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
2
Q
When does jaundice usually become visible on the sclera?
A
FIRST
34 to 51 μmol/L
(2-3 mg/dl)
3
Q
When does jaundice become visible on the face?
A
68 to 86 μmol/L
( about 4 to 5 mg/dL)
4
Q
Jaundice advances in a
A
head-to-foot direction
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)
6
Q
How many neonates become visibly jaundiced in the first week of life?
A
Slightly more than half
7
Q
Hyperbilirubinemia may be harmless or harmful depending on
A
its cause and the degree of elevation
8
Q
The threshold for concern for jaundice varies by
A
- Age
- Degree of prematurity
- Health status
9
Q
Jaundice threshold for healthy term infants
A
more than 308 μmol/L
( 18 mg/dL )
10
Q
Infants who are premature, small for gestational age, or ill (sepsis, hypothermia, hypoxia) are at
A
much greater risk than healthy newborns
11
Q
Treament for hyperbilirubinemia is given based on
A
- age
- clinical factors
12
Q
what is the major consequence of neonatal hyperbilirubinemia
A
Neurotoxicity
13
Q
How does neurotoxicity manifest
A
- acute encephalopathy
- can be followed by neuro problems eg
- cerebral palsy
- sensorimotor deficits
- cognition is usually spared
14
Q
What is the most severe form of neurotoxicity
A
Kernicterus
15
Q
Does kernicterus still occur?
A
Yes, although rare
16
Q
What is kernicterus?
A
- brain damage
- Also known as Bilirubin encephalopathy
17
Q
Bilirubin is normally bound to
A
- Serum albumin
- therfore stays in the vascular space
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)
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).
20
Q
Risk of hyperbilirubinemia in neonates ≥ 35 weeks gestation
A
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
22
Q
Mechanisms of hyperbilirubinemia
A
- Increased production of bilirubin
- Decreased hepatic uptake
- Decreased conjugation
- Impaired excretion
- Impaired bile flow (cholestasis)
- Increased enterohepatic circulation
23
Q
Most cases of jaundice involve
A
unconjugated hyperbilirubinemia.
24
Q
What may cause a conjugated or mixed hyperbilirubinemia.
A
LIVER PROBLEMS
- Liver dysfunction
- neonatal sepsis
- neonatal hepatitis
25
**Physiologic hyperbilirubinemia main points**
* 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.
26
What is **Breastfeeding Jaundice** also known as?
* **starvation jaundice**
* **breast-non-feeding jaundice**
27
What is **breast milk jaundice?**
* different from breastfeeding jaundice
* Usually in healthy, thriving infants
28
**Pathologic hyperbilirubinemia** in term infants is diagnosed if
* 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
29
Some of the most common causes of pathologic hyperbilirubinemia are
* hemolytic anemia
* G6PD deficiency (inc RBC breaskdown)
* Hematoma resorption
* Sepsis
* Hypothyroidism
30
What findings may indicate pathological jaundice?
* Jaundice in the **first day of life**
* **Jaundice after 2 wk of age**
* **Lethargy, irritability, respiratory distress**
31
Jaundice that develops in the first 24 to 48 h, or that persists \> 2 wk, is most likely
pathologic
32
aundice that does not become evident until after 2 to 3 days is more consistent with
physiologic, breastfeeding, or breast milk jaundice
33
Diagnosis of hyperbilirubinemia
Diagnosis is suspected by the infant’s color and is confirmed by measurement of serum bilirubin
34
What bilirubin concentration in infants warrants further testing?
* **\> 10 mg/dL (\> 170 μmol/L)** in preterm infants
* or **\> 18 mg/dL** in term infants
35
Treatment of hyperbilirubinemia is directed at
the underlying disorder.
36
Treatment for **physiologic jaundice**
* 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.
37
with **breastfeeding jaundice,** it is not advisable to supplement with
* water or dextrose
* it may disrupt the mother’s production of milk.
38
in **breastfeeding jaundice,** assure mother that
hyperbilirubinemia has not caused any harm and that she may safely resume breastfeeding.
39
in **breastfeeding jaundice,** stopping breastfeeding is necessary for
* only 1 or 2 days
* mother should continue to express
40
in **breastfeeding jaundice,** what may be appropriate at higher bilirubin levels?
phototherapy
41
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
42
**breastfeeding jaundice** may be prevented or reduced by
increasing the frequency of feedings
43
Treatment for **breastfeeding jaundice**
* 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.
44
Definitive treatment of hyperbilirubinemia involves
* Phototherapy
* Exchange transfusion
45
What is phototherapy
* 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.
46
What is an exchange teansfucion
* For severe hyperbilirubinemia,
* rapidly removes bilirubin
* Small amounts of blood drawn and replaced through umbilical vein catheter
47
48
Where does bilirubin come from?
* 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
49
50
Amount of jaundice in a newborn depends on
the balance of bilirubin production and elimination.
51
the balance of bilirubin production and elimination may be upset because of
* (a) increased bilirubin production
* (b**) decreased ability to metabolize** the bilirubin for elimination
* (c) **decreased elimination and increased absorption** of bilirubin in the intestines.
52
What leads to additional produciton of bilirubin in the neonate?
* 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
53
what causes Increased bilirubin production after birth?
* blood is transferred from the placenta to the newborn, further increasing blood volume and hemoglobin concentrations.
* Immature or inactive RBCs are destryed --\> inc bilirubin
54
In the newborn, unconjugated bilirubin enters the liver cells
slower than in an older chil
55
Conjugation of bilirubin is necessary for
bilirubin to be transferred into bile and moved into the small intestine and stool.
56
Decreased Elimination and Increased Absorption of Bilirubin in the Intestines
* 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
In healthy, Caucasian, term intants, bilirubin levels peak on what days?
2-3
58
Jaundice resolves in most formula-fed infants by what day?
day 7
59
Breastmilk jaundice onset
* Usually after day 5
* (extension of physiological jaundice)
* potentially existing for many weeks
60
What type of baby might get starvation/breastfeeding/breast-non feeding jaundice?
breasfed baby who is not getting enough milk
61
POtential causes of breastmilk jaundice
* Increase in intestinal absorption of bilirubin
* Due to an as yet unknown substance in milk
62
Causes of breastfeeding jaundice
* 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
Solution for breastfeeding jaundice
* Correct the breastfeeding problem
* restore fluid and caloric intake.
64
65
What factors have been associated with exaggerated hyperbilirubinemia (Pathological Hyperbilirubinemia) ?
* 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
What is the initial presentation of kernicterus?
* Lethargy
* poor feeding
* vomiting
* irregular respirations
67
How can kernicterus be reversed in the early stages?
Removing bilirubin from the circulation and brain by **exchange transfusion**
68
If severe hyperbilirubinemia continues
the infant manifests severe neurologic signs
69
Survivors of kernicterus almost always bave
significant permanent neurologic damage
70
What was used to determine levels of jaundice in the past?
Inspection/visual estimation
71
Why is visual estimation no longer used for jaundice assesment?
unreliable and inaccurate
72
Experts now recommend what assessment for jaundice?
screen all infants by serum or transcutaneous level of bilibrubin prior to discharge
73
Where is serum bilirubin plotted?
On the nomogram
74
What is the purpose of the nomogram?
to determine an infant’s risk for significant hyperbilirubinemia.
75
In addition to plotting on the nomogram, what else must be done before discharge?
Adequate breastfeeding must be established and documented
76
Follow-up assessments for jaundice
* A follow-up visit with HCP at 3 to 5 days of age
* for further assessment, teaching, and support of the family
77
What are considered when managing jaundice?
* The baby’s age
* general condition
* serum bilirubin level
* cause of the hyperbilirubinemia
78
While it is known that there is an association between breastfeeding and jaundice...
* breastfeeding must be optimized and supported
* it is important to convey that breastfeeding is helpful, not harmful.
79
In managing jaundice, it is important to help mothers and their babies with the following:
* 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
81
Infants receiving phototherapy should continue to
breastfeed
82
Do infants receiving phototherapy require IV fluids
Not unless they show signs of dehydration
83
phototherapy has been found to increase the baby’s
fluid requirements
84
Why are babies’ eyes are covered during phototherapy treatments
toavoid corneal damage.
85
Very high or rapidly increasing bilirubin levels may need to be controlled with
an exchange transfusion.
86
Physiologic hyperbilirubinemia occurs in
almost all neonates
87
Physiologic hyperbilirubinemia generally resolves when?
* first week of life (formula fed)
* first few weeks (breastfed)
88
Physiologic hyperbilirubinemia is caused by
* 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
Physiologic hyperbilirubinemia
bilirubin levels
* up to 18 mg/dL by 3 to 4 days of life (7 days in Asian infants)
* fall afterward
90
Breastfeeding jaundice is also known as
* starvation jaundice
* breast-non-feeding jaundice
91
Breastfeeding jaundice develops in what infants?
* develops in one sixth of breastfed infants during the first week of life
92
Breastfeeding jaundice is usually seen on what day of life?
May be seen in first few days after birth, but **not before 24 hrs**
93
Breastfeeding jaundice usually occurs in babies who have not established effective breastfeeding because of
* sleepiness
* prematurity
* poor position
* poor latch with inadequate milk transfer.
94
What is the standard of treatment for hyperbilirubinemia?
phototherapy
95
How does phototherapy work?
The light is absorbed by bilirubin, making it water soluble and able to be excreted in the stool and urine
96
Breastfeeding jaundice may be prevented or reduced by
increasing the frequency of feedings
97
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
98
Most cases of jaundice involve
unconjugated hyperbilirubinemia
99
Once in the liver, bilirubin must be conjugated with
* glucuronic acid
* to form a water-soluble bilirubin
* but the newborn, due to its immature liver, has limited ability to do this
100
Conjugation is necessary for bilirubin to be
transferred into bile and moved into the small intestine and stool.
101
To manage jaundice, breastfeeding must be started early to promote what?
the passage of meconium.
102
Important parts of breastfeeding to manage jaundice
* 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
**Causes of patholotical jaundice**
Decreased elimination of bilirubin caused by
* genetic conjugation disorders
* low intake at feedings
* prematurity/immature liver metabolism
* breastmilk feedings
104
**Causes of patholotical jaundice**
metabolic disorders
* galactosemia
* hypothyroidism
105
**Causes of patholotical jaundice**
Liver diseases
* hepatitis
* Crigler-Najjar syndrome
* Rotor’s syndrome
* liver damage from CMV
* toxoplasmosis
* rubella
* syphilis
* congenital biliary atresia
106
**Causes of patholotical jaundice**
reduction in the number of carrier proteins (albumin) or binding sites caused by
* prematurity
* sepsis
* hypoxia
* use of certain drugs
107
**Causes of patholotical jaundice**
Risk factors
* prematurity
* maternal diabetes
* urinary tract infection
* G6PD deficiency
* Asian race
108
**Causes of patholotical jaundice**
Increased production of bilirubin related to
**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
Pathologic jaundice is diagnosed if infant shows
symptoms or signs of a serious illness
110
Pathologic jaundice is diagnosed if TSB
* rises by more than 5 mg/dL/day
* TSB is more than 18 mg/dL
111
Pathologic jaundice is diagnosed if it appears
* in the first 24 h
* after the first week of life
* lasts \> 2 wk
112
Jaundice in the first day of life is usually
pathological
113
TSB rate in pathological jaundice
**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
Conjugated bilirubin concentration in pathological jaundice
* 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
Jaundice after two weeks of age is usually
pathological
116
Infants with pathological jaundice show signs of
Lethargy, irritability, respiratory distress
117
What causes kernicterus?
* unconjugated bilirubin deposition in **basal ganglia and brain stem nuclei**
* due to either acute or chronic hyperbilirubinemia
118
Most bilirubin is produced from
the breakdown of Hb into unconjugated bilirubin
119
Unconjugated bilirubin binds to what in blood for transport to liver?
albumin
120
what happens to bilirubin in the liver?
taken up by hepatocytes and conjugated (made water-soluble) by an enzyme
121
Where is bilirubin excreted after conjugation?
excreted in bile into the duodenum
122
What happens to conjugated bilirubin in adults?
reduced by gut bacteria into urobilin and excreated
123
Why don't neonates excrete bilirubin as efficiently as adults?
have fewer gut bacteria, so excrete less bilirubin -
124
In addition to fewer gut bacteria to aid in bilirubin excretion, neonates also have
an enzyme that deconjugates bili
125
In the neonate, what happens to unconjugated bilirubin?
* reabsorbed and recycled into circulation
* This is called **enterohepatic circculation of bilirubin**
126
Some of the most common types of of neonatal jaundice include
* Physiologic hyperbilirubinemia
* Breastfeeding jaundice
* Breast milk jaundice
* Pathologic hyperbilirubinemia due to hemolytic disease
127
What causes physiological jaundice?
* 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
Breastfeeding jaundice main points
* 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
Breastfeeding jaundice mainly occurs in what babies?
those who have not established effective breastfeeding because of:
* sleepiness
* prematurity
* poor position
* poor latch with inadequate milk transfer
130
Breast **MILK** Jaundice usually develops in
first 5 to 7 days of life (usually around transition to mature milk)
131
Breast MILK jaundice usually peaks at
about 2 wk
132
Breast MILK jaundice is considered
Normal
133
What is thaught to cause breast MILK jaundice?
* increased concentration of β-glucuronidase in breast milk, causing
* INCREASED DECONJUGATIO and INCREASED RESORPTION of bili
134
The bilirubin produced after birth is insoluble and must be transported
to the liver bound to serum albumin
135
Once in the infant's liver, in order to be excreted, bilirubin must be
conjugated with glucuronic acid to form a water-soluble bilirubin
136
ConjDue to its immature, liver, the newborn has limited abliity to do what?
Conjugate bilirubin for elimination
137
Conjugation is necessary for bilirubin to be
transferred into bile and moved into the small intestine and stool.
138
When is the onset of breastfeeding jaundice?
* earlier than physiologic jaundice
* but still after day 1
139
What TSB levels may indicate pathological jaundice?
* 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)
