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