Neonatal Jaundice Flashcards
Jaundice is the ___________ discolouration of the skin, sclera, mucous membranes and plasma.
Hyperbilirubinaemia becomes clinically evident when serum value reaches ______mg/dl
yellowish
5-7
Jaundice in the newborn derives its clinical importance from 2 facts
•It can be toxic to the developing _______
•It may be symptomatic of an underlying disease e.g. ________,___________
brain
sepsis, hypothyroidism
_____________ is the commonest neonatal emergency
Neonatal jaundice
Jaundice is seen in _____% of term babies, and in _______ % of all preterms
Animashaun et al found that _____% of a cohort of children with cerebral palsy had severe NNJ
60
80-100
Metabolism of bilirubin
Bilirubin is the by-product of ______ metabolism (Haemoglobin)
__________ is the major source of bilirubin (75%)
25% of bilirubin is from _________________ and ___________ heme such as catalase, cytochrome, peroxidase
heme
Red cell heme
ineffective erythropoiesis ; non-red cell heme
Bilirubin Metabolism: reticuloendothelial system
_____________ converts heme to __________ + CO + Fe . This is reduced to __________ by _________________.
1g of heme produces _____mg of bilirubin
This bilirubin is bound to ________ and transported to the liver for ___________
, which makes the bilirubin ________________
Heme oxygenase ; biliverdin
bilirubin ; biliverdin reductase.
35mg ; albumin ; conjugation
water soluble
Bilirubin metabolism: liver
Bilirubin transported into hepatocyte cytosol is bound by ________
_____________________ converts the bilirubin to polar water soluble forms: bilirubin _________________ for easier excretion in the urine and GIT
Some of the conjugated forms of bilirubin are excreted as part of ______ into the intestine
ligandin
UDP glucuronyl transferase
bilirubin mono/di-glucuronide
bile
Bilirubin Metabolism: intestine
In the GIT phase, the _________ bilirubin comes out of the ___________ into the intestines, and gets converted to ___________ and ___________ by the intestinal bacteria.
___________ gives stool the brown colour. ___________ is carried to the kidneys for excretion.
If ___________ by ___________ in the GIT, bilirubin becomes available for enterohepatic circulation as unconjugated bil (more jaundice)
conjugated ; canaliculi
urobilinogen ; stercobilinogen
Stercobilinogen ; Urobilinogen
deconjugated ; beta-glucuronidases
Bilirubin metabolism: peculiarities of the newborn
Jaundice is common in the newborn due to the following reasons
Increased ____________
Reduced ___________ (to ____ days)
Increased __________________
Decreased ________ concentration of ligandin and decreased activity of _________
Increased activity of _______________
Decreased intestinal flora
red cell per Kg
red cell lifespan ; 90 days
ineffective erythropoiesis
hepatic concentration
UDP glucuronyl transferase
beta-glucuronidase
Hyperbilirubinemia & Clinical Outcomes:
List 3
Jaundice
Kernicterus
Acute bilirubin encephalopathy
Jaundice -???
Kernicterus -??
Acute bilirubin encephalopathy -???
Deposits in skin and mucous membranes
Permanent neuronal damage
Unconjugated bilirubin deposits in the brain
Physiologic Vs Pathologic
Physiologic jaundice is one that starts within _________ of life, peaks on the _________ day and resolves by the _________ day. It usually does not exceed ____mg/dl in full terms. In preterm baby, it maybe as high as ___mg/dl and may take up to __________ to resolve.
Baby is apparently well. Pathologic jaundice is the reverse
24 hours ; 4th-5th
6th-7th ; 12mg/dl
15mg/dl ; 2 weeks
Conjugated Vs Unconjugated
In conjugated hyperbilirubinaemia the conjugated or direct fraction is _____% or more of the total serum bilirubin
If the conjugated or direct fraction is less than _____% it is unconjugated hyperbilirubinaemia
20
20
Early-onset Vs Late-onset Vs Prolonged Jaundice
Early-onset starts _________________
Late –onset jaundice starts ____________________ e.g. breastmilk jaundice, biliary atresia
Prolonged jaundice ____________________ e.g. hypothyroidism, breastmilk jaundice, galactosaemia, prematurity, Down’s syndrome
within the first week
after the first week
lasts beyond the 2nd week
Breastfeeding jaundice
Breastfeeding jaundice occurs early
It is due to __________ of breast milk feeds
It is often associated with ___________________ and increased __________ of bilirubin
Treatment should be aimed at supporting __________ while __________ as needed to avoid extreme weight loss, dehydration, and worsening jaundice.
delayed initiation
poor passage of meconium
enterohepatic circulation
breastfeeding ; supplementing
Breast milk jaundice
Breast milk jaundice is a different, (more or less?) benign entity, which tends to occur late in the __________ or afterwards.
It is actually due to ? Hormonal /enzymes in the breast milk which ____________________.
Usually weight gain is ________, and the baby is otherwise well.
Jaundice might persist as late as _________ , but usually will peak by _________.
Treatment is to sometimes ________ breastfeeding for _________ if severe
more ; first week
delay UDPT conjugation ; good
3-4 weeks ; 2 weeks.
interrupt ;48hrs
Commonest Medical Causes of hyperbilirubinemia
_____________ is an important cause of severe NNJ
_______ incompatibility Preterm/ LBW
____________ alone or in combination w/other factors is also very important
______ incompatibility is not as common as ABO
G6PD deficiency
ABO
Septicemia
Rh incompatibility
Why so much neonatal jaundice/ABE/kernicterus in Nigeria?
Perception/Practices of Caregivers
Lack of ________
____________________ for inborn
____________ usually after 5- 7th day!!..dark skin leading to largest numbers of ABE/kernicterus in out born infants
awareness
Early hospital discharge
Late detection
Practices of caregivers
Use of __________ /mentholated rub/dusting powder & __________ persists despite a knowledge of the hazards of such practices in populations w/high incidence of ______ deficiency
Using herbal medications and other treatments delaying seeking definitive therapy
naphthalene/mentholated rub
eucalyptus oil
G6PD deficiency
Clinical Presentation
The aim of history and physical examination is to seek to establish
The presence and extent of jaundice (__________ chart)
Possible aetiology
Presence of features suggestive of __________
Kramer’s
encephalopathy
Physical Features
Extent of jaundice
Presence of ________,____________ —- hemolytic process
Presence of ________—- sepsis
Presence of ___________ or extensive ________
Look for abnormal facies
Test the integrity of the CNS
pallor, hepatosplenomegaly
fever; hematoma; bruising
Investigation
Unconjugated Hyperbilirubinaemia
Serum __________ : both total and direct
Mother’s and baby’s ________/__________
_______ assay especially in males
FBC/ESR , blood culture
_____________ test
bilirubin
ABO/rhesus blood group
G6PD
Direct Coomb’s
Investigations
Conjugated Hyperbilirubinaemia
Serum _________: Total and direct
_______ function test: SGOT, SGPT,Alk phosphatase
___________ screen
Abdominal USS.
Urine for _________
_______ biopsy
_________ scan
bilirubin; Liver
TORCHES ; reducing sugar
Liver ; Hepatic
Treatment:
The over-riding goal is to prevent _________ by reducing the serum level of __________ bilirubin. This can be achieved by:
Observation/monitoring _____ level
_______therapy
__________________
Others –Agar, IV Immunoglobulins
Zinc or Tin mesoporphyrins
Hepatic enzyme inducers such as phenobarbitone
Treatment of the underlying cause should go on concurrently
bilirubin encephalopathy
unconjugated
Serum bilirubin; Photo
Exchange blood transfusion
Phototherapy
It converts _____________________ to ________________ forms that are principally excreted in the _______
Absorption of light by bilirubin occur at wavelength between _____-_____ nm, hence lights with maximum energy output near these wavelengths are effective as phototherapy lamps esp _______ light
water-insoluble bilirubin
polar water soluble forms
stools; 450-460 nm
blue light
Phototherapy: mechanism of action
3 mechanisms of action
__________ isomerisation
________-isomerisation
_________________
Structural
Photo
Photo-oxidation
Phototherapy - indications
Serum bilirubin level ___________________
Treatment of jaundice after phototherapy
less than that required for EBT
Phototherapy is contraindicated in conjugated hyperbilirubinaemia
Why?
because in this state it can cause bronze-baby syndrome
Phototherapy: complications
____________ from increased insensible loss and diarrhoea (osmotic diarrhoea)
Hyper________
Possible damage to the ______ and ___________
Disruption of _____________
___________ syndrome if the jaundice is conjugated
Dehydration
thermia
retina and gonads
mother-child bonding
Bronze baby
Phototherapy-Daily care
Daily ______ check
_________ check
Maximum exposure of the body
Shielding of the _______ and __________
Increase maintenance fluid by ______%
The distance between the lamp and the baby should be 15-20cm and 8-10cm between the lamp and the incubator
Serum bilirubin
Temperature
eyes and testes
10-20
Therapeutic challenges
_____________ of functional phototherapy
__________ phototherapy
_________ phototherapy techniques
Monitoring devices not available..radiometers
Unavailability
Ineffective
Faulty
EBT: Indications
SB>____mg/dl in term baby
SB>____ times the weight of the preterm in Kg
Rate of rise of SB >____mg/dl per day
In Rhesus isoimmunisation, cord SB>4mg/dl and Hb <12g/dl
20; 10
5
EBT :
Double volume exchange (___x ____ x __mls) is commonly done
Aliquots of exchange is < ___% of total blood volume
Fresh whole blood compatible with _______________ should be used
Anticoagulant for the blood is ___________________________
Ideal time for a double volume EBT is ____________
The __________ method is the technique commonly used
2; wright; 80
mother and baby
citrate phosphate dextrose acetate
1 hour; push-pull
EBT: Complications
Those associated with blood transfusion
Transmission of ___________
Electrolyte derangement e.g. _________
Metabolic derangement e.g. ————-,_________
infective organisms
hyperkalemia
hypocalcemia, hypoglycaemia
EBT: Complications
Those associated with the procedure
Hypo______
Cardiac ________
_______ overload
Vascular ________
Necrotising enterocolitis
thermia; arrhythmias
Fluid ; rupture
Kernicterus
This is the (acute or chronic?) (temporary or permanent?) manifestation of _____________________ . Initially referred to pathologic yellowish staining of the brain by bilirubin
The major sites affected are the __________, cranial nerve nuclei (______,__________), cerebellar nuclei, brainstem nuclei, hippocampus and anterior horn cells
chronic permanent
bilirubin encephalopathy
basal ganglia
cochlear, occulomotor
ABE: Clinical features
Acute bilirubin encephalopathy refers to early acute clinical manifestation of bilirubin brain damage.
There are 3 phases:
Early: ______,_______ suck and __________ cry
Intermediate: _____tonia, ______, __________ , wind milling movts, fever, retrocollis
Late: _______tonia
Lethargy ; poor; high pitched
Hypo; seizure ; opistotonus
Hyper
ABE can be evaluated using the _______ Score ( ________________________________ )
BIND
Bilirubin induced Neurological dysfunction
Chronic Bilirubin Encephalopathy: Kernicterus
This is characterised by
Choreoathetotic or dyskinetic cerebral palsy
Partial or complete sensorineuronal deafness
Paralysis of upward gaze
Dysconjugate gaze
Usually minimal or NO mental retardation
Dental dysplasia and loss of scalp hair are sometimes seen
Maybe not now
