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CHAPTER 5

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1
The term “hemolytic” is derived from the Latin word for _______
“destruction” (lysis) of red blood cells.
2
Whatt is it called When there is an abnormal destruction of red blood cells
hemolytic disease
3
it is an excessive levels of accumulated serum bilirubin (indirect) greater than 12-13 mg/dl in the term newborn characterized by jaundice or icterus
HYPERBILIRUBINEMIA
4
it is the yellowish discoloration of the skin and sclera and mucous membranes due to accumulation of bilirubin pigment
Jaundice
5
Approximately __% full term infants and about __% of premature infants develop some degree of jaundice.
- 60%
- 80%
6
It is the most common physiologic problem in newborns and is of concern because of the current early hospital discharge patterns. Most cases of this will not occur until the infant is at home.
Jaundice
7
a yellow pigment produced as a byproduct of the breakdown of hemoglobin in red blood cells is transported to the liver, where it is processed and excreted in the bile
Bilirubin
8
The presence of bilirubin in neonates are from:
o ___%- from catabolism of circulating RBCs
o ___%- from ineffective erythropoiesis (bone marrow) and from turnover of heme
proteins and free heme
o 75%
o 25%
9
after the birth of a child, the fetus has a high hemoglobin and hematocrit due to what
Due to low oxygen tension in fetal blood
10
after the birth of a child, what does increase and what are no longer needed?
oxygen tension increases and the extra RBCS are no longer needed
11
after the birth of a child, what does the infant begin to break down?
excessive RBCs
12
nonpolar, lipid- soluble bilirubin; end product of heme- protein catabolism from a series of enzymatic reactions in the reticuloendothelial cells; potentially neurotoxic
UNCONJUGATED BILIRUBIN
13
polar, water-soluble glucuronide of bilirubin (direct reacting); end product from indirect, unconjugated bilirubin that has undergone conjugation in the liver cell microsome by the enzyme uridine diphosphoglucuronic acid )UDP(-glucuronyl transferase; not neurotoxic
CONJUGATED BILIRUBIN
14
It breaks down heme to become iron & biliverdin
HEME OXYGENASE
15
What transports UB into the hepatocytes
LIGANDIN
16
What converts biliverdin to UB
BILIVERDIN REDUCTASE
17
It is a liver enzyme that conjugates bilirubin by combining with glucuronic acid
GLUCORONYL TRANSFERASE
18
It is an intestinal enzyme in the NB that converts CB to UB
BETA-GLUCORONIDASE
19
Physiologic factors afecting hyperbilirubenemia
a. Increased production of bilirubin
b. Decreased removal of bilirubin due to transient liver enzyme insufficiency
c. Increased reabsorption of bilirubin
20
a primary mechanism of physiologic jaundice (Wong)
Enterohepatic shunting
21
what is it called when there is Delayed passage of meconium leading to an Increased glucuronidase activity
Less motile intestines
22
Factors Likely To Make Physiological Jaundice Worse In A Given Baby
1. Breastfeeding difficulties
2. Prematurity
3. Dehydration
4. Polycythemia
5. Delayed passage of meconium
6. Enterohepatic shunting
7. possible factors in breast milk that prevent bilirubin conjugation
8. Genetic predisposition to increased production (Native Americans, Asians,
Mediterranean)
23
It can slow the processing of bilirubin and lead to a higher bilirubin level.
Dehydration
24
what is it called when hematocrit (RBC volume percentage in blood) of greater than 65%.
Polycythemia
25
possible factors in breast milk that prevent bilirubin conjugation
 Pregnanediol
 B-glucuronidase
 Lipase
26
inhibits hepatic glucuronyl transferase which suppresses now the bilirubin conjugation
Pregnanediol
27
The most common pathologic causes of indirect hyperbilirubinemia include:
 Infection (sepsis)
 Hemolytic disorders
 Traumatic birth injuries
 Polycythemia
 Some disease states
28
this can increase the rate of red blood cell destruction and lead to an
increase in bilirubin levels.
nfection (sepsis)
29
it is the destruction of red blood cells (hemolysis) and lead to a higher bilirubin level.
Hemolytic disorders
30
it causes bruising at delivery, cephalohematoma (vacuum extraction, forceps increased production of RBCs
Traumatic birth injuries
31
Some disease states of indirect hyperbilirubenemia
a. G6PD deficiency
b. Thyroxine deficiency
c. Galactosemia
d. Substrate deficiency (Hypoglycemia)
32
it results from X-linked enzymopathy due to enzyme deficiency in production. This
defect makes RBCs more vulnerable to lysing under oxidative stress
G6PD deficiency
33
This increases the activity of glucuronyl transferase which promotes conjugation of bilirubin.
Thyroxine
34
It occurs when there is an Absent or deficient galactose 1-phosphate uridyl transferase which is needed in glucuronidation of indirect bilirubin.
Galactosemia
35
It is the precursor of glucuronic acid which is involved in bilirubin conjugation
Glucose
36
The most common pathologic causes of direct hyperbilirubinemia include:
 Prolonged use of parenteral nutrition
 Disturbed capacity of the liver to secrete conjugated bilirubin
 Infections
37
most common inherited intrahepatic metabolic disorder
alpha1-antitrypsin deficiency
38
the most common cause of billiary obstruction
Bile duct obstruction
39
What is the primary concern in neonatal jaundice
prevention of kernicterus / bilirubin encephalopathy.
40
It is the yellow staining of brain cells that may result in bilirubin encephalopathy
Kernicterus
41
It is a syndrome of severe brain damage from the deposition of bilirubin in the brain cells.
Bilirubin encephalopathy
42
The occurrence of this is related to the amount of diffusible, loosely bound bilirubin and availability of albumin binding sites.
kernicterus
43
This easily crosses the bloodbrain barrier and is transferred into the brain cells, causing obvious yellow staining of the brain tissue, similar to its effect on the skin.
Free bilirubin
44
Factors That Enhance Bilirubin Encephalopathy Despite Lower Serum Bilirubin Level
1. Respiratory/Metabolic acidosis
2. Decreased serum albumin
3. Drugs which displace bilirubin from albumin (esp. sulphonamides and related
compounds; salicylates)
4. Infections
45
It is Any condition that increases metabolic demands for oxygen and glucose: fetal distress, hypoxia, hypothermia, hypoglycemia, sepsis (H+ and free fatty acids compete with binding sites for bilirubin; also opens BBB)
Respiratory/Metabolic acidosis
46
MANIFESTATIONS OF BILIRUBIN ENCEPHALOPATHY/KERNICTERUS
 CNS excitation/depression
 Appears after peak plasma bilirubin has been established for several hours
47
Early signs of kernicterus
 Lethargy /decreased activity
 Poor feeding
 Listlessness /irritability
48
Late signs of kernicterus
 Opisthotonus
 Spasticity
 Seizures
 High-pitched cry
 Serum bilirubin levels are 30 mg/dl or greater (in term infants)
49
The lifelong damage from kernicterus may cause long-term:
 Movement problems
 Hearing loss or deafness
 Learning problems and other developmental disabilities.
 Problems moving the eyes, especially looking upward.
 Sequelae to kernicterus.
50
What is it called when Some babies may seem to have normal hearing, but they
develop a problem processing sounds
auditory neuropathy or auditory dyssynchrony
51
lifelong damage from kernicterus where it includes mental retardation, sensorineural hearing impairment and cerebral palsy, often with ataxia and chorioathetosis.
Sequelae to kernicterus
52
DIAGNOSIS for babies with MANIFESTATIONS OF BILIRUBIN ENCEPHALOPATHY/KERNICTERUS
1. Visual assessment (Kramer Rule)
2. Serum bilirubin levels
3. Timing of appearance of jaundice
4. CBC; Hgb/Hct; reticulocyte count
5. Blood type, Rh and Coomb’s
53
a diagnosis in which it describes the relationship between serum bilirubin levels and the progression of skin discoloration
Visual assessment (Kramer Rule)
54
what is the Normal indirect bilirubin
0.2-1.4 mg/dL
55
It is a useful screening device to detect neonatal jaundice in full term infants that is done through a device which measures the amount of yellow colour in subcutaneous tissue, converting it into an estimate of total serum bilirubin leve
Transcutaneous bilirubinometry
56
This is a non-invasive test that can be done at the bedside, and thus can be a useful
screening tool to determine if serum measurement is necessary.
Transcutaneous bilirubinometry
57
what diagnosis has this limitations:
 affected by race, gestational age and birth weight
 intensity of jaundice not always related to the degree of hyperbilirubinemia
 once phototherapy started, no longer useful as a screening tool
Transcutaneous bilirubinometry
58
when does jaundice usually appear?
within 24 hours after birth
59
Persistent jaundice after:
1 week (____)
2 weeks (____)
1 week (term)
2 weeks (preterm)
60
It is when Reticulocytes are newly produced, relatively immature red blood cells (RBCs).
CBC; Hgb/Hct; reticulocyte count
61
This kind of test determines the number and/or percentage of reticulocytes in the blood and is a reflection of recent bone marrow function or activity.
reticulocyte test
62
Goals in preventing bilirubin encephalopathy/kernicterus and reverse hemolytic process in blood incompatibility
1. Prevention is the best treatment
2. Encourage frequent breastfeeding (early onset)
3. Offer supplemental feedings of pumped breast milk or formula.
4. Interrupt breastfeeding temporarily-(late onset)
5. Periodic assessment and serial bilirubin levels
6. Direct sunlight to speed metabolism of bilirubin
7. Phototherapy
63
in phototherapy, what kind of light is more effective but it alters coloration of infant so normal fluorescent light is preferred for better observation
Blue light
64
in phototherapy, what alters structure of bilirubin to soluble form (LUMIRUBRIN) for easier excretion
Photoisomerization
65
types of phototherapy
a. Conventional=2-3 lights over and under
b. Fiberoptic blanket or panel
66
a type of phototherapy where it consist of a light generating illuminator, a bundle of plastic fibers affixed to a panel that distributes the energy and a soft disposable light permeable cover to protect the infant
Fiberoptic blanket or panel
67
Drawbacks to this include noise from the fan in the light source and damage and/or breakage of the optic fibers
fiberoptic phototherapy units
68
side effeccts of phototherapy
- altered activity
- altered fluid status
- altered GI function
- altered hematological function
- ocular effects
- skin changes
- altered thermal/metabolic function
69
In extreme cases, this occurs to replace the baby’s damaged blood with fresh blood
Exchange transfusion
70
2 Pharmaceutical Therapy
a. Intravenous immunoglobulin G (IVIG)
b. Heme oxygenase production inhibitor
71
A Pharmaceutical Therapy where it is used in Rh and ABO hemolytic disease, and has been demonstrated to significantly reduce the need for exchange transfusion.
Intravenous immunoglobulin G (IVIG)
72
A Pharmaceutical Therapy where it Inhibits heme oxygenase that are microsomal enzymes that cleave heme to produce the antioxidant biliverdin, inorganic iron and carbon monoxide (CO).
Heme oxygenase production inhibitor
73
What happens when ther is Less than Body Requirements related to poor feeding and dehydration in newborns.
Imbalanced Nutrition
74
Nursing diagnosis for those with MANIFESTATIONS OF BILIRUBIN ENCEPHALOPATHY/KERNICTERUS
a. Risk for Injury related to elevated bilirubin levels, which can cause brain damage and jaundice.
b. Imbalanced Nutrition: Less than Body Requirements related to poor feeding and dehydration in newborns.
c. Deficient Fluid Volume related to fluid loss through increased urine output and decreased oral intake
d. Altered Tissue Perfusion related to elevated bilirubin levels, which can interfere with oxygen delivery to body tissues.
e. Altered Parenting related to the need for increased monitoring and interventions for the affected newborn.
75
what conditions should be Avoided for these enhances bilirubin encephalopathy
 Infection
 Metabolic acidosis
 Hypothermia-keep warm to reduce metabolic needs
 Hypoxia
 Hypoglycemia
76
HEMOLYTIC DISEASE OF THE NEWBORN | MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
1. PHYSIOLOGIC JAUNDICE
2. BREAST-FEEDING-JAUNDICE (early onset)
3. BREAST-MILK JAUNDICE (late onset)
4. HEMOLYTIC JAUNDICE
77
What HEMOLYTIC DISEASE OF THE NEWBORN when the ff occurs:
 immature hepatic function plus increased bilirubin load from red blood cell hemolysis
PHYSIOLOGIC JAUNDICE
78
What HEMOLYTIC DISEASE OF THE NEWBORN when the ff occurs:
 decreased milk intake related to fewer calories consumed by infant before mother milk is well established
 enterohepatic shunting
BREAST-FEEDING-JAUNDICE (early onset)
79
What HEMOLYTIC DISEASE OF THE NEWBORN when the ff occurs:
 possible factors in breast milk thatprevent bilirubin conjugation
 less frequent stooling
BREAST-MILK JAUNDICE (late onset)
80
What HEMOLYTIC DISEASE OF THE NEWBORN when the ff occurs:
 blood antigen incompatibility causes hemolysis of large number of RBC
 liver unable to conjugate and excrete bilirubin from hemolysis
HEMOLYTIC JAUNDICE
81
RBC destruction which results from an antigen-antibody reaction; characterized by hemolytic anemia and hyperbilirubinemia
ERYTHROBLASTOSIS FETALIS
82
defined as the development of antibodies against the antigens of another individual of the same species
Isoimmunization
83
Isoimmunization Occurs by 2 main mechanisms:
a. When Rh (-) mother is exposed to Rh (+) fetal RBC
b. When female receives Rh (+) blood transfusion
84
It is most commonly caused by Rh incompatibility between the mother and fetus, but can also occur with other blood group incompatibilities.
Erythroblastosis fetalis
85
What happens when the mother's immune system is exposed to fetal blood cells, it may produce antibodies that attack and destroy the fetal red blood cells
Antibody formation
86
It is The destruction of fetal red blood cells leads to hemolysis, or the breakdown of
red blood cells, which releases bilirubin into the fetal bloodstream.
Hemolysis
87
This can cause jaundice, brain damage, and other serious complications in the developing fetus.
elevated bilirubin levels
88
It occurs when there is loss of red blood cells, or a decreased number of red blood
cells in the fetal bloodstream, which can impair oxygen delivery to the fetus and other tissues
anemia
89
The accumulation of bilirubin and other waste products in the fetal bloodstream can which can further impair the delivery of oxygen and nutrients to the developing fetus.
placental dysfunction
90
It involves the destruction of fetal red blood cells and the accumulation of bilirubin and other waste products, leading to serious complications for the developing fetus.
erythroblastosis fetalis
91
Diagnosis for ERYTHROBLASTOSIS FETALIS
1. Anti D antibody titer
2. Coomb’s test
3. Polymerase Chain Reaction
4. Fetal blood sampling/cordocentesis
92
a diagnosis where it measures the concentration or level of anti-D antibodies in a person's blood, indicating their immune response to the RhD antigen
Anti D antibody titer
93
a diagnosis where it determines whether a person has antibodies attached to the surface of their red blood cells, which can cause hemolytic anemia
Coomb’s test
94
2 categories of Coomb’s test
a. Indirect-uses maternal blood
b. Direct-uses neonatal cord
95
a diagnosis that includes detection of free fetal RHD DNA sequences in maternal plasma or serum using PCR
Polymerase Chain Reaction
96
a iagnosis test for signs of anemia usin an ultrasound transducer is used to show the position of the fetus and umbilical cord on a monitor. Then a fetal blood sample is withdrawn from the umbilical cord for testing
Fetal blood sampling/cordocentesis
97
what happens when heme is broken down to photoporphyrin making it indirect bilirubin
Pathologic Jaundice
98
it is when the liver and spleen may be enlarged from an attempt to destroy damaged blood cells.
Hepatosplenomegaly
99
What occurs when An infant needs to use glucose stores to maintain metabolism in the presence of anemia
Hypoglycemia
100
This occurs If the number of red cells has significantly decreased, the blood in the vascular circulation may be hypotonic to interstitial fluid; fluid will shift from the lower to higher isotonic pressure by the law of osmosis, causing extreme edema
Hydrops fetalis
101
It can result in heart failure as the heart has to beat so fast to push the dilute blood forward.
severe anemia
102
a commercial preparation of passive antibody, do not cross placenta because
not an Ig G given to prevent formation of antibodies that will react to Rh component
RhoGam (Rho D Human Immunoglobulin)
103
can a mother receive RhoGam to protect future pregnancy If both indirect and direct Coomb’s test are (-), that is, there are no antibodies,
yes, mother can receive RhoGam to protect future pregnancy
104
RhoGam (Rho D Human Immunoglobulin) must be injected within how many hours after delivery to an unsensitized mother of an Rh(+) infant (most antibodies are formed at this stage)
72 hours
105
it is the necrosis of the bowel as a result of poor perfusion
Necrotizing Enterocolitis
106
RBC lifespan for:
- adult
- newborn
- adult: 120 days
- newborn: 70 to 90 days
107
causes of hyperbilirubenemia
1. decreased production of bilirubin
2. Decreased removal of bilirubin
3. Increased reabsorption of bilirubin
108
it is the process whereby urobilinogen in the small intestine is converted back to nconjugated bilirubin
enterohepatic shunting
109
it contains substances to prevent bilirubin conjugation
breastmilk
110
what is it called when thereis lower-than-normal levels of protein in the body
hypoproteinemia
111
what ocurs when there is delayed cord clamping, erythrocyte transfusion, and placental insufficiency
polycythemia
112
Causes of Indirect hyperbilirubenemia
a. infection
b. hemolytic disorder
c. traumatic birth injury
113
alpha1-antitrypsin deficiency
most common genetic liver disease in children
114
it is the most common cause of billiary obstruction
Billary atrasia
115
patho or physio
- within 24 hrs
- after 24hrs
- pathology
- physiology
116
what is the primary concern in neonatal jaundice
prevention of kernicterus
117
up to how many mg/dL is when the unconjugated bilirubin becomes toxic to:
- Term infants
- Preterm/LBW
- Term infants: 25-30 mg/dL
- Preterm/LBW: 8-12 mg/dL
118
Factors that enhance bilirubin encephalopathy despite lower serum bilirubin level
1. respiratory/metabolic acidosis
2. drugs
3. decrease seru albumin level
4. intracranial infection
119
increases hydrogen ions and free acids compete with the binding sites for bilirubin
respiratory/metabolic acidosis
120
spasm of the muscles causing backward arching of the head, neck, and spine
opisthotonus
121
- muscles are continously contracted
- contraction causes stiffness or tightness of the muscles and can interfere with normal movement, speech, and gait
spasticity
122
it is the occurence of involuntary movements in a combination of choreo (irregular migrating contractions) and athetosis (twisting and writhing)
choreoathetosis
123
CBC (complete blood count)
can help determine level of ed blood cell destruction, hemolytic anemia, sepsis, or polycythemia
124
this test is used for testing RH incompatibility
Coomb's test
125
it is effective in decreasing rates of exchange transfusion and in preventing progression to severe hyperbilirubenemia in infants with moderately elevated levels
phototherapy
126
mainstay of treatment for hyperbilirubenemia and the application of fluorescent light is used to infant's exposed skin
phototherapy
127
it is when baby lies on a blanket that incorporates fibreoptic cables; light travels through the fibreoptic cables and shines on the baby's back
Fiberoptic blanket or panel
128
conventional
it is when baby is held under a halogen or fluorescent lamp with their eyes covered
129
amount of the infant's blood are removed, and equal amounts of donor whole blood are transfused
exchange transfusion
130
- a therapy treatment for patients with antibody deficiencies
- prepared from a pool of immunoglobulins (antibodies) from the plasma of thousands of healthy donors
Intravenous immunoglobulin G (IVIG)
131
theya re made by the immune system of healthy people for the purpose of fighting infections
immunoglobulins
132
a condition from genitalia being exposed to sunlight in infants
priapism
133
if this is not observed, "remove shields at least once per shift to inspect eye
infection/irritation and to allow eye contact," what might happen to the baby?
SENSORY DEPRIVATION
134
How often do we need to Feed baby to prevent metabolic acidosis-removed and cuddled for feeding
regularly (every 2-3 hours)
135
a syndrome making grayish discoloration of skin
brown baby syndrome
136
hemolytic disease of the newborn that results from maternal-fetal blood incompatibility specifically involving the Rh factor
ERYTHROBLASTOSIS FETALIS
137
what kind of Ig does:
- can pass through placenta
- cannot pass through placenta
- IgG
- IgM
138
hemolytic disease of the newborn that results from maternal-fetal blood group incompatibilty specifically involving the Rh factor
ERYTHROBLASTOSIS FETALIS
139
thin covering of antigens that surrounds the RBCs
Rh Factor
140
why is it that fetus must be monitored every 2 weeks
for probability that IgG may kill the baby
141
this test looks for antibodies that may bind to fetal blood cells and causes premature RBC destruction (hemolysis)
Coomb's Test
142
direct or indirect Coomb's Test:
- detects antibodies on mother's serum
- uses maternal blood
- done at 1st visit then at 28 week
indirect
143
direct or indirect Coomb's Test:
- detects antibodies attached to circulating RBCs of infants
- uses cord blood sample
- done at delivery
direct
144
it is when an ultrasound transducer is used to show the position of the fetus and umbilical cord on a monitor. then a fetal blood samle is withdrawn from the umbilical cord for testing
cordocentesis
145
what color of the amniotic fluid is when:
- infant is mildly or not affected
straw colored
146
what color of the amniotic fluid is when:
- severely affected
Deep yellow
147
what color of the amniotic fluid is when:
- extremely ill or still born from Hydrops Fetalis
Brown/Green
148
What does these mean?:
- Hydrops
- Fetalis
- Edema
- Lethal State
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