Common Newborn Problems Flashcards
Physiologic hyperbilirubinemia: predictable rise in serum bilirubin after birth that is not associated with harm to the newborn.
Aka physiologic jaundice, nonpathologic unconjugated hyperbilirubinemia, or icterus neonatorum.
Ultimately, this definition is based on serum bilirubin, and is NOT associated with a statistical likelihood of kernicterus.
Generally ___ bilirubin
Physiologic hyperbilirubinemia: predictable rise in serum bilirubin after birth that is not associated with harm to the newborn.
Aka physiologic jaundice, nonpathologic unconjugated hyperbilirubinemia, or icterus neonatorum.
Ultimately, this definition is based on serum bilirubin, and is NOT associated with a statistical likelihood of kernicterus.
Generally unconjugated bilirubin
Features of pathologic hyperbilirubinemia
Features include jaundice before 24 hours of age, rapid elevation of serum bilirubin greater than 80uM per day, and peak bilirubin greater 350 uM (lower for special circumstances and preterm infants)
breast feeding vs breast milk jaundice
breast feeding jaundice: physiologic hyperbilirubiemia in an infant who is breast feeding, thought to be related to decreased lfuid and caloric intake.
- mainly unconjugated bilirubin (because it is a physiologic jaundice)
- If persistently yellow at 2-3 weeks, also rule out conjugated hyperbilirubinemia. (conjugated fraction of bilirubin is greater than 20% of the total bilirubin or greater than 20uM absolute).
Mechanism: Fluid intake is reduced (starvation, feeding frequency, weight loss/dehydration compared to in the womb), inhibition of hepatic excretion of bilirubin, and delayed intestinal reabsorption of bilirubin.
breast milk jaundice: persistent unconjugated hyperbilirubinemia after one week of age assocaited with continueed breast feeding. it tends to resolve within 12 weeks.
T/f in bilirubin encephalopathy, intellect and IQ is often affected
false. most bilirubin encephalopathy features involve motor retarfation and seizurse. intellect is largely spared
outline the differences in bilirubin metaboism in utero vs after birth
In utero, the baby doesn’t deal with its bilirubin– the mother excretes and conjugates it.
After birth, the new organs need to start processing bilirubin.
When hemoglobin is metabolized, it becomes unconjugated bilirubin. It joins with albumin and gets picked up and conjugated by the liver and then excreted in the form of stercobilin and urobilin . In a fetus, the fetus’s unconjugated bilirubin gets taken up by the mother. The mother’s liver then conjugates it and excretes it.
Vast majority of bilirubin in the newborn is the unconjugated state.
WHy do babies get jaundice? (6 reasons)
- reduced blood cell lifespan
- increase shunt of bilirubin production recylcing of nonRBC heme sources
- persistant portal venous blood flow through ductus venosus (bilirubin rich blood misses the liver– the liver can’t grab the bilirubin, leaving a build up of onconjugated bilirubin in the blood)
- decresae in Y proteins so that the liver can’t steal bilirubin from the serum
- more bilirubin production overall
- breast mildf actors that interfere with enter-heaptic circulation along with the gut flora
- there is a decrease iN UDP activity which is one of the first steps for conjugating bilirubin
DDx for xauses of jaundice by age of onset <24 hours
if below 24 hours, it’s due to hemolysis
- Rh incompatibility
ABO incompatibility
G6PD deficiency
hereditary spherocytosis
IFNECTION/SEPSOIS
The presence of hemolysis makes jaundice more likely pathologic.
African descent decreases the likelihood of jaundice.
Early passage of meconium is protective against jaundice.
The more mature the delivery (>40 weeks), the more ready organs are to conjugate/function.
Pathologic Jaundice Risk Factors/Causes: RBC intrinsic factor anomalies, RBC extrinsic factor anomalies
Due to RBC intrinsic factors like:
Isoimmunization (ABO incompatibility, rH incompatibility)
- ABO incompatibility: most commonly identified cause of hemolytic jaundice, usually because mother is O and baby is A or B. No prior sensitisation is required, DAT (coombs) may be positive. Degree of hemolysis may be modest; may have more spherocytes, may have retics.
- RBC enzyme deficiencies (G6PD deficiency)
- RBC structural abnormalities (hereditary spherocytosis or elliptocytosis)
Due to RBC Extrinsic like:
Extravascular blood: cephalohematoma, subgaleal hematoma, bruising, occult hematoma, swallowed maternal blood
Polycythemia due to maternal diabetes, fetomaternal/twin to twin transfusion
DIC/Sepsis
Pathological jaundice Risk Factors/Causes: Decreased bilirubin metabolism anomalies
UDPGT enzyme immaturity due to prematurity)
Gilbert Syndrome
Sepsis (UTI)
Neonatal hypothyroidism, drugs.
onset of physiologic vs pathologic pre-hepatic/unconjugated jaundice
physiologic; onsert 2-3 days. Ddx is breast feeding jaundice, breast milk jaundice, hypothyroidism, decreased intestinal transit
pathological: onset first 24 hours of life. LCinicall yunwell with risk factors.
Treatment Options of jaundice
Observation
Feeding (breast +/- hydrolysed formula)
Phototherapy
- 460nm light photoisomerazes bilirubin
- Allows baby to pee it out.
- Highly dependent on intensity/dose and surface area exposed.
IVIG if isoimmunization
Exchange transfusion; takes bilirubin out of blood.
T/F cephalohematoma crosses suture line
false.
Distinct margins, continuing to grow for the first day and a half.
Takes a long time to totally go away– the blood has to be hydrolyzed and evacuated from the subperiosteal space.
Periosteum can start to deposit bone above the level of the skull bone. It will leave a little bump– rarely severe
Caput succadaneum: location of bleed, characteristic findings, timing, volume of blood
at point of contact; can extend across sutures.
- findings: pitting edema that shifts with grabity
- maximal size and firmness at birth
- volume: minimal.
-
compare and contrast location of caput succedaneum, cephalohematoma, subgalelal hemorrhae: location, characteristic findings, timing, volume of blood.
caput succedaneum vs chignon
caput succedaneum: swelling (almost pitting), chignon: swelling of head due to vacuum
a brachial plexus injury is associated with ___ fracture
clavicular fracture
signs of brachial plexus injury
Seen in 0.1% of births, mostly with vaginal birth, but higher percentage with breech delivery.
Signs: asymmetric Moro reflex –> Can test with Moro response; “drop” the baby and they will elevate their arms in a “scared” response. If they don’t do this, it is possible that it’s Erb’s palsy (C5-C6).
Three patterns: Erb Palsy, Klumpe (C8-T1), and complete.
Rarely diaphragmatic involvement in horner syndrome**really uncommon.
Recovery can be within weeks, months, and incomplete.
Dependent on if nerves were just a little stretched/bruised, or if complete shear forces/severing happened.
T/f there is a set defined normal BG for neonates
Lowest normal glucose for a newborn baby:
A normal range for BG values in the newborn has not been properly defined. Values are influenced by birth weight, gestational age, feeding method and postnatal age.
Controversy over the definition of a safe blood glucose concentration (ie a value below which there is risk of long-term neurodevelopmental impairment)
Neonatal hypoglycemia is not a medical condition in itself, but a feature of illness or of failure to adapt from the fetal state of continuous transplacental glucose consumption to the extrauterine pattern of intermittent nutrient supply
Serum glucose: <2.6mM (<72 hrs of life) is considered neonatal hypoglycemia.
Risks for Infant Hypoglycemia
- Prematurity: lower glycogen stores, lower fat stores, increased heat loss– large BSA to mass ratio (similar reason for hypothermia), impaired liver function– glycolysis, gluconeogenesis (from alanine and other proteins) and lipolysis (to make ktone bodies for brain fuel), higher metabolic rate, immature glucose regulation of insulin– causes relative hyperinsulinism.
- Hypothermia
- hypoxia/asphyxia
- Maternal diabetes
- Maternal medication (beta blockers)
- Intrauterine growth restriction
- Inuit
- Sepsis
- Respiratory distress syndrome
- Polycythemia
- Cardiac failure/cyanotic congenital heart disease
- Interruption of intravenous infusions
Clinical Features of Neonatal hypoglycemia
Preventing Hypoglycemia in newborns
Identification and monitoring of infants at risk– preterm, SGA, IDDM, Poor adaptation (low Apga), and maternal beta-blocker.
Early and frequency feeding
Lactation support
Monitoring and Treatment plan for neonatal hypoglycemia
- Symptomatic infants are assessed with Bedside glucometer or lab glucose measurement
- At risk infants are tested at regular intervals beginning within 1-3 hours of birth. Duration of monitoring is determined by the risk variables and the measured glucose
- Any abnormal glucose [2.6 mM] results in additional feeding
- Post feed glucose needs to be >/= 2.6mM
- There should be 2 sequential glucose measures >/= 2.6mM before monitoring stops
- High risk infants are monitored 24-35 hours
- Severe hypoglycaemia <1.8mM or sequential ac feed glucose <2.6mM require assessment and possible IV dextrose
Treatment
- Oral (breast milk or infant formula or dextrose gel)
- 2ml/kg of D10W IV then continuous infusion of glucose at 6-8 mg/kg/min. Adjust after repeat glucose measures. May need to increase to 15 mg/kg/min
- Glucagon, steroids, growth hormone may be necessary
- Diazoxide, octreotide (somatostatin analogue) or calcium channel blockers in hyperinsulinemic HI states
- Sub- total pancreatectomy in refractory HI states.
