Final Case Study-bili (ReVISED)
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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
9
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.