Jaundice - Hepatic and Biliary Disorders - Merck Manuals Professional Edition

10/25/2015
NeonatalHyperbilirubinemiaPediatricsMerckManualsProfessionalEdition
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Neonatal Hyperbilirubinemia
(Jaundice in Neonates)
by Alan Lantzy, MD
Jaundice in Neonates : A Merck Manual of Patient Symptoms podcast
Jaundice is a yellow discoloration of the skin and eyes caused by hyperbilirubinemia
(elevated serum bilirubin concentration). The serum bilirubin level required to cause
jaundice varies with skin tone and body region, but jaundice usually becomes visible on
the sclera at a level of 2 to 3 mg/dL (34 to 51 mol/L) and on the face at about 4 to 5 mg/dL
(68 to 86 mol/L). With increasing bilirubin levels, jaundice seems to advance in a head-tofoot direction, appearing at the umbilicus at about 15 mg/dL (258 mol/L) and at the feet
at about 20 mg/dL (340 mol/L). Slightly more than half of all neonates become visibly
jaundiced in the first week of life.
Consequences of hyperbilirubinemia
Hyperbilirubinemia may be harmless or harmful depending on its cause and the degree of
elevation. Some causes of jaundice are intrinsically dangerous whatever the bilirubin level.
But hyperbilirubinemia of any etiology is a concern once the level is high enough. The
threshold for concern varies by
Age
Degree of prematurity
Health status
Among healthy term infants, the threshold typically is considered to be a level > 18 mg/dL
(> 308 mol/L); see Figure: Risk of hyperbilirubinemia in neonates = 35 wk gestation..
However, infants who are premature, small for gestational age, and/or ill (eg, with sepsis,
hypothermia, or hypoxia) are at much greater risk. In such infants, although risk increases
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with increasing hyperbilirubinemia, there is no level of hyperbilirubinemia that is

considered safe; treatment is given based on age and clinical factors. There are now
suggested operational thresholds to initiate phototherapy based on gestational age.
Neurotoxicity is the major consequence of neonatal hyperbilirubinemia. An acute
encephalopathy can be followed by a variety of neurologic impairments, including cerebral
palsy and sensorimotor deficits; cognition is usually spared. Kernicterus is the most severe
form of neurotoxicity. Although it is now rare, kernicterus still occurs and can nearly
always be prevented. Kernicterus is brain damage caused by unconjugated bilirubin
deposition in basal ganglia and brain stem nuclei, caused by either acute or chronic
hyperbilirubinemia. Normally, bilirubin bound to serum albumin stays in the intravascular
space. However, bilirubin can cross the blood-brain barrier and cause kernicterus in
certain situations:
When serum bilirubin concentration is markedly elevated
When serum albumin concentration is markedly low (eg, in preterm infants)
When bilirubin is displaced from albumin by competitive binders
Competitive binders include drugs (eg, sulfisoxazole, ceftriaxone, aspirin) and free fatty
acids and hydrogen ions (eg, in fasting, septic, or acidotic infants).
Risk of hyperbilirubinemia in neonates 35 wk gestation.

Risk is based on total serum bilirubin levels. (Adapted from Bhutani VK, Johnson L, Sivieri
EM: Predictive ability of a predischarge hour-specific serum bilirubin for subsequent
significant hyperbilirubinemia in healthy term and near-term newborns. Pediatrics 103
(1):614, 1999.)
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Pathophysiology
The majority of bilirubin is produced from the breakdown of Hb into unconjugated
bilirubin (and other substances). Unconjugated bilirubin binds to albumin in the blood for
transport to the liver, where it is taken up by hepatocytes and conjugated with glucuronic
acid by the enzyme uridine diphosphogluconurate glucuronosyltransferase (UGT) to make
it water-soluble. The conjugated bilirubin is excreted in bile into the duodenum. In adults,
conjugated bilirubin is reduced by gut bacteria to urobilin and excreted. Neonates,
however, have less bacteria in their digestive tracts, so less bilirubin is reduced to urobilin
and excreted. They also have the enzyme -glucuronidase, which deconjugates bilirubin.
The now unconjugated bilirubin can be reabsorbed and recycled into the circulation. This
is called enterohepatic circulation of bilirubin (see also Bilirubin metabolism).
Mechanisms of hyperbilirubinemia
Hyperbilirubinemia can be caused by one or more of the following processes:
Increased production
Decreased hepatic uptake
Decreased conjugation
Impaired excretion
Impaired bile flow ( cholestasis)
Increased enterohepatic circulation
Etiology
Classification
There are several ways to classify and discuss causes of hyperbilirubinemia. Because
transient jaundice is common among healthy neonates (unlike adults, in whom jaundice
always signifies a disorder), hyperbilirubinemia can be classified as physiologic or
pathologic. It can be classified by whether the hyperbilirubinemia is unconjugated,
conjugated, or both. It also can be classified by mechanism (see Table: Causes of Neonatal
Hyperbilirubinemia).
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Causes
Most cases involve unconjugated hyperbilirubinemia. Some of the most common causes
of neonatal jaundice include
Physiologic hyperbilirubinemia
Breastfeeding jaundice
Breast milk jaundice
Pathologic hyperbilirubinemia due to hemolytic disease
Liver dysfunction (eg, caused by parenteral alimentation causing cholestasis, neonatal
sepsis, neonatal hepatitis) may cause a conjugated or mixed hyperbilirubinemia.
Physiologic hyperbilirubinemia occurs in almost all neonates. Shorter neonatal RBC life
span increases bilirubin production; deficient conjugation due to the deficiency of UGT
decreases clearance; and low bacterial levels in the intestine combined with increased
hydrolysis of conjugated bilirubin increase enterohepatic circulation. Bilirubin levels can
rise up to 18 mg/dL by 3 to 4 days of life (7 days in Asian infants) and fall thereafter.
Breastfeeding jaundice develops in one sixth of breastfed infants during the first week of
life. Breastfeeding increases enterohepatic circulation of bilirubin in some infants who
have decreased milk intake and who also have dehydration or low caloric intake. The
increased enterohepatic circulation also may result from reduced intestinal bacteria that
convert bilirubin to nonresorbed metabolites.
Breast milk jaundice is different from breastfeeding jaundice. It develops after the first 5
to 7 days of life and peaks at about 2 wk. It is thought to be caused by an increased
concentration of -glucuronidase in breast milk, causing an increase in the deconjugation
and reabsorption of bilirubin.
Pathologic hyperbilirubinemia in term infants is diagnosed if
Jaundice appears in the first 24 h, after the first week of life, or lasts > 2 wk
Total serum bilirubin (TSB) rises by > 5 mg/dL/day
TSB is > 18 mg/dL
Infant shows symptoms or signs of a serious illness
Some of the most common pathologic causes are
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Immune and nonimmune hemolytic anemia

G6PD deficiency
Hematoma resorption
Sepsis
Hypothyroidism
Causes of Neonatal Hyperbilirubinemia

Mechanism
Causes
Breast milk (breast milk jaundice)
Breastfeeding failure (breastfeeding jaundice)
Drug-induced paralytic ileus (magnesium sulfate or morphine)
Increased
enterohepatic
circulation
Fasting or other cause for hypoperistalsis

Hirschsprung disease
Intestinal atresia or stenosis, including annular pancreas
Meconium ileus or meconium plug syndrome
Pyloric stenosis*
Swallowed blood
Overproduction
Breakdown of extravascular blood (eg, hematomas; petechiae; pulmonary, cerebral, or

occult hemorrhage)
Polycythemia due to maternofetal or fetofetal transfusion or delayed umbilical cord
clamping
Certain drugs and agents in neonates with G6PD deficiency (eg, acetaminophen, alcohol,
antimalarials, aspirin, bupivacaine, corticosteroids, diazepam, nitrofurantoin, oxytocin,
penicillin, phenothiazine, sulfonamides)
Overproduction due
to hemolytic anemia
Maternofetal blood group incompatibility (eg, Rh, ABO)

RBC enzyme deficiencies (eg, of G6PD or pyruvate kinase)
Spherocytosis
Thalassemias (, )
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1 -Antitrypsin deficiency*
Biliary atresia*
Undersecretion due
to biliary obstruction
Choledochal cyst*
Cystic fibrosis* (inspissated bile)
Dubin-Johnson syndrome and Rotor syndrome*
Parenteral nutrition
Tumor or band* (extrinsic obstruction)
Crigler-Najjar syndrome (familial nonhemolytic jaundice types 1 and 2)
Drugs and hormones
Gilbert syndrome
Hypermethioninemia
Undersecretion due
Hypopituitarism and anencephaly
to metabolicendocrine conditions Hypothyroidism
Lucey-Driscoll syndrome
Maternal diabetes
Prematurity
Tyrosinosis
Asphyxia
Intrauterine infections
Maternal diabetes
Mixed overproduction Respiratory distress syndrome
and undersecretion
Sepsis
Severe erythroblastosis fetalis
Syphilis
TORCH infections
*Jaundice may also occur outside the neonatal period.
TORCH =toxoplasmosis, other pathogens, rubella, cytomegalovirus, and herpes simplex.
Adapted from Poland RL, Ostrea EM Jr: Neonatal hyperbilirubinemia. In Care of the High-Risk Neonate , ed. 3,
edited by MH Klaus and AA Fanaroff. Philadelphia, WB Saunders Company, 1986.
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Evaluation
History
History of present illness should note age of onset and duration of jaundice. Important
associated symptoms include lethargy and poor feeding (suggesting possible kernicterus),
which may progress to stupor, hypotonia, or seizures and eventually to hypertonia.
Patterns of feeding can be suggestive of possible breastfeeding failure or underfeeding.
Therefore, history should include what the infant is being fed, how much and how
frequently, urine and stool production (possible breastfeeding failure or underfeeding),
how well the infant is latching on to the breast or taking the nipple of the bottle, whether
the mother feels that her milk has come in, and whether the infant is swallowing during
feedings and seems satiated after feedings.
Review of systems should seek symptoms of causes, including respiratory distress, fever,
and irritability or lethargy (sepsis); hypotonia and poor feeding (hypothyroidism, metabolic
disorder); and repeated episodes of vomiting (intestinal obstruction).
Past medical history should focus on maternal infections (toxoplasmosis, other
pathogens, rubella, cytomegalovirus, and herpes simplex [TORCH] infections), disorders
that can cause early hyperbilirubinemia (maternal diabetes), maternal Rh factor and blood
group (maternofetal blood group incompatibility), and a history of a prolonged or difficult
birth (hematoma or forceps trauma).
Family history should note known inherited disorders that can cause jaundice, including
G6PD deficiency, thalassemias, and spherocytosis, and also any history of siblings who
have had jaundice.
Drug history should specifically note drugs that may promote jaundice (eg, ceftriaxone,
sulfonamides, antimalarials).
Physical examination
Overall clinical appearance and vital signs are reviewed.
The skin is inspected for extent of jaundice. Gentle pressure on the skin can help reveal
the presence of jaundice. Also, ecchymoses or petechiae (suggestive of hemolytic anemia)
are noted.
The physical examination should focus on signs of causative disorders.
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The general appearance is inspected for plethora (maternofetal transfusion); macrosomia

(maternal diabetes); lethargy or extreme irritability (sepsis or infection); and any
dysmorphic features such as macroglossia (hypothyroidism) and flat nasal bridge or
bilateral epicanthal folds (Down syndrome).
For the head and neck examination, any bruising and swelling of the scalp consistent with
a cephalohematoma are noted. Lungs are examined for crackles (rales), rhonchi, and
decreased breath sounds (pneumonia). The abdomen is examined for distention, mass
(hepatosplenomegaly), or pain (intestinal obstruction). Neurologic examination should
focus on signs of hypotonia or weakness (metabolic disorder, hypothyroidism, sepsis).
Red flags
The following findings are of particular concern:
Jaundice in the first day of life
TSB > 18 mg/dL
Rate of rise of TSB > 0.2 mg/dL/h (> 3.4 mol/L/h) or > 5 mg/dL/day
Conjugated bilirubin concentration > 1 mg/dL (> 17 mol/L) if TSB is < 5 mg/dL or >
20% of TSB (suggests neonatal cholestasis)
Jaundice after 2 wk of age
Lethargy, irritability, respiratory distress
Interpretation of findings
Evaluation should focus on distinguishing physiologic from pathologic jaundice. History,
physical examination, and timing can help, but typically TSB and conjugated serum
bilirubin levels are measured.
Timing
Jaundice that develops in the first 24 to 48 h, or that persists > 2 wk, is most likely
pathologic. Jaundice that does not become evident until after 2 to 3 days is more
consistent with physiologic, breastfeeding, or breast milk jaundice. An exception is
undersecretion of bilirubin due to metabolic factors (eg, Crigler-Najjar syndrome,
hypothyroidism, drugs), which may take 2 to 3 days to become evident. In such cases,
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bilirubin typically peaks in the first week, accumulates at a rate of < 5 mg/dL/day, and can
remain evident for a prolonged period. Because most neonates are now discharged from
the hospital or nursery within 48 h, many cases of hyperbilirubinemia are detected only
after discharge.
Physical Findings in Neonatal Jaundice

Findings
Timing of Jaundice
Cause
General examination
First 24 h
Fever, tachycardia, respiratory
distress
Lethargy, hypotonia
Accumulates >5
mg/dL/day (> 86
mol/L/day)
May appear in the
first 2448 h
Can be prolonged
(> 2 wk)
Pneumonia, TORCH infection, sepsis
Hypothyroidism, metabolic disorder
2448 h
Macrosomia
Can accumulate > 5

mg/dL
First 24 h
Petechiae
Accumulates >5
mg/dL
First 24 h
Plethora
Accumulates >5
mg/dL
Maternal diabetes
Hemolytic states (eg, maternofetal blood group

incompatibility, RBC enzyme deficiencies, hereditary
spherocytosis, thalassemias, sepsis)
Maternofetal or fetofetal transfusion, delayed umbilical

cord clamping
Head and neck examination

Bilateral slanting palpebral
fissures, flat nasal bridge,
macroglossia, flattened occiput
First 23 days
Down syndrome (possible duodenal atresia,

Hirschsprung disease, intestinal obstruction, wide
spacing between 1st and 2nd toes)
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Cephalohematoma
2448 h
Can accumulate > 5
mg/dL
Birth trauma
2448 h
Macroglossia
Can be prolonged
(> 2 wk)
Hypothyroidism
Abdominal examination
Abdominal distention, decreased

bowel sounds
Possible delayed
manifestation (23
days or later)
Intestinal obstruction (eg, cystic fibrosis, Hirschsprung

disease, intestinal atresia or stenosis, pyloric stenosis,
biliary atresia)
TORCH =toxoplasmosis, other pathogens, rubella, cytomegalovirus, and herpes simplex.
Testing
Diagnosis is suspected by the infants color and is confirmed by measurement of serum
bilirubin. Noninvasive techniques for transcutaneous measurement of bilirubin levels in
infants are being used increasingly, with good correlation with serum bilirubin
measurements. Risk of hyperbilirubinemia is based on age-specific TSB levels.
A bilirubin concentration> 10 mg/dL (> 170 mol/L) in preterm infants or > 18 mg/dL in
term infants warrants additional testing, including Hct, blood smear, reticulocyte count,
direct Coombs test, TSB and direct serum bilirubin concentrations, and blood type and Rh
group of the infant and mother.
Other tests, such as blood, urine, and CSF cultures to detect sepsis and measurement of
RBC enzyme levels to detect unusual causes of hemolysis, may be indicated by the history
and physical examination. Such tests also may be indicated for any neonates with an initial
bilirubin level > 25 mg/dL (> 428 mol/L).
Treatment
Treatment of hyperbilirubinemia is directed at the underlying disorder. In addition,
treatment for hyperbilirubinemia itself may be necessary.
Clinical Calculator: Newborn Hyperbilirubinemia Assessment
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Physiologic jaundice usually is not clinically significant and resolves within 1 wk. Frequent
formula feedings can reduce the incidence and severity of hyperbilirubinemia by
increasing GI motility and frequency of stools, thereby minimizing the enterohepatic
circulation of bilirubin. The type of formula does not seem important in increasing bilirubin
excretion.
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, and the mother should be encouraged to continue
expressing breast milk regularly so she can resume nursing as soon as the infants bilirubin
level starts to decline. She also should be assured that the 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 mothers production of
milk.
Definitive treatment of hyperbilirubinemia involves
Phototherapy
Exchange transfusion
Phototherapy
This treatment remains the standard of care, most commonly using fluorescent white light.
(Blue light, wavelength 425 to 475 nm, is most effective for intensive phototherapy.)
Phototherapy is the use of light to photoisomerize unconjugated bilirubin into forms that
are more water-soluble and can be excreted rapidly by the liver and kidney without
glucuronidation. It provides definitive treatment of neonatal hyperbilirubinemia and
prevention of kernicterus.
For neonates born at 35 wk gestation, phototherapy is an option when unconjugated
bilirubin is >12 mg/dL (> 205.2 mol/L) and may be indicated when unconjugated bilirubin
is > 15 mg/dL at 25 to 48 h, 18 mg/dL at 49 to 72 h, and 20 mg/dL at> 72 h (see Figure: Risk
of hyperbilirubinemia in neonates = 35 wk gestation.). Phototherapy is not indicated for
conjugated hyperbilirubinemia.
For neonates born at < 35 wk gestation, threshold bilirubin levels for treatment are lower
because premature infants are at a greater risk of neurotoxicity. The more preterm the
infant, the lower the threshold (see Table: Suggested Thresholds* for Starting
Phototherapy or Exchange Transfusion in Infants < 35 wk Gestation).
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Suggested Thresholds* for Starting Phototherapy or Exchange

Transfusion in Infants < 35 wk Gestation
Exchange
Phototherapy Transfusion
Gestational Age (wk)
(total serum
bilirubin,
mg/dL)
(total
serum
bilirubin,
mg/dL)
< 28
56
1114
28 to < 30
68
1214
30 to < 32
810
1316
32 to < 34
1012
1518
34 to < 35
1214
1719
*Consensus-based recommendations adapted from Maisels MJ, Watchko JF, Bhutani

VK, Stevenson DK: An approach to the management of hyperbilirubinemia in the
preterm infant less than 35 weeks of gestation. Journal of Perinatology 32:660664,
2012.
Because visible jaundice may disappear during phototherapy even though serum bilirubin
remains elevated, skin color cannot be used to evaluate jaundice severity. Blood taken for
bilirubin determinations should be shielded from bright light, because bilirubin in the
collection tubes may rapidly photo-oxidize.
Exchange transfusion
This treatment can rapidly remove bilirubin from circulation and is indicated for severe
hyperbilirubinemia, which most often occurs with immune-mediated hemolysis. Small
amounts of blood are withdrawn and replaced through an umbilical vein catheter to
remove partially hemolyzed and antibody-coated RBCs as well as circulating Igs. The blood
is replaced with uncoated donor RBCs that do not have the RBC membrane antigen that
binds the circulating antibodies. That is, type O blood is used if the neonate is sensitized to
AB antigens and Rh-negative blood is used if the neonate is sensitized to Rh antigen.
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Because adult donor RBCs have more ABO antigen sites than fetal cells, type-specific
transfusion will intensify the hemolysis. Only unconjugated hyperbilirubinemia can cause
kernicterus, so if conjugated bilirubin is elevated, the level of unconjugated rather than
total bilirubin is used to determine the need for exchange transfusion.
For term infants, specific indications are serum bilirubin 20 mg/dL at 24 to 48 h or 25
mg/dL at > 48 h and failure of phototherapy to result in a 1- to 2-mg/dL (17- to 34-mol/L)
decrease within 4 to 6 h of initiation or at the first clinical signs of kernicterus regardless of
bilirubin levels. If the serum bilirubin level is > 25 mg/dL when the neonate is initially
examined, preparation for an exchange transfusion should be made in case intensive
phototherapy fails to lower the bilirubin level.
Thresholds have been suggested for neonates born at < 35 wk gestation (see ). Previously,
some clinicians used criteria based solely on patient weight, but these criteria have been
replaced by the more specific guidelines described above.
Most often, 160 mL/kg (twice the infants total blood volume) of packed RBCs is exchanged
over 2 to 4 h; an alternative is to give 2 successive exchanges of 80 mL/kg each over 1 to 2
h. To do an exchange, 20 mL of blood is withdrawn and then immediately replaced by 20
mL of transfused blood. This procedure is repeated until the total desired volume is
exchanged. For critically ill or premature infants, aliquots of 5 to 10 mL are used to avoid
sudden major changes in blood volume. The goal is to reduce bilirubin by nearly 50%, with
the knowledge that hyperbilirubinemia may rebound to about 60% of pretransfusion level
within 1 to 2 h. It is also customary to lower the target level by 1 to 2 mg/dL in conditions
that increase the risk of kernicterus (eg, fasting, sepsis, acidosis). Exchange transfusions
may need to be repeated if bilirubin levels remain high. Finally, there are risks and
complications with the procedure, and the success of phototherapy has reduced the
frequency of exchange transfusion.
Key Points
Neonatal jaundice is caused by increased bilirubin production, decreased bilirubin
clearance, or increased enterohepatic circulation.
Some jaundice is normal in neonates.
Risk varies with postnatal age, TSB value, prematurity, and health of the neonate.
Treatment depends on cause and degree of bilirubin elevation; the more preterm the
infant, the lower the threshold level for treatment.
Definitive treatments include phototherapy and exchange transfusion.
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Last full review/revision August 2015 by Alan Lantzy, MD

Metabolic, Electrolyte, and Toxic Disorders in Neonates
Neonatal Hyperbilirubinemia
Kernicterus
Neonatal Hypercalcemia
Neonatal Hypocalcemia
Neonatal Hyperglycemia
Neonatal Hypoglycemia
Neonatal Hypernatremia
Neonatal Hyponatremia
Prenatal Drug Exposure
Fetal Alcohol Syndrome
Perinatal Polycythemia and Hyperviscosity Syndrome
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Jaundice - Hepatic and Biliary Disorders - Merck Manuals Professional Edition

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10/25/2015

* This is the Professional Version. *

with increasing hyperbilirubinemia, there is no level of hyperbilirubinemia that is

Risk of hyperbilirubinemia in neonates 35 wk gestation.

Immune and nonimmune hemolytic anemia

Causes of Neonatal Hyperbilirubinemia

Fasting or other cause for hypoperistalsis

Breakdown of extravascular blood (eg, hematomas; petechiae; pulmonary, cerebral, or

Maternofetal blood group incompatibility (eg, Rh, ABO)

The general appearance is inspected for plethora (maternofetal transfusion); macrosomia

Physical Findings in Neonatal Jaundice

Pneumonia, TORCH infection, sepsis

Hypothyroidism, metabolic disorder

Can accumulate > 5

Hemolytic states (eg, maternofetal blood group

Maternofetal or fetofetal transfusion, delayed umbilical

Head and neck examination

Down syndrome (possible duodenal atresia,

Abdominal distention, decreased

Intestinal obstruction (eg, cystic fibrosis, Hirschsprung

TORCH =toxoplasmosis, other pathogens, rubella, cytomegalovirus, and herpes simplex.

Suggested Thresholds* for Starting Phototherapy or Exchange

*Consensus-based recommendations adapted from Maisels MJ, Watchko JF, Bhutani

Last full review/revision August 2015 by Alan Lantzy, MD

* This is a professional Version *

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