Physiologic jaundice is a common cause of hyperbilirubinemia in newborns resulting from increased bilirubin production, shortened RBC lifespan, and hepatic immaturity. It presents between 2-10 days of life with indirect bilirubin levels <12 mg/dL in term infants peaking on day 3. Kernicterus is a neurological syndrome caused by bilirubin deposition in the brain and can be prevented by avoiding excessively high indirect bilirubin levels >25 mg/dL. Diagnosis of hyperbilirubinemia involves history, physical exam, and laboratory tests including total, direct and indirect bilirubin levels as well as blood typing if levels are
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
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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Hyperbilirubinemia didactics at Neonatal Intensive Care Unit
Source: Nelson's Textbook of Pediatrics 19th edition
Most pictures were taken from Google images
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
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
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.
follow me on my YouTube channel :- medic o mania
Hyperbilirubinemia didactics at Neonatal Intensive Care Unit
Source: Nelson's Textbook of Pediatrics 19th edition
Most pictures were taken from Google images
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
neontal joudice is is a yellowish discoloration of the skin, sclerae, mucous membranes and nails.
Hyperbilirubinemia is a common and, in most cases, benign problem in neonates.
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
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
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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
3. Definition:is a yellowing of the skin and sclera
of a newborn infant caused by accumulation of
Bilirubin( Hyperbilirubinemia) in the skin &
mucous mambrene
4. Hyperbilirubinemia is a common and in most
cases benign problem in neonates. Jaundice is
observed during the 1st wks. of life in
approximately 50- 60% of term newborns and
80% of premature infants.
Its clinically visible when exceeds 5 mgm/dl.
5. Metabolism and secretion of bilirubin
Bilirubin -breakdown of hemoglobin
Unconjugated bilirubin (insoluble in water)
transported to liver- Bound to albumin
Transported into hepatocyte (Ligandin / y- protein ) &
conjugated - With glucuronic acid → now water
soluble
Secreted into bile
In ileum & colon, converted to stercobilin
10-20% (Deconjugated by β glucuronidase)
reabsorbed into portal circulation (Enterohepatic
circulation )and re-excreted into bile or into urine by
kidneys - urobilinogen
6.
7. Clinical Manifestations
• Yellow skin and sclera
• Poor feeding
• Brown urine
• Fever
• High pitch cry
• Vomiting
• without treatment
can progress to acute
bilirubin
Encephalopathy
(kernicterus)
8. Physiologic jaundice : (Icterus Neonatorum)
Physiologic jaundice is a common cause of
hyperbilirubinemia among newborns. It is adiagnosis
of exclusion, made after careful evaluation has ruled
out more serious causes of jaundice, such as
hemolysis, infection, and metabolic diseases.
10. Characteristics:-
1-The clinical pattern of physiologic jaundice in
term infants includes a peak indirect-reacting
bilirubin level of no more than 12 mg/dL on day 3
of life. In premature infants, the peak is higher (15
mg/dL) and occurs later (fifth day).
2-its disappears by one weak in full term infants &
two weeks in preterm infants.
3-serum bilirubin is rarly rising at
a rate faster than 5 mg/dL/24 hr
4- Healthy baby.
11. Pathologic jaundice
• Appears within 24 hours of age
• Increase of bilirubin > 5 mg / dl / day
• Total Serum bilirubin > 13 mg / dl in term
infant or 10 mg/dl in preterm
.The direct bilirubin fraction is greater than
1.5 mg/dL
May associated with
acute hemolysis
• Signs of an
underlying illness
12. Risk factors for jaundice
1-low birth wt & prematurity
2-polycythemia
3-A sibling affected
4-male sex
5-hemolytic conditions
6-sepsis
7-ABO incompatibility
15. In Hemolytic disease of the
newborn (ABO / Rh)
Rh incompitability:
• is the most common cause
• < 1 mL of Rh-positive fetal blood is sufficient to sensitize the
Rh negative mother
• 90% sensitization during delivery/abortion
So , most first born infants are not affected due to the short
period of exposure which is insufficient to produce a
significant maternal IgG antibody response.
Sensitized mother produces Ab –IgG types—crosses placenta
sensitized –small doses of Ag stimulate high Ab titer .
So, risk and severity of sensitization response increases with
each subsequent pregnancy with Rh-positive blood fetus
16. Not all mother produce hemolysis in their
baby ??
1. The baby may be Rh negative
2. Not all mother produce enough Abs
3. The mother might have been immunized
by anti D immunoglobin
4. Fetomaternal trasfusion occurs only in 50%
of preg
5. When mother and baby ABO
incompatibale
17. ABO incompatibility
• if Mother is type O and the baby is either type A
or B. O +ve Mothers makes antibodies which are
IgM & IgG types , IgG types crosses the placenta
• No effects if the mother & baby have same blood
group or baby is grp O, as there is nothing to
make antibodies against.
• If mother - type A or B Makes antibodies (IgM)
type so does not cross the placenta
So, even if baby has a different blood type no effect
18. Physiologic jaundice is a common cause of hyperbilirubinemia
among newborns. It is a diagnosis of exclusion, made
after careful evaluation has ruled out more serious causes of
jaundice, such as hemolysis, infection, and metabolic diseases.
Physiologic jaundice is the result of many factors that
are normal physiologic characteristics of newborns:
1- increased bilirubin production resulting from an increased RBC
mass,
2- shortened RBC life span,
3- hepatic immaturity of ligandin and glucuronosyltransferase.
Physiologic jaundice
19. Crigler-Najjar syndrome is a serious, rare, autosomal
recessive, permanent deficiency of glucuronosyltransferase
that results in severe indirect hyperbilirubinemia.
Type II
responds to enzyme induction by phenobarbital, producing
an increase in enzyme activity and a reduction of bilirubin
levels.
Type I
does not respond to phenobarbital and manifests
as persistent indirect hyperbilirubinemia, often leading to kernicterus
Gilbert disease is caused by a mutation of the promoter
region of glucuronosyltransferase and results in a mild
indirect hyperbilirubinemia. In the presence of another icterogenic
factor (hemolysis), more severe jaundice may develop
20. Breast milk jaundice
may be associated with unconjugated hyperbilirubinemia without
evidence of hemolysis during thefirst to second week of life.
Bilirubin levels rarely increase to more than 20 mg/dL.
Interruption of breastfeeding for 1 to 2 days results in a rapid decline
of bilirubin levels, which do not increase significantly after
breastfeeding resumes.
Breast milk may contain an inhibitor of bilirubin conjugation or may
increase enterohepatic recirculation of bilirubin because of
breast milk glucuronidase
21. Direct-reacting hyperbilirubinemia (defined as a direct bilirubin
level >2 mg/dL or >20% of the total bilirubin) is never
physiologic and should always be evaluated thoroughly
according to the diagnostic categories
Etiology of Direct Conjugated Hyperbilirubinemia
Direct-reacting bilirubin (composed mostly
ofconjugated bilirubin) is not neurotoxic to the
infant but signifies a serious underlying
disorder involving cholestasis or hepatocellular
injury.
22.
23. Best classified by age of onset and duration:
Early: within 24 hrs of life
Intermediate: 2 days to 2 weeks
Late: persists for >2 weeks
Causes of neonatal jaundice
25. Kernicterus ( bilirubin encephalopathy):
is a neurologic syndrome results when indirect bilirubin is
deposited in brain cells and disrupts neuronal metabolism and
function, especially in the basal ganglia.
Indirect bilirubin may cross the blood-brain barrier because of
its lipid solubility. Other theories propose that a disruption of
the blood-brain barrier permits entry of a bilirubin-albumin
or free bilirubin–fatty acid complex
Its characterized by severe athetoid
cerebral palsy, paralysis of upward gaze,
hearing loss & intellctual impairment
& its preventable
Kernicterus
26. Kernicterus usually is noted when the bilirubin level is
excessively high for gestational age. It usually does not
develop
in term infants when bilirubin levels are less than 20 to25
mg/dL, but the incidence increases as serum bilirubin levels
exceed 25 mg/dL
27. Pathalogy
Yellow staining of the brain with neuronal injury, there are necrosis, neuronal
loss and gliosis
Its commonly seen in the basal ganglia, hypocampus,cerebellum,brainstem &
spinal cord
28. Risk factor for Kernicterus
1. Sever hyperbilirubinemia
2. Prematurity
3. Asphyxia
4. Acidosis ,hemolysis, hypoxia, hypothermia
5. Hypoglycemia, sepsis, meningitis,
Other risks for kernicterus in term infants are
hemolysis, jaundicenoted within 24 hours of birth, and
delayed diagnosis of hyperbilirubinemia
29. Clinical feature
The earliest clinical manifestations of kernicterus are
lethargy
Hypotonia
irritability
poor Moro response
poor feeding.
A high-pitched cry and emesis also may be present.
Early signs are noted after day 4 of life.
Later signs include
bulging fontanelle
opisthotonic posturing
pulmonary hemorrhage
Fever
Hypertonicity
paralysis of upward gaze and seizures
30. Complication of Kernicterus
Infants with severe cases of kernicterus die in the neonatal
period.
Spasticity resolves in surviving infants, who may
manifest later nerve deafness
choreoathetoid cerebral palsy
mental retardation
enamel dysplasia
and discoloration of teeth as permanent sequelae
Prevention
Kernicterus may be prevented by
-avoiding excessively high indirect bilirubin levels
-avoidingconditions or drugs that may displace bilirubin from
albumin.
32. :
• History
ask about Antenatal history
Drugs
Trauma
Family H/O of jaundice
Liver disease
H/O delayed feeding
Sepsis
Sibling jaundice
Splenectomy in family
33. Examination :
• Look for yellowish discoloration of the skin,
sclera and mucous membrane
• Gently pressing by finger on the tip of the
nose
• Examination of liver and spleen for
hepatosplenomegaly
• Look for the color of urine and
• stool
35. LABORATORY TESTS
Physical evidence of jaundice is observed in infants when
bilirubin levels reach 5 to 10 mg/dL (versus 2 to 3 mg/dL in
adults). When jaundice is observed, the laboratory evaluation
for hyperbilirubinemia should include
a total bilirubin measurement to determine the magnitude of
hyperbilirubinemia.
Bilirubin levels greater than 5 mg/dL on the first day of life
or greater than 13 mg/dL thereafter in term infants should be
evaluated further with
measurement of indirect and direct bilirubin levels
blood typing
Coombs test
complete blood count, blood smear
and reticulocyte count.
36. These tests must be
performed before treatment of hyperbilirubinemia with
phototherapy
or exchange transfusion. In the absence of hemolysis
or evidence for either the common or the rare causes of
nonhemolytic indirect hyperbilirubinemia,
the diagnosis is
either physiologic or breast milk jaundice. Jaundice present
after 2 weeks of age is pathologic and suggests a direct-reacting
Direct-reacting hyperbilirubinemia (defined as a direct
bilirubin
level >2 mg/dL or >20% of the total bilirubin) is never
physiologic and should always be evaluated thoroughly
according to the diagnostic categories
Direct-reacting bilirubin (composed mostly of conjugated
bilirubin)
is not neurotoxic to the infant but signifies a serious underlying
disorder involving cholestasis or hepatocellular injury.
38. phototherapy
•is an effective and safe method for reducing indirect bilirubin
levels, particularly when initiated before serum bilirubin increases
to levels associated with kernicterus.
•In term infants, phototherapy is begun when indirect
bilirubinlevels are between 16 and 18 mg/dL.
• Under the effects of phototherapy light with maximal
irradiancein the 425- to 475-nm wavelength band, bilirubin is
transformed into isomers that are water soluble and easily
excreted.
• Blue lights and white lights are effective in reducing bilirubin
39. The therapeutic effect of phototherapy depends on
1. the light energy emitted in the effective range of wavelengths
2. the distance between the lights and the infant
3. the surface area of exposed skin,
4. the rate of hemolysis
During phototherapy :
1. Cover the eyes and Genitals
2. Supplemental hydration
3. monitoring for side effects
4. Monitering of bilirubin level
40. Serum bilirubin levels and hematocrit should be monitored every
4-8 hr in infants with hemolytic disease and those with
bilirubin levels near toxic range .
Complications of phototherapy
Early complication:
1. loose stools
2. erythematous macular rash
3. dehydration (increased insensible water loss, diarrhea)
4. bronze baby syndrome (which occurs in the presence of direct
hyperbilirubinemia)
5. lethargy, masking of cyanosis, nasal obstruction by eye pads
41. Late complication:
• Risk of skin malignancies
• Damage to intracellular DNA
• Retinal damage
• Testicular damage
42. Intensive phototherapy
using light source above and beneath the infant using
in sever cases with risk of kernicterus
Home phototherapy
This is an option way of treatment where facilities are
available and fiber optic blankets are commonly used
.the family should be well instructed and a well trained
nurse should be present it is usually used for simple
jaundice
43. Intravenous Immunoglobulin
The administration of intravenous immunoglobulin
use in treatment for hyperbilirubinemia due to
isoimmune hemolytic disease.
(0.5-1.0 g/kg/dose; repeat in 12 hr) has been shown to
reduce the need for exchange transfusion in both ABO
and Rh hemolytic disease, by reducing hemolysis
44. Exchange blood transfusion
usually is used for infants with dangerously high
indirect bilirubin levels who are at risk for kernicterus .
The exchange transfusion usually is performed
through an umbilical venous catheter placed in the
inferior vena cava or,if free flow is obtained, at the
confluence of the umbilical veinand the portal system.
45. Indication:
• The appearance of clinical signs suggesting
kernicterus
• Rh and ABO incompatibility
• Unconjugated billirubin > 20 -25mg/dl in
term, >15 -18mg/dl preterm babies.
• Other disease :Septicemia ,DIC,Severe
anemia,…
46. Complications
1. Problems related to the blood (transfusion reaction,
metabolic instability,or infection)
2. Problems related to the catheter (vessel perforation or
hemorrhage)
3. problems related to the procedure (hypotension or
necrotizing enterocolitis )
4. Unusual complications include thrombocytopenia and
graft-versus-host disease.
47. Prevention of neonatal jaundice :
1. Promote and support breast feeding
2. Establish nursery protocols for identifying and evaluating
hyperbilirubinemia
3. Measure bilirubin levels in all neonate with jaundice in the first 24
hrs
4. Recognize that visual estimation of bilirubin level inaccurate
5. Interpret all bilirubin levels according to baby age in hrs
6. Identify preterm ,breast fed infant and provide close monitoring
7. Risk assessment for all newborn baby .
8. Give written and verbal information to familly
9. Treat newborns when indicated and appropriate follow up
Blood group incompatibility:
Maternal antibodies crosses placenta (IgG), reacts against RBC antigens of infant and causes haemolysis +/- anaemia
Most severe cases - hydrops fetalis
Breast milk jaundice
Early: due to lower calorie intake (so check weight gain) and slower passage of meconium
Late: due to beta-glucoronidase in milk leads to deconjugated of bilirubin in the bowel and increased enterohepatic circulation
Management: usually reassurance - do not stop breast feeding unless very severe!