This document provides information on neonatal jaundice including definitions, incidence, pathophysiology, risk factors, clinical presentation, diagnosis, management, and prevention of kernicterus. Some key points include:
- Neonatal jaundice is diagnosed if the total serum bilirubin is >5 mg/dL in a full-term newborn or >7 mg/dL in a preterm newborn.
- Jaundice occurs in 60% of full-term and 80% of preterm infants due to the immature liver's inability to sufficiently conjugate and excrete bilirubin.
- Risk factors for pathological jaundice include jaundice in the first 24 hours of life or
Definition of neonatal sepsis,type of neonatal sepsis ,early onset neonatal sepsis,late onset neonatal sepsis,Pathophysiology of neonatal sepsis,,sign and symptoms of neonatal sepsis, diagnosis of neonatal sepsis,management of neonatal sepsis, antibiotic used for neonatal sepsis,prevention of neonatal sepsis, prognosis of neonatal sepsis ,and A summary
Neonatal jaundice (hyperbilirubinemia) by Rajiv MavachiRajiv Mavachi
Jaundice is the most common condition that requires medical attention in newborns. The yellow coloration of the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin.
Growth charts in Neonates- Preterm and termSujit Shrestha
Growth charts in Newborn, Preterm and term neonates. All historically used charts in NICU are discussed here.
Presented by Dr Sujit, in Sir Ganga Ram Hospital
Congenital hypothyroidism is quite common in Indians and is the most common reversible congenital cause of mental retardation.
Early identification and intervention is important as Thyroid dependent brain development is complete by 3 years of age.
Universal screening is ideal as most cases are sporadic.
Positive cases on screening by filter paper test should be confirmed by serum levels estimation.
Serum Thyroid hormone levels are of primary importance in diagnosing and managing this condition, other investigations are ancillary.
Age based reference values must be followed in interpreting the results.
Timely monitoring (serum hormone levels, compliance, growth & development) and adequate counseling of care givers are key in managing this condition.
Jaundice is the yellow color seen in the skin of many newborns. Jaundice happens when a chemical called bilirubin builds up in the baby’s blood. During pregnancy, the mother’s liver removes bilirubin for the baby, but after birth the baby’s liver must remove the bilirubin. In some babies, the liver might not be developed enough to efficiently get rid of bilirubin. When too much bilirubin builds up in a new baby’s body, the skin and whites of the eyes might look yellow. This yellow coloring is called jaundice.
When severe jaundice goes untreated for too long, it can cause a condition called kernicterus. Kernicterus is a type of brain damage that can result from high levels of bilirubin in a baby’s blood. It can cause athetoid cerebral palsy and hearing loss. Kernicterus also causes problems with vision and teeth and sometimes can cause intellectual disabilities. Early detection and management of jaundice can prevent kernicterus.
Centers for Disease Control and Prevention:
Definition of neonatal sepsis,type of neonatal sepsis ,early onset neonatal sepsis,late onset neonatal sepsis,Pathophysiology of neonatal sepsis,,sign and symptoms of neonatal sepsis, diagnosis of neonatal sepsis,management of neonatal sepsis, antibiotic used for neonatal sepsis,prevention of neonatal sepsis, prognosis of neonatal sepsis ,and A summary
Neonatal jaundice (hyperbilirubinemia) by Rajiv MavachiRajiv Mavachi
Jaundice is the most common condition that requires medical attention in newborns. The yellow coloration of the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin.
Growth charts in Neonates- Preterm and termSujit Shrestha
Growth charts in Newborn, Preterm and term neonates. All historically used charts in NICU are discussed here.
Presented by Dr Sujit, in Sir Ganga Ram Hospital
Congenital hypothyroidism is quite common in Indians and is the most common reversible congenital cause of mental retardation.
Early identification and intervention is important as Thyroid dependent brain development is complete by 3 years of age.
Universal screening is ideal as most cases are sporadic.
Positive cases on screening by filter paper test should be confirmed by serum levels estimation.
Serum Thyroid hormone levels are of primary importance in diagnosing and managing this condition, other investigations are ancillary.
Age based reference values must be followed in interpreting the results.
Timely monitoring (serum hormone levels, compliance, growth & development) and adequate counseling of care givers are key in managing this condition.
Jaundice is the yellow color seen in the skin of many newborns. Jaundice happens when a chemical called bilirubin builds up in the baby’s blood. During pregnancy, the mother’s liver removes bilirubin for the baby, but after birth the baby’s liver must remove the bilirubin. In some babies, the liver might not be developed enough to efficiently get rid of bilirubin. When too much bilirubin builds up in a new baby’s body, the skin and whites of the eyes might look yellow. This yellow coloring is called jaundice.
When severe jaundice goes untreated for too long, it can cause a condition called kernicterus. Kernicterus is a type of brain damage that can result from high levels of bilirubin in a baby’s blood. It can cause athetoid cerebral palsy and hearing loss. Kernicterus also causes problems with vision and teeth and sometimes can cause intellectual disabilities. Early detection and management of jaundice can prevent kernicterus.
Centers for Disease Control and Prevention:
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
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.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
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.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
3. • The normal TSB level is < 1 mg/dl
• Neonatal clinical jaundice is Dx. If the TSB is
> 5 mg/dL in FT NB.
> 7 mg/dL in preterm NB .
4. Definition :
Is an elevation of TSB level is > 2mg /dl ,
it is a common condition among NB babies ,and most of
the cases are benign problem
However, untreated sever unconjugated
hyperbilirubinemia is potentially neurotoxic,
whereas conjugated hyperbilirubinemia is often
signifies a serious underling illnesses
Definition of Jaundice :
Yellowish discoloration of skin , mucous membranes , and
sclera
6. Source of Bilirubin
75% comes from breakdown of Hb
25% comes from breakdown of free heme , non-
Hb proteins and ineffective erythropoisis
• 1gm of Hb produce about 34-35mg of bilirubin
• 1gm of albumin bind 8.5 mg of bilirubin
8. RBC catabolism •Heme-proteins
•Infective erythropoisis
Biliverdin
Accepter protein (Y or Z)
Glucronyl
transferase
Smooth RES
Bilirubin glucuronideB-
glucuronidase
Fecal bilirubin
Bilirubin
+
Albuimn
25%Heme
75%Heme
Hemeoxidase
RES
Biliverdin reductase
Enterohepatic
Recirculation
Of bilirubin
Intestinal
Bacteria
urobilinoids
9.
10. • unconjugated hyperbilirubinemia
Elevation of serum UCB 2 mg/dl or more
• conjugated hyperbilirubinemia
Is increase level of CB > 20% of the total serum
bilirubin
It is a sign of hepatobiliry dysfunction
11. Lipid-soluble
Can not be excreted by the
kidney
Can enter the CNS
particularly in NB
(neurotoxic)
Skin color lemon yellow or
orange yellow
Physiological & pathological
Water soluble
Can be excreted by
the kidney
Can not enter the
CNS ( non neurotoxic)
Skin color greenish or
muddy yellow
Always pathological
12. 1. Increased bilirubin production
Physiological jaundice
Pathological jaundice
Hemolytic diseases
immune ( RH, ABO incompatibility )
or subgroup
non-immune ( G6PD deficinciecy
H. spherocytosis)
Extravasated blood
(cephalhematoma, extensive bruises )
polycythemia
sepsis
2. Defective transport of bilirubin in the
circulation
Hypoalbuminemia ( prematurity ,
postnatal malnutrition )
Drugs e.g. synthetic vit. K,
sulfonamide , salicylate ,
gentamicin , aminophyline
furosemide , and digoxin .)
by displacement of bilirubin
from its albumin binding sites
3. Defective bilirubin uptake by the liver
Physiological jaundice
Pathological jaundice
prematurity
deficiency of lgandin ( Y and Z proteins )
sepsis
breast milk jaundice
4. Defective conjugation of bilirubin
Physiological jaundice
Pathological jaundice
Hypothyroidism
sepsis
Crigler-Najjar syndrome (Type I and II)
Lucey – Driscoll syndrome
5. Increased enterohepatic circulation
Bowel obstruction ( meconum ileus)
Delayed passage of meconum
( meconum plug , delayed feeding
( breast feeding jaundice ) and
hypothyroidism
13.
14. criteria
• Onset after 36 hr of age ( 2nd – 3rd day )
• Rate of bilirubin rise < 5mg/dl /day
• Peak of bilirubin con. Up to 12mg/dl in FT &
Up to 14mg/dl in preterm
• Duration 8 days in FT NB. & 14 days in preterm
• Serum CB level < 2mg/dl at any time
• The NB. Looks normal not anemic not sick active
with normal color of urine and stool
• It dose not require any treatment
16. PATHOLOGICAL JAUNDICEPHYSIOLOGICAL JAUNDICE
At any time, even 1st hrAfter 36hr ( 2nd – 3rd day )ONSET
>5 mg/dl per 24hr or
>0.5mg/dl/hr
< 5 mg/dl per 24hr
RATE OF
BILIRUBIN
RISE
>12 mg/dl in FT NB
>14 mg/dl in preterm NB
Up to 12mg/dl in FT NB
Up to 14mg/dl in preterm
NB
PEAK
BILIRUBIN
CONC.
> 1 wk in FT NB
> 14 days in preterm NB
8 days in FT NB
14 days in preterm NB
DURATION OF
PERSISTENCE
> 2 mg/dl at any time< 2 mg/dl at any time
SERUM CB
LEVEL
Looks abnormal , anemic
sick & abnormal color of
urine & stool
Looks normal not anemic
not sick normal urine & stool
color
CINICALLY
NB.
17. Two types of jaundice may occur in newborns who are
breast fed. Both types are usually harmless.
Breastfeeding jaundice
• Occurs in babies who do not nurse well or if the
mother's milk is slow to come in.
• Poor weight gain , Delayed stooling
Breast milk jaundice
• appear in some healthy Infant show good weight gain ,
normal LFT no evidence of hemolysis or illness
18. Breast milk jaundiceBreast feeding jaundice
2% of breast-fed term infant
develop UCHB after 1st wk. (10-
30mg/dl) during 2nd – 3rd wk. & if
BF. Continued slow UCB (3-10 wk)
30% of breast-fed infant Have
higher UCB level (>12mg/dl) during
the first week of life
After 7 days ( late onset )(early onset)during the first week
Breast milk has increased B-
glucuronidase enzyme activity ,has
pregnanediol or unknown
substance or FFA that interfere
or inhibit H uptake or conjugation
Milk intake , dehydration ,Occurs
due to delayed stooling or
reduced caloric intake
ttt. stop breast feeding for 1-2
days & give other milk formula
then resume breast feeding
Rapid UCB in 48 hr
ttt. Frequent breast feeding
( >10 feeding/day)
Do not supplement with
glucose water
19. • Major risk factors
– jaundice in first 24 hours (always
pathologic)
– ABO or Rh incompatibility and
positive coombs test
– G6PD deficiency
– Delivery at 35 to 36 weeks
gestation
– Significant Birth trauma
• Cephalhematoma
• Large hematomas
– Infant Breast feeds only (especially
before milk let-down occurs)
– F.H/O sibling who required
phototherapy for Neonatal
jaundice
– Serum bilirubin in high risk range
for age in hours
• Minor risk factors
– Male gender
– Maternal age over 25 years old
– Macrosomic IDM
– Delivery at 37 to 38 weeks
gestation
– Serum bilirubin in intermediate
range for age in hours
• Other risk factors
– Polycythemia
– Medication exposure
• Mother: Diazepam, Oxytcin
• Infant: Pediazole,
Chloramphenicol
20.
21. Within 1st 24hr of life
• Erythroblastsis fetalis
• TORCH infection
• Extravascular hematoma
• Sepsis
• polycythemia
On the 2nd -3rd day
• Physiological
• Crigler-Najjar syndrome
• Early onset Breast feeding
jaundice
After 3rd day and Within the 1st
wk
• Bacterial sepsis
• TORCH + Enterovirus
• Hematoma
After 1st wk of life
• Breast milk jaundice
• Extrahepatic Biliary atresia
• Hypothyroidism
Persistent jaundice during the 1st mo
of life
• Inpsissated bile syndrome (post-
hemolytic cholestasis )
• Hyperalimenation-associated
cholestasis
• Hypothyroidism
• pyloric stenosis
• Hepatitis (TORCH infection)
• Extrahepatic Biliary atresia
• Galactsemia
• Breast milk jaundice
• Crigler-Najjar syndrome
22. NOTE :
• Jaundice due to hemolytic anemia , in utero
infection (TORCH) and sepsis may present
at any time after birth
23. History
1. Family H/O jaundice , anemia , splenectomy (chronic
hemolytic anemia), liver disease
2. Previous sibling with jaundice (blood group incompatibility)
or Breast milk jaundice
3. Maternal illness during pregnancy : TORCH infection or DM
febrile illness
24. 4. Maternal drugs : sulphonamides , antimalaria or
salicylate (may cause hemolysis in G6PD-def. infant )
5. Maternal blood group and RH ,
6. Hx. Of abortion or SB & use of Anti-D if she was Rh – ve
7. Labor history : use of forceps vacuum asphyxia ,delayed
cord clamping
8. Postnatal H/O day of Onset, general condition, vomiting,
infrequent stooling , light colored stool, delayed Breast
feeding, whether the infant is breast-fed or formula-fed
25. Physical Examination
• Color of Jaundice (lemon yellow or orange yellow UCB type ,
greenish or muddy yellow CB type)
• (face =5mg/dl, mid abdomen =15mg/dl, sole = 20mg/dl )
• Pallor , plethora , petechiae
• Signs of Prematurity
• SGA (polycythemia ,TORCH infection )
• Microcephaly (TORCH infection)
• Cephalhematoma , bruises
• Hepatospleomegaly ( hemolytic anemia , infection )
• Signs of Hypothyroidism
• Signs of neonatal sepsis
• Omphalitis ( septicemia )
• Signs of Kernicterus
26. Laboratory investigation & other paraclinical
• Serum bilirubin total & direct
• blood group and RH of the infant & mother
• Coombs test
• CBC (Hb, Hct ,WBC )& Red cell morphology, S. electrolyte, RBS
• Reticulocyte count , G6PD enzyme assay ,osmotic fragility test
• Screening for TORCH infection
• Screening for sepsis (CRP, Blood cultures & other sites cultures , ESR )
• LFT ( serum albumin )
• Stool & urine analysis
• CXR
• Abdominal U/S
• ERCP
• Thyroid Stimulating Hormone
• Galactosemia Screen
27.
28. Definition ( Bilirubin Encephalopathy )
Neurological syndrome resulting from the
deposition of UCB in the
• Basal ganglia
• Brainstem nuclei
• Various cranial nerve nuclei
• Cerebellar nuclei
29. Incidence
30% in of infant of all gestational age with
untreated hemolytic disease
Total Bilirubin > 25 to 30 mg/dl
30. Risk factors
• UCB level > 30mg/dl but the range is wide (21-
50mg/dl)
• Duration of exposure to hyperbilirubinaemia
• Hypoproteinemia , Drugs , free FA
• Prematurity , Asphyxia , hyperosmlarity ,Seizures ,
hypertension , infection ( increase permeability of
BBB to bilirubin )
33. Phase 3 ( after the 1st wk )Phase 2 ( middle of 1st wk )Phase 1 ( 1st 12 days )
HypotoniaHypertoniaHypotonia
apneaIrritabilityLethargy
opisthotonusRDPoor feeding
SeizuresFeverVomiting
If pt. recover show few
abnormality (hypertonia)
Bulging FontanelHigh – pitched cry
Seizuresloss of Moro reflex
opisthotonusSeizures
DeathDeathDeath
Acute form
34. Chronic form
• Kernicterus (Residual deficits)
– Spasticity
– Severe athetoid Cerebral Palsy
– High frequency Hearing Loss or Deafness
– Mild Mental Retardation
– Upward gaze paralysis
• Dental dysplasia
35. American academy of pediatrics has identified potentially preventable
causes of Kernicterus :
• Early discharge (<48hr ) with no early follow-up within 48hr
• Failure to check the bilirubin level in infant noted to be jaundiced in
the 1st 24hr
• Failure to recognize the presence of risk factors for hyperbilirubinaemia
• Underestimation of the severity of jaundice by clinical ( visual )
assessment
• Lack of concern regarding the presence of jaundice
• Delay in measuring S.Bilirubin level despite marked jaundice or delay
in initiating phototherapy in presence of elevated Bilirubin level
• Failure to respond to parental concern regarding jaundice , poor
feeding or lethargy
36. Recommendation
• Any infant who is jaundiced before 24hr requires measurement of TSB
level & if it is elevated then should evaluated for possible hemolytic
disease
• Follow-up within 2-3 days of discharge to all NB discharged earlier
than 48hr after birth esp. < 38 wk gestation
• Avoid routine supplementation with water or glucose water
• Provide parents with written &verbal information about NB jaundice
37. • The goal of therapy is to prevent kernicterus
• Interpret all bilirubin levels according to the
infants age in hours
• Treat newborn ,when indicated with
phototherapy or exchange
38. 1. Phototherapy
2. Exchange Transfusion
3. Treatment of the Etiological factor :
Hypothyroidism
Stop drugs
Correction any factor that increase the
permeability of UCB eg. Acidosis
Increase frequency & volume of milk feeding
39. A . Conventional Phototherapy
A blue light and day light with wave 425-475nm
and 550-600 consequently is best
B . Intensive phototherapy
Fluorescent blue , fiberoptic blanket phototherapy
NOTE : Phototherapy decrease the need for exchange
transfusion & decrease No. of exchange transfusion, but it
is not substitute for exchange transfusion
40. The effectiveness of phototherapy in reducing
UCB depends on :
A. The light emitted in the effective range of
wavelengths (240- 470nm)
B. The distance between light source and infant
(most effective if 45cm)
C. The surface area of skin exposed
D. The rate of hemolysis and excretion
41. In premature NB without of significant of
hemolysis, UCB level usually declines 1-3
mg/dl after 12- 24hr of exposure
43. • Phototherapy is usually started at 50 – 70 % of
the maximal indirect level
• If the values exceed this level ,if Phototherapy
is unsuccessful in reducing the maximal
indirect level ,or if signs of kernicterus are
evident EXCHANGE TRANSFUION is indicated
44.
45.
46. Indication of Phototherapy
1. Abnormal rise of UCB level
2. While waiting for & in between exchange
transfusion
3. Prophylactic in some cases :
a. VLBW infant
b. Hemolytic disease of NB
c. Severely bruised premature infant
47. Procedure
• It is applied continuously except during feeding
• Infant kept naked except for eyes bandage and a diaper
• The infants are turned every 2 hr
• Monitoring of Temp. /2hr , UCB level & Hct. /4-8hr in
case of hemolysis and 12-24hr for other cases , and
body Wt. daily
• The Lamps should be changed after 2,000 hr of use
48. When discontinue phototherapy ?
When the level of UCB is low to eliminate
concern about toxic effects of UCB
• TSB level should be followed for at least 24hr
after discontinue phototherapy
• Risk factors for toxic level of UCB are absent
• The baby is old enough to handle the bilirubin load
• Usually at the level < 13-14 mg/dl in term NB
49. Guidelines for phototherapy in hospitalized infants of 35 or more weeks’ gestation. Note:
These guidelines are based on limited evidence and the levels shown are approximations.
51. Side effects of phtoyherapy
1. Dehydration
2. GIT ( loose or watery Diarrhea )
3. Damage of Corneal
4. Dermatitis (erythemtous macular rash &
purpuric rash )
5. DNA damage
6. Decrease maternal-infant interaction
7. Dark grayish-brown discoloration of skin (bronze
baby syndrome)
52. 2- Exchange transfusion
The goals of exchange transfusion in immune
Hemolytic disease :
o To correct anemia
o To remove the sensitized RBCs
o To remove the antibodies
o To reduce the UCB level
53. Indications
A. Severe hyperbilirubinaemia refractory to phototherapy
B. Hemolytic disease of NB
C. Others :
Septicemia
DIC
Polycythemia
IEM
Hypomagnesaemia
Respiratory depression
54. Procedure
Start phototherapy until Exchange transfusion
• Estimate the BWt , GA, vital signs and CVP
• Pre-exchange blood sample labs
Serum bilirubin total & direct
blood group and RH of the infant
Coombs test
CBC (Hb, Hct ,WBC )& Red cell morphology
Reticulocyte count
S,Ca ,RBS
LFT
ABG
55. • Aspirate 20 cc of infant's blood
• Infuse 20 cc of donors blood
• Exchange transfusion should carried out over (45-60 min )
• Monitoring during Exchange transfusion:
Body temp., CVP , Bp , PaO2 , pH,BS, S.Ca ,
• Blood Volume is double the blood volume of the infant
= 2 × 85 ml /kg = 170 ml /kg
• Umbilical Venous Catheter placed at 7 cm or less
• Alternate aspiration and infusion
56. Blood used in exchange transfusion :
• Fresh , warm , washed and irradiated
• Grouping :
in Rh incompatibility use infant’s ABO group, Rh – ve
in ABO incompatibility use group O, infant’s Rh type
For others infant’s ABO, Rh group.
57.
58.
59. Guidelines for exchange transfusion in infants 35 or more weeks’ gestation. Note that these
suggested levels represent a consensus of most of the committee but are based on limited
evidence, and the levels shown are approximations.
62. Other therapies
• Phenobarbital:
as adjunct management It is recommended only in Crigler-Najjar
type II
• Metalloporphyrins :
by inhibits conversion of heme to biliverdin, so reduce UCB level
in (ABO incompatibility or G6PD deficiency)
• Intravenous immunoglobulin
0.5 – 1 g/kg/dose over 4 hr repeated in 12 hr it is
recommended in persist isoimmune hemolytic disease (both ABO
& Rh ).
63. Crigler-Najjar Disease :
• Congenital deficiency or absence of glucuronyl
transferase enzyme
• Autosomal recessive
Type I : Congenital absence of the enzyme
kernicterus develops early leading to death
Type II : partial deficiency of the enzyme
the condition improves on administration of
phenobarbitone & kernicterus is unusual
64. Gilbert’s syndrome
• Benign disorder
• Can result from mutations to genes coding for
UDP-glucuronyl transferase
65.
66.
67. Definition
An increased level of direct bilirubin >20% of the
total serum bilirubin
It is a sing of hepatobiliry dysfunction
68. Hepatic
Idiopathic neonatal hepatitis
intrahepatic cholestasis with paucity
of bile duct (Alagille syndrome )
Infections
Sepsis
Viral Hepatitis
TORCH infections
Metabolic
Galactosemia
Alpha-1-antitrypsin deficiency
Cystic fibrosis
Drugs
Total parenteral nutrition
Post-hepatic
Biliary atresia
Bile duct obstruction
Choledochal cyst
causes
Others
Dubin-Johnson syndrome
Rotor s syndrome
69. Clinical manifestations
• Greenish jaundice due to CB
• The stool are clay in color while urine is dark
• Hepatospleomegaly
• Other clinical manifestations of the etiology may
be present e.g. refuse feeding purpura ... etc.
Guidelines for exchange transfusion in infants 35 or more weeks’ gestation.Note that these suggested levels represent a consensus of most of the committee but are based on limited evidence, and the levels shown are approximations. See ref. 3 for risks and complications of exchange transfusion. During birth hospitalization, exchange transfusion is recommended if the TSB rises to these levels despite intensive phototherapy. For readmitted infants, if the TSB level is above the exchange level, repeat TSB measurement every 2 to 3 hours and consider exchange if the TSB remains above the levels indicated after intensive phototherapy for 6 hours.The following B/A ratios can be used together with but in not in lieu of the TSB level as an additional factor in determining the need for exchange transfusion52: If the TSB is at or approaching the exchange level, send blood for immediate type and crossmatch. Blood for exchange transfusion is modified whole blood (red cells and plasma) crossmatched against the mother and compatible with the infant.53