cm.

 Symmetric chest

 Chest wall intact

 No lumps, masses or areas of tenderness

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  Use of accessory muscles upon breathing

Cardiovascular System

 Normal heart sounds upon auscultation

 Capillary refill after 2 seconds

 Regular and rhythmic heart rate

Digestive System

 Abdominal circumference of 35 cm.

 Unblemished abdominal contour

 Flat abdominal contour

 No tenderness, lumps or masses palpated

Musculoskeletal System

 (+) moro/startle reflex

 (+) palmar grasp reflex

 (+) suckling reflex

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 IV. DIAGNOSTIC AND LABORATORY PROCEDURES

Diagnostic / Indications Date Results Normal Analysis and

Laboratory or Purpose Ordered Values (units Interpretation
Procedures Date Results used in the of the Results
were hospital)
released
Hematology Hematology February 27, Leucocyte 11,200/cu.mm 5-10,000
tests can help 2010 count
diagnose Hemoglobin 13.14 12-16
anemia, Hematocrit 40 40-50
hemophilia, Platelets 220,000 150-500,000
blood- Segmenters 75% 55-70
clotting Lymphocytes 25% 25-35
disorders, and
leukemia.
Complete Hemoglobin February 27, 15.4 12-16 Hemoglobin is
Blood Count
measures the 2010 in the normal
test (CBC)
Hemoglobin amount of range.
oxygen
carrying
protein in the
blood.
White Blood This is done February 27, 4,900 5-10,000 The WBC is
Cells
to determine 2010 slightly lower
the presence than the
of infection normal value
and
inflammation.

Hematocrit Hematocrit is February 46 40-50 The

15
 tested to 27,2010 Hematocrit is
monitor the within the
patient’s normal range
hydration
status and
oxygen level.
Platelet To identify February 200,000 150,000- Platelet count
the cause of 27,2010 500,000 is within
excess normal range
bleeding.
Eosinophils Eosinophil February 1 2-4 Eosinophils is
test is used to 27,2010 slight lower
diagnose than the
allergy, drug normal range
reactions,
Parasitic
infections,
collagen
disease,
Hodgkins
disease,
Myelo-
proliferative
diseases.
Monocytes This test is February 1 2-8 Eosinophils is
used to 27,2010 slight lower
evaluate and than the
manage blood normal range
disorders,
certain
problems
with the

16
 immune
system, and
cancers.
Lymphocytes Are responsible February 44 25-35 Lymphocytes
for the storage
27,2010 is higher than
of immunologic
normal, it
memory. This
means that a
indicates that
second contact the patient has
with an antigen infection
elicits an
accelerated and
increased
response.
Segmenters This is to February 54 55-70 The level of
identify the 27,2010 segmenters is
levels of slightly below
mature WBC the normal
whether it is values which
increase or comparison
decrease together with
together with the WBC.
the WBC.

Nursing Responsibilities:

Prior:

• Explain test Procedures; explain that slight discomfort maybe felt when skin is punctured.

• Avoid stress if possible because altered physiologic status influences and changes normal

hemogram values.

17
 • Dehydration or over dehydration can dramatically alter values, for example large volume

of IV fluids can dilute the blood and values will appear as lower counts. The presence of

either of these states should be communicated to the laboratory.

• Fasting is not necessary; however fat meals may alter some test results as a result of

lipidemia.

During the procedure

• Prepare all the equipments to be used.

• Tell the mother when to insert the needle to her baby.

• Assist the patient if necessary

• Ensure a sterile blood sample from the patient.

After:

• Apply manual pressure and dressings to the puncture site on removal of the needle

• Monitor the puncture site for oozing or hematoma formation Maintain pressure dressings

on the site if necessary. Notify physician of unusual problems with bleeding.

• Resume normal activities and diet.

• Bruising on the puncture site is not uncommon; Signs of inflammation are unusual and

should be reported if the inflamed area appears larger, if red streaks develop or if

drainage occurs.

V. THE PATIENT AND HER ILLNESS

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BILIRUBIN

Bilirubin (formerly referred to as hematoidin) is the yellow breakdown product of normal

heme catabolism. Heme is found in hemoglobin, a principal component of red blood cells.

Bilirubin is excreted in bile and urine, and elevated levels may indicate certain diseases. It is

responsible for the yellow color of bruises, urine, and the yellow discoloration in jaundice.

Bilirubin is created by the activity of biliverdin reductase on biliverdin, a green

tetrapyrrolic bile pigment which is also a product of heme catabolism. Bilirubin, when oxidized,

reverts to become biliverdin once again. This cycle, in addition to the demonstration of the

potent antioxidant activity of bilirubin, has led to the hypothesis that bilirubin's main physiologic

role is as a cellular antioxidant.

Cell type structure Occurrence in Cell Anatomy Function

blood

(per mm3)

Erythrocytes 4,000,0000 to Salmon colored Transport

5,000,000 bicarbonate oxygen to
( Red Blood
disks; literally hemoglobin
Cell)
sacs of molecules; also
hemoglobin; transport small
most organelles amount of
have been carbon dioxide.
ejected.

19
 Erythrocytes (red blood cells) generated in the bone marrow are disposed of in the spleen

when they get old or damaged. This releases hemoglobin, which is broken down to heme as the

globin parts are turned into amino acids. The heme is then turned into unconjugated bilirubin in

the reticuloendothelial cells of the spleen. This unconjugated bilirubin is not soluble in water. It

is then bound to albumin and sent to the liver.

In the liver it is conjugated to glucuronic acid by the enzyme Glucuronosyltransferase,

making it soluble in water. Much of it goes into the bile and thus out into the small intestine.

Some of the conjugated bilirubin remains in the large intestine and is metabolised by colonic

bacteria to urobilinogen, which is further metabolized to stercobilinogen, and finally oxidised to

stercobilin. This stercobilin gives feces its brown color. Some of the urobilinogen is reabsorbed

and excreted in the urine along with an oxidized form, urobilin.

Normally, a tiny amount of bilirubin is excreted in the urine, accounting for the light

yellow color. If the liver’s function is impaired or when biliary drainage is blocked, some of the

conjugated bilirubin leaks out of the hepatocytes and appears in the urine, turning it dark amber.

The presence of this conjugated bilirubin in the urine can be clinically analyzed, and is reported

as an increase in urine bilirubin. However, in disorders involving hemolytic anemia, an increased

number of red blood cells are broken down, causing an increase in the amount of unconjugated

bilirubin in the blood. As stated above, the unconjugated bilirubin is not water soluble, and thus

one will not see an increase in bilirubin in the urine. Because there is no problem with the liver

or bile systems, this excess unconjugated bilirubin will go through all of the normal processing

mechanisms that occur (e.g., conjugation, excretion in bile, metabolism to urobilinogen,

reabsorption) and will show up as an increase in urine urobilinogen. This difference between

20
increased urine bilirubin and increased urine urobilinogen helps to distinguish between various

disorders in those systems.

LIVER

The liver is a vital organ present in vertebrates and some other animals. It has a wide

range of functions, including detoxification, protein synthesis, and production of biochemicals

necessary for digestion. The liver is necessary for survival; there is currently no way to

compensate for the absence of liver function.

This organ plays a major role in metabolism and has a number of functions in the body,

including glycogen storage, decomposition of red blood cells, plasma protein synthesis, hormone

production, and detoxification. It lies below the diaphragm in the thoracic region of the

abdomen. It produces bile, an alkaline compound which aids in digestion, via the emulsification

of lipids. It also performs and regulates a wide variety of high-volume biochemical reactions

requiring highly specialized tissues, including the synthesis and breakdown of small and

complex molecules, many of which are necessary for normal vital functions.

The liver produces and excretes bile (a greenish liquid) required for emulsifying fats.

Some of the bile drains directly into the duodenum, and some is stored in the gallbladder. The

liver also breaks down hemoglobin, creating metabolites that are added to bile as pigment

(bilirubin and biliverdin).

21
BILE

Bile or gall is a bitter-tasting, dark green to yellowish brown fluid, produced by the liver

of most vertebrates, that aids the process of digestion of lipids in the small intestine. In many

species, bile is stored in the gallbladder between meals and upon eating is discharged into the

duodenum.

Bile acts to some extent as a surfactant, helping to emulsify the fats in the food. Bile salt

anions have a hydrophilic side and a hydrophobic side, and therefore tend to aggregate around

droplets of fat (triglycerides and phospholipids) to form micelles, with the hydrophobic sides

towards the fat and hydrophilic towards the outside. The hydrophilic sides are positively charged

due to the lecithin and other phospholipids that compose bile, and this charge prevents fat

droplets coated with bile from re-aggregating into larger fat particles. Ordinarily, the micelles in

the duodenum have a diameter of around 14-33 μm.

22
 The dispersion of food fat into micelles thus provides a largely increased surface area for

the action of the enzyme pancreatic lipase, which actually digests the triglycerides, and is able to

reach the fatty core through gaps between the bile salts. A triglyceride is broken down into two

fatty acids and a monoglyceride, which are absorbed by the villi on the intestine walls. Without

bile salts, most of the lipids in the food would be passed out in feces, undigested.

Since bile increases the absorption of fats, it is an important part of the absorption of the

fat-soluble substances, such as the vitamins D, E, K and A. Besides its digestive function, bile

serves also as the route of excretion for bilirubin, a byproduct of red blood cells recycled by the

liver. Bilirubin derives from hemoglobin by glucuronidation.

Biliary Flow

The term biliary tree is derived from the arboreal branches of the bile ducts. The bile

produced in the liver is collected in bile canaliculi, which merge to form bile ducts. Within the

liver, these ducts are called intrahepatic (within the liver) bile ducts, and once they exit the liver

they are considered extrahepatic (outside the liver). The intrahepatic ducts eventually drain into

the right and left hepatic ducts, which merge to form the common hepatic duct. The cystic duct

from the gallbladder joins with the common hepatic duct to form the common bile duct.

Bile can either drain directly into the duodenum via the common bile duct or be

temporarily stored in the gallbladder via the cystic duct. The common bile duct and the

pancreatic duct enter the second part of the duodenum together at the ampulla of Vater.

23
2. PATHOPHYSIOLOGY (A. BOOK BASED)

Modifiable Factors Non –modifiable

Infant weight Factors
Nutrition Age (newborn)
Exposure to Race
environment Genetics
Immature Hepatic Familial risk
System

Too much bilirubin in the blood

RBC breakdown

Bilirubin is formed

Newborn’s body is not easily able

to get rid of the bilirubin
Bilirubin is build up in the blood &
other tissues & fluids of newborn’s
body

Causes yellowing of the skin and

tissues (jaundice)

Physiologic jaundice Pathologic jaundice

24

Factors that alter the usual process

in bilirubin metabolism
 Factors that are seen as normal
response to the body’s ability to
excrete bilirubin in the first days of
life

hyperbilirubinemia
Unconjugated hyperbilirubinemia
Conjugated hyperbilirubinemia

Water soluble which metabolized Fat soluble which are not yet
by the liver metabolized by the liver
Not excreted easily
Excreted in stool and some in urine
If not converted, can be deposited
in the skin

Lead to kernicterus (yellowing int

the brain)
B. SYNTHESIS OF THE DISEASE (Book Based)
Neonatal Sepsis
b.1 Definition of the Disease

Hyperbilirubinemia (also known as jaundice) is an increased level of bilirubin in the

blood. It may occur due to physiologic factors that are seen as “normal” in the newborn. It may

be due to pathologic factors that alter the usual process in bilirubin metabolism.

PREDISPOSING FACTORS

Age

A premature baby may not be able to process bilirubin as quickly as full-term babies do.

Also, he or she may feed less and have fewer bowel movements. These conditions result in less

bilirubin eliminated in your baby's stool.

Race

25
 Race is a predictor of health outcomes and risk for some clinical conditions, for example,

mother's race predicts risk for hyperbilirubinemia in newborns, with blacks at lowest risk. Little

is known about the correlation of race as recorded in medical records with self-reported race.

Also, use of maternal race to predict newborn risk for hyperbilirubinemia has not been tested for

multiracial mothers and newborns. We sought to examine how maternal race documented in

medical records correlates with self-reported race and to examine the correlation between

mothers' and newborns' race in the context of risk for neonatal hyperbilirubinemia, focusing on

multiracial mothers and newborns.

Genetics and Familial Risk

Some variations in the UDP-glucuronosyltransferase 1A1 (UGT1A1) gene are involved

in the development of unconjugated hyperbilirubinemia. We hypothesize that other genetic

factors may also be associated with this disease.

PRECIPITATING FACTORS

Infant Weight

Delayed enteral feedings - if feedings are delayed it decreases intestinal motility and

removal of meconium, which leads to reabsorption of direct bilirubin, which is converted back to

indirect bilirubin. Which means bilirubin increases in the blood and leads to hyperbilirubinemia?

Immature Hepatic System

26
 Immature hepatic system - leads to decreased elimination of bilirubin from the system;

therefore, higher levels of indirect bilirubin are in the blood which leads to hyperbilirubinemia.

Exposure to environment
The environment affects the child’s immunity due to exposure.

PATHOPHYSIOLOGY (B. CLIENT BASED)

Modifiable Factors
Non –modifiable
Jaundice
Factors
Nutrition (formula
Age (newborn)
feeding)
Familial risk

Too much bilirubin in the blood

RBC breakdown

Bilirubin is formed

Newborn’s body is not easily able

to get rid of the bilirubin

Bilirubin is build up in the blood &

other tissues & fluids of newborn’s
body

Causes yellowing of the skin and

tissues (jaundice) 27

Neonatal Sepsis
 Physiologic jaundice Pathologic jaundice

Factors that are seen as normal Factors that alter the usual process
response to the body’s ability to in bilirubin metabolism
excrete bilirubin in the first days of
life

hyperbilirubinemia
Unconjugated hyperbilirubinemia
Conjugated hyperbilirubinemia

Water soluble which metabolized Fat soluble which are not yet
by the liver metabolized by the liver

Excreted in stool and some in urine Not excreted easily

If not converted, can be deposited

in the skin

Lead to kernicterus (yellowing in

B. SYNTHESIS OF THE DISEASE (Client Based) the brain)
The breakdown of RBC into bilirubin is deposited in the skin and excreted in urine when

present in the blood in excessive amounts (hyperbilirubinemia). This characteristic makes

jaundice a valuable indicator of a variety of disorders involving either hemolysis or biliary

obstruction. When there is an obstruction blocking the flow into the intestine, jaundiced clients

may have clay-colored stools owing to lack of bilirubin and its metabolites in the intestine.

Jaundice or icterus, is the yellow pigmentation of the sclera, skin, and deeper tissues

caused by excessive accumulation of bile pigments in the blood. The cause of jaundice may be

described according to the location of the pathologic change. It may occur outside the liver in

which the accumulated bilirubin is predominantly unconjugated and may also in the liver cause

by hereditary cholestatic syndromes or biliary obstruction.

28
 One of the modifiable factors affecting the child’s condition was the unsterile technique

of some health care providers because of just limited resources in the hospital. Another factor

was the child’s environment where in the time the child was admitted in the hospital, he was

placed in the corridor where there were many people who passed by in that place.

One thing that you cannot change or improve is the child’s age since the patient is only

seven days old, his immune system is still not stable and other organs were not yet fully

developed to fight for such infections or diseases that trigger his immunity.

VI. THE PATIENT AND HER CARE

1. Medical Management

Medical General Indications / Date Ordered / Client’s

Management Description Purpose Performed / Response to
Changed / Treatment
Discontinued

D5 IMB 85cc D5 IMB is Appropriate Date ordered Not assessed.

+D50 10cc x typically the for fluid and and started:
11-12 choice for electrolyte
uggts/min via maintenance replacement March 01, 2010
soluset fluid and
electrolytes D/C:
replacement for

29
 pediatric patients
while D50 is an
IV bolus used to
reversed
hypoglycemia.

a.1 Nursing Responsibilities:

Prior to Administration:
• Check doctor’s order
• Check the amount of IV fluid ordered and how long will be consumed
• Explain the procedure to be conducted and its importance to the patient.
• Obtain the necessary materials needed for IV insertion.

During Administration
• Check again the IV fluid ordered and hours to run in the doctor’s order to avoid
medication errors.
• Check for backflow by lowering the IV bottle. The bottle should be lower than the
IV site.
• Regulate as ordered.
• Use sterile technique in venipuncture and equipment assembly.
• Do not use solution if outdated, cloudy or the seal is not intact, as with all IV
solutions.
• Label the IV bottle with the name of the IV fluid, route and time of the
administration and your signature

After Administration:
• Document the procedure given
• Observe the IV site at least every hour for signs of infiltration
or other complication such as thrombhoplebitis, fluid or electrolytes
overload and air embolism. Remove dislodged IV and inform for reinsertion.
30
 • Monitor for fluid under/over load.
• Always check if the IVF is infusing well, intact and free from infiltration.
• Always check for its patency.
• Monitor patient’s skin integrity.
• Check for fluids to follow.

B. Drugs

Medical General Indications / Date Ordered / Client’s

Management Description Purpose Performed / Response to
Changed / Treatment
Discontinued
Ampicilin It has in vitro For treatment of Date ordered and
activity against infection
started: Not assessed.
gram-positive and (Respiratory, GI,
gram-negative UTI and
aerobic and meningitis) due
February 26,2010
anaerobic to E. coli, P.
bacteria. The mirabilis,
D/C:
bactericidal enterococci,
activity results Shigella, S.
from the typhosa and
inhibition of cell other
wall synthesis Salmonella,
and is mediated nonpenicillinase-
through producing N.
Ampicillin gononhoeae, H.
binding to influenzae,
penicillin binding staphylococci,
proteins (PBPs). streptococci
Ampicillin is including
stable against streptococcus
hydrolysis by a
variety of beta-
lactamases,
including
penicillinases,
and
cephalosporinases
and extended

31
 spectrum beta-
lactamases.
Nursing responsibilities before, during and after the medication administration
• Do not give the medication if the patient is allergic.
• Obtain a history before initiating therapy to determine previous use of and reactions to
penicillins or cephalosporins. Persons with a negative history of penicillin sensitivity may
still have an allergic response.
• Obtain specimens for culture and sensitivity before therapy. First dose may be given
before receiving results.
• Observe patients for signs and symptoms of anaphylaxis (rash, pruritus, laryngeal edema,
wheezing). Discontinue the drug and notify the physician immediately if these occur.
Keep epinephrine, an antihistamine, and resuscitation equipment close by in the event of
an anaphylactic reaction.

Medical General Indications / Date Ordered / Client’s

Management Description Purpose Performed / Response to
Changed / Treatment
Discontinued
Amikacin Aminoglycosides Short-term Date ordered and
work by binding treatment of
started: Not assessed.
to the bacterial serious
30S ribosomal susceptible
subunit, causing infections,
February 26,2010
misreading of t- including
RNA, leaving the septicemia,
D/C:
bacterium unable respiratory tract,
to synthesize bones and joints,
proteins vital to CNS (eg,
its growth. meningitis), skin
and skin
structure, intra-
abdominal (eg,
peritonitis),
burns and
postoperative

32
 infections,
complicated and
recurrent UTIs
or
uncomplicated
UTIs not
susceptible to
other antibiotics.

Nursing responsibilities before, during and after the medication administration

• A history of hypersensitivity or serious toxic reactions to aminoglycosides may

contraindicate the use of any other aminoglycoside because of the known cross-

sensitivities of patients to drugs in this class.

• Observe site for extravasation during administration.

• Observe for signs of renal, hepatic and haematological dysfunction during prolonged

therapy.

Medical General Indications / Date Ordered / Client’s

Management Description Purpose Performed / Response to
Changed / Treatment
Discontinued
Cefotaxime Inhibits bacterial Cefotaxime Date ordered and
cell wall exerts its action
started: Not assessed.
synthesis by against most
binding to one or gram negative
more of the aerobic bacteria
February 28, 2010
penicillin-binding as well as some
proteins (PBPs) gram positive
D/C:
which in turn bacteria.
inhibits the final
transpeptidation
step of
peptidoglycan
synthesis in
bacterial cell
walls, thus

33
 inhibiting cell
wall biosynthesis.

Nursing responsibilities before, during and after the medication administration

• Do not give this medication if the patient is allergic to cefotaxime sodium, any

component of CLAFORAN, or the cephalosporin group antibiotics.

• Read product insert three(3) times: before, during and after administering the drug.

• Check IV site carefully for signs of thrombosis or drug reaction

• Once administered the nurse should observe for any reactions the patient has to the

medication and take appropriate observations.

Medical General Indications / Date Ordered / Client’s

Management Description Purpose Performed / Response to
Changed / Treatment
Discontinued
Paracetamol The mechanism It is indicated in Date ordered and
of action is disease
started: Not assessed.
related to manifesting with
depression of the pain and fever
prostaglandin headache, high
February 28, 2010
synthesis by temperature,
inhibition of the infectious
D/C:
specific cell diseases and
cyclooxygenase chills (acute
and depression of catarrhal
the inflammations of
thermoregulatory the upper
center in the respiratory tract,
medulla flu etc.)
oblongata.

Nursing responsibilities before, during and after the medication administration

34
• Paracetamol should not be used in hypersensitivity to the preparation and in severe liver
disease
• Long-term treatment with high doses may cause a toxic hepatitis with following initial
symptoms: nausea, vomiting, sweating and discomfort
• In rare cases hypersensitivity reactions, predominantly skin allergy (itching and rash)
• Occasionally a gastrointestinal discomfort may be seen
• Once administered the nurse should observe for any reactions the patient has to the
medication and take appropriate observations of the patient.

35