Neonatal + infant

Question 1

What are the benefits of breast feeding?

Answer 1

• Immune: reduced gastroenteritis + bronchiolitis + ENT infection + NEC
• Reduced SIDs
• Reduced allergy when there is a FH of allergy
• Reduced childhood obesity
• Maternal benefits: reduced PND, T2DM, breast and ovarian cancer
• Family benefits: all the above, financial (free!)
• Public health: the above, fewer admissions

Question 2

Properties of breast milk?

Answer 2

Immunological: secretory IgA, lysozymes, lactoferrin (inhibits growth of E coli)

Nutrition: more easily-digested lipid + protein, more calcium, low renal solute load, iron more bio-available

First milk - colostrum - v high in energy to make up for physiologically stressful birth process, then gets more watery

Question 3

Complications of breast feeding?

Answer 3

• Unknown intake
• Transmission of maternal BBV
• Breast milk jaundice (unconjugated, self limiting, continue bf)
• Transmission of drugs
• Nutrient deficiency if prolonged
• Potential transmission of environmental contaminants e.g. nicotine, caffeine
• Less flexibility e.g. the dad can’t do the feeding
• Emotional difficulties if it doesn’t succeed

Question 4

How long should women ideally BF for?

Answer 4

6m ebf, then alongside foods until 2y

Question 5

Physiology of breast feeding?

Answer 5

Oxytocin (PP) stimulates letdown reflex: supply + demand (not much comes out initially)

Prolactin (AP) is the other hormone involved

If mother gives bottle top ups at beginning cos baby is hungry, it interrupts the hormone production and can mean they stop making milk

Question 6

Know a bit about formula feeding too

Answer 6

Modified cow’s milk with other nutrients added

Normal values:

• Day 1 around 50ml/kg/day
• End of W1 150ml/kg/day
• Milk bottles not standardised, most mums use ounces (on the tins), 1 ounce is about 30ml, most feed around 8x per day

Question 7

Group B Streptococcus infection

Answer 7

GBS carried by 10-30% of women in faeces/vagina, and up to 50% of the babies get colonised

Comps: early + late onset sepsis (usually pneumonia but may be meningitis), late onset disease up to 3m old (usually meningitis)

RF for infection if mother colonised: preterm, PROM, maternal fever >38 during labour, maternal chorioamnionitis, previously infected infant –> if any of these happen mother given prophylactic IV Abx intrapartum

Question 8

What are the types of IUGR?

Answer 8

IUGR=growth not reaching its genetic potential

• Asymmetrical: more common, head spared at expense of liver+fat. Due to placenta not supplying enough nutrition in late pregnancy e.g. pre-eclampsia, smoking, multiple pregnancy. Rapid weight gain after brith (higher risk of later T2DM)
• Symmetrical: rarer, HC+AC equally reduced suggesting longer period of poor growth. May be small but normal, or a chromosomal disorder/congenital infection/maternal drug or alcohol/chronic medical issue in mother/malnutrition in mother. Likely to always be small

Question 9

What issues are more likely in a baby born with IUGR?

Answer 9

Intrauterine hypoxia, IUD, asphyxia during birth + delivery, hypothermia (as large SA), hypoglycaemia (less fat + glycogen stores), hypocalcaema, polycythaemia

Question 10

Early onset sepsis <48h old

Answer 10

Due to bacteria from birth canal entering amniotic fluid which fetus inhales – so causes pneumonia + sepsis

Causes: viral, early-onset listeria, GBS

RF: prolonged/premature ROM, chorioamnionitis

CF: RDS, temp high/low, poor feeding, vomiting, apnoea, bradycardia, abdo distension, jaundice, neutropenia, hypo/hyperglycaemia, shock, irritability, seizures, lethargy, signs of meningitis (tense/bulging fontanelle, head retraction)

Ix: CXR, septic screen

M: benzylpenicillin/amoxicillin (G+ cover) and gentamicin (G- cover). Can stop after 48h if no sign of infection and cultures negative

Question 11

Late onset sepsis >48h old

Answer 11

Cause: often environmental like invasive procedures, S epidermidis commonest, can also be GBS

CF: usually non specific

M: cover G+ and G- e.g. fluxcloxacillin + gentamicin, or broad spec e.g. meropenem

Question 12

What specific infections are neonates at risk of?

Answer 12

• GBS
• Listeria monocytogenes: uncommon, transmitted to mother in unpasteurised milk/soft cheese/undercooked poultry, mother mild illness + bacteraemia, but can cause IUD/preterm/neonatal sepsis
• Conjunctivitis: when there is discharge with redness.
• Umbilical infection if skin around inflamed
• HSV: through infected birth canal, up to 4w old localised herpetic lesions on skin/eye, encephalitis, disseminated
• Hepatitis B (if mother positive then give neonate vaccination soon after birth, complete course)

Question 13

What is neonatal jaundice?

Answer 13

A common disorder (>50% newborns), when bili reaches 80 (CF not reliable)

Common in newborns because when they start breathing the Hb starts to reduce meaning more breakdown products

Question 14

What are the causes of neonatal jaundice>

Answer 14

• Early <24h: abnormal
• Haemolytic disorders: unconjugated bili. Rhesus or ABO incompatibility, G6PD deficiency (mostly boys), spherocytosis
• Congenital infections: conjugated bili
• Between 24h-2w: likely physiological, or haemolysis
• Physiological: normal as Hb falling + hepatic bili metabolism less efficient
• Breast milk jaundice: unconjugated, multifactorial, can be normal up to 3w
• Dehydration
• Infection e.g. UTI. Unconjugated. From poor fluid intake, haemolysis, reduced LFT
• Haemolysis as above
• Bruising
• Polycythaemia (venous haematocrit >0.65
• Crigler-Najar syndrome: v rare
• Prolonged >2w: never normal
• Unconjugated: commonest, from breast milk or infections like UTI
• Conjugated: dark urine pale stools poor weight gain hepatomegaly –> things like biliary atresia, neonatal hepatitis

Question 15

What is kernicterus?

Answer 15

Unconjugated bili deposited in basal ganglia + brainstem nuclei, when there isn’t enough albumin left to bind excessive levels to stop it crossing BBB

Rare now cos of anti-D Ig

Acute - lethargy, poor feeding, severe causes irritable/hypertonia/seizures/coma

Long term can cause cerebral palsy cos of damaged basal ganglia; also sensorineural HL or LD

Question 16

How do you assess neonatal jaundice?

Answer 16

Press skin to blanch it - but harder to see in darker skinned babies

Obstructive - dark urine pale stools

Generally by time: if <24h likely haemolysis, if 24h-2w assess but usually normal, if >2w not normal

If unwell check for sepsis + dehydration

Charts to assess the rise which usually is linear then a plateau - can use to estimate the need for intervention before a dangerous level is reached, different charts by age so for pre-terms there is a lower threshold

Question 17

How is neonatal jaundice managed?

Answer 17

• Plot bili on the graph (right graph for right age)
• Phototherapy: visible light in a specific wavelength makes unconjugated bili water-soluble so it gets excreted (don’t use indiscriminately as disrupts normal care of infant)
• Exchange transfusion: blood removed from arterial line/umbilical vein and replaced with donor blood via a peripheral/umbilical vein, usually exchange 2x infant’s blood volume. CMV screening
• IV immunoglobulins - when there is an immune haemolysis

Question 18

How do babies born at 23-27w differ to term neonates?

Answer 18

• Skin v thin, dark red colour
• Male undescended testes, female prominent external genitalia
• No coordinated suckling reflex, usually needs tube feeding
• Faint cry, eyelids may be fused, doesn’t interact
• Startles to loud noise as opposed to any sound
• Limbs extended, jerky movements

Question 19

Long term problems of prematurity?

Answer 19

• LD, cerebral palsy
• Difficulties with other areas of development
• Hearing and vision impairments

Question 20

Medical complications of prematurity?

Answer 20

• Resuscitation more likely needed
• RDS
• Pneumothorax - from over distended alveoli in RDS or if they are ventilated, if tension chest drain
• Apnoea + bradycardia
• Hypotension
• Patent ductus arteriosus
• Hypoxia, hypoglycaemia, hypocalcaemia, electrolyte imbalances
• Osteopenia of prematurity (prevented now by giving phosphate calcium + vitamin D to support mineralisation)
• High nutritional requirements, at risk of deficiencies
• Infection as they receive less of the IgG that gets transferred mostly in T3, most hospital-induced
• Jaundice
• IVH + PVL
• NEC
• Retinopathy of prematurity
• Bronchopulmonary dysplasia
• Inguinal herniae

Question 21

Respiratory distress syndrome?

Answer 21

Surfactant deficiency - lowered surface tension - alveolar collapse + impaired gas exchange

Usually occurs in pre-terms, if this anticipated mother given glucocorticoids to stimulate surfactant production (which also reduces BPD + IVH)

CF: occurs up to 4h post-deliver with tachypnoea >60, laboured breathing, chest wall recession, expiratory grunting, cyanosis

CXR: diffuse ground glass appearance, air bronchogram, indistinct heart border

M: oxygen, surfactant into lungs, NIV with CPAP/high flow nasal cannula/invasive ventilation

Question 22

Apnoea + bradycardia

Answer 22

Common until around 32w gestational age
Brady when breathing stops for <30s or glottis closed - usually cos immature resp control (but check for hypos, HF, aspiration from GOR), breathing starts after gentle physical stimulation
Caffeine often given to help
May need ventilation

Question 23

Patent ductus arteriosus

Answer 23

RF: RDS main

CF: bounding pulse due to increase pulse pressure, systolic murmur, prominent precordial impulse

M: if symptoms treat with ibuprofen which is a prostaglandin synthetase inhibitor (as PGs keep it open)

Question 24

Nutritional problems in premature babies

Answer 24

High requirements cos of fast growth

<35w they need tube feeding as too immature to suck, preferably breast milk + fortification

if v ill or immature <1kg need parenteral nutrition (risks of sepsis + thrombosis)

iron stores mostly transferred during T3 + lose blood from regular sampling + inadequate EPO response – iron def most common

Question 25

Intraventricular haemorrhage + periventricular leukomalacia

Answer 25

These mostly occur within 72h. RF are perinatal asphyxia, severe RDS + pneumothorax

IVH: can lead to parenchymal infarction causing hemiplegia, or impair CSF flow causing hydrocephalus - cranial sutures separate + tense fontanelle. Over half develop CP

PL: WM brain injury from ischaemia/inflammation, if takes >1w to resolve then CP risk is increased

Both of these may have no clinical signs

Question 26

Necrotising enterocolitis

Answer 26

Bowel ischaemic injury + bacterial invasion

RF: premature (bowel wall thinner etc), formula fed

CF: feed intolerance, vomiting (may be bile-stained), abdo distension, fresh blood in stool, shock

XR: distended loops of bowel, thickened bowel wall with intra-mural gas, gas in portal venous tract

M: stop oral feeds, broad spec Abx, parenteral nutrition, often need ventilation, surgery for perforation

Comps: 20% mortality, strictures, malabsorption from resection, neurodevelopment delay

Question 27

Retinopathy of prematurity

Answer 27

Developing bv damaged - retinal detachment - fibrosis - blindness

Screen eyes of susceptible infants

Laser therapy + intra-vitreal VEGF can help

Question 28

Bronchopulmonary dysplasia (prev name chronic lung disease)

Answer 28

Infants who still need oxygen after a length of time (Depends on severity) cos of delayed maturation + trauma from artificial ventilation or infection

CXR: widespread opacification, cystic changes

M: CPAP/high flow NC (may be for months), short course low dose steroids to help wean off O2

Comps: infection, pulmonary HTN, higher risk of resp infections like pertussis

Question 29

What is the Apgar score?

Answer 29

Done at 1 and 5 minutes to check newborn health. 7-10 good, 4-6 moderately low, 0-3 v low

Score 2 for each normal parameter: pulse (>100), respiratory effort (strong + crying), colour (pink), muscle tone (active movement) and reflex irritability (cries on stimulation, sneezes/coughs)

Question 30

Outline the newborn physical examination

Answer 30

Done within 72h of birth, to screen for congenital abnormalities, make referrals for tests/treatment, reassure parents. They have enough one at 6-8w usually at GP. Documented online system print out for notes

Basic outline:

1. Brief history: maternal + newborn, parental concerns
2. Weight
3. General inspection: pallor, cyanosis, jaundice, rashes etc
4. Tone: gently passively move limbs
5. Head: microcephaly, sutures, shape (moulding to birth canal common), injuries, anterior fontanelle
6. Skin: document any birth marks of lacerations in case of future child protection concerns
7. Face: dysmorphic features, asymmetry like CNVII palsy, nose patency
8. Eyes: signs of conjunctivitis, sclera for jaundice, position + shape, epicanthic folds, red reflex, subconjunctival haemorrhage (common from delivery)
9. Ears: pinna symmetry, accessory auricles, hearing screen test before discharged
10. Mouth: visualise whole palate + central uvula, look for tongue-tie (ankyloglossia)
11. Neck: appearance e.g. Turner’s, swellings e.g. cystic hygroma, clavicular# from delivery
12. Upper limb symmetry, digits, palms (2 palmar creases per hand), brachial pulses
13. ChesT: deformities, air entry, murmurs, pulse oximetry
14. Abdo: distension, herniae, liver (should be no more than 2cm below costal margin), spleen (may be just about palpable), kidneys, bladder (shouldn’t be palpable), umbilical discharge/hernia/erythema
15. Genitalia ambiguity, meatal position in boys, palpate scrotum to ensure both present, in girls ensure labia not fused (may have some white DC from maternal oestrogen)
16. Lower limbs symmetry, tone, movement, femoral pulses (CoA), ankle deformity (talipes), digits
17. Hips: examine individually with nappy off, Barlow’s + Ortolani’s tests
18. Back for scoliosis, hair tufts, sacral pits
19. Anus patency
20. Reflexes

Question 31

What are the main conditions screened for on the NIPE?

Answer 31

DDH
Small 
Floppy baby
Birth trauma
Birth marks
Dysmorphic features 
Extra/missing digits
Cleft palate
Ambiguous genitalia
Testicular maldescent
Coarctation of the aorta
Scoliosis
Neural tube defects
Hirschsprung disease

Question 32

Signs of respiratory distress at term

Answer 32

Tachypnoea, laboured breathing (sternal + subcostal indrawing, nasal flaring), expiratory grunting, cyanosis

Question 33

Causes of respiratory distress at term

Answer 33

• TTN
• Meconium aspiration
• Pneumonia: RF are PROM >24h, chorioamniontiis, low bw
• Pneumothorax - usually asymptomatic tho
• RDS as in premature but much less common at term as usually have enough surfactant
• Persistent pulmonary hypertension of the newborn
• Milk aspiration: more in prem/neuro damage/cleft palate
• Rare things like CDH, tracheo-oesophageal fistula, pulmonary hypoplasia, choanal atresia
• Non-lung causes like CHD, HIE, severe anaemia, metabolic acidosis

Question 34

Transient tachypnoea of the newborn

Answer 34

Commonest cause of resp distress at term - delayed resorption of lung liquid

More risk after CS

M: usually settles in first few days but may need O2

Question 35

Meconium aspiration

Answer 35

More common post-term, fetal hypoxia, asphyxiated

Lung irritant + mechanical obstruction + chemical pneumonitis + infection predisposition

CXR: hyper inflated lungs, patches of collapse or consolidation, air leak (predisposes to pneumothorax)

M: if cries + fine no resus, if doesn’t cry start lung inflation within 1st minute, quickly suction oropharynx but if bradycardic start PPV even if meconium present. Often needs mechanical ventilation. may develop PPHTN

Question 36

Persistent pulmonary hypertension of the newborn

Answer 36

Life threatening, a/w asphyxia/meconium aspiration/sepsis/RDS

R-L shunting due to high pulmonary vascular resistance - cyanosis without murmur or signs of HF

M: ventilation, inhaled nitric oxide (vasodilator), sometimes sildenafil

Question 37

Outline neonatal resuscitation

Answer 37

• Dry + cover baby, if don’t breathe/cry put on resus table with heater and partially cover
• If irregular breathing in first min but HR >100 just encourage with airway opening (neutral position, chin lift/jaw thrust if needed), suctioning of visible secretions/blood
• if no breathing/HR <100 need airway positioning, lung inflation by mask ventilation, consider O2
• if HR <60 after 5 effective inflation breathes do chest compressions ratio 15:2 breaths
• drugs not usually needed
• if unresponsive tracheal intubation, this usually works but if not consider DOPE (Displaced tube, Obstructed tube [meconium], Patient [obstruction in the trachea, perinatal asphyxia etc] Equipment failure)

If pre-term put in plastic bag except face to keep warm, lower [O2] cos of free-radicals can damage tissues, CPAP if wanting to avoid intubation

Question 38

Neonatal seizures

Answer 38

Startle/tremor when stimulated/sleeping-normal

Seizures: unstimulated, usually repetitive rhythmic movements of limbs persisting despite restraint, often also eye movements + changes in breathing

Causes: HIE, cerebral infarct, sepsis, meningitis, metabolic, ICH, cerebral malformation, drug withdrawal e.g. maternal opiates, congenital infection, kernicterus

Question 39

Blood group incompatibility

Answer 39

Rhesus: usually antenatal detection @ booking and 28w, if D-neg given anti-D immunisation, also if have a sensitising event. Can treat via antenatal umbilical fetal transfusion

ABO incompatibility : now more common, most IgM antibodies so don’t cross placenta but some group O have IgG antibodies which can haemolyse red cells by crossing placenta. Haemolysis less severe, no hepatosplenomegaly, positive DAT

Question 40

Biliary atresia

Answer 40

Progressive fibrosis + obliteration of biliary tree - die within 2y if don’t intervene!

CF: mild jaundice, pale stools, faltering growth, hepato/splenomegaly, raised conjugated bili + abnormal LFT

Ix: US abdo may show contracted/absent gallbladder, ERCP to confirm

M: Kasai surgery temporary then liver transplant

Question 41

What are the common types of birth mark?

Answer 41

• Slate grey naevus: benign flat birthmark, irregular, often over sacrum, may look like a bruise. go by 3-5y
• Naevus simplex: stork bite/salmon patch. A capillary malformation, often eyelid/back of neck/glabella, goes by about 1y
• Naevus flammeus (port wine stain): vascular malformation, doesn’t regress
• milia: not a birth mark but like tiny white cysts on the face go within weeks
• erythema toxicum: v common, benign, erythematous macules/papules/pustules

Question 42

What are the possible traumatic injuries a baby can acquire from birth?

Answer 42

RF: malpositioned, larger than pelvic outlet, instrumental delivery

• Soft tissue injuries: caput succedaneum (oedema beyond margins), cephalhaematoma (confined to sutures, soft), chignon (oedema + bruise from Ventouse), bruising to face/butocks from face/breech presentation, abrasions from scalp electrodes, forceps marks
• Nerve palsies: Erb palsy (C5-6, resolves by 2-3m), CN VII palsy from compression (u/l weakness on crying, eye stays open, transient), damage to cervical spine (rare)
• # : clavicle from shoulder dystocia, humerus/femur from breech

Question 43

Cleft lip + palate

Answer 43

• CL: failed fusion of frontonasal + maxillary processes. surgery at 3m
• CP failed fusion of palatine processs + nasal septum. surgery at 6-12m

Some a/w syndromes or maternal AED, usually polygeneic

CF: may make feeding harder, prone to AOM + secretory OM, avoid adenoidectomy as makes gap bigger

Question 44

Pierre Robin sequence

Answer 44

posterior displacement of tongue and midline cleft of the soft palate

may cause feeding issues + cyanotic episodes (as tongue falls back it obstructs upper airways)

Question 45

Oesophageal atresia

Answer 45

Usually a/w tracheo-oesophageal fistula

RF: polyhydramnios, absent stomach bubble on antenatal screening, other congenital malformations (almost half, VACTERL)

CF: persistent salivation, choking/coughing when feed, cyanotic episodes, aspiration

Ix: pass feeding tube after birth and check on XR if it reaches stomach

M: continuous suction to reduce aspiration then surgery

Later comps: GORD, chronic cough

Question 46

Exomphalos (omphalocele) vs gastroschisis

Answer 46

Exomphalos: abdo contents through umbilical ring, covered with amniotic membrane + peritoneum, often a/w other abnormlaities

Gastroschisis: bowel protrudes through defect in anterior abdo wall adjacent to umbilicus, no covering. Not a/w other abnormalities but high risk of dehydration + protein loss so cover with a wrap, NG tube + aspirates, IV fluids

Question 47

What are the typical features of congenital infections?

Answer 47

Growth restriction, intracerebral calcification, hydrocephalus, microcephaly, deafness, eye problems, pneumonitis, cardiomegaly, PDA< hepatomegaly, jaundice, rashes e.g. blueberry muffin, bone abnormalities, BM suppression

Question 48

What are the major congenital infections?

Answer 48

• Rubella: infection <8w worst (deafness, CHD, cataracts), 13-16w usually hearing issues, >18w minimal risk
• CMV: commonest, no screening or vaccine and asymptomatic in woman, in 5% of infected infants they can have SNHL/cerebral palsy/epilepsy. M-antiviral to the infant
• Toxoplasma gondii: from cat faeces or raw meat, spreads via placenta. If infant gets CF is retinopathy, cerebral calcification or hydrocephalus + long term neuro disability, if asymptomatic they are at long term risk of chorioretinitis
• Syphilis: rash on feet + hands, bone lesions, if mother fully treated within 1m of delivery infant will be fine, if doubt give infant penicillin
• Varicella zoster: at risk if mother develops chickenpox. Risky time is within 5d before + after delivery as not protected by maternal antibodies so can get a serious vesicular rash
• Parvovirus B19: can rarely cause fetal hydrops + death from severe anaemia, so if mother affected serial US monitoring

Question 49

Hypoxic-ischaemic encephalopathy

Answer 49

Perinatal asphyxia –> brain injury (‘birth asphyxia’ medicolegal implications so only use if certain things present)

Causes: failure of gas exchange (e.g. abruption, ruptured uterus), interrupted umbilical blood flow cord compression from dystocia, cord prolapse), inadequate maternal perfusion e.g. hypotension/hyperttension, fetal compromise e.g. IUGR/anaemia, failure of cardioresp adaptation at birth

CF: irritability, staring eye, hyperventilation, hypertonia (milder stages), moderate - hypotonic/can’t feed/seizures/markedly abnormal movement, severe (no spontaneous movement or response to pain, fluctuating tone, prolonged seizures, MOF)

Can cause immediate neuronal injury or secondarily from reperfusion injury

M: resp support, anticonvulsants, fluid restriction (transient renal impariment), monitor glucose + electrolytes, inotropes, mild hypothermia

Comps: >2w of CF they are likely to remain that way, death, major disability, cerebral palsy, PPHN, seizures

Question 50

Meconium delay

Answer 50

• SBO: also /pw persist vomiting usually bile stained (unless above AoV). Causes include duodenal atresia/stenosis (a/w T21), ileal/jejunal stenosis or atresia, malrotation, meconium ileus (impacted thick meconium, majority CF), meconium plug
• LBO: Hirschsprung disease, rectal atresia

Question 51

Neonatal hypoglycaemia risk factors

Answer 51

SFGA (insufficient brown fat), maternal diabetes (baby used to high sugar of maternal blood so pancreas still makes lots f insulin), traumatic birth (use up lots of glucose), sepsis, transient hyper-insulinaemia of prematurity

Question 52

CF of neonatal hypoglycaemia

Answer 52

Drowsiness, not waking for feeds, jitters which stop if put hand on it (so not seizure), vit D deficiency

Glucose below 2 (babies more tolerant of lower sugars as they have the brown fat for energy)

Question 53

How would you manage neonatal hypoglycaemia?

Answer 53

M: dextrose, promote feeding

May need ix if suspect a rare cause like CAH

Question 54

Ambiguous genitalia

Answer 54

Excessive androgens - CAH (F)
Inadequate androgens - androgen insensitivity syndromes (M)
Gonadotrophin insufficiency e.g. Prader-Willi syndrome
Ovo-testicular DSD (prev called true hermaphroditism): both XX and Y cells so both tissues present + complex external phenotype, rare

Question 55

Inborn errors of metabolism

Answer 55

Many types, some diagnosed on heelprick, wide range of presentations

CF: usually early childhood. Consider in an unexpectedly severe presentation of an illness, unexplained metabolic abnormalities, hypoglycaemia, HF/cardiomyopathy, early onset seizures, dysmorphic features, developmental regression

FH of IEM, sudden unexplained death, epilepsy, LD, consanguinity

M: symptomatic like AEDs, specific like enzyme replacement, dietary is often a major aspect like supplying a deficiency (e.g. regular feeding in glycogen storage disease) or restriction which is usually protein (e.g. phenylalanine restriction in PKU), preventing catabolism when ill as metabolic demands increased (emergency regimen put in place), ketogenic diets for GLUT1 deficiency (as they cant transport glucose into CNS so rely on ketones as alternative energy source)

Question 56

What is screened for on the newborn blood spot test at day 5-7?

Answer 56

• Cystic fibrosis
• Sickle cell disease
• TSH (to detect congenital hypothyroidism)
• PKU (cause LD, seizure, microcephaly; M-restrict phenylalanine)
• MCAD (causes encephalopathy + death; M-avoid fasting + emergency regimen)
• Glutaric acuduria type 1 (causes macrocephaly + encephalopathy criss aged 6-18m + movement disorder; M-daily carnitine + avoid fasting)
• Isovaleric academia (causes metabolic acidosis, high ammonia; M-low protein, carnitine + glycine)
• Homocystinuria (causes marfanoid appearance/LD/lens dislocation/osteporosis; M-low protein + pyridoxine + folic acid)
• Maple syrup urine disease (causes encephalopathy in first week; M-low protein)

Question 57

HIV infection in the neonate diagnosis

Answer 57

• > 18m anti-HIV antibodies

* <18m: DNA PCR (as they will have maternal HIV antibodies confirming exposure but not infection)

Question 58

CF of HIV infection

Answer 58

Varies with degree of immunosuppression

Suspect in persistent lymphadenopathy, parotid swelling, recurrent fever, recurrent bacterial/candidal/unusual infections, hepatosplenomegaly, chronic diarrhoea, lymphocytic interstitial pneumonitis

Question 59

Management of HIV

Answer 59

ART: start in all infants as they have highest risk for progression, in older children depends on viral load + CD4
PCP prophylaxis - co-trimoxazole
Vaccinations except BCG

Question 60

How is vertical transmission of HIV prevented?

Answer 60

*ART during pregnancy + intrapartum: aim for undetectable viral load at delivery
PEP to infant
*Avoid breast feeding (tho in developing world prob continue + give ART)
*Actively manage labour to avoid prolonged ROM + unnecessary instrumentation
*If VL detectable near EDD do a pre-labour CS

Question 61

Talipes

Answer 61

Positional - from intrauterine compression, easily correctible

Talipes equinovarus: clubfoot. Complex, entire foot inverted, forefoot adducted, heel rotated + planter flexed, foot shorter, calf muscles thinner. M: Ponseti method casting usually works or surgery but usually not complete

Talipes calcaneovalgus: foot dorsiflexed + everted, usually due to intra-uterine moulding, usually self-corrects or can adv passive foot exercises. A/w DDH

Question 62

Sticky eyes

Answer 62

Common from day 3 onwards, clean with water/saline

Discharge + redness may be conjunctivitis

Question 63

neonatal conjunctivitis

Answer 63

• Staph/strep (topical ointment like chloramphenicol/neomycin).
• With purulent discharge: if within 48h may be gonococcal infection (IV cephalosporins as can cause vision loss) or within 1-2w may be Chlamydia (M-oral erythromycin)

Question 64

Skull problems?

Answer 64

• Caput succedaneum: SC fluid collection, may cross suture lines, resolves in a a few days is from pressure during delivery
• Cephalhaematoma: sub-periosteal haemorrhage, may get bigger but bound by suture lines, RF-instrumental delivery
• Subgaleal haemorrhage: between aponeurosis of scalp + periosteum, cross suture lines, rare but can cause life threatening loss
• Craniosynostosis: fibrous suture prematurely fuses changing growth patter of head, needs surgery

Question 65

What are the tests for DDH?

Answer 65

o Barlow’s test – adduct hip whilst applying light pressure on knee with thumb, direct force posteriorly. If unstable, femoral head will slip over posterior rim of acetabulum – palpate sublux/dislocation
o Ortolani’s test – done to confirm posterior dislocation from +ve Barlow’s. Flex hips + knees to 90 degrees, abduct legs using thumbs, +ve test is ‘clunk’ heard + felt

Question 66

Neonatal reflexes

Answer 66

o Palmar grasp reflex – object placed in infant’s hand their fingers close + they grasp
o Sucking reflex – instinctively suck anything that touches roof of mouth
o Rooting reflex – goes around 4m, turn head toward anything that strokes its cheek or mouth
o Stepping reflex – soles of feet touch flat surface they appear to walk by placing one foot in front of another
o Moro reflex – support infant’s upper back with one hand, then drop back once/twice into other hand. Legs + head extend whilst arms jerk up with fingers extended. Arms then brought together, hands clench into fists + infant cries.
 Asymmetry – hemiparesis, brachial plexus injury, # clavicle

Question 67

After delivery involving meconium what signs would prompt the need for neonatal medics to review?

Answer 67

RR > 60 per minute
the presence of grunting
heart rate <100 or >160
capillary refill time >3 seconds
temperature of 38°C or above, or 37.5°C on 2 occasions 30 minutes apart
oxygen saturation <95%
central cyanosis