Christine Piper, BSN, RN, CPN cpiper79@wi.rr.com
Alverno College
MSN 621
May 2006
• Each page will have action buttons that allow the user to “go back” or to “move forward” found in the lower right hand corner
• There are action buttons on the main page that allow the user to navigate to main topics, reference pages, and other internet links that might be of interest
• To reach the main page after you are in a topic, there will be a home button located in the lower left hand corner that allows the user to go back to the main page
• Throughout this tutorial all italicized words are defined if you roll over the word with the mouse
• Please note there are sound effects throughout the presentation
• The purpose of this tutorial is to provide information regarding the pathophysiology, risk factors, symptoms, diagnosis, and current treatment recommendations regarding hyperbilirubinemia in infants
• To understand the pathophysiology of hyperbilirubinemia
• To identify risk factors for hyperbilirubinemia
• To identify signs and symptoms of hyperbilirubinemia
• To understand diagnosing of hyperbilirubinemia in infants
• To understand current treatment recommendations
• 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
factors that alter the usual process in bilirubin
(1)
An increase in the amount of bilirubin in the blood
A decrease in the amount of bilirubin in the blood
There is no change in the amount of bilirubin in the blood
Hyperbilirubinemia is an increase of bilirubin in the blood
Try again
If you break the word apart it helps you to define the word. For example hyper = high, excessive bilirubin = bilirubin emia = blood
Try again
If you break the word apart it helps you define the word. For example hyper = high, excessive bilirubin = bilirubin emia = blood
• Bilirubin is the by product of the breakdown of
which is found in red blood cells (1)
• Normal red blood cell destruction accounts for
80% of daily bilirubin produced in the newborn
(10)
• Infants produce twice as much bilirubin per day than as an adult (1)
• There are two types of bilirubin - unconjugated
(indirect) bilirubin and conjugated (direct) bilirubin
• Unconjugated (indirect) bilirubin
– Fat-soluble
by by the liver
– Is not easily excreted
– Is the biggest concern for newborn jaundice
– If it is not converted it can be deposited into the skin which causes the yellowing of the skin or into the brain which can lead to
(1)
• Conjugated (direct) bilirubin
– Water soluble
– It is
by the liver
– It is mostly excreted in stool and some in the urine
Unconjugated (indirect) bilirubin is bilirubin that is broken down by the liver and is excreted through the urine and stool
Unconjugated
(indirect) bilirubin is bilirubin that has not yet been broken down by the liver
Conjugated (direct) bilirubin is bilirubin that is broken down by the liver and is excreted in urine or stool
Reticuloendothelial System
Iron
Globin Red blood cells Hemoglobin
Heme
Biliverdin
Liver
Conjugated bilirubin
Bilirubin albumin complex
Unconjugated bilirubin
Urobilinogen
Stercobilin
Red blood cells are broken down in the
Red blood cells break down to
further broken down to iron,
Reticuloendothelial System
Iron
Globin Red blood cells Hemoglobin
is further broken down to
then to unconjugated bilirubin by the
enzyme biliverdin reductase (1)
Heme
Biliverdin
Liver
Conjugated bilirubin
Bilirubin albumin complex
Unconjugated bilirubin
Urobilinogen
Stercobilin
Unconjugated bilirubin is then carried to the liver by
(1)
The liver then converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines (1)
Reticuloendothelial System
Iron
Globin Red blood cells Hemoglobin
Heme
Biliverdin
Liver
Conjugated bilirubin
Bilirubin albumin complex
Unconjugated bilirubin
Urobilinogen
Stercobilin
The intestines then convert the conjugated bilirubin into
and
(1)
Reticuloendothelial System
Iron
Globin Red blood cells Hemoglobin
Heme
Biliverdin
Liver
Conjugated bilirubin
Bilirubin albumin complex
Unconjugated bilirubin
Urobilinogen
Stercobilin
is excreted in the urine (1)
is excreted in the stool (1)
Click On The Correct Response To
Complete The Diagram
Red blood cells are broken down to hemoglobin
Hemoglobin is further broken down to iron, globin, and heme
Liver converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines
Unconjugated bilirubin is carried to the liver by albumin
Stercobilin is excreted in the stool
Intestines convert conjugated bilirubin into urobilinogen and stercobilin
Urobilinogen is excreted in the urine
Click On The Correct Response To
Complete The Diagram
Red blood cells are broken down to hemoglobin
Hemoglobin is further broken down to iron, globin, and heme
Stercobilin is excreted in the stool
Liver converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines
Intestines convert conjugated bilirubin into urobilinogen and stercobilin
Urobilinogen is excreted in the urine
Unconjugated bilirubin is carried to the liver by albumin
Click On The Correct Response To
Complete The Diagram
Red blood cells are broken down to hemoglobin
Hemoglobin is further broken down to iron, globin, and heme
Stercobilin is excreted in the stool
Heme is further broken down to bilverdin then to unconjugated bilirubin by the enzyme biliverdin reductase
Liver converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines
Intestines convert conjugated bilirubin into urobilinogen and stercobilin
Urobilinogen is excreted in the urine
Unconjugated bilirubin is carried to the liver by albumin
Click On The Correct Response To
Complete The Diagram
Red blood cells are broken down to hemoglobin
Hemoglobin is further broken down to iron, globin, and heme
Stercobilin is excreted in the stool
Heme is further broken down to bilverdin then to unconjugated bilirubin by the enzyme biliverdin reductase
Liver converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines
Intestines convert conjugated bilirubin into urobilinogen and stercobilin
Unconjugated bilirubin is carried to the liver by albumin
Urobilinogen is excreted in the urine
Click On The Correct Response To
Complete The Diagram
Red blood cells are broken down to hemoglobin
Hemoglobin is further broken down to iron, globin, and heme
Stercobilin is excreted in the stool
Heme is further broken down to bilverdin then to unconjugated bilirubin by the enzyme biliverdin reductase
Unconjugated bilirubin is carried to the liver by albumin
Liver converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines
Intestines convert conjugated bilirubin into urobilinogen and stercobilin
Urobilinogen is excreted in the urine
Click On The Correct Response To
Complete The Diagram
Red blood cells are broken down to hemoglobin
Hemoglobin is further broken down to iron, globin, and heme
Stercobilin is excreted in the stool
Heme is further broken down to bilverdin then to unconjugated bilirubin by the enzyme biliverdin reductase
Urobilinogen is excreted in the urine
Unconjugated bilirubin is carried to the liver by albumin
Liver converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines
Intestines convert conjugated bilirubin into urobilinogen and stercobilin
Click On The Correct Response To
Complete The Diagram
Red blood cells are broken down to hemoglobin
Hemoglobin is further broken down to iron, globin, and heme
Stercobilin is excreted in the stool
Heme is further broken down to bilverdin then to unconjugated bilirubin by the enzyme biliverdin reductase
Unconjugated bilirubin is carried to the liver by albumin
Liver converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines
Intestines convert conjugated bilirubin into urobilinogen and stercobilin
Urobilinogen is excreted in the urine
Click On The Correct Response To
Complete The Diagram
Red blood cells are broken down to hemoglobin
Hemoglobin is further broken down to iron, globin, and heme
Heme is further broken down to bilverdin then to unconjugated bilirubin by the enzyme biliverdin reductase
Unconjugated bilirubin is carried to the liver by albumin
Liver converts unconjugated bilirubin to conjugated bilirubin where it is excreted in the intestines
Intestines convert conjugated bilirubin into urobilinogen and stercobilin
Urobilinogen is excreted in the urine
Stercobilin is excreted in the stool
jaundice is an exaggerated normal process seen in 60% of term
infants (1)
• It normally occurs during the first week of life
• It is normally benign and self-limiting
• Associated with a bilirubin level greater than 5-7mg/dL (1)
Prematurity & Hyperbilirubinemia
infants are more susceptible to hyperbilirubinemia due to:
• Immature
system
feedings
levels
Prematurity & Hyperbilirubinemia
system leads to decreased elimination of bilirubin from the system; therefore, higher levels of indirect bilirubin are in the blood which leads to hyperbilirubinemia
Reticuloendothelial System
Iron
Globin Red blood cells Hemoglobin
Heme
Biliverdin
Liver
Conjugated bilirubin
Bilirubin albumin complex
Unconjugated bilirubin
Urobilinogen
Stercobilin
Prematurity &
Hyperbilirubinemia
• Delayed
feedings if feedings are delayed it decreases intestinal motility and removal of
, 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 (10)
Reticuloendothelial System
Iron
Red blood cells Hemoglobin Globin
Heme
Biliverdin
Liver
Bilirubin albumin complex
Unconjugated bilirubin
Conjugated bilirubin
Urobilinogen
Stercobilin
Prematurity & Hyperbilirubinemia
• Decrease in serum
levels - if there is a decrease in the amount of albumin receptors available, bilirubin does not bind to the albumin; therefore, is considered “free” bilirubin. Which means bilirubin increases in the blood and leads to hyperbilirubinemia (1)
Reticuloendothelial System
Iron
Red blood cells Hemoglobin Globin
Heme
Biliverdin
Liver
Conjugated bilirubin
Bilirubin albumin complex
Unconjugated bilirubin
Urobilinogen
Stercobilin
• Polycythemia is an increased level of red blood cells (RBCs) in the
• A infant has more RBCs than an adult, and the lifespan of an RBC is shorter in neonates (1)
• Increased RBCs and a shorter lifespan leads to increased destruction of RBCs, which leads to more bilirubin in the blood, which leads to hyperbilirubinemia
Please try again
Please try again
60% of term infants have physiologic
jaundice
jaundice is due to factors that alter the process of bilirubin
• It usually appears within 24 hours of life
• Associated with a bilirubin level increase of 0.5 mg/dL/ hour or 5mg/dL per day
(10)
• Persists for longer than 7 to 10 days (10)
• Hemolytic anemia
• Rh incompatibility
• ABO incompatibility
• G6PD (glucose-6-phosphate deficiency) deficiency
• Hemolytic anemia is an incompatibility between the blood of the mother and her fetus
• This can occur due to Rh incompatibility or ABO blood incompatibility
• Rh incompatibility is when the mother lacks the Rh factor on the surface of her red blood cells and her baby is born with the Rh factor on his or her red blood cells
(13)
• This occurs in about 15% of the
Caucasian population and 7% of the
African American population (13)
• It does not occur with the first born child
• In Rh incompatibility there is potential for the infant’s blood to enter the mother’s system (13)
• If this happens the mother will develop
against the fetal blood cells which
may cross the placenta and destroy the infant’s
red blood cells (13)
• Increased destruction of red blood cells leads to increased bilirubin in the blood; therefore, leading to hyperbilirubinemia
Treatment for Rh Incompatibility
• There is an injection called Rh immune globulin (also known as Rhogam) which is given to pregnant women at 28 weeks of pregnancy and within 72 hours of delivering an infant who is born Rh positive (13)
• This injection prevents the mother’s body from forming
against the Rh factor found on fetal red blood cells (13)
• If the mother is already sensitized, meaning her body has already made antibodies against the Rh factor, the injection will be ineffective (13)
• This injection prevents sensitization in more than 95% of Rh negative women (13)
• ABO incompatibility occurs with any blood type; however, it is more common if the mother has type O blood and the infant has blood type A, B, or AB
• Fetal cells cross the placenta
and enter the mother’s bloodstream (6)
• When this occurs the mother’s body forms
against the fetal cells (6)
• Those antibodies are then small enough to cross back through the placenta into the baby’s circulation and cause destruction of red blood cells (6)
• Increased destruction of red blood cells leads to increased bilirubin in the blood; therefore, leading to hyperbilirubinemia
Glucose-6-Phosphate Dehydrogenase
G6PD
• The function of G6PD enzyme is to initiate an oxidation/reduction reaction (3)
• An oxidation/reduction reaction is transferring electrons from one molecule to the next (3)
• Oxidation is the loss of electrons and reduction is the gain of electrons (3)
Pentose Phosphate Pathway
Retrieved from http://www.malariasite.com/malaria/g6pd.htm
Used with permission (11)
The G6PD enzyme is responsible for reducing NADP+
(nicotinamide adenine dinucleotide phosphate) to
NADPH (reduced nicotinamide adenine dinucleotide phosphate
) (3)
• Without adequate levels of NADPH, red blood cells are more prone to stress and
oxidation, which leads to hemolysis
of red blood cells (3)
• If there is a G6PD deficiency there will not be adequate levels of NADPH; therefore, leading to increased hemolysis of red blood cells
• Increased hemolysis of red blood cells leads to increased levels of bilirubin, which then leads to hyperbilirubinemia
Physiologic Jaundice versus
Pathologic Jaundice
Physiologic
Occurs 24 hours after birth
Prematurity
Polycythemia
Pathologic
Occurs less than
24 hours after birth
Hemolytic anemia
G6PD deficiency
Hemolytic anemia
ABO incompatibility
Increased fluid intake
G6PD deficiency
Prematurity
Polycythemia
Rh incompatibility
Headache
is a rare, irreversible complication of hyperbilirubinemia
• If bilirubin levels become markedly elevated, the unconjugated bilirubin may cross into the
and stain the brain tissues
(1)
• If staining of the brain tissues occurs there is permanent injury sustained to areas of the brain which leads to neurological damage (10)
is used to describe the yellow staining of the brain nuclei as seen on autopsy (kern means nuclear region of the brain; icterus means jaundice)” (Juretschke, 2005, p. 10)
Picture Of A Brain With
Kernicterus
Yellow staining in the brain due to increased unconjugated bilirubin passing
through the blood brain barrier
Retrieved April 30, 2006, from http://www.urmc.rochester.edu/neuroslides/sli de156.html
Used with permission (9)
are:
feeding, temperature instability, and
(1)
• Symptoms then progress to:
,
opisthotonos and arching, fever, seizures, and
high pitched cry (10)
, and upward gaze
(10)
Genetics play a part in hyperbilirubinemia
There are studies that link genetic mutations in enzymes to increased risk for hyperbilirubinemia
There are studies that link genetic mutations in enzymes to increased risk for hyperbilirubinemia
• A study done from 2001 to 2003 looked at three enzymes with possible genetic defects that were linked to increased rates of hyperbilirubinemia in the Asian population (7)
• The study was conducted in Taiwan
• The reason for this is because the Asian population has twice the incidence of hyperbilirubinemia than the Caucasian population (7)
• They were looking to identify potential genetic defects that contribute to the higher incidence of hyperbilirubinemia
The three enzymes are:
• G6PD - glucose-6-phosphate dehydrogenase
• OTAP 2 - organic anion transporter 2
• UGT1A1 - UDPglucuronsyltransferase 1A1
Pentose Phosphate Pathway
Retrieved from http://www.malariasite.com/malaria/g6pd.htm
Used with permission (11)
The G6PD enzyme is responsible for reducing NADP+
(nicotinamide adenine dinucleotide phosphate) to
NADPH (reduced nicotinamide adenine dinucleotide phosphate
) (3)
Glucose-6-Phosphate Dehydrogenase
G6PD
• The function of G6PD enzyme is to initiate an oxidation/reduction reaction (3)
• An oxidation/reduction is transferring electrons from one molecule to the next
(3)
• Oxidation is the loss of electrons and reduction is the gain of electrons (3)
• G6PD is also responsible for maintaining adequate levels of NADPH inside the cells (3)
• If there is a G6PD deficiency there will not be adequate levels of NADPH
• Without adequate levels on NADPH, red blood cells are more prone to stress and oxidation, which leads to
of red blood cells (3)
• If there is increased hemolysis of red blood cells, there will be increased levels of bilirubin, which then leads to hyperbilirubinemia
Retrieved April 8, 2006, from http://www.rcsb.org/pdb/explore.do?structureId=1QKI
Used with permission
Organic Anion Transporter 2
• The function of the OATP 2 enzyme is
uptake of unconjugated bilirubin (7)
Reticuloendothelial System
Iron
Globin Red blood cells Hemoglobin
Heme
Biliverdin
Liver
Conjugated bilirubin
Bilirubin albumin complex
Unconjugated bilirubin
Urobilinogen
Stercobilin
Organic Anion Transporter 2
OATP 2
• In the study done, the authors identified
in the OATP 2 enzyme, which led to increased risk for hyperbilirubinemia in the Asian population (7)
• If the enzyme activity is delayed there will be increased levels of unconjugated bilirubin in the blood, therefore leading to hyperbilirubinemia
UDP - Glucuronsyltransferase 1A1
UGT1A1
• The function of UGT1A1 is to convert unconjugated or indirect bilirubin to conjugated or direct bilirubin (7)
Reticuloendothelial System
Iron
Globin Red blood cells Hemoglobin
Heme
Biliverdin
Liver
Conjugated bilirubin
Bilirubin albumin complex
Unconjugated bilirubin
Urobilinogen
Stercobilin
UDP - Glucuronsyltransferase 1A1
UGT1A1
• In the study done, the authors identified
in the UGT1A1 enzyme which, led to increased risk for hyperbilirubinemia in the Asian population (7)
• If the enzyme activity is delayed there will be increased bilirubin in the blood, therefore leading to hyperbilirubinemia
What enzyme is responsible for converting unconjugated (indirect) bilirubin to conjugated (direct) bilirubin?
The UGT1A1 is responsible for converting unconjugated (indirect) bilirubin to conjugated (direct) bilirubin
Please try again!
The G6PD enzyme is responsible for maintaining adequate levels of NADPH in the red blood cells which helps prevent
of red blood cells
Please try again!
The OATP 2 enzyme is involved in the
uptake of unconjugated bilirubin
What enzyme is responsible for maintaining adequate levels of NADPH in the red blood cells which helps prevent
of red blood cells?
The G6PD enzyme is responsible for maintaining adequate levels of NADPH in the red blood cells which
of red blood cells
Please try again!
The OATP 2 enzyme is involved in the
uptake of unconjugated bilirubin
Please try again!
The UGT1A1 is responsible for converting unconjugated
(indirect) bilirubin to conjugated (direct) bilirubin
What enzyme is involved in the
uptake of unconjugated bilirubin?
The OATP 2 enzyme is involved in the
uptake of unconjugated bilirubin
Please try again!
The G6PD enzyme is responsible for maintaining adequate levels of
NADPH in the red blood cells which helps prevent
of red blood cells
Please try again!
The UGT1A1 is responsible for converting unconjugated
(indirect) bilirubin to conjugated (direct) bilirubin
Major Risk Factors for Hyperbilirubinemia in Full-Term Newborns
• J aundice within first 24 hours after birth
• A sibling who was jaundiced as a neonate
• U
such as ABO blood type incompatibility or Rh incompatibility
• N onoptimal sucking/nursing
• D eficiency in glucose-6-phosphate dehydrogenase, a genetic disorder
• I nfection
/bruising
• E ast Asian or Mediterranean descent
Retrieved April 18, 2006, from http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5023a4.htm
Used with permission (2)
• Poor feeding
• Increased sleepiness
• Increased yellowing of the skin or sclera
• Increased bilirubin level
•Check bilirubin level
•Check complete blood count
•Check reticulocyte count
•Coombs test
•Blood groups & types
•G6PD level
level
•Visual assessment (least reliable)
• This test is to measure the amount of bilirubin in the blood
• Increased bilirubin = hyperbilirubinemia
• In term infants a normal bilirubin level is between 1.0 - 10.0 mg/dL (4)
• There is NO safe bilirubin level identified
• This test will determine if the infant has increased red blood cells in the
(polycythemia)
• If an infant has a
greater than
65% this places that infant at risk for hyperbilirubinemia (16)
• This test measures young non-nucleated red blood cells (4)
• If the reticulocyte count is greater than
5% in the first week of life, this identifies the infant as trying to replace destroyed red blood cells (16)
• ABO grouping and Rh types are confirmed by examining RBCs for
presence of blood group antigens
and
against these antigens (4)
Retrieved April 18, 2006, from http://en.wikipedia.org/wiki/Image:Coombs_test_schematic.png
Used with Permission (15)
• “The direct coombs test is a direct measure of the amount of maternal
coating the infant’s red blood cell” (Blackburn, 1995, p. 21)
• If the antibody is present, the test is positive
Retrieved April 18, 2006, from http://en.wikipedia.org/wiki/Image:Coombs_test_schematic.png
Used with Permission (15)
• “The indirect coombs test measures the effect of a sample of the infant’s serum (which is thought to contain maternal
adult RBCs” (Blackburn, 1995, p. 21)
• “If the infant’s serum contains antibodies, they will interact with and coat these adult RBCs
(positive test)” (Blackburn, 1995, p. 21)
• The G6PD level is done to identify neonates at risk for G6PD deficiency
• “The Beutler fluorescent spot test is a rapid and inexpensive test that visually identifies
NADPH produced by G6PD under ultraviolet light. When the blood spot does not fluoresce, the test is positive; it can be false-positive in patients who are actively
therefore only be done several weeks after a hemolytic episode” (Glucose-6-phosphatedehydrogenase deficiency, n.d., ¶ 16)
• This test indicates the reserve amount of
available for binding indirect bilirubin (16)
• A normal albumin level in a term infant is between 2.6 - 3.6 g/dL (4)
• “Visual assessment of jaundice is most accurate when the infant’s skin is blanched with light digital pressure in a welllit room” (Juretschke, 2005, p. 11)
• “As bilirubin levels rise, the accuracy of visual assessment decreases”
(Juretschke, 2005, p. 11)
Zones Showing Kramer’s
Progression Of Jaundice
• Jaundice proceeds in a cephalopedal progression, meaning jaundice progresses from the head down to the toes (10)
• This diagram demonstrates what level the bilirubin is at depending on what areas of the infant’s body is jaundiced
• For example, if the infant was noted to be jaundiced from the head to the neck that would be zone 1 and the bilirubin level would be between 4 – 8 mg/dL
Zone 1 2 3 4 5
Bilirubin 4-8 5-12 8-16 11-18 >15
Level (mg/dL)
After Kramer, 1969 (12)
• Phototherapy is treatment of choice
• Encourage frequent feedings
• Intravenous hydration
• Intravenous immune globulin
• Exchange transfusion
• “In the mid-1950s, Sister Jean at Rochford
General Hospital in England noted that infants exposed to sunlight were less jaundiced in the uncovered skin areas than their nonexposed counterparts” (17)
• Phototherapy works by converting indirect bilirubin to lumirubin, a water-soluble compound that is a more excretable form of bilirubin (10)
• “Only certain wavelengths (colors) of light are absorbed by bilirubin; as bilirubin is a yellow pigment, blue is absorbed more effectively, however, green light is more deeply absorbed into the skin” (17)
An infant undergoing phototherapy
Retrieved April 24, 2006, from http://en.wikipedia.org/wiki/Image:Infant_jaundice_treatment.jpg
Used with permission
• Encouraging frequent feedings at least eight times per day helps to stimulate intestinal motility and removal of
meconium , thus reducing reabsorption of
direct bilirubin into the system (1)
• Intravenous hydration of infants with hyperbilirubinemia was thought to decrease bilirubin levels, however, unless an infant is dehydrated intravenous hydration is not indicated (17)
• Intravenous immune globulin (IVIG) has been used to decrease bilirubin levels due to hemolytic anemia
• It is thought that IVIG interferes with receptors in the
that are necessary for
to occur (10)
• An exchange transfusion is used only in extreme cases when phototherapy has failed
• The process for an exchange transfusion involves small amounts of blood being removed from the infant and then replaced with the same amount of donor RBCs and plasma
(1)
• The process continues until twice the circulating volume has been replaced (1)
• The exchange replaces ~ 87% of the circulating blood volume and decreases the bilirubin level by ~ 55% (1)
• For information on kernicterus there is a website entitled Parents of Infants and children with Kernicterus. Their website is http://www.pickonline.org/
• A Sentinel Alert was issued in April 2001 by the Joint Commission on Accreditation of Healthcare Organizations on
Kernicterus. The website address is http://www.jointcommission.org/SentinelE vents/SentinelEventAlert/sea_18.htm
References
1.
Blackburn, S. (1995). Hyperbilirubinemia and neonatal jaundice.
Neonatal Network , 14(7), 15-29.
2.
Center for Disease Control and Prevention. (2001). Kernicterus in fullterm infants-United States, 1994-1998. Morbidity and Mortality Weekly
Report , 50(23), p. 494. Retrieved April 18, 2006, from http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5023a4.htm
3.
Ethnasios, R. (2003). Physiology of G6PD. Retrieved March 2, 2006, from http://www.rialto.com/g6pd/physiolo.htm
4.
Fischbach, F. Nurses’ quick reference to common laboratory and diagnostic tests (2 nd ed.). Philadelphia: Lippincott-Raven.
5.
Glucose-6-phosphate dehydrogenase deficiency. (n.d.). Wikipedia .
Retrieved May 1, 2006, from Answers.com Web site: http://www.answers.com/topic/glucose-6-phosphate-dehydrogenasedeficiency
6.
Hull, J. (2006). ABO incompatibility. Retrieved March 31, 2006, from http://www.drhull.com/EncyMaster/A/ABO_incompatibility.html
References
7.
Huang, M., Kua, K., Teng, H., Tang, K., Weng, H., & Huang, C. (2004).
Risk factors for severe hyperbilirubinemia in neonates. Pediatric
Research , 56(5), 682-89.
8.
Infant undergoing home phototherapy for jaundice. (2005). Retrieved
April 25, 2006, from http://en.wikipedia.org/wiki/Image:Infant_jaundice_treatment.jpg
9.
Józefowicz, R., Miller, J., & Powers, J. (2000). Neuropathy and neuroimaging laboratory: Mind, brain, and behavior course. University of Rochester School of Medicine and Dentistry. Retrieved April 30,
2006 from http://www.urmc.rochester.edu/neuroslides/slide156.html
10.
Juretschke, L. (2005). Kernicterus: Still a concern. Neonatal Network ,
24(2), 7-19.
11.
Kakkilaya, B., M.D. (2005). Glucose 6 phosphate dehydrogenase deficiency. Retrieved March 18, 2006, from http://www.malariasite.com/malaria/g6pd.htm
12.
Kramer, L. (1969). Advancement of dermal icterus in the jaundiced newborn. American Journal of Diseases of Children , 118(3), 454-458.
Copyright
© (1969), American Medical Association, All Rights
Reserved.
13.
March of Dimes Birth Defects Foundation. (2001). Quick reference and fact sheets: Rh disease . Retrieved February 28, 2006, from http://www.marchofdimes.com/printableArticles/681_1220.asp?printabl
e=true
14.
PDB ID: 1QKI (Identification of the enzyme in the database)
Au, S.W.N., Gover, S., Lam, V.M.S., & Adams, M.J.
Human Glucose-6-Phosphate Dehydrogenase: The Crystal Structure
Reveals a Structural Nadp+ Molecule and Provides Insights Into
Enzyme Deficiency.
Stucture v8 pp. 293 (2000).
Retrieved April 8, 2006, from http://www.rcsb.org/pdb/explore.do?structureId=1QKI
15.
Rad, A. (2006). Coombs test. Retrieved May 1, 2006, from http://en.wikipedia.org/wiki/Coombs_test
16.
Schwobel, A. & Sakraida, S. (1997). Hyperbilirubinemia: new approaches to an old problem. Journal of Perinatal & Neonatal
Nursing , 11(3), 78-98.
17.
Steffensrud, S. (2004). Hyperbilirubinemia in term and near term infants: Kernicterus on the rise? Newborn and Infant Nursing Reviews ,
4(4), 191-200.
18.
Venes, D. (Ed.). (2005). Taber’s cyclopedic medical dictionary
(20 th ed.), Philadelphia: F.A. Davis Company.
• Thank you for taking the time to complete this tutorial on neonatal jaundice
• If there are any questions, please contact me at cpiper79@wi.rr.com