Section 4: Jaundice and the Breastfed Infant Flashcards

1
Q

What is jaundice?

A

a yellow discoloration of the skin and sclera caused by hyperbilirubinemia

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2
Q

When does jaundice usually become visible on the sclera?

A

FIRST

34 to 51 μmol/L

(2-3 mg/dl)

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3
Q

When does jaundice become visible on the face?

A

68 to 86 μmol/L

( about 4 to 5 mg/dL)

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4
Q

Jaundice advances in a

A

head-to-foot direction

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5
Q

When does jaundice appear at the umbilicis and feet?

A
  • umbilicus at about 258 μmol/L (15 mg/dL)
  • at the feet at about 340 μmol/ (20 mg/dl)
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6
Q

How many neonates become visibly jaundiced in the first week of life?

A

Slightly more than half

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7
Q

Hyperbilirubinemia may be harmless or harmful depending on

A

its cause and the degree of elevation

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8
Q

The threshold for concern for jaundice varies by

A
  • Age
  • Degree of prematurity
  • Health status
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9
Q

Jaundice threshold for healthy term infants

A

more than 308 μmol/L

( 18 mg/dL )

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10
Q

Infants who are premature, small for gestational age, or ill (sepsis, hypothermia, hypoxia) are at

A

much greater risk than healthy newborns

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11
Q

Treament for hyperbilirubinemia is given based on

A
  • age
  • clinical factors
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12
Q

what is the major consequence of neonatal hyperbilirubinemia

A

Neurotoxicity

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13
Q

How does neurotoxicity manifest

A
  • acute encephalopathy
  • can be followed by neuro problems eg
    • cerebral palsy
    • sensorimotor deficits
  • cognition is usually spared
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14
Q

What is the most severe form of neurotoxicity

A

Kernicterus

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15
Q

Does kernicterus still occur?

A

Yes, although rare

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16
Q

What is kernicterus?

A
  • brain damage
  • Also known as Bilirubin encephalopathy
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17
Q

Bilirubin is normally bound to

A
  • Serum albumin
  • therfore stays in the vascular space
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18
Q

When can bilirubin cross the blood-brain barrier and cuase kernicterus?

A

WHEN ALBUMIN ISN’T KEEPING IT IN THE VASCULAR SPACE

  • VERY HIGH serum bilirubin
  • VERY LOW serum albumin (eg preteruM)
  • BILIRUBIN displaced from Albumin (competitive binders)
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19
Q

What are competitive binders for bilirubin?

A
  • drugs (eg, sulfisoxazole, ceftriaxone, aspirin)
  • free fatty acids
  • hydrogen ions (eg, in fasting, septic, or acidotic infants).
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20
Q

Risk of hyperbilirubinemia in neonates ≥ 35 weeks gestation

A
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21
Q

Patho of jaundice

A
  • most bilirubin produced from breakdown of Hb into unconjugated bilirubin
  • U. bilirubin binds to albumin in blood for transport to liver
  • in liver, it is taken up by hepatocytes and conjugated (made water-soluble) by an enzyme
  • Conjugated bilirubin is excreted in bile into duodenum
  • In adults, Con. Bili is reduced by gut bacteria into urobilin and excreated
  • Neontates have fewer gut bacteria, so excrete less bilirubin -
    • they also have an enzyme that deconjugates bili
  • Unconjugated bili is reabsorbed and recycled into circulation
  • This is called enterohepatic circculation of bilirubin
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22
Q

Mechanisms of hyperbilirubinemia

A
  • Increased production of bilirubin
  • Decreased hepatic uptake
  • Decreased conjugation
  • Impaired excretion
  • Impaired bile flow (cholestasis)
  • Increased enterohepatic circulation
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23
Q

Most cases of jaundice involve

A

unconjugated hyperbilirubinemia.

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24
Q

What may cause a conjugated or mixed hyperbilirubinemia.

A

LIVER PROBLEMS

  • Liver dysfunction
  • neonatal sepsis
  • neonatal hepatitis
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25
Q

Physiologic hyperbilirubinemia main points

A
  • occurs in almost all neonates
  • Generally resolves in first 1-3 weeks of life
  • Bilirubin levels can rise up to 18 mg/dL by 3 to 4 days of life (7 days in Asian infants) and fall thereafter.
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26
Q

What is Breastfeeding Jaundice also known as?

A
  • starvation jaundice
  • breast-non-feeding jaundice
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27
Q

What is breast milk jaundice?

A
  • different from breastfeeding jaundice
  • Usually in healthy, thriving infants
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28
Q

Pathologic hyperbilirubinemia in term infants is diagnosed if

A
  • Jaundice appears
    • in the first 24 h
    • after the first week of life,
    • lasts more than 2 wks
  • Total serum bilirubin (TSB) rises by more than 5 mg/dL/day
  • TSB is more than 18 mg/dL
  • Infant shows symptoms or signs of a serious illness
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29
Q

Some of the most common causes of pathologic hyperbilirubinemia are

A
  • hemolytic anemia
  • G6PD deficiency (inc RBC breaskdown)
  • Hematoma resorption
  • Sepsis
  • Hypothyroidism
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30
Q

What findings may indicate pathological jaundice?

A
  • Jaundice in the first day of life
  • Jaundice after 2 wk of age
  • Lethargy, irritability, respiratory distress
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31
Q

Jaundice that develops in the first 24 to 48 h, or that persists > 2 wk, is most likely

A

pathologic

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32
Q

aundice that does not become evident until after 2 to 3 days is more consistent with

A

physiologic, breastfeeding, or breast milk jaundice

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33
Q

Diagnosis of hyperbilirubinemia

A

Diagnosis is suspected by the infant’s color and is confirmed by measurement of serum bilirubin

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34
Q

What bilirubin concentration in infants warrants further testing?

A
  • > 10 mg/dL (> 170 μmol/L) in preterm infants
  • or > 18 mg/dL in term infants
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35
Q

Treatment of hyperbilirubinemia is directed at

A

the underlying disorder.

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36
Q

Treatment for physiologic jaundice

A
  • usually is not clinically significant and resolves within 1 wk
  • Frequent formula feedings can reduce the incidence and severity ( by increasing GI motility and frequency of stools)
  • The type of formula does not seem important in increasing bilirubin excretion.
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37
Q

with breastfeeding jaundice, it is not advisable to supplement with

A
  • water or dextrose
  • it may disrupt the mother’s production of milk.
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38
Q

in breastfeeding jaundice, assure mother that

A

hyperbilirubinemia has not caused any harm and that she may safely resume breastfeeding.

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39
Q

in breastfeeding jaundice, stopping breastfeeding is necessary for

A
  • only 1 or 2 days
  • mother should continue to express
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40
Q

in breastfeeding jaundice, what may be appropriate at higher bilirubin levels?

A

phototherapy

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41
Q

If the bilirubin level continues to increase > 18 mg/dL in a term infant with early breastfeeding jaundice

A

a temporary change from breast milk to formula may be appropriate

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42
Q

breastfeeding jaundice may be prevented or reduced by

A

increasing the frequency of feedings

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43
Q

Treatment for breastfeeding jaundice

A
  • may be prevented or reduced by increasing the frequency of feedings
  • If the bilirubin level continues to increase > 18 mg/dL in a term infant with early breastfeeding jaundice, a temporary change from breast milk to formula may be appropriate
  • phototherapy also may be indicated at higher levels.
  • Stopping breastfeeding is necessary for only 1 or 2 days (mother should continue to exress)
  • assure mother that hyperbilirubinemia has not caused any harm and that she may safely resume breastfeeding.
  • It is not advisable to supplement with water or dextrose because that may disrupt the mother’s production of milk.
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44
Q

Definitive treatment of hyperbilirubinemia involves

A
  • Phototherapy
  • Exchange transfusion
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45
Q

What is phototherapy

A
  • Standard of care for hyperbilirubinemia
  • most commonly uses fluorescent white light
  • Blue light, wavelength 425 to 475 nm, is most effective for intensive phototherapy
  • The light is absorbed by bilirubin, making it water soluble and able to be excreted in the stool and urine
  • It provides definitive treatment of neonatal hyperbilirubinemia and prevention of kernicterus.
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46
Q

What is an exchange teansfucion

A
  • For severe hyperbilirubinemia,
  • rapidly removes bilirubin
  • Small amounts of blood drawn and replaced through umbilical vein catheter
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47
Q
A
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48
Q

Where does bilirubin come from?

A
  • disintegration of red blood cells and the breakdown of hemoglobin into globin and heme
  • Heme is further broken down to iron, biliverdin, and carbon monoxide
  • Biliverdin is reduced to bilirubin
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49
Q
A
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50
Q

Amount of jaundice in a newborn depends on

A

the balance of bilirubin production and elimination.

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51
Q

the balance of bilirubin production and elimination may be upset because of

A
  • (a) increased bilirubin production
  • (b) decreased ability to metabolize the bilirubin for elimination
  • (c) decreased elimination and increased absorption of bilirubin in the intestines.
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52
Q

What leads to additional produciton of bilirubin in the neonate?

A
  • In utero, low O2 environment stimulates production of extra RBCs
  • LIfespan of fetal RBCs shorter than adult
  • Large volume of heme + shorter lifespan produces additional bilirubin
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53
Q

what causes Increased bilirubin production after birth?

A
  • blood is transferred from the placenta to the newborn, further increasing blood volume and hemoglobin concentrations.
  • Immature or inactive RBCs are destryed –> inc bilirubin
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54
Q

In the newborn, unconjugated bilirubin enters the liver cells

A

slower than in an older chil

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55
Q

Conjugation of bilirubin is necessary for

A

bilirubin to be transferred into bile and moved into the small intestine and stool.

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56
Q

Decreased Elimination and Increased Absorption of Bilirubin in the Intestines

A
  • Conjuigated bili must be eliminated in stool
  • Neonates have a high level of an enzyme in the intestinal mucosa that removes the glucuronide from the conjugated bilirubin and makes it water insoluble (unconjugated) and available for transport back across the intestinal lumen into the neonate’s circulation
  • This bilirubin, now at elevated levels, is transported to the immature liver cells and the cycle continues.
57
Q

In healthy, Caucasian, term intants, bilirubin levels peak on what days?

A

2-3

58
Q

Jaundice resolves in most formula-fed infants by what day?

A

day 7

59
Q

Breastmilk jaundice onset

A
  • Usually after day 5
  • (extension of physiological jaundice)
  • potentially existing for many weeks
60
Q

What type of baby might get starvation/breastfeeding/breast-non feeding jaundice?

A

breasfed baby who is not getting enough milk

61
Q

POtential causes of breastmilk jaundice

A
  • Increase in intestinal absorption of bilirubin
  • Due to an as yet unknown substance in milk
62
Q

Causes of breastfeeding jaundice

A
  • Breastfeeding increases enterohepatic circulation of bilirubin in infants who have decreased milk intake+ dehydration or low caloric intake
  • also may result from reduced intestinal bacteria that convert bilirubin to nonresorbed metabolites.
63
Q

Solution for breastfeeding jaundice

A
  • Correct the breastfeeding problem
  • restore fluid and caloric intake.
64
Q
A
65
Q

What factors have been associated with exaggerated hyperbilirubinemia (Pathological Hyperbilirubinemia) ?

A
  • Increased production of bilirubin related to an increased hemolysis of red blood cells due to:
    • blood group incompatibility
    • inherited red blood cell abnormalities
    • birth trauma
    • genetic factors
    • prematurity
    • polycythemia
  • Decreased elimination of bilirubin caused by genetic disorders of conjugation, low oral intake of feedings, prematurity with immature hepatic metabolism, breastmilk feedings
  • Risk factors such as prematurity, maternal diabetes, urinary tract infection, G6PD deficiency, Asian race
  • A reduction in the number of carrier proteins (albumin) or binding sites caused by such things as prematurity, sepsis, hypoxia, and the use of certain drugs
  • Liver diseases such as hepatitis, Crigler-Najjar syndrome, Rotor’ssyndrome, liver damage from CMV, toxoplasmosis, rubella, syphilis, congenital biliary atresia
  • Metabolic disorders such as galactosemia and hypothyroidism
66
Q

What is the initial presentation of kernicterus?

A
  • Lethargy
  • poor feeding
  • vomiting
  • irregular respirations
67
Q

How can kernicterus be reversed in the early stages?

A

Removing bilirubin from the circulation and brain by exchange transfusion

68
Q

If severe hyperbilirubinemia continues

A

the infant manifests severe neurologic signs

69
Q

Survivors of kernicterus almost always bave

A

significant permanent neurologic damage

70
Q

What was used to determine levels of jaundice in the past?

A

Inspection/visual estimation

71
Q

Why is visual estimation no longer used for jaundice assesment?

A

unreliable and inaccurate

72
Q

Experts now recommend what assessment for jaundice?

A

screen all infants by serum or transcutaneous level of bilibrubin prior to discharge

73
Q

Where is serum bilirubin plotted?

A

On the nomogram

74
Q

What is the purpose of the nomogram?

A

to determine an infant’s risk for significant hyperbilirubinemia.

75
Q

In addition to plotting on the nomogram, what else must be done before discharge?

A

Adequate breastfeeding must be established and documented

76
Q

Follow-up assessments for jaundice

A
  • A follow-up visit with HCP at 3 to 5 days of age
  • for further assessment, teaching, and support of the family
77
Q

What are considered when managing jaundice?

A
  • The baby’s age
  • general condition
  • serum bilirubin level
  • cause of the hyperbilirubinemia
78
Q

While it is known that there is an association between breastfeeding and jaundice…

A
  • breastfeeding must be optimized and supported
  • it is important to convey that breastfeeding is helpful, not harmful.
79
Q

In managing jaundice, it is important to help mothers and their babies with the following:

A
  • Breastfeeding early to promote the passage of meconium.
  • Positioning and latching-on to ensure effective suckling at the breast.
  • Understanding the importance of frequent and unrestricted breastfeeding.
  • Teaching mothers methods of encouraging a drowsy baby.
  • Assessing infant’s stools for colour change (typically passing from meconium to brown-green [transitional stool] to green-yellow and mustard yellow with soft curds); consistent colour change would indicate adequate milk intake.
  • Avoiding the use of complementary and supplementary feedings of formula, water, or glucose water.
  • Feeling encouraged, positive, and supported.
80
Q
A
81
Q

Infants receiving phototherapy should continue to

A

breastfeed

82
Q

Do infants receiving phototherapy require IV fluids

A

Not unless they show signs of dehydration

83
Q

phototherapy has been found to increase the baby’s

A

fluid requirements

84
Q

Why are babies’ eyes are covered during phototherapy treatments

A

toavoid corneal damage.

85
Q

Very high or rapidly increasing bilirubin levels may need to be controlled with

A

an exchange transfusion.

86
Q

Physiologic hyperbilirubinemia occurs in

A

almost all neonates

87
Q

Physiologic hyperbilirubinemia generally resolves when?

A
  • first week of life (formula fed)
  • first few weeks (breastfed)
88
Q

Physiologic hyperbilirubinemia is caused by

A
  • Shorter neonatal RBC life span increases bilirubin production
  • deficient conjugation due to the deficiency of UGT decreases clearance
  • low bacterial levels in the intestine combined with increased hydrolysis of conjugated bilirubin increase enterohepatic circulation
89
Q

Physiologic hyperbilirubinemia

bilirubin levels

A
  • up to 18 mg/dL by 3 to 4 days of life (7 days in Asian infants)
  • fall afterward
90
Q

Breastfeeding jaundice is also known as

A
  • starvation jaundice
  • breast-non-feeding jaundice
91
Q

Breastfeeding jaundice develops in what infants?

A
  • develops in one sixth of breastfed infants during the first week of life
92
Q

Breastfeeding jaundice is usually seen on what day of life?

A

May be seen in first few days after birth, but not before 24 hrs

93
Q

Breastfeeding jaundice usually occurs in babies who have not established effective breastfeeding because of

A
  • sleepiness
  • prematurity
  • poor position
  • poor latch with inadequate milk transfer.
94
Q

What is the standard of treatment for hyperbilirubinemia?

A

phototherapy

95
Q

How does phototherapy work?

A

The light is absorbed by bilirubin, making it water soluble and able to be excreted in the stool and urine

96
Q

Breastfeeding jaundice may be prevented or reduced by

A

increasing the frequency of feedings

97
Q

If the bilirubin level continues to increase > 18 mg/dL in a term infant with early breastfeeding jaundice

A

a temporary change from breast milk to formula may be appropriate

98
Q

Most cases of jaundice involve

A

unconjugated hyperbilirubinemia

99
Q

Once in the liver, bilirubin must be conjugated with

A
  • glucuronic acid
  • to form a water-soluble bilirubin
  • but the newborn, due to its immature liver, has limited ability to do this
100
Q

Conjugation is necessary for bilirubin to be

A

transferred into bile and moved into the small intestine and stool.

101
Q

To manage jaundice, breastfeeding must be started early to promote what?

A

the passage of meconium.

102
Q

Important parts of breastfeeding to manage jaundice

A
  • Positioning and latching-on to ensure effective suckling at the breast.
  • Understanding the importance of frequent and unrestricted breastfeeding.
  • Teaching mothers methods of encouraging a drowsy baby.
103
Q

Causes of patholotical jaundice

Decreased elimination of bilirubin caused by

A
  • genetic conjugation disorders
  • low intake at feedings
  • prematurity/immature liver metabolism
  • breastmilk feedings
104
Q

Causes of patholotical jaundice

metabolic disorders

A
  • galactosemia
  • hypothyroidism
105
Q

Causes of patholotical jaundice

Liver diseases

A
  • hepatitis
  • Crigler-Najjar syndrome
  • Rotor’s syndrome
  • liver damage from CMV
  • toxoplasmosis
  • rubella
  • syphilis
  • congenital biliary atresia
106
Q

Causes of patholotical jaundice

reduction in the number of carrier proteins (albumin) or binding sites caused by

A
  • prematurity
  • sepsis
  • hypoxia
  • use of certain drugs
107
Q

Causes of patholotical jaundice

Risk factors

A
  • prematurity
  • maternal diabetes
  • urinary tract infection
  • G6PD deficiency
  • Asian race
108
Q

Causes of patholotical jaundice

Increased production of bilirubin related to

A

increased hemolysis of red blood cells

This can be due to:

  • blood group incompatibility
  • inherited red blood cell abnormalities
  • birth trauma
  • genetic factors
  • prematurity
  • polycythemia
109
Q

Pathologic jaundice is diagnosed if infant shows

A

symptoms or signs of a serious illness

110
Q

Pathologic jaundice is diagnosed if TSB

A
  • rises by more than 5 mg/dL/day
  • TSB is more than 18 mg/dL
111
Q

Pathologic jaundice is diagnosed if it appears

A
  • in the first 24 h
  • after the first week of life
  • lasts > 2 wk
112
Q

Jaundice in the first day of life is usually

A

pathological

113
Q

TSB rate in pathological jaundice

A

more than 18 mg/dL

  • TSB rate rises more than 0.2 mg/dL/ per hour (> 3.4 μmol/L/h)
  • or more than 5 mg/dL/day
114
Q

Conjugated bilirubin concentration in pathological jaundice

A
  • greater than 1 mg/dL(> 17 μmol/L) if TSB is more than 5 mg/dL
  • greater than 20% of TSB(suggests neonatal cholestasis)
115
Q

Jaundice after two weeks of age is usually

A

pathological

116
Q

Infants with pathological jaundice show signs of

A

Lethargy, irritability, respiratory distress

117
Q

What causes kernicterus?

A
  • unconjugated bilirubin deposition in basal ganglia and brain stem nuclei
  • due to either acute or chronic hyperbilirubinemia
118
Q

Most bilirubin is produced from

A

the breakdown of Hb into unconjugated bilirubin

119
Q

Unconjugated bilirubin binds to what in blood for transport to liver?

A

albumin

120
Q

what happens to bilirubin in the liver?

A

taken up by hepatocytes and conjugated (made water-soluble) by an enzyme

121
Q

Where is bilirubin excreted after conjugation?

A

excreted in bile into the duodenum

122
Q

What happens to conjugated bilirubin in adults?

A

reduced by gut bacteria into urobilin and excreated

123
Q

Why don’t neonates excrete bilirubin as efficiently as adults?

A

have fewer gut bacteria, so excrete less bilirubin -

124
Q

In addition to fewer gut bacteria to aid in bilirubin excretion, neonates also have

A

an enzyme that deconjugates bili

125
Q

In the neonate, what happens to unconjugated bilirubin?

A
  • reabsorbed and recycled into circulation
  • This is called enterohepatic circculation of bilirubin
126
Q

Some of the most common types of of neonatal jaundice include

A
  • Physiologic hyperbilirubinemia
  • Breastfeeding jaundice
  • Breast milk jaundice
  • Pathologic hyperbilirubinemia due to hemolytic disease
127
Q

What causes physiological jaundice?

A
  • Shorter neonatal RBC life span = INCREASED BILIRUBIN PRODUCTION
  • deficient conjugation due to the deficiency of UGT = DECREASED BILIRUBIN CLEARANCE
  • low bacterial levels in the intestine combined with increased hydrolysis of conjugated bilirubin INCREASED ENTEROHEPATIC CIRCULATION
128
Q

Breastfeeding jaundice main points

A
  • develops in one sixth of breastfed infants during week 1
  • May be seen in first few days after birth, but not before 24 hrs
129
Q

Breastfeeding jaundice mainly occurs in what babies?

A

those who have not established effective breastfeeding because of:

  • sleepiness
  • prematurity
  • poor position
  • poor latch with inadequate milk transfer
130
Q

Breast MILK Jaundice usually develops in

A

first 5 to 7 days of life (usually around transition to mature milk)

131
Q

Breast MILK jaundice usually peaks at

A

about 2 wk

132
Q

Breast MILK jaundice is considered

A

Normal

133
Q

What is thaught to cause breast MILK jaundice?

A
  • increased concentration of β-glucuronidase in breast milk, causing
  • INCREASED DECONJUGATIO and INCREASED RESORPTION of bili
134
Q

The bilirubin produced after birth is insoluble and must be transported

A

to the liver bound to serum albumin

135
Q

Once in the infant’s liver, in order to be excreted, bilirubin must be

A

conjugated with glucuronic acid to form a water-soluble bilirubin

136
Q

ConjDue to its immature, liver, the newborn has limited abliity to do what?

A

Conjugate bilirubin for elimination

137
Q

Conjugation is necessary for bilirubin to be

A

transferred into bile and moved into the small intestine and stool.

138
Q

When is the onset of breastfeeding jaundice?

A
  • earlier than physiologic jaundice
  • but still after day 1
139
Q

What TSB levels may indicate pathological jaundice?

A
  • more than 18 mg/dL
  • Rate of rise of TSB > 0.2 mg/dL/h (> 3.4 μmol/L/h)
    • or > 5 mg/dL/day
  • Conjugated bilirubin concentration > 1 mg/dL (> 17 μmol/L) if TSB is < 5 mg/dL or
  • > 20% of TSB (suggests neonatal cholestasis)