Final Case Study-bili (ReVISED)

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I. INTRODUCTION 1. De scr ipt ion 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) p er day or is higher than 17 mg per dL (290 mol per L), or an infant has signs and symptoms suggestive of serious 1

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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

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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.

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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.

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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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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

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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.

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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.

- 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

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Lolo Tits Lola Peks Lola TingLolo Toy

LOL BRB Baktong Bakti LMAO BB

Baby Supti

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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

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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 /

Laboratory

Procedures

Indications

or Purpose

Date

Ordered

Date Results

were

released

Results Normal

Values (units

used in the

hospital)

Analysis and

Interpretation

of the Results

Hematology Hematology

tests can help

diagnose

anemia,

hemophilia,

 blood-

clotting

disorders, and

leukemia.

February 27,

2010

Leucocyte

count

Hemoglobin

Hematocrit

Platelets

Segmenters

Lymphocytes

11,200/cu.mm

13.14

40

220,000

75%

25%

5-10,000

12-16

40-50

150-500,000

55-70

25-35

Complete

Blood Count

test (CBC)Hemoglobin

Hemoglobin

measures theamount of 

oxygen

carrying

 protein in the

 blood.

February 27,

2010

15.4 12-16 Hemoglobin is

in the normalrange.

White Blood

Cells

This is done

to determine

the presence

of infection

and

inflammation.

February 27,

2010

4,900 5-10,000 The WBC is

slightly lower 

than the

normal value

Hematocrit Hematocrit is February 46 40-50 The

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tested to

monitor the

 patient’s

hydration

status and

oxygen level.

27,2010 Hematocrit is

within the

normal range

Platelet To identify

the cause of 

excess

 bleeding.

February

27,2010

200,000 150,000-

500,000

Platelet count

is within

normal range

Eosinophils Eosinophil

test is used to

diagnose

allergy, drug

reactions,

Parasitic

infections,

collagen

disease,

Hodgkins

disease,

Myelo-

 proliferative

diseases.

February

27,2010

1 2-4 Eosinophils is

slight lower 

than the

normal range

Monocytes This test is

used to

evaluate and

manage blood

disorders,

certain

 problems

with the

February

27,2010

1 2-8 Eosinophils is

slight lower 

than the

normal range

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immune

system, and

cancers.

Lymphocytes Are responsible

for the storage

of immunologic

memory. This

means that a

second contact

with an antigen

elicits an

accelerated and

increased

response.

February

27,2010

44 25-35 Lymphocytes

is higher than

normal, it

indicates that

the patient has

infection

Segmenters This is to

identify the

levels of 

mature WBC

whether it is

increase or 

decrease

together with

the WBC.

February

27,2010

54 55-70 The level of  

segmenters is

slightly below

the normal

values which

comparison

together with

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.

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• 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

 blood

(per mm3)

Cell Anatomy Function

Erythrocytes

( Red Blood

Cell)

4,000,0000 to

5,000,000

Salmon colored

 bicarbonate

disks; literally

sacs of 

hemoglobin;

most organelles

have beenejected.

Transport

oxygen to

hemoglobin

molecules; also

transport small

amount of 

carbon dioxide.

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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

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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).

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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.

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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 .

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Modifiable FactorsInfant weight

 Nutrition

Exposure to

environment

Immature HepaticSystem

 Non –modifiable

FactorsAge (newborn)

Race

Genetics

Familial risk 

2. PATHOPHYSIOLOGY (A. BOOK BASED)

 

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Too much bilirubin in the blood

Bilirubin is build up in the blood &

other tissues & fluids of newborn’s body

 Newborn’s body is not easily able

to get rid of the bilirubin

Bilirubin is formed

RBC breakdown

Pathologic jaundice

Causes yellowing of the skin andtissues (jaundice)

Physiologic jaundice

Factors that alter the usual processin bilirubin metabolism

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B. SYNTHESIS OF THE DISEASE (Book Based)

 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

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hyperbilirubinemia

Factors that are seen as normal

response to the body’s ability to

excrete bilirubin in the first days of 

life

Conjugated hyperbilirubinemiaUnconjugated hyperbilirubinemia

Water soluble which metabolized

 by the liver 

Fat soluble which are not yet

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 intthe brain)

 Neonatal Sepsis

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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

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Modifiable Factors

Jaundice

 Nutrition (formulafeeding)

 Non –modifiable

Factors

Age (newborn)Familial risk 

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)

 

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Too much bilirubin in the blood

Bilirubin is build up in the blood &

other tissues & fluids of newborn’s

 body

 Newborn’s body is not easily able

to get rid of the bilirubin

Bilirubin is formed

RBC breakdown

Causes yellowing of the skin and

tissues (jaundice)

 Neonatal Sepsis

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B. SYNTHESIS OF THE DISEASE (Client Based)

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.

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Pathologic jaundicePhysiologic jaundice

hyperbilirubinemia

Factors that are seen as normalresponse to the body’s ability to

excrete bilirubin in the first days of 

life

Conjugated hyperbilirubinemia

Factors that alter the usual processin bilirubin metabolism

Unconjugated hyperbilirubinemia

Water soluble which metabolized by the liver 

Fat soluble which are not yetmetabolized 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 inthe brain)

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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

Management

General

Description

Indications /

Purpose

Date Ordered /

Performed /

Changed /

Discontinued

Client’s

Response to

Treatment

D5 IMB 85cc

+D50 10cc x

11-12

uggts/min via

soluset

D5 IMB is

typically the

choice for 

maintenance

fluid and

electrolytes

replacement for 

Appropriate

for fluid and

electrolyte

replacement

Date ordered

and started:

March 01, 2010

D/C:

 Not assessed.

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 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.

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• 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

Management

General

Description

Indications /

Purpose

Date Ordered /

Performed /

Changed /

Discontinued

Client’s

Response to

Treatment

Ampicilin It has in vitro

activity againstgram-positive and

gram-negative

aerobic andanaerobic

 bacteria. The

 bactericidalactivity results

from theinhibition of cell

wall synthesisand is mediated

through

Ampicillin binding to

 penicillin binding

 proteins (PBPs).Ampicillin is

stable against

hydrolysis by avariety of beta-lactamases,

including

 penicillinases,and

cephalosporinases

and extended

For treatment of 

infection(Respiratory, GI,

UTI and

meningitis) dueto E. coli, P.

mirabilis,

enterococci,Shigella, S.

typhosa andother 

Salmonella,nonpenicillinase-

 producing N.

gononhoeae, H.influenzae,

staphylococci,

streptococciincluding

streptococcus

Date ordered and

started:

February 26,2010

D/C:

 Not assessed.

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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

Management

General

Description

Indications /

Purpose

Date Ordered /

Performed /

Changed /

Discontinued

Client’s

Response to

Treatment

Amikacin Aminoglycosideswork by binding

to the bacterial

30S ribosomalsubunit, causing

misreading of t-

RNA, leaving the bacterium unable

to synthesize

 proteins vital to

its growth.

Short-termtreatment of 

serious

susceptibleinfections,

including

septicemia,respiratory tract,

 bones and joints,

CNS (eg,

meningitis), skinand skin

structure, intra-

abdominal (eg, peritonitis),

 burns and

 postoperative

Date ordered and

started:

February 26,2010

D/C:

 Not assessed.

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infections,

complicated andrecurrent UTIs

or 

uncomplicated

UTIs notsusceptible 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

Management

General

Description

Indications /

Purpose

Date Ordered /

Performed /

Changed /

Discontinued

Client’s

Response to

Treatment

Cefotaxime Inhibits bacterial

cell wall

synthesis by

 binding to one or more of the

 penicillin-binding

 proteins (PBPs)

which in turninhibits the final

transpeptidationstep of 

 peptidoglycan

synthesis in bacterial cell

walls, thus

Cefotaxime

exerts its action

against most

gram negativeaerobic bacteria

as well as some

gram positive

 bacteria.

Date ordered and

started:

February 28, 2010

D/C:

 Not assessed.

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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

Management

General

Description

Indications /

Purpose

Date Ordered /

Performed /

Changed /

Discontinued

Client’s

Response to

Treatment

Paracetamol The mechanismof action is

related to

depression of the prostaglandin

synthesis by

inhibition of thespecific cell

cyclooxygenase

and depression of 

the

thermoregulatorycenter in the

medullaoblongata.

It is indicated indisease

manifesting with

 pain and fever headache, high

temperature,

infectiousdiseases and

chills (acute

catarrhal

inflammations of 

the upper respiratory tract,

flu etc.)

Date ordered and

started:

February 28, 2010

D/C:

 Not assessed.

Nursing responsibilities before, during and after the medication administration

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• 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.