Neonatology Flashcards by Em RA

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.

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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

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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

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What is the treatment for DDH that hasn’t resolved by 6 weeks?

-long-term splinting in flexion abduction in a Pavlik harness

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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

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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

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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)

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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

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What is the preferred treatment of talipes equinovarus, starting ASAP but changing gradually.

-Ponseti method: foot manipulated in a long leg plaster cast

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If ponseti method fails to correct talipes, what surgery is carried out?

-soft tissue release

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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

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Name 2 ways in which bilirubin can me measured in suspected neonatal jaundice:

transcutaneous bilirubinometres

- serum bilirubin measurements

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Name 3 pathological causes of early neonatal jaundice (!)

sepsis
rhesus incompatibility
ABO incompatibility
red cell anomalies: spherocytosis, eliptocytosis, G6PD def.

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In ABO incompatibility in neonate, what IgG antibody is always present?

Maternal anti-A or anti-B haemolysin

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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

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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)

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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

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What pathological causes of neonatal jaundice (24hr-2wks ) exist (name 2+)

polycythaemia
cephalohaematoma resorption
hypothyroidism
haemoglobinopathies
viral hepatitis

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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

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How is kernicterus prevented?

phototherapy
exchange transfusion
IV Ig (if cause is isoimmune haemolytic disease)

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What are signs of ABE (acute bilirubin encephalopathy) in neonates.

lethargy, poor feeding
hypotonia, shrill cry -> irritability, hypertonicity
then apnoea, seizures, coma, death

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Phototherapy works by using light energy to convert __ to __ products (lumirubin etc) that can be excreted without __.

bilirubin
soluble
conjugation

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Side effects of phototherapy for jaundice:

high/low temperature
eye damage (give protection)
diarrhoea, fluid loss
separation from mother

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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

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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

Neonatology Flashcards

(76 cards)