Hyperbilirubinemia didactics at Neonatal Intensive Care Unit
Source: Nelson's Textbook of Pediatrics 19th edition
Most pictures were taken from Google images
Please find the power point on Phototherapy in jaundice . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Please find the power point on Phototherapy in jaundice . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Neonatal jaundice occurs in 60% of term and 80% of preterm babies. Despite Neonatal jaundice is one of the commonest neonatal conditions, there are no national practice guidelines for its management in our country. Lack of uniform guidelines and standard practice parameters for diagnosis and management of neonatal jaundice often leads many babies to develop unnoticed hyperbilirubinemia causing kernicterus and long term poor neurological sequelae. This review after briefly discussing the epidemiology and pathophysiology of neonatal jaundice provides evidence-based pragmatic guidelines for the diagnosis and management of neonatal jaundice in resource-limited countries like Afghanistan
Management of child with neonatal jaundiceNEHA MALIK
Newborn jaundice is a yellowing of a baby's skin and eyes. Newborn jaundice is very common and can occur when babies have a high level of bilirubin, a yellow pigment produced during normal breakdown of red blood cells.
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Icterus neonatorum presentation for studentsNehaNupur8
Introduction
Definition
Metabolism and excretion of bilirubin
Causes
Symptoms
Types
Physiological jaundice
Pathological jaundice
Breast milk jaundice
Neo natal jaundice is a yellow discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin level.
Neo natal jaundice becomes apparent at serum bilirubin concentration of 5-7mg / dL.
Shoulder and trunk 8-10mg/dl
Lower body – 10-12mg/dl.
Entire body 12-15 mg /DL
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...
Hyperbilirubinemia
1. Jackie Lou C. Acha
West Visayas State University College of Medicine
Neonatal Intensive Care Unit
2. Hyperbilirubinemia
The state of excessive amount of bile
pigment billirubin in the blood visibly
manifested as jaundice.
Jaundice
Yellowish discoloration of
the skin, sclerae, and
mucous membranes due
to accumulation of
bilirubin pigment
3. Hyperbilirubinemia
Unconjugated bilirubin (Normal: 0.2 to 1.4 mg/dL)
- indirect bilirubin
- nonpolar
- lipid soluble (indirect reacting)
Conjugated bilirubin (Normal: 0.1 to 0.4 mg/dL)
- direct bilirubin
- polar
- water soluble (direct reacting)
5. Bilirubin (bile pigment)
- end product of hemoglobin
metabolism that is excreted in bile.
- Neonates
75% - from catabolism of circulating
RBC
25% - from ineffective erythropoeisis
(bone marrow)
- from turnover of heme proteins
and free heme (liver)
9. Bilirubin Formation
When the heme portion of hemoglobin is
metabolized beliverdin is formed
When beliverdin is reduced it becomes
bilirubin, which immediately combines
with plasma protein and becomes free
bilirubin
10. Free bilirubin is absorbed by the hepatic
cells and is then released from the
plasma protein by glucuronide to form
bilirubin glucuronide or sulfate which
forms bilirubin sulfate.
11. The conjugated bilirubin is excreted in
the bile and is transformed by bacterial
flora to urobilinogen which is very
soluble.
5% of reabsorbed urobilinogen is
excreted in the urine by the kidneys and
the rest is re excreted in the liver.
14. Manifested as yellowing of the:
Face ~5 mg/dl
Abdomen ~15mg/dl
Soles ~20 mg/dl
Jaundice usually becomes apparent in a
cephalocaudal progression.
15. Bright yellow/ orange= indirect bilirubin
in the skin
Greenish/ muddy yellow cast= jaundice
of the obstructive type (direct bilirubin)
17. Risk Factors for Neonatal
Hyperbilirubinemia
J A U N D I C E
Jaundice visible on the 1st day of life
A sibling with neonatal jaundice or anemia
Unrecognized hemolysis (ABO, Rh incompatibility); UDP-glucoronyl
transferace deficiency (Crigler-Najjar, Gilbert disease)
Nonoptimal feeding (formula or breast-feeding)
Deficiency of G6PD
Infection, Infant of diabetic mother, Immaturity (prematurity)
Cephalhematoma or bruising, Central hematocrit >65% (polycythemia)
East Asian, Mediterranean, Native American heritage
18. Physiologic Jaundice
a.k.a. ICTERUS NEONATORUM
Transient
Occurs during the 1st week of life
(usually on the 2nd and 3rd day)
A result of:
1. increased bilirubin production
2. decreased ability of the liver to clear
the bilirubin from plasma
19. 6-7% of full-term infants have indirect
bilirubin levels >12.9 mg/dL
<3% have levels >15 mg/dL
20. Physiologic Jaundice
I. Increased bilirubin production
Normal bilirubin production in newborn
8-10 mg/kg/day (twice the rate of normal daily
production in the adult)
Normal level of indirect-reacting bilirubin in
umbilical cord serum= 1-3mg/dL
Rises at a rate of <5mg/dL/24hr
Peak= between 2nd and 4th days at 5-6mg/dL
21. Factors that result to increased
bilirubin production
1. Larger circulating red blood cell volume in
the newborn
2. Shortened RBC life span (70-90 days vs
120 days in adult)
3. Substantial production from sources other
than senescent red cells
4. Increased enterohepatic circulation of
bilirubin
22. Physiologic Jaundice
II. Decreased clearance of bilirubin from
plasma
Factors:
1. Deficient Ligandin, a protein
responsible from binding bilirubin in the
hepatocyte
2. Decreased activity of the conjugating
enzyme, UDP-glucuronosyl
transferase (<1% of adult activity
during the first 10 days of life)
23. Non-physiologic Jaundice
A. Overproduction Hyperbilirubinemia
Blood Group Incompatibilities
Maternal-fetal or feto-fetal transfusions
Non Immune Hemolytic Anemias
Structurally Abnormal Red Cells
Extravascular Hemolysis
24. Non-physiologic Jaundice
B. Undersecretion Hyperbilirubinemia
Enzymatic Deficiency
Hormonal Suppression (Breastmilk
Jaundice)
Inhibition of Conjugation
Hepatic Cell Injury Due to Infections
Substrate Deficiency (hypoglycemia)
Mechanical Obstruction
26. Maternal antibodies are developed from
the infant’s antigens which results into
hemolysis.
Strongly considered if there is presence
of jaundice in the first 24 hours of life.
27. B. Maternal-fetal or Feto-fetal
Transfusion
Results into increased number of red
cells, the degradation of which the infant
liver may not be able to handle.
28. C. Non Immune Hemolytic Anemias
G6PD Deficieny
G6PD deficiency dec. NADPH dec
GSH dec. protection of RBCs from
oxidants dec. red cell integrity
hemolysis
Excess of Vitamin K given IM
29. D. Structurally Abnormal Red Cells
Pyknocytes –RBC are smaller than
normal and have irregular borders with
spiny projection.
Spherocytic Anemia –Sphere shaped
RBC
30. E. Extravascular Hemolysis
Results in infants with extensive
petechiae or large hematomas which
leads to severe jaundice due to
increased hemoglobin catabolism at
these sites.
31. Undersecretion of Bilirubin
Majority of infants with undersecretion
hyperbilirubinemia become jaundiced on
the second or third day of life.
32. A. Enzymatic Deficiency
Deficient Glucuronyl Transferase –
no longer considered physiologic if the
duration is longer than 2 weeks and
bilirubin levels >12mg/dl in FT and
15mg/dl in PT.
33. B. Hormonal Suppression
Pregnandiol (breastmilk Jaundice)
- Present in maternal breast milk which
suppresses bilirubin conjugation.
-Breast feeding may be stopped and
restarted in a period of 48 hours.
34. Breastfeeding Jaundice versus
Breastmilk Jaundice
Parameters Breastfeeding Jaundice Breastmilk Jaundice
Onset 3rd-4th day of life Late- start to rise on day 4; may reach
20-30mg/dL on day 14 then decrease
slowly, Normal by 4-12 weeks
Pathophysiology Decrease milk intake
resulting to increase
enterohepatic circulation
Unknown; probably due to B-
glucuronidase in breastmilk which
increase enterohepatic circulation;
Normall Liver Function Test, (-)
Hemolysis
Management Fluid and caloric
supplementation
If breastfeeding is stopped, rapid
decrease in bilirubin level in 48 hours,
if resumed may rise to 2-4mg/dL but
not to previous level
36. C. Inhibition of Conjugation
Sulfonamides and Vitamin K –results in
competitive conjugation inhibition of
bilirubin.
Galactosemia –absent or deficient
galactose 1-phosphate uridyl
transferase which is needed in
glucuronidation of indirect bilirubin.
37. D. Hepatic Cell Injury Due to Infections
-Results in the destruction of liver
parenchyma thus reducing liver mass
available for bilirubin excretion.
38. E. Substrate Deficiency (hypoglycemia)
Glucose is the precursor of glucuronic
acid which is involved in bilirubin
conjugation.
39. F. Mechanical Obstruction
Biliary Atresia
- obstruction of the bile ducts
Idiopathic Neonatal Hepatitis
- giant cell transformation, increased
extramedullary hematopoiesis, and
inflammation
40. Diagnostic Approach to neonatal
Jaundice
Jaundice
Measure total and direct bilirubin
Jaundice not physiological
Blood
types, Rh, Coombs’,
hematocrit, RBC
morphology, Reticulo
cyte count
41. Increased direct bilirubin
Intrauterine Infections
Toxoplasmosis
Rubella
CMV
Herpes simplex
Syphilis
Biliary atresia
Paucity of intrahepatic bile
ducts
Giant cell hepatitis
Alpha-antitrypsin deficiency
Sepsis
Bile Plugs
Choledochal cyst
Cystic fibrosis
Galactosemia
Tyrosinosis
Hypermethioninemia
Increased indirect bilirubin
Coombs’ test
positive
•isoimmunization
Rh
ABO
Minor blood
group
Coombs’ test
negative
Hematocrit
42. Hematocrit
Normal or low
Red cell morphology
and reticulocyte count
Abnormal
Specific
morphological
abnormalities
Spherocytosis
Elliptocytosis
Stomatocytosis
Pyknocytosis
Non specific
abnormalities
ABO incompatibility
G6PD deficiency
Pyruvate kinase
deficiency
Alpha-thalassemia
DIC
High
Twin-twin transfusion
Maternal-fetal transfusion
Delayed cord clamping
Small for dates
Normal
Extravascular blood
Cephalhematoma, bruising, other
hemorrhage
Increased Enterohepatic circulation
Breast feeding
Pyloric stenosis
Small or large bowel obstruction
Swallowed blood
Metabolic-endocrine
Congenital glucuronyl transferase
deficiency
Galactosemia
Hypothyroidism
Breast milk jaundice
Others: Infants of DM mother; inadequate
43. Kernicterus
If untreated, hyperbilirubinemia can
result to kernicterus or the deposition of
bilirubin in the brain.
Usually occurs if the bilirubin levels are
25mg/dl or higher in term infants
Toxicity starts at 8-12 mg/dl in sick or
low birth weights
44. Clinical Features of Kernicterus
ACUTE FORM
Phase 1(1st 1–2 days):
poor sucking, stupor, hypotonia, seizures
Phase 2 (middle of 1st wk):
hypertonia of extensor
muscles, opisthotonos, retrocollis, fever
Phase 3 (after the 1st wk):
hypertonia (hypotonia in Spitzer)
45. Kernicterus
CHRONIC FORM
First year: hypotonia, active deep tendon
reflexes, obligatory tonic neck
reflexes, delayed motor skills
After 1st yr: movement disorders
(choreoathetosis, ballismus, tremor), up
ward gaze, sensorineural hearing loss
46.
47. Phototherapy
- Primary treatment
- infant is unclothed and is exposed to 20 watt
daylight or blue fluorescent light at 30 inches.
48. Principle
Bilirubin absorbs light maximally in the
blue range (420–470 nm).
Phototherapy detoxifies bilirubin by
converting it to photoproducts that are
less lipophilic than bilirubin and that can
then be excreted without further
metabolism
49. Reactions in phototherapy
1. Photo-isomerization (reversible)
- toxic native unconjugated 4Z, 15Z-
bilirubin is converted into an unconjugated
configurational isomer 4Z,15E-bilirubin
-comprises about 20% of TSB in a baby
under phototherapy
2. Structural isomerization (irreversible)
-Bilirubin becomes Lumirubin
-cleared from the serum much more rapidly
50. Usually continued for 5 days, the time
wherein physiologic jaundice subsides.
- Baby’s eyes are shielded to avoid retinal
degeneration
52. Management
Double volume exchange transfusion
-160-180 ml/kg
- the quickest way of clearing the
bilirubin from circulation.
53. Phenobarbital given to mothers at 30-60
mg/kg/day 2 to 3 wks prior to delivery or
to infants at 5 mg/kg/day after birth is
effective in reducing neonatal jaundice.
55. Go forth and get one forth!
1. True or False
The incidence of hyperbilirubinemia is
higher in term compared to preterm
babies
56. 2. Based on clinical examination, which of
the following reflects the highest serum
concentration of bilirubin
a. Yellowing of the face
b. Yellowing of the teeth
c. Yellowing of the abdomen
d. Yellowing of the soles
57. 3-4
Give at least 2 risk factors for neonatal
hyperbilirubinemia
Clue: J A U N D I C E
58. 5. What is the level of serum bilirubin in
mg/dL that can usually cause
kernicterus
61. A premature infant developed a grey-brown
coloration during phototherapy. The infant
had haemolytic jaundice due to Rhesus
incompatibility complicated by cholestasis
of thick bile fluid.
8. What is this condition called?
9. Should phototherapy be discontinued?
Yes/No
62. 10. What is the enzyme that catalyzes the
hepatic conjugation of bilirubin to form
bilirubin diglucoronide?
Bilirubin + 2UDP-Diglucuronide
enzyme?
Bilirubin Diglucuronide + 2UDP
Editor's Notes
Hyperbilirubinemia is a common and, in most cases, benign problem in neonates. Nonetheless, untreated, severe indirect hyperbilirubinemia is potentially neurotoxic, and conjugated-direct hyperbilirubinemia often signifies a serious hepatic or systemic illness.Jaundiceit may also be due in part to deposition of the pigment after it has been converted in the liver cell microsome by the enzyme uridinediphosphoglucuronic acid (UDP)-glucuronyltransferase to the polar, water-soluble ester glucuronide of bilirubin (direct reacting).
The unconjugated form is neurotoxic in infants at certain concentrations and under various conditions. Conjugated bilirubin is not neurotoxic but indicates a potentially serious disorder.
usually becomes apparent in a cephalocaudal progression starting on the face and progressing to the abdomen and then feet, as serum levels increase. Dermal pressure may reveal the anatomic progression of jaundice
but clinical examination cannot be depended on to estimate blood levels.
By pathologic criteria, kernicterus will develop in ⅓ of infants (all gestational ages) with untreated hemolytic disease and bilirubin levels >25–30 mg/dL. bilirubin interferes with oxygen utilization by cerebral tissue, possibly by injuring the cell membrane; antecedent hypoxic injury increases the susceptibility of brain cells to injury.
The term bronze baby syndrome refers to a sometimes-noted dark, grayish-brown skin discoloration in infants undergoing phototherapy. Almost all infants observed with this syndrome have had significant elevation of direct-reacting bilirubin and other evidence of obstructive liver disease. The discoloration may be due to photo-induced modification of porphyrins, which are often present during cholestatic jaundice and may last for many months. Despite the bronze baby syndrome, phototherapy can continue if needed.