CBL 7 – Jaundice Flashcards
BF for late preterm infant?
Lots of support lol
What are late preterm infants at risk of? (5)
Often have less successful BF rates than term or earlier preterm babes, because they seem sturdy but are actually developmentally immature, so don’t get adequate support
Increased risk for
jaundice
hypoglycemia
slow weight gain
dehydration
formula use
Calculation for feeding baby on feeding plan?
150 mLs per kilo per day /divided by number of feeds (ends up being A LOT)
Define jaundice
Definition: Yellow coloration of sclera and skin due to increased levels of bilirubin (which is a byproduct of red blood cells breaking down) in the bloodstream
Defined physiological jaundice
Normal jaundice with transition from intrauterine to extrauterine life with no adverse sequelae
Usually after 24 hours - 6 days (visible)
Define Pathological Jaundice
When jaundice occurs for reasons other than normal newborn transition and/or when circulating bilirubin levels reach a level of neurotoxicity that result in adverse sequalae
Often within the first 24 hours
Types of pathological hyperbilirubinemia?
Severe and critical
Define severe hyperbilirubinemia
total serum bilirubin (TSB) > 340 μmol/L in first 28 days of life
Define critical hyperbilirubinemia
TSB > 425 μmol/L in first 28 days of life (1)
What numbers are needed for TSB for adverse neurological sequale?
Adverse neurological sequale have not been documented with TSB <340 μmol/L
Adverse neurological sequale are very rare 340 μmol/L to <425 μmol/L, less rare >425 μmol/L
Etiology of Physiological Jaundice
· Newborns have more red blood cells than adults and the fetal red blood cells still circulating have a shorter life span than adult red blood cells, which results in a higher level of red blood cells and then a higher level of bilirubin than adults have (1,2)
· Immature liver that can’t conjugate (process where the liver makes bilirubin water soluble) bilirubin as quickly as adult livers which makes for slower excretion of bilirubin (1,2)
· Conjugated bilirubin is broken down further by bacteria in the gut that newborns aren’t as colonized with, making the excretion slower than in adults (2)
4 main reasons for pathological jaundice?
- Hemolytic
- non hemolytic
- impaired bilirubin conjugation
- impaired bilirubin excretion
Some examples of hemolytic jaundice? (4)
Isoimmunization
RBC enzyme defects
RBC membrane defects
Hemoglobinopathies (thalassemia and sickle cell)
Some examples of non-hemolytic jaundice? (3)
Extravascular blood (hematoma, etc)
Polycythemia (intrauterine hypoxia)
Exaggerated enterohepatic circulation (cystic fibrosis, breastmilk jaundice)
Some examples of impaired bilirubin conjugation? (3)
- Gilbert syndrome – genetic mutation that leads to reduced activity of UDP-glucoronyl transferase (fairly common, 3-7 % incidence) (1)
- Crigler-Najjar syndromes – autosomal recessive genetic mutation reduces levels of UDP-glucoronyl transferase (rare, 0.6 per million) (1)
- Congenital hypothyroidism – decreases bilirubin conjugation and decreases gut motility (1
Some examples of impaired bilirubin excretion? (4)
- Biliary obstruction – biliary atresia (40-50 % of all biliary obstructions), gallstones, bile duct abnormalities (1)
- Infection – examples cholestasis (impaired bile flow between liver and small intestines) from sepsis, meningitis, TORCH infections (1)
- Chromosomal differences – Trisomy 18 and 21, Turner’s syndrome – all have reduction of intrahepatic bile ducts (1)
- Metabolic disorders – causing cholestasis (1)
How long physiological jaundice last?
Sometimes so long, months especially if breastfed
Incidence of jaundice term?
60 %
Incidence of jaundice preterm?
80%
What is the rate of rise?
Helps determine how severe risk is bw two TSB values
Formula for rate of rise?
(TSB 2 – TSB 1)/Time
Most common type of jaundice?
Physiological
What is a bad rate of rise?
Greater than 3.4 micromols per L per hour (requires immediate Tx)
When routine jaundice screening/testing offered?
Within 24-72 hours of life
Incidence of severe hyperbili?
1.2/100 000
Long term disability from hyperbili?
0.3/100 000
What are risk factors for severe hyperbilirubinemia? (11)
● Visible jaundice less than 24 hours
● Preterm
● G-6-PD (prevalent in Mediterranean descent among others)
● Male
● Asian ethnicity
● ABO isoimmunization (O birthing person)
● Maternal age greater than 25
● BF
● Dehydration
● Babe significantly bruised following birth
● Babe born to a family with a history of previous children with severe hyperbilirubinemia requiring treatment
Visual assessment of jaundice/different skin tones?
Hold in sunlight
Depress skin with finger
Look at mucosa and whites of eyes
What would be use to see if TCB/TSB is high?
Age specific nomogram (and secretly bili tool lol)
Risk factors for severe hyperbilirubinemia ?
o Jaundice in first 24 hours after birth (pathological jaundice)
o Dehydration / inadequate feeding (note weight loss over 10%)
o Late-preterm newborns
o Birth weight under 2500g
o Bruising
o Cephalohematoma
o Hemolysis due to maternal isoimmunization, maternal glucose-6-phosphate dehydrogenase deficiency, or spherocytosis
o Siblings who had severe hyperbilirubinemia
o Asian ethnicity
o Male newborns
o Resuscitation after birth
o Sepsis
o Subgaleal hemorrhage
What is kernicterus?
- In simple terms, kernicterus is neurological damage caused by excess levels of bilirubin (1-6)
- This type of brain damage is very rare and most commonly occurs in newborns due to the neurotoxic effect of bilirubin in extreme cases of jaundice (1-6)
- It is considered a preventable disease (1-6)
- Incidence: CPS suggests 1:10,000 (1)
How is kernicterus identified?
- Signs and symptoms of kernicterus include the signs and symptoms of severe hyperbilirubinemia/bilirubin encephalopathy:
o Extreme lethargy, difficult to rouse or keep awake
o Weak or floppy muscle tone
o Unnatural high-pitched cry, irritability
o A fever combined with any of the above (1-2,6) - Signs and symptoms specific to kernicterus include:
o Opisthotonos, an unnatural position of arching backwards with the head back
o Seizures (1) - Kernicterus can also be identified by finding yellow staining of the basal ganglia of brain tissue during an autopsy (1)
- Jaundice
- Abnormal cry (shrill & high pitched)
- Loss of Moro reflex
- Lethargic
- Poor feeding
- Floppy/Poor Tone
How is kernicterus treated?
- Unfortunately, Kernicterus is incurable and causes permanent brain damage (3-4,6)
- However, early identification and quick treatment may prevent further damage to the brain (6)
- Treatment is the same as for severe hyperbilirubinemia, including light therapy, administration of intravenous fluids, and/or a feeding tube with specialized formula (2,6)
- Blood transfusion or exchange transfusion therapy in order to remove some of the excess bilirubin in the bloodstream (2,6)
- Administration of intravenous immunoglobulins in cases of hemolysis due to isoimmunization (2)
- Long term treatment may include speech therapy, physiotherapy, and special education depending on the extent of neurological damage (6)
What can we do for prevention of kernicterus?
The main way to prevent kernicterus is to screen and treat for jaundice before it becomes severe; screening may occur through visual assessment, testing total serum bilirubin (TSB) levels, and screening for risk factors (1-6)
Rh immunoglobulin
Feeding support
Adequate follow up and surveillance
TCB vs TSB accuracy?
TCB is a good screen but not diagnostic.
TSB is gold standard for diagnosing and determining levels of Tx.
What is TCB?
Use of a bilimetre (light metre) to screen for jaundice. Non-invasive, pain-free, simple bilirubin measurement tool to help categorize the level of jaundice in the newborn. First 72 hours of life. Screening tool.
What is TSB?
Consists of collecting blood via a capillary heel blood sample to determine the amount of bilirubin circulating in blood. 24-72 hours. Precise bili levels
What’s a DAT?
Direct Coombs Test (direct antiglobulin test) – detects antibodies attached to RBCs which an indicate immune mediated hemolysis
How does DAT relate to jaundice?
Strength of result may add to severity of jaundice
Standard treatment of hyperbilirubinemia?
Phototherapy and adequate feeding
Who gets a DAT? (6)
- Birther with blood group O
- Birther, who is Rh Negative
- Hx of hemolytic disease-previous babies
- Birther with unknown blood group
- ABO incompatibility between birther and baby
- Concerns about the baby potentially developing anemia
Who doesn’t get a DAT?
Rh neg birthers who have received WinRho
Those with none of the previously mentioned risk factors
What does a posi DAT mean?
Presence of antibodies in babes RBCs but doesn’t mean babe will develop jaundice OR if neg doesn’t mean babe WONT develop jaundice.
Input up to 3 weeks?
BF: 8 or more times per day (1-3 hours, including 2-3 night feeds)
Gains 2-3 weeks?
120-240 g per week OR 4-8 ounces per week
Output for first week?
VOIDs: day 1:1, day 2:2, day 3:3, day 4:4, day 5,6,7:5
SOILED: day 1-2: 1-2; day 3-4: 2-3 brown, green, yellow; day 5,6,7: 2-3 soft/yellow
Output 2-3 weeks?
VOIDs: 2-3 (or more) soft and yellow
SOILED: At least 6 wet
