Neonatology Flashcards
DDH affects 1-3% newborns, what are risk factors and which hip is most affected?
Anything causing crowding in uterus eg. large birth weight, oligohydramnios
-female, first born babies,
-breech position, sibling(s) affected
Left hip most affected.
When should babies have their hips examined? (NB: if high risk US is done at 2-4weeks)
in first days of life and at 6weeks
If neonatal exam suggests hip instability what should you and in what timeframe? If hips still unstable at x weeks=requires rx.
- arrange an US by 2-4weeks
- x = 6weeks
What is the treatment for DDH that hasn’t resolved by 6 weeks?
-long-term splinting in flexion abduction in a Pavlik harness
If DDH is detected from 6-18months how is it treated? And if after 18months?
6-18mnths: exam under anaesthesia, arthrography and closed reduction
18mnths+: open reduction with corrective osteotomies to maintain joint stability
What Test and Manoeuvre are used to examine the neonates hip?
- The Ortolani Test: clunk as femoral head relocated
- The Barlow Manoeuvre: attempt to dislocate an unstable hip with pressure on femoral head w thumb
What is the main risk with a Pavlik harness to treat DDH? How can you monitor this? What age are these contraindicated in?
- AVN of fem head from excess abduction
- US and making sure fit is good
- CI >4.5 months (or if hips are irreducible)
Talipes equinovarus is club foot, most idiopathic but 20% associated with genetic conditions. What is the 3 abnormalities of foot?
- inversion
- adduction of forefoot relative to hindfoot
- equinus=plantarflexion deformity
What is the preferred treatment of talipes equinovarus, starting ASAP but changing gradually.
-Ponseti method: foot manipulated in a long leg plaster cast
If ponseti method fails to correct talipes, what surgery is carried out?
-soft tissue release
Neonatal jaundice is divided into: early, jaundice and prolonged jaundice, describe each in terms of mostly pathological or physiological and time frames
Early - <24hrs, most pathological (!) action needed
Jaundice - 24hr-14days mostly physiological
Prolonged - 14days+ (>21 if preterm) can be phys or pathological
Name 2 ways in which bilirubin can me measured in suspected neonatal jaundice:
- transcutaneous bilirubinometres
- serum bilirubin measurements
Name 3 pathological causes of early neonatal jaundice (!)
- sepsis
- rhesus incompatibility
- ABO incompatibility
- red cell anomalies: spherocytosis, eliptocytosis, G6PD def.
In ABO incompatibility in neonate, what IgG antibody is always present?
Maternal anti-A or anti-B haemolysin
Based on differentials, what tests are important when investigating early neonatal jaundice?
- septic screen: FBC, CRP, blood culture
- packed cell vol, blood film
- group and save
- DAT, maternal blood group, G6PD level
For what reasons does neonatal jaundice often occur between 24hrs-2weeks?
- shorter RBC lifespan so more bilirubin produced
- less bilirubin conjugated (hepatic immaturity)
- absence of gut flora impedes bile pigment elimination
- breastfeeding w difficulties -> dehydration and less elimination of bilirubin (more enterohepatic circulated)
In physiological neonatal jaundice the bilirubin is __ and rises in first few days then resolves over 2weeks, levels should be monitored to prevent___
- unconjugated
- kernicterus
What pathological causes of neonatal jaundice (24hr-2wks ) exist (name 2+)
- polycythaemia
- cephalohaematoma resorption
- hypothyroidism
- haemoglobinopathies
- viral hepatitis
What is kernicterus? Levels of unconjugated bilirubin >350umol high risk(!)
Permanent neurological sequelae of severe hyperbilirubinaemia and acute bilirubin encephalopathy (deposited in basal ganglia and brainstem nuclei)
e.g. cerebral palsy, deafness, low IQ
How is kernicterus prevented?
- phototherapy
- exchange transfusion
- IV Ig (if cause is isoimmune haemolytic disease)
What are signs of ABE (acute bilirubin encephalopathy) in neonates.
- lethargy, poor feeding
- hypotonia, shrill cry -> irritability, hypertonicity
- then apnoea, seizures, coma, death
Phototherapy works by using light energy to convert __ to __ products (lumirubin etc) that can be excreted without __.
- bilirubin
- soluble
- conjugation
Side effects of phototherapy for jaundice:
- high/low temperature
- eye damage (give protection)
- diarrhoea, fluid loss
- separation from mother
Exchange transfusion to treat jaundice uses __ blood, xml/kg given via __ vein and removed via the __ artery. Aim is to removed bilirubin.
- warmed (37degrees)
- umbilical vein, umbilical artery
Prolonged jaundice is often physiological/breastmilk jaundice, what red flags alert a more serious pathology?
- pale stool
- hepatosplenomegaly, ascites
- bruising/bleeding
- neurological signs
Crigler-Najjar and Gilbert S. are unconjugated bilirubin causes of prolonged jaundice, name some conjugated causes:
clues: gland related, chole-related, aemia/blood related and deficiency
- hypothyroidism, CF
- biliary atresia
- choledochal abnormalities
- galactosaemia
- a1 anti-trypsin def
- neonatal haemochromatosis
Biliary atresia = biliary tree occlusion due to progressive cholangiopathy, it is rare but serious and earlier identified better prognosis, what signs?
- jaundice, dark urine, pale stools
- spleen palpable by ~4wks
- liver may become hard and enlarged
RDS (Resp. distress S.) is when a deficiency of __ leads to lower __ causing widespread __ __ and inadequate __
- surfactant
- surface tension
- alveolar collapse
- gas exchange
Surfactant is a mixture of ___ and proteins excreted by the __ of the alveolar epithelium
- phospholipids
- type II pneumocytes
The more preterm the infant the higher chance of RDS, if preterm is anticipated what can be done? What does this trigger? timeframe -24-34wks
- give antenatal glucocorticoids to mother
- stimulates fetal surfactant production
At delivery/within 4hrs, what signs will be present in a baby with RDS? and when severe?
NB: atelectasis then re-inflation w each breath exhausts the baby..
- tachypnea (>60breaths/min)
- laboured breathing, chest wall recession, subcostal indrawing and nasal flaring
- expiratory grunting (trys to create a positive airway pressure)
- (severe ->cyanosis, hypoxia, low co, low BP, acidosis & renal failure)
How is RDS treated?
- delay clamping cord to promote placenta-fetal circulation
- oxygen via 02-air blender start at 30% and increase
- surfactant therapy
- CPAP, NIPPV or mechanical ventilation
Name 3 ddx of increased work of breathing within hours of birth other than RDS.
- sepsis, meconium aspiration, congenital pneumonia
- tracheo-oesophageal fistula
- TTN
Describe an RDS typical CXR appearance:
-X-ray: ground glass diffuse granular lungs +/- air bronchograms (large airways outlined), heart border indistinct
Based on preterm gestation weeks and FiO2 %, you can intubate and give RDS prophylactic .. via..
surfactant ET (endotrachal) tube
Bronchopulmonary dysplasia (BPS) complicates ventilation in some __ baby’s especially with a birth weight
- RDS, <1kg
- ante and postnatal steroids
- surfactant
Pulmonary hypoplasia is rare, suspect in infants with persisting __ +/- feeding difficulties. Some degree occurs with an early elective delivery for early spontaneous ROMs
-neonatal tachypnoea
Define : preterm, low birthweight (LBW), very LBW, extremely LBW and small for gest. age (SGA).`12
Preterm: neonate <37weeks gestational age (GA)
LBW: <2500g regardless of GA
VLBW: <1500g regardless of GA
ELBW: <1000g “”
SGA: birthweight below the 10th percentile for GA
IUGR = a reduction of expected fetal growth in utero, most commonly is __ when weight centile is __ compared to length and head circumference -ie. __. (usually due to an insult __ in pregnancy e.g. __)
- asymmetrical
- reduced
- head sparing
- later in pregnancy e.g. pre-eclampsia
Less common symmetrical IUGR suggest foetus was affected from __ pregnancy, seen in babies with __ or constitutionally small and are more likely to remain __
- early
- chromosomal abnormalities
- small permanently
Poverty accounts largely for variance in birthweights, what other factors can cause IUGR?
- malformation, twins, congenital infection
- placental insufficiency (maternal HD, high BP, smoking, diabetes, sickle cell..)
Other than shorter adult stature and possibly health, what are major complications of IUGR? -risks from infection/malformation if present..
- hypogylcaemia (poor fat/glycogen stores)
- hypothermia (larger SA)
- polycythaemia 2dry to chronic hypoxia
- NEC
- meconium aspiration
~40% prematurity causes are unknown, what are some possible causes?
- smoking, malnutrition, poverty
- PMH of prematurity, GU infectio/chorioamnionitis
- PT, DM, polyhydramnios, multiple pregnancy
- uterine malformation
- placenta disorders, premature ROM
What are pre-term babies likely to require support with after birth?
- thermoregulation
- nutrition
In RDS air from overdistended alveoli can track into the interstitium -> pulmonary interstitial __ .
In 10% ventilated infants, air leaks into pleural cavity causing a _
- emphysema
- pneumothorax
How can you thermoregulate a pre-term baby?
- put in plastic bag at birth
- stabilise under a radiant warmer +/- heated matress
- humidified incubator
What can stimulate respiration for a preterm with periods of bradycardia/apnnoea?
Caffeine
Patent ductus arteriosus with shunting of blood from left to right is common in preterm infants with__ and can cause difficulty __
RDS
-difficulty weaning the infant from artificial ventilation
If symptomatic how can a patent DA be closed medically in a pre-term?
-a prostaglandin sythetase inhibitor, indomethacin or ibroprofen
Why are preterm babys at risk of iron deficiency? (same reason they are at increased risk of infection) and 2 other reasons..
- iron is mostly transferred in the last trimester and from loss of blood from sampling and inadequate EPO response
- iron supplements are started at several weeks
NEC (Necrotising Enterocolitis) is higher in preterms due to the bowel being vulnerable to _, what is beneficial in preventing this disease?
- ischaemic injury and bacterial invasion
- breast milk = (can add pre+probiotics too)
what are signs of NEC in the infant? What can NEC progress to?
- feed intolerance, vomiting, bile may be stained
- distended abdomen, stool +/- blood
- pain
- can –> bowel perforation
NEC treatment? NB: mechanical ventilation and circulatory support may be needed
- stop oral feeding
- give broad-spec Abx vs aerobic and anerobes
- parenteral nutrition
20% VLBW infants have haemorrhages in the brain, these can be detected with _. RFs include:
US scans of craium
-asphyxia, severe RDS, pneumothorax
Retinopathy of prematurity affects developing blood vessels at the junction of the __& __ __. There is vascular __ which can progress to retinal __ , fibrosis and __.
vascularised and non-vascularised retina
proliferation
retinal detatchment
blindness
Retinopathy of prematurity affects 35% VLBW infants so infants at risk (
<1500g or <32 weeks GA
Laser therapy reduces visual impairment in retinopathy of prematurity, what injections may prove beneficial?
-intravitreal anti-VEGF
At birth name 3 things the growth-restricted infant is at risk of:
- hypo
- hypo
- hypo
- p____
- hypothermia (large SA:V ratio esp w large head)
- hypoglycaemia (from poor fat and glycogen stores)
- hypocalcaemia
- polycythaemia Ht > 0.65
name 3 problems associated w being large for gestational age infants (>90th centile) (most = normal but may be from mother T1/gest.DM or congenital disease)
- birth ___ e.g. from ___ ___, or birth ____
- hypo___ due to _____
- p____
- birth trauma e.g. shoulder dystocia, birth asphyxia
- hypoglycaemia due to hyperinsulinemia
- polycythaemia
Give 5 scenarios in which hypoglycaemia is more likely in first 24hrs of life:
..babies:
- with IUGR
- who are pre-term
- who are born to mothers with DM
- who are large-for-dates
- hypothermic, polycythaemic, or ill for any reason
Preterm/IUGR babies may have hypoglycaemia due to: ___?
vs. infants of a DM mother –> hypoglycaemia due to: ___?
- IUGR: poor glycogen stores
- DM: sufficient stores but hyperplasia of the islet cells -> high insulin levels
Name 3 sx of hypoglycaemia in the newborn:
- jitteriness
- irritability
- apnoea
- lethargy
- drowsiness
- seizures
- how is hypoglycaemia usually prevented?
- if BMs are low on 2 occasions despite this, what/how do we give?
- prevent by early and frequent milk feeding
- if still low, give IV dextrose infusion (aim maintain BM > 2.6mmol/l)
NB: to correct hypoglycaemia in a new born dextrose is usually given IV infusion, if v high conc e.g. 20% is needed, how should it be given due to what risk?
-high concs give via central venous catheter (avoids extravasation into tissues can -> tissue necrosis)
If in a hypoglycaemic neonate there has been a significant difficulty or delay in starting IV dextrose what can be given instead?
-Glucagon
Explain what birth asphyxia is? Risk?
- lack of oxygen in labour/delivery
- risk of brain injury and death
What gasping is seen in birth asphyxia and what do we call it? and how does HR change?
- fetus O2 deprived in utero -> gasps, primary apnoea (HR maintained)
- if lack of O2 continues, –> irregular gasping then 2nd period of apnoea (secondary) with this HR and BP falls
In secondary apnoea from birth asphyxia (-if lack of O2 continues, –> irregular gasping then 2nd period of apnoea), what is the only way infant can recover upon delivery?
-needs help with lung expansion upon delivery: positive pressure ventilation or tracheal tube to lungs directly
Name 2 causes of a continuous asphyxia insult (rare)
and 1 v common cause of intermittent birth asphyxia:
- continuous: after placental abruption, or cord prolapse
- intermittent: during labour from prolonged and frequent contractions
HIE (Hypoxic-Ischaemic Encephalopathy) clinical manifests ~48hrs post asphyxia, state a ft of:
- mild
- moderate
- severe
mild: irritable infant, +/- hyperventilation, hypertonia, impaired feeding, stary eyes
mod: abnormal movements, hypotonic, can’t feed, +/- seizures
severe: no normal spontaneous movement/response to pain, fluctuating limb tone, multi-organ failure, seizures
Name 4 ways you can manage infants with HIE (different aspects of their care)
-respiratory support
-rx clinical seizures w anti-convulsant
-fluid restrict due to transient renal impairment
-rx hypotension by volume and inotrope support
-monitor and rx hypoglycaemia, electrolyte imbalance esp low Ca2+
-
What is the standard therapy for mod-severe HIE?
Neuroprotection achieved how?
- inducing mild therapeutic hypothermia (cool to 33-34 rectal temperature for 72hrs by wrapping in a cooling blanket)
- reduces brain damage if started within 6hrs of birth in an infant >36weeks’ gestation
Trisomy 18: small babies, short sternum (resp problems), small chin and rockerbottom feet, heart and renal abnormalities
What syndrome and prognosis?
- Edward’s Syndrome
- 90% die within first year
Polydactyly, severe developmental malformations, heart, renal, midlife defects, rarely survive >1 month, what is this rarer trisomy syndrome?
-trisomy 13: Patau Syndrome
What would the karyotype be for a female child with Turner’s Syndrome?
45X
Williams syndrome is a 7q11.23 deletion that often presents with congenital heart defects (AS, PS) with bulbous tipped nose, wide mouth and widely spaced teeth, developmental delay…
- what is the personality?
- 15% have a what electrolyte abnormality
- overfriendly personality
- hypercalcaemia
