Neonatal Flashcards
What is the NIPE?
Newborn exam: diagnose health problems soon after birth. All should have within 72 hours (ideally at 6-24 hours to allow period of physiological transition).
Screening may be carried out by trained midwives or by paediatricians & is governed by the National Newborn & Infant Physical Examination (NIPE) screening program.
Acceptable obs for a neonate?
HR 120-160
Systolic 50-70 mmHg
RR 40-60
Temp 36.5-37.5°C
What are different steps of the NIPE? (15)
- General Inspection
- Head
- Face
- Ears
- Mouth
- Eyes
- Neck & clavicles
- Arms & hands
- Chest
- Abdomen
- Groin & genitals
- Pelvis & legs
- Feet
- Spine
- Neuro: tone, head lag, cry, sucking, symmetrical movement & reflex (Moro & stepping)
What should be checked in the ‘general inspection’ part of the NIPE?
Colour: polycythaemia (redness), jaundice, cyanosis, traumatic cyanosis (tight wrapped cord causing local petechiae & cyanosis - no central cyanosis).
Skin: stawberry naevi, Erythema Toxicum Neonatorum (~50%!), mongolian blue spot, milia (milk spots), naevus simplex, benign pustular melanosis, congenital melanocytic naevi, port wine stain, collodion baby, napkin rash
Obs
What should be checked when doing head examination in NIPE?
Sutures palpable and fontanelles soft and flat (tense/bulging = raised ICP, sunken = dehydration).
Head Shape: moulding = overlapping skull bones due to passage through birth canal, usually resolves 2-3 days. Plagiocepahly + brachycephaly - both forms of ‘flat head syndrome’ (~1 in 5 babies, most cases no concerns– improves over time). Craniosynostosis (rare, premature fusion of bones + palpable ridged suture > abnormal growth of head). Scaphocephaly (premature fusion of sagittal suture - form of craniosynostosis).
Bleeds: caput succedaneum, cephalohaematoma, subhaleal haemorrhage, EDH and intracerebral bleed (very rare, may cause life-threatening bleeding. Most likely traumatic delivery but may also be associated with NAI).
- Largest circumference: take largest of 3 readings; should be 0.1-0.2cm accuracy.
When do the fontanelles close?
Anterior closes 18-24 months (closure at birth due to microcephaly or moulding). Posterior closes birth-2 months.
What is caput succedaneum?
Oedematous swelling + bruising on presenting part. Associated with ventouse, serosanginous and subcutaneous, crosses suture line (effusion overlies periosteum) pitting oedema.
Resolves without Tx (few days) but may need analgesia.
What is a cephalohaematoma?
Subperiosteal swelling limited to surface of one bone (usually parietal), does not cross suture lines (but can be bilateral!).
Common in prolonged second stage deliveries + assisted deliveries. Usually mild, but severe cases risk jaundice or anaemia. Maximal on the 2nd day + resolves over days-weeks. Resolution linked with calcification which can lead to it feeling like there is a prominent ring of bone around a central defect. These may exacerbate jaundice.
What is a subgaleal haemorrhage?
Diffuse swelling of scalp (boggy appearance), may represent serious blood loss (bleeding between periosteum + scalp galea aponeurosis).
Rare, but potential to be serious (hypovolaemia). May be associated with traumatic delivery e.g. vacuum extraction or with coagulopathies in the infant.
What should be checked when doing face examination in NIPE?
Abnormal facies: e.g. Fetal Alcohol, Down’s, Turner’s, Cushing, Noonan, Weaver, Sotos and Russell-Silver Syndromes
Facial nerve palsy: forceps injury or birth trauma – often manifests with asymmetrical facial expression when crying (care must be taken to ensure infant can completely close eye of affected side!!)
What should be checked when doing ear examination in NIPE?
Position, shape & skin tags / pits / abnormalities.
Pre-auricular skin tags + pre-auricular skin pits - both often normal but can be associated with hearing loss or renal abnormalities
What should be checked when doing mouth examination in NIPE?
Open to check for swellings
Gently insert finger to assess hard + soft palate
(if soft palate cleft: specialist cleft teams who support feeding + plan surgical correction)
Asses suck reflex
Neonatal teeth may need review by dentist as some can become loose and cause airway hazard
What should be checked when doing eye examination in NIPE?
Bilateral red reflex (+6 setting, 12 inches from face)
Absence may indicate retinoblastoma (white reflex) or congenital cataracts - 2 week referral to ophthalmologist
If not co-operative, placing baby over mothers’ shoulder will encourage baby to fully open eyes.
Subconjunctival haemorrhage: small bleeds due to delivery – resolve spontaneously
What should be checked when doing neck/clavicle examination in NIPE?
Palpate clavicles for evidence of birth trauma (fracture relatively common birth injury, especially in assisted delivery e.g. shoulder dystocia)
Check for signs of brachial plexus injury (more common in breech & shoulder dystocia)
Erb’s palsy: injury to C5-C6 peripheral nerves, weakness in elbow flexion & supination
Klumpke’s Palsy: injury to C8-T1 – weak extensors of arm and intrinsic muscles of hand, may be associated with Horner’s syndrome
Examine skin folds of neck for evidence of infection or other abnormalities
What should be checked when doing arm/hand examination in NIPE?
- Brachial Pulses (+ exclude humeral fracture)
- Palmar Creases: transverse palmar crease is found in ~5%; inherited trait associated with Down’s syndrome and other genetic disorders, but can reassure in absence of other abnormalities.
- Fingers: polydactyly often hereditary and most commonly isolated finding. Whole, functional fingers may be kept but finger segments surgical removed. Post-axial polydactyly usually isolated, but pre-axial (rare) is more likely to be related to an underlying medical condition. Syndactyly usually an isolated finding with no impact on function (easily missed so check carefully), but more severe cases can significantly affect function. Polysyndactyl: combination of both extra digits + webbing.
Also check hypoplasia / aplasia / formation of nail beds.
- Grasp Reflex
What should be checked when doing chest examination in NIPE?
- Inspection: symmetry & pulsation
Neonatal gynaecomastia:
- Apex heart: heaves & thrills
- Auscultate 4 regions
- Breath sounds: Noisy breathing common in newborns but should not be increased WOB. Stridor can indicate laryngomalacia, aortic vascular ring, haemangioma nodule of the vocal cord or external compression from a neck lump.
What is neonatal gynaecomastia / how is it managed?
Breast tissue in up to 90% neonates (transfer of maternal oestrogen + progesterone). Enlarged tissue: normal response to falling oestrogen at end of pregnancy (triggers prolactin release from neonatal pituitary).
Usually normal, associated with milky discharge (usually resolving ~few weeks & squeezing out increases complications including infection).
Persistence >1-2 months may indicate pituitary tumour.
Usually bilateral, may be asymmetrical; if unilateral consider abscess or mastitis, especially if heat or erythema.
In the NIPE, what should be considered when assessing for murmurs?
Not all neonates with congenital heart disease will have detectable murmurs and not all those with murmurs will have congenital heart disease.
Risk factors: CHD in first degree relative, T21 or abnormality on USS.
If murmur, reassuring signs are: o Pink, no cyanosis, with normal pre-and-post ductal oxygen saturations o No respiratory distress o Quiet, intermittent, positional murmur o Feeding well o Normal four limb blood pressures
Common causes of pathological murmurs: PDA + VSD. If murmur detected >24 hours of age, senior opinion must be sort: local guidelines likely to include senior review, ECG, pre-and-post ductal saturations (4 limb BP not useful). If suspicion of pathology ?inpatient echo. If not suspected, follow up by consultant or GP.
What should be checked when doing abdo examination in NIPE?
- Inspection
Cord: clean & dry with no redness to surrounding skin
Symmetry / distention / masses - Palpation
Iliac fossae > hypochondrial regions (ensures enlarged liver/spleen not missed). Feel independently for spleen & liver (liver: soft edge up to 1cm below costal margin). Ballot kidneys (often easy to feel in first day of life).
What should be checked when doing groin + genital examination in NIPE?
- Femoral Pulses
Note any difference in quality compared to brachial pulses. In coarctation: pulses absent or difficult to feel (radio-femoral delay is not present as a sign in infancy). If absent: ECHO, 4 limb BPs / saturations & refer to cardiac surgeons.
- Hernial orifices
Umbilical Hernia (usually benign but can be associated with genetic syndromes e.g. Beckwith-Wiedemann Syndrome), Inguinal Hernia.
- Genitalia & anus
Establish if passed urine & meconium. Anorectal malformation: check anus for patency (note: passage of meconium does not equate to patent anus or anus in correct place – anorectal malformations are commonly associated with urogenital malformations)
Undescended testes (first degree relative cryptorchidism - risk factor)
Ambiguous genitalia
Hypospadias
Scrotal & groin swellings
Palpable Bladder: requires prompt evaluation as may be sign of urinary obstruction (e.g. due to posterior urethral valves in males).
How should undescended testes be managed?
Palpable but undescended needs routine follow-up, if not descended at 2 years old will likely require surgical correction to reduce chance of later malignacy. If impalpable on just one side laparoscopy required to identify position. If bilateral undescended & impalpable, urgent review for ambiguous genitalia required.
What does ambiguous genitalia indicate?
CAH or other endocrine abnormalities - urgent senior review. Genetic, biochemical + endocrine work ups are to ascertain cause + aid decisions regarding the sex of the baby. Informing parents as soon as concerns arise reduces the emotional trauma associated with these complex cases.
What types of hypospadias are there and how is it managed?
May be glandular (on the glans penis), distal (on the penile shaft), or proximal (on the scrotum)
Always important to ensure there is a good urinary stream, educate the parents not to circumcise their baby (foreskin is often used in the repair), and ensure paediatric surgical follow up. In case of proximal hypospadias, may be necessary to complete chromosomal and endocrine workup, as severe cases may be difficult to differentiate from ambiguous genitalia.
How are suspected hydroceles managed?
Scrotal swellings that transilluminate: normally resolve spontaneously but may be followed up for parental reassurance. Care should be taken not to miss an inguinal hernia as these require surgical referral. If doubt about whether lump is inguinal hernia or hydrocele, USS helpful.
What causes neonatal withdrawal bleeds / discharge?
Exposure to maternal hormones can make the outside of the vagina (i.e. labia majora and clitoris) a little swollen and prominent, and can cause a thick, milky discharge.
More dramatically, at 2-3 days of age there may be a little bit of bleeding caused by withdrawal of the hormones exposed to in the womb – can reassure that this will be the first and last menstrual period until puberty. Requires no treatment.
What should be checked when doing pelvis + leg examination in NIPE?
Relaxed on firm surface. When pelvis stabilised, hip + knee flexed 90 degrees.
Barlow: stabilise non-test hip + adduct hip being tested. Push femur into acetabulum (pressure towards bed, downward pressure on knee) – posterior movements suggest it is possible to dislocate the hip out of the acetabulum. Dislocation will give a ‘click’
Ortolani: stabilise pelvis by firmly holding symphysis pubis and coccyx between thumb & middle finger. Index finger of other hand on greater trochanter + abduct hip: palpable ‘clunk’ signifies relocation of posteriorly dislocated hip.
Also check: equal length upper & lower leg segments, exclude femur fracture
Examine skin creases – differences may indicate hip asymmetry
How should hip abnormalities on NIPE be managed?
If congenital dislocation of hip: hip USS + urgent review (2 weeks) in neonatal or specialist hip clinic for follow up. Treatment in first instance is with Pavlik harness.
Developmental dysplasia of the hips (1-2/10,000): risk factors first degree relative with hip problem as baby or young child (requiring splint, harness or operation), breech at or after 36 weeks (or at delivery if before 36 weeks).
If normal examination but risk factors present: hip USS within 6 weeks. If ‘clicky’ but not dislocated or dislocatable then local practice varies regarding USS.
What should be checked when doing feet examination in NIPE?
Mobility
Talipes Equinovarus: fully dorsiflex feet to shin and invert & evert to 90°. Fixed talipes = inversion of feet which cannot be manually corrected with dorsiflexion. Requires referral to physiotherapy. Positional talipes which can be brought to a normal position with very little pressure may not need treatment beyond gentle straightening exercises which can be done by the parents with each nappy change.
Skin creases & toes: count toes & check sandal gap
What should be checked when doing neuro examination in NIPE?
- Spine: ventral suspension position: midline defects down back
Stalk mark / naevus flamius on nape of neck is a common normal finding. Pigmentations or unusual lesions potentially significant: may suggest underlying spinal defect
Buttocks parted to check for sacral dimples – may be normal but dimples that are deep, discharging, or associated with abnormal neurology / skin discolouration are more likely to indicate spinal cord tethering > MRI / USS.
Hairy tufts may be associated with spina bifida occulta.
- Tone
- Head Lag
- Cry
- Sucking
- Symmetrical movements
- Reflexes (stepping, morrow)
Main reflexes in neonates?
Moro (birth - 3/4 months)
grasp (birth - 4/5 months)
rooting (birth - 4 months)
stepping (birth - 2 months)
What is early jaundice?
presenting <24 hours
Causes: rhesus incompatibility, ABO incompatibility (Group O mothers most at risk), G6PD deficiency, hereditary spherocytosis, infection (always suspect)
May be more severe (significant) in: preterm, sepsis, severe haemolysis (due to Rh-incompatibilty, ABO incompatibility, G6PD deficiency, spherocytosis) and bruising (cephalohaematoma or subgaleal haemorrhage – blood in haematoma breaks down).
What is physiological jaundice?
Presenting after 24 hours + resolving 2 weeks (or in 21 days if preterm).
Usually presents day 2 – 3. VERY common: most babies appear enteric (yellow) to some extent. Although may appear very yellow, usually not a problem.
However, very high bilirubin can cross BBB & cause kernicterus. If physiological may still require phototherapy (especially as infants may have become more tired and feeding may suffer). Rarely: may require immunoglobulin or exchange transfusion.
Term neonate can have level >300 on day 4 of life and not require any treatment
Causes:
Breastfeeding jaundice (unclear aetiology, resolves without treatment or complication, continue breastfeeding)
Polycythaemia: babies have naturally high packed cell volume (PCV); more red cells = greater breakdown
Resolving cephalohaematoma
How does phototherapy work?
Light in blue region most effective
Converts insoluble trans-bilirubin > photoisomers (cis-bilirubin) that can be excreted into the bowel (without requiring conjugation by liver).
What is prolonged jaundice?
> 14 days or >21 days if preterm
Causes: BREASTFEEDING jaundice (most common but diagnosis of exclusion), BILE DUCT obstruction (e.g. biliary atresia, choledochal cysts), HYPOTHYROIDISM, UTI, neonatal hepatitis, metabolic issues (e.g. galactosaemia, alpha-1-antitrypsin deficiency, glucogen storage disease), genetic (e.g. CF, trisomy 21/18), toxic (drugs, TPN).
- Bile duct obstruction e.g. biliary atresia (congenital absence of biliary tree): most important condition to exclude, requires urgent surgical assessment : pale stools + dark urine worrying: implies limited or no passage of bile into gut, delay in diagnosis > worse prognosis (does not resolve spontaneously, often requires liver transplant unless prompt identification + surgical correction)
- Hypothyroidism : possible presentation but should usually picked up earlier as part of screening programs
- UTI: undiagnosed may present with jaundice as only symptom
- Neonatal hepatitis: liver inflammation > biliary flow obstruction
- Physiological / breast feeding jaundice: most common cause of prolonged jaundice, but diagnosis of exclusion
What causes breastmilk jaundice?
Some bilirubin in the bowel reverts to the unconjugated form in the presence of bacteria. Conjugated form then reabsorbed by the enterohepatic circulation.
This can be exaggerated if exclusively breastfed > breastmilk jaundice (most common form of prolonged jaundice).
How should jaundice be investigated?
All require transcutaneous bilirubinometer check (heel prick also possible). If < 2 weeks old: plot onto treatment threshold graph.
May also consider (based on suspicion) blood film & FBC (red cell anomalies, inflammatory markers), DAT or Coombs test (for haemolysis), CRP (for infection but can be normal in neonates despite overwhelming sepsis!), blood cultures (if starting Abx must be done first).
Ask: pigmentation of stools & dark urine, whether infant is thriving, mode of feeding, Fhx of jaundice.
Prolonged jaundice: check Total Bilirubin including the conjugated fraction: (↑ conjugated fraction suggests biliary atresia).
Prolonged jaundice screen: FBC, blood film, DAT / Coombs, CRP, blood cultures, thyroid function, liver function (including conjugated bilirubin) & clean catch or catheter urine sample for bacteria.
How is jaundice managed?
If <2 weeks old: plot onto treatment threshold graph. Separate graphs for 38+ weeks and for each week between 23 & 37 weeks.
- UV Phototherapy: maximum skin exposure, keep eyes covered, ensure good feeding & regular monitoring of bilirubin – rebound bilirubin should be checked (after phototherapy stopped)
- Exchange transfusion: done in small aliquots over several hours to a total of 2x baby’s blood volume (replaces 85% of baby’s blood), usually requires venous & arterial access
- IV immunoglobin (haemolytic disease)
Prognosis / complications of jaundice?
Well treated, then good prognosis with no long-term effects, kernicterus is in theory completely avoidable with early detection + treatment
Kernicterus: encephalopathy resulting from deposition of unconjugated bilirubin in the brain. Unconjugated bilirubin crosses BBB & binds irreversibly to neuroreceptors in basal ganglia + brainstem nuclei > permanent neurological effects (e.g. choreoathetoid CP, learning disability, deafness). Occurrence rare in developed countries as neonatal jaundice tends to get identified & treated early. Mild cases present with poor feeding & lethargy, whilst more severe cases are associated with irritability, hypertonia, seizures & coma.
Consequences: lethargy, poor feeding, irritability, hypertonia, seizures, coma, CP + learning disability, deafness. Long-term effects of kernicterus mimic a parkinsonian picture due to effects on basal ganglia and severe developmental delay.
Why is neonatal sepsis so important?
Leading cause of neonatal mortality worldwide
High index of suspicion + early treatment when suspected.
Blood inflammatory markers highly unreliable in neonates (especially in early stages of sepsis).!
What is early onset neonatal infection?
When is it treated?
Onset within 48 hours, usually vertical transmission
Babies often given Abx based on pre-delivery risk factors:
o Invasive GBS in previous pregnancy
o Current pregnancy: maternal GBS colonisation, bacteriuria or infection
o Prolonged rupture of membranes
o Preterm birth
o Intrapartum fever or suspected chorioamnionitis
o Suspected or confirmed infection in other baby if multiple pregnancy
o Suspected or confirmed invasive bacterial infection in mother
How may early onset neonatal infection present? What are the likely causes?
May present non-specifically, but possible signs: temp instability, poor feeding, vomiting, respiratory distress, apnoeas, brady/tachycardia, shock, hypo/hyperglycaemia, irritability, lethargy / drowsiness, seizures, jaundice (particularly first 24 hours) + ↓ urine output
Likely: Group B Strep (most common cause of serious bacterial infection in 1st week of life) other strep species, coliforms
Rarer: Listeria, Klebsiella, Pseudomonas
Investigations and management for neonatal infection?
Blood cultures, baseline inflammatory markers (if raised, or worrying clinical signs: further assessment + lumbar puncture). If respiratory signs: CXR
If possible infection: broad-spectrum Abx e.g. gentamicin + benzylpenicillin.
Duration dependent on: bacteria isolated from baby or mother, whether any rise in inflammatory markers, and whether symptoms present at onset or during treatment
Minimum duration 36-48 hours, pending culture results
What is late onset neonatal infection? What causes it?
> 48 hours
More likely environmental, particularly if inpatient (staff / visitors, indwelling lines, poor aseptic technique in performing neonatal procedures).
GBS can present after 48 hours (including those discharged to community)
Staphylococcal infections (including aureus) are increasing: Coagulase-negative Staphylococcus = most common infecting organism on neonatal unit, particularly if long lying venous catheters (although also part of normal skin flora). Coliforms & pseudomonal species are also causes.
How is late onset neonatal infection managed?
Wide variability in this group: likely broad spectrum to cover gram positive + negative (e.g. flucloxacilin + gentamicin). Important to target therapy based on sensitivity data which may vary between populations.
Start Abx if: 1 red flag or 2 risk factors or clinical indicators
NICE: IV benzypenicillin + IV gentamicin recommended (many centres use cefotaxime after local discussion), take blood cultures + CRP at start of Abx, repeat CRP at 18-24 hours.
Abx can be stopped if negative cultures + no rise in CRP 36 hours after first dose. Consider LP if baby very unwell, CRP is >10 or positive culture. Many centres have a higher CRP threshold.
What are the red flags for starting Abx in late onset neonatal infection?
Parenteral antibiotic treatment given to mother for confirmed or suspected invasive bacterial infection at an time during labour or in 24 hour periods before and after birth (does not refer to intrapartum antibiotic prophylaxis)
Suspected or confirmed infection in another baby if multiple pregnancy
Respiratory distress starting >4 hours after birth
Seizures
Need for mechanical ventilation in a term baby
Signs of shock
(Note: if 2 or more non-red flag risk factors, this also indicates Abx, but too many of them to list!)
Why is Group B strep so important in neonates?
How common is it?
Most common cause of serious bacterial infection (e.g. septicaemia pneumonia) in 1st week of life, and of meningitis in first 3 months of life.
Infection: 10% mortality, ½ of survivors suffer neurodisability due to GBS meningitis.
21% women carry GBS, but incidence of neonatal infection just 0.5/1000 live births, (2.3 if born to colonised mothers & 0.9 if colonisation presents in a previous pregnancy).
How may group B strep infection present in neonates?
May occur early (< 7 days: vertical transmission during labour or after rupture of membranes) or late (>7 days: presumable acquired after delivery, frequent meningitis).
Respiratory distress, temperature instability, hypoglycaemia, seizures.
Can we prevent neonatal GBS infection?
Prevention remains controversial
Intrapartum IV Abx prophylaxis effective at reducing infection but would mean administering Abx to many well women (may also not be time to do this).
In England, decision to treat mothers or babies (benzylpenicillin or cefotaxmine) is present on number of risk factors: premature, mother colonised or previously had a child with infection, evidence of maternal infection (pyrexia or raised CRP), prolonged rupture of membranes (>24 hours) or evidence of fetal distress.
This usually results in infants having IV line inserted (Abx) until blood culture results are available and all other results (including CRP) are normal.
How is congenital herpes simplex managed? How does it present?
Usually transmitted via birth canal: if mother has primary infection / active vaginal herpes at >28 weeks gestation, elective C-section advised.
Women with recurrent herpes should be treated with suppressive therapy & advised of low transmission risk.
Presentation in neonate: skin lesions, encephalitis or disseminating disease.
Treatment with acyclovir, however, congenital herpes has high mortality.
How is congenital syphilis managed? How does it present?
Picked up by antenatal screening, congenital syphilis presents as: fever, irritability, saddle nose, rashes, ulceration. Babies born to mothers with active syphilis: penicillin (even in the absence of symptomatic infection).
How does congenital listeria present? How is it managed?
Gram +ve, maternal infection via soft cheese, unpasteurised milk. Classically associated with preterm delivery complicated by meconium passage. Associated with stillbirth + miscarriage.
In neonate: presents as early sepsis or as listeria meningitis. Treatment is with amoxicillin.
How does congenital hep B present? How is it managed?
Vertical transmission – in congenital hep B, commonly develop chronic infection (25% of these infants will die of cirrhosis or liver cancer).
Vaccination if mother is HBsAg positive. If born to higher risk mother (e.g. active hepatitis B in pregnancy, ‘e’ antigen positive or ‘e’ antibody negative): Hep B immunoglobulin in addition to the live vaccine.
How does congenital hep C present? How is it managed?
Hep C: transmission linked to maternal viral RNA load & neonatal diagnosis by measuring HCV RNA. In neonates: often spontaneously clears / asymptomatic, small proportion have chronic infection. Treatment coordinated with paediatric liver & infectious disease specialists – options include interferon & antiretrovirals.
How does congenital HIV present? How is it managed?
HIV: vertical transmission + via breast milk.
Antenatal screening: if detected viral load useful for predicting risk (low load= low vertical transmission rates). In UK: all women advised not to breastfeed, C-section if viral load >50 at 36 weeks (with zidovudine infusion 4 hours before). In neonate, initial tests can be inaccurate: serial tests over several months required to confirm baby is HIV negative.
Oral zidovudine after birth if maternal load >50 (reduces risk). If >50, triple therapy ART for 4-6 weeks.
How does congenital VZV present? How is it managed?
Maternal VZV (Chicken Pox): human herpes type 3
If mother contracts chicken pox during pregnancy, risk of transmission. However, if develops >7 days before birth, antibodies likely transmitted via placenta + additional treatment not required for baby.
Congenital varicella: atypical scarring of skin + IUGR. May also have cataracts, cerebral cortical atrophy + global developmental delay.
If mother develops chicken pox within 7 days of delivery (or up to 4 days post delivery) then VZV immunoglobulin should be administered (mother + baby should be isolated). Vesicular lesions should be treated with IV acyclovir.
What is CMV? How is it managed?
Around 50% have been exposed but only transmitted when ‘active’ i.e. when caught for 1st time (usually nursery children) or if re-activated (immunocompromise) or re-infected with different strain.
Usually asymptomatic, may get flu-like symptoms.
Congenital: microcephaly, hepatosplenomegaly, IUGR, cardiac defects, jaundice, pinpoint petechial ‘blueberry muffin’ skin lesions, sensorineural deafness, encephalitis (seizures). High mortality rate.
Postnatal (acquired) infection can result in neurological deficit, feed intolerance, hepatorenal failure + eye disease.
Postnatally treated with ganciclovir.
What is rubella? How is it managed?
‘German measles’ caused by togovirus. Very rare in UK after MMR vaccine introduced. Outbreaks more common winter-Spring. Incubation 14-21 days, infectious from 7 days before symptoms to 4 days after rash.
Features: prodrome (low grade fever), maculopapular rash initially on face > whole body (usually fades 3-5 days), suboccipital and postoccipital lymphadenopathy.
Complications: arthritis, thrombocytopenia, encephalitis, myocarditis.
How is rubella in pregnancy managed?
What is congenital rubella syndrome?
If contracted during pregnancy, in first 8-10 weeks damage to fetus as high as 90%, but rare after 16 weeks.
~30% risk of transplacental infection (5-10% risk of fetal loss). Clinically difficult to distinguish rubella from parvovirus B19.
Suspected cases > local Health Protection Unit (type/timing investigations vary): if raised IgM antibodies - recent exposure to virus. Immunity no longer routinely checked at booking but if ever tested + not found to have immunity, advised to avoid those who may have rubella + offered post-natal MMR vaccination.
Congenital rubella syndrome: cataracts, deafness, congenital heart disease (e.g. PDA), growth retardation, hepatosplenomegaly, purpuric skin lesions, ‘salt and pepper’ chorioretinitis, microphthalmia, CP.
What is toxoplasmosis?
Toxoplasma gondii = protozoa infecting via GI tract, lung or broken skin. Oocysts release trophozoites which migrate widely: including eye, brain + muscle. Usually cats although other animals e.g. rats carry the disease.
Most asymptomatic, if symptomatic usually self-limiting. Clinical features resembling infectious mononucleosis (fever, malaise, lymphadenopathy). Other less common manifestations: meningoencepahlitis + myocarditis.
Investigation: antibody test, Sabin-Feldman dye test.
Treatment usually reserved for severe cases or immunosuppressed (pyrimethamine plus sulphadiazine for at least 6 weeks).
Transplacental: congenital toxoplasmosis: microcephaly, hepatosplenomegaly, IUGR, hepatitis, chorioretinitis, cerebral calcification, hydrocephalus, hydrops (excess fluid e.g. ascites or pleural effusion), hydrocephalus, foetal anaemia.
What is parvovirus B19? Can it harm fetus?
Spread by respiratory route, variety of presentations:
Erythema infectiosum (slapped-cheek syndrome): may have mild feverish illness (barely noticeable) or in others, rose-red rash after a few days. This may spread to other parts but only rarely involves palms/soles (unlike other rashes)! Begin to feel better as rash appears, rash peaks after a week then fades. Infectious 3-5 before rash occurs (not infectious during rash therefore no school exclusion). Most children recover without treatment.
Months afterwards: warm bath, sunlight, heat or fever will trigger recurrence.
In first 20 weeks of pregnancy can cause harm to foetus, if exposed <20 weeks – advise from obstetrician.
Adults: may cause acute arthritis, or in immunosuppressed patients – pancytopenia. Aplastic crises (e.g. in sickle-cell disease is also possible as parvovirus B19 suppress erythropoiesis for ~1 week – aplastic anaemia rare unless there is a chronic haemolytic anaemia).
What is neonatal conjunctivitis? Management?
Most ‘sticky eyes’ in neonatal period are non-bacterial in origin & often represent blocked tear ducts that resolve with simple cleaning.
Persistent discharge or signs of inflammation should be swabbed for microbiological examination.
Chlamydia should be suspected in presence of maternal history or ulceration of the corneas.
What is the newborn hearing screening program?
~1-2 / 1000 infants are born with deafness.
Screening in first 2 weeks of life, usually on post-natal ward. OtoAcoutic Emissions (OAE) test, and may perform Automated Auditory Brainstem Responses (AABR).
Children with abnormal responses will be referred for audiology follow-up but abnormal responses do not confirm deafness (this is a screening test).
What is the newborn blood spot screening?
9 conditions?
Heel prick: Days 5-7 for all infants
- Phenylketonuria (PKU): cant to metabolise phenylalanine, untreated > LD / behavioural problems – dietary management
- Medium Chain Acyl-CoA Dehydrogenase Def (MCADD): 1 in 10,000 – autosomal recessive, cant metabolise certain fat, can be acutely unwell when starved or stressed – diagnosis allows education & planning
- Maple Syrup Urine Disease (MSUD): autosomal recessive, unable to metabolise leucine, isoleucine and valine AAs
- Congenital Hypothyroidism: 1 in 3,000 – not usually inherited, untreated leads to learning deficits, thyroxine replacement (detected by high TSH levels)
- CF: 1 in 2500, test for immunoreactive trypsin (IRT)
- Homocystinuria (HCU): autosomal recessive, cant metabolise homocysteine AA, pyridoxine unresponsive
- Sickle cell disease: 1 in 2000, well at birth due to HbF, affected children require Pen V prophylaxis and f/u, may detect B thalassaemia.
- Isovaleric acidaemia: autosomal recessive, cant metabolise leucine AA
- Glutaric aciduria type 1 (GA1): autosomal recessive, cant metabolise lysine + tryptophan AAs
How common is prematurity? When should they be admitted?
England & Wales: 7% born <37 weeks i.e. ~50,000/year
Admission if:
Require breathing support: likely if <32, term with meconium aspiration, transient tachypnoea of the newborn or congenital lung abnormalities
Feeding support: likely if <33-34 (NG feeds or even IV feeds), reduced tone, genetic problems)
Temperature support: smaller infants (<2kg) and those <34 weeks will likely have difficulty maintain body temperature and will often need to be managed in an incubator or with a heated mattress
Other problems: severe sepsis, profound jaundice, surgical abnormalities, safeguarding concerns, drug withdrawal
Define: premature, extremely premature, VLBW, ELBW, SGA, IUGR
Premature <37 weeks
Extremely premature <28 weeks (<2% of prematurity)
Very low birth weight <1.5kg
Extremely low birth weight <1kg
SGA: weight <10th centile
IUGR: growth velocity falls during pregnancy causing foetal weight to cross gestation related weight centiles on serial scans
What are risk factors for prematurity and low birth weight?
Risk Factors: prematurity & low birth weight
- Placental: placenta prævia, placental abruption, placental insufficiency
- Uterine: uterine malformation, cervical incompetence
- Maternal: pre-eclampsia, chronic illness e.g. CKD, infection, smoking & drug abuse
- Fœtal: fœtal distress, multiple pregnancy, chromosomal abnormalities, foetal / neonatal infection
- Other: premature rupture of membranes, trauma, iatrogenic
General prognosis of prematurity?
Prognosis: No problems (31%), glasses / squints (30%), severe disability (11%), moderate disability (13%), mild neurological problems (11%), mild hearing losses (4%)
List complications of prematurity
IVH, PVL
Retinopathy of prematurity
Hearing deficit (all premature infants require pre-discharge hearing check)
Poor feeding
Respiratory distress syndrome
Chronic lung disease (bronchopulmonary dysplasia)
Apnoea of prematurity
Pneumothoraces
PDA
Hypotension
Anaemia of prematurity
NEC
Inguinal hernia (should always be repaired as high risk of strangulation)
Jaundice (weaker BBB so lower treatment threshold)
Hypocalcaemia, Hyponatraemia, Hyper or hypoglycaemia (renal salt losses due to immature kidneys, poor absorption of enteral feeds and immature insulin secreting pathways, therefore often require supplements)
Metabolic bone disease
Hypothermia
Infection Risk
What is IVH? Risk factors and investigations?
<32 weeks: bleeding into ventricular spaces, usually from germinal matrix (many found to have blood within first 72 hours of life)
Diagnosis: USS probe onto fontanelle (bedside)
Risk factors:
- prematurity (rare >32 weeks)
- low birth weight
- sepsis
- lack of antenatal steroids (given for both lung maturation & IVH)
- hypotension or hypertension (swings in BP: surge through germinal matrix)
- respiratory distress syndrome
- hypoxia
How is IVH graded?
Grade 1: limited to germinal matrix (similar to bruising)
Grade 2 into non-dilated ventricle (1-2 = good prognosis; would not expect long-term issues)
Grade 3 into dilated ventricle
Grade 4: involves parenchyma
Higher grades (3-4): poor prognosis: increased risk of cerebral palsy, post-haemorrhagic hydrocephalus & developmental delay
What is PVL?
High risk 24-26 weeks, greatest risk if <32 weeks
White matter injury characterised by necrosis of the white matter near lateral ventricles. Caused by ischaemia in the developing brain (difficultly in neonatal period: high risk).
Prognosis: neurological deficits, often motor
Small cysts in periventricular regions highly suggestive of long-term developmental delay.
What is retinopathy of prematurity?
Risk factors, diagnosis, treatment?
<32 weeks
Abnormal proliferation of retinal blood vessels causing visual impairment (can get bleeding & retinal detachment).
Risk factors: prematurity, low birth weight, excess supplemental oxygen
Diagnosis: routine screening fundoscopy for infants at risk. Carefully targeting SaO₂ in preterm infants to reduce their exposure to oxygen. UK: Routine surveillance has greatly reduced blindness associated with this condition.
More central (near fovea) = worse visual outcome.
Treatment: laser photocoagulation (sacrifices some vision but prevents progression).
What is RDS? Risk factors, diagnosis and Tx?
Surfactant deficiency (protein by type 2 pneumocytes – coats inner surface of lung & increases compliance).
Risk factors: preterm, lack of antenatal steroids, male, Caucasian, hypothermia, diabetes in pregnancy
CXR: dense lung fields, ground glass
Tx: antenatal steroids, animal-derived surfactant via endotracheal tube after delivery, positive pressure ventilation / CPAP
Complications: pneumothorax (due to inflation of stiff lung), pulmonary haemorrhage, chronic lung disease
What is chronic lung disease (broncho-pulmonary dysplasia)? Risk factors, diagnosis, treatment, prognosis?
Oxygen requirement at 28 days OR 36 weeks corrected (due to lung disease acquired in early premature life).
Risk factors: preterm, lack of antenatal steroids, exposure to high ventilation pressures, exposure to high levels of supplemental oxygen, poor nutritional status
CXR: finer lung fields (not as dense as RDS)
Prevention: minimising pressure used during ventilation
Respiratory support + oxygen as required, consider diuretics, long-term home oxygen, palivizumab (RSV) + immunise family against influenza.
Many babies will get better as they grow, some go home on oxygen & perhaps remain ventilator dependent or die subsequently of the disease.
What is apnoea of prematurity?
Poor central respiratory drive
Reduce risk by administration of caffeine to stimulate respiratory drive
Why do pneumothoraces occur in prematurity?
‘Stiff’ surfactant deficient lungs
artificial surfactant has reduced incidence of pneumothorax in preterm babies
What is PDA?
Clinical features, diagnosis, treatment and complications
<33-34 weeks
Persistent fetal structure: increased left to right shunting + pulmonary oedema. In post-natal life, aortic pressure > pulmonary arterial pressure: blood from aorta –> pulmonary artery –> increased volume of blood to lungs.
Signs: respiratory distress, tachycardia, active precordium, bounding pulses, wide pulse pressure, signs of pulmonary oedema, murmur
Diagnosis: ECHO
May spontaneously resolve: fluid restriction, closed by giving NSAIDs (ibuprofen), paracetamol . May require surgical ligation
Complications: chronic lung disease, NEC
Why does prematurity cause hypotension? Management?
Immature CV system less able to compensate for changes in intravascular volume: exacerbated by increased fluid loss from immature kidneys
Treatment includes giving more volume + inotropic support
What causes anaemia of prematurity?
How is it managed?
Lack of transfer of maternal iron stores, reduced erythropoietin production (immature bone marrow), high metabolic demand + shorter RBC half-life.
Multiple blood tests. May lead to repeated transfusions throughout the neonatal period (packed red blood cells)
What is NEC?
Presentation, management and complications?
Inflammation & necrosis of intestinal tissues, likely related to breakdown of gut epithelial barrier, bacterial translocation across gut wall, immature innate immunity, intestinal ischaemia
Blood in stool, abdo distention + discolouration, ↓ bowel sounds, bilious gastric aspirates, feed intolerance, shock & collapse, apnoeas
XR: dilated bowel loops, bowel wall oedema + thumbprinting, pneumatosis (intramural gas), portal venous gas, pneumoperitoneum secondary to perforation, football sign(?)
Management:
- Stop feeding + broad spectrum Abx (triple)
- Supportive: TPN, blood products, ventilation
- Surgical resection
Complications: mortality ~20%, strictures, malabsorption, short gut syndrome, intestinal failure
What is metabolic bone disease?
Preterm: lack of Ca²⁺ / PO₄ transfer from mother (usually occurs last 3 months of pregnancy).
Signs: rising ALP, decreased PO₄, osteopenia, fractures
Management: PO₄ supplements or breast milk fortifier (contains Ca²⁺ & PO₄). No long term complications
Why do preterm infants get hypothermia? Management?
Large surface area, less muscle mass + immature skin
Incubator support, often to weight of 1.4-1.6kg
Why are preterm infants susceptible to infection?
Degree of immunodeficiency, immature skin barrier (poor integrity, readily broken), increased medical input with indwelling devices, immature gut response, poor neutrophil production, incomplete transfer of maternal antibodies
Risk factors: PPROM, maternal infection with GBS, maternal sepsis & chorioamnionitis
May lead to repeated transfusions throughout the neonatal period (packed red blood cells)
What are Signs of Sepsis in Preterm infants?
Treatment?
May be non-specific / difficult to detect • Tachypnoea • Respiratory distress • Apnoeas & bradycardias • Tachycardia • Temperature instability • Feed intolerance • Hypo / hyperglycaemia • Jaundice • Local signs of meningitis or soft tissue infection
Low threshold for Abx, consider antivirals, consider lumbar puncture if ↑ CRP
Any baby <1 month with fever: FBC, CRP, blood cultures, LP, urine sample
At what gestational age is resuscitation usually NOT carried out?
23 weeks
If 23+0 - 23 + 6: assessment + care dependent on parental wishes (resus or palliative care)
If 24+0 - 24 + 6: resuscitation followed by reassessment > intensive or palliative care
If 25+0 - 25+ 6: resuscitation followed by intensive care
(> palliative if necessary)
What are signs of respiratory distress in a term neonate?
What could cause this?
Tachypnoea (>60), recessions, nasal flaring, grunting (some may mistake for crying), tachycardia, poor feeding
Causes: infection, TTN, meconium aspiration syndrome, sepsis, pneumonia, persistent pulmonary hypertension of the newborn (PPHN), pneumothorax (air in pleural space), respiratory distress syndrome (RDS), congenital diaphragmatic hernia (CDH - bowel in chest cavity), congenital cardiac disease.
What is Transient tachypnoea of the newborn (TTN)?
Risk factors, diagnosis and management?
Most common cause of respiratory distress in term babies, due to delay in clearance of foetal lung fluid. Usually begins at birth & resolves within first 4 hours of life (fluid only takes days to clear).
Risk factors: delivery without labour (‘cold section’)
XR: may include cardiomegaly, pleural effusion, fluid in the horizontal fissure & prominent perihilar interstitial markings
Management: observation if sats/blood gas ok, respiratory support (CPAP, high flow, sometimes ventilation), IV antibiotics in case of infection, NG feeding if too breathless to suck, IV fluids if feeds cause RDS.
What is meconium aspiration syndrome?
diagnosis and management?
Hypoxia or stress in labour > meconium (sign of fetal distress) > gasping inspirations > aspiration (during or after birth) > chemical irritation + pneumonitis of the airways > poor gas exchange + surfactant impairment, pulmonary hypertension
Initial mechanical obstructive disease (which itself can be fatal) + after some hours, inflammatory cells into lungs which causes chemical pneumonitis + further prevents gas exchange. Symptoms typically present in first 4 hours of life: respiratory distress with hypoxia.
Diagnosis: observed meconium in liqour, respiratory distress + radiographic changes. XR: classical areas of over-inflation and heterogenous opacification - air pockets, ‘honeycomb’, hyperinflated lungs.
Management (supportive): supplemental oxygen, high flow therapy, ventilation, consider inhaled nitric oxide (vasodilator to prevent progression to PPHN), surfactant therapy + inotropic support of BP
What is Respiratory Distress Syndrome (ARDS)?
(term infants)
how is it treated?
Extremely premature most at risk but rarely can affect term infants + term neonatal RDS can be classified in 3 ways:
- Acute respiratory distress syndrome (ARDS) – associated with asphyxia, meconium aspiration, shock, sepsis and DIC
- Idiopathic respiratory distress syndrome (IRDS)
- RDS relating to inherited surfactant disorders.
Treatment is different to preterm infants: broad spectrum Abx given as perinatal acquired infection is leading cause of term neonatal RDS. Mechanical ventilatory support and exogenous surfactant are also extremely important.
What is bronchopulmonary dysplasia?
term infants
Persistent oxygen requirement from birth > 28 days or 36 weeks corrected gestation.
Extremely premature most likely affected, however, infection + postnatal lung injury from ventilatory support are also associated risk factors.
XR: begins with RDS picture but can evolve into that of pulmonary interstitial oedema.
Management: nutrition optimisation, oxygen, ventilator support as required. Corticosteroid therapy and/or diuretic therapy may be helpful in improving lung function.
Many babies with chronic lung disease will get better with growth, others go home on oxygen & perhaps remain ventilator-dependent or die subsequently of the disease.
What causes pneumothorax in term infants?
Management?
May occur spontaneously or secondary to respiratory distress syndrome, meconium aspiration syndrome or mechanical ventilation.
May be asymptomatic but may require aspiration or chest-drain insertion.
XR classification: simple or tension.
Should be nursed in higher concentrations of oxygen as this can aid spontaneous resolution, however, larger pneumothoraces or those under tension will require aspiration and/or chest drain insertion.
What causes pneumonia in term neonates?
Management?
Congenital or acquired after birth, more common in babies with risk factors for infection e.g. prolonged rupture of membranes or chorioamnionitis.
Usually bacterial, most commonly Gram-negative bacilli (e.g. E coli, Klebsiella, pseudomonas), Group B streptococcus & staphylococcus.
CXR: heterogenous opacity
Management: broad-spectrum Abx, supportive care with oxygen & ventilatory support as needed, IV fluids and/or an NG tube may reduce respiratory distress.
What is PPHN (Persistent Pulmonary Hypertension of the Newborn)?
Pathophysiology / causes / presentation
Lungs filled with fluid in utero + pulmonary vessels constricted (high pressure). At birth: breathing dilates, pulmonary vessels, vascular resistance (PVR) drops significantly.
In PPHN: pulmonary vessels don’t dilate, elevated PVR + subsequent persistence of fetal intracardiac shunts > systemic hypoxaemia.
ACUTE EMERGENCY: worsening cyanosis, tachypnoea + hypoxia despite increasing oxygen & ventilatory support. Spectrum of severity ranges from mild + transient respiratory distress to severe hypoxia & cardiopulmonary instability.
Mainly affects infants close to term + shortly after birth: almost all diagnosed within first 72 hours of life.
Can be primary or secondary to lung disease e.g. meconium aspiration, RDS (lungs redirect flow to oxygen rich parts by vasoconstricting in low oxygen – if homogenous lung disease vasculature constricts globally across both lungs > high pulmonary pressure > right-to-left shunting through foramen ovale & ductus arteriosus)
Can also be caused by pulmonary hypoplasia
How is PPHN managed?
Ventilation + intubation with high conc. oxygen (oxygen = most potent pulmonary vasodilator)
Pulmonary vasodilators (iNO, sildenafil – directly to lungs via endotracheal tube)
Inotropes to maintain systemic blood pressure (must be kept higher than pulmonary pressure to avoid right>left shunting)
In extreme cases ECMO (extracorporeal membrane oxygenation) can be used to bypass the lungs outside the body (complications can be serious: large vascular catheters + heparinisation of blood flow to prevent clotting in the ECMO circuit – preterm babies not suitable due to increased risk of haemorrhage + difficult to place vascular catheters).
What are Congenital Pulmonary Airway Malformations?
Congenital cystic adenomatoid malformations (CCAMs): rare congenital condition involving error in lung development (leaving part of the lung as non-functional cystic tissue).
Paediatric surgeons usually remove these if large or symptomatic, timing depends on symptoms in the infants at time of birth vs the anaesthetic risk (reduces with age of the infant).
Severe cases may require urgent surgery.
What is Broncho-Pulmonary Sequestration?
Rare condition: normal lung tissue supplied with blood vessels from the systemic circulation rather than the pulmonary circulation & not attached to the bronchial tree. Usually surgically removed.
What are neonatal seizures? Causes?
Repetitive, rhythmic movements that if isolated to a limb, continue even when that body part is restrained.
Causes: infection (particularly meningitis), hypoglycaemia, IHV, neonatal cerebrovascular events, cerebral malformation, HIE, withdrawal from maternally ingested drugs, electrolyte imbalances, pyridoxine deficiency (rare but treatable cause of intractable neonatal seizures).
How are neonatal seizures diagnosed? (differentials)
Jitteriness in a baby can be a normal finding, but may be associated with hypoglycaemia, hypocalcaemia or neonatal abstinence syndrome (physiological withdrawal experienced by an infant exposed to opiate drugs antenatally by maternal ingestion).
These can be excluded by careful history taking, examination & investigation.
Myoclonic jerks can occur during sleep + periods before waking – normal finding + needs no treatment.
How are neonatal seizures managed?
All require admission to NICU - cranial ultrasound as well as electrode monitoring of cerebral activity [CFAM] is available
Should be treated for meningoencephalitis, with broad spectrum Abx and antiviral agents – if the seizures persist, antiepileptic medication may be required e.g. phenobarbitone.
How is cerebral infarction diagnosed / managed in neonates?
Rare event in neonates, may occur secondary to thrombosis, most commonly MCA– babies do not usually develop encephalopathy, instead present with isolated seizures. Diagnosis confirmed by MRI scan, prognosis often good, demonstrating plasticity of the neonatal brain.
Why are neonates susceptible to hypoglycaemia?
Term infants have brown fat (generates energy & heat).
Neonates can tolerate far lower blood sugars than the adult population. Accepted normal in immediate neonatal period: 2.6mmol/L. However, in presence of risk factors, may be unable to metabolise glycogen effectively or absorb enough milk enterally to sustain normal blood glucose.
Risk factors all requiring blood sugar monitoring:
- Preterm (↓ glycogen)
- SGA (↓ glycogen)
- Maternal diabetes in pregnancy (hyperinsulinism)
- Large for gestational age (hyperinsulinism)
- Infection (↑ metabolic demand)
- Hypothermia (↑ metabolic demand)
- Resuscitation required at birth (↑ metabolic demand)
- Poor cord gases (↑ metabolic demand)
(Additional risk factor: Maternal beta blocker use - crosses placenta, ↑ insulin and ↓ glycogen stores?)
What are signs of neonatal hypoglycaemia?
Prognosis?
Lethargy, hypotonia, poor feeding, jittering, seizures, apnoea. Note: hypoglycaemia may also be a sign of sepsis in the newborn infant.
Mild asymptomatic = excellent prognosis.
Prolonged exposure, particularly if symptomatic has been shown to have detrimental effect on development. Severe symptomatic: associated with developmental delay and MRI brain changes, particularly in the occipital regions. > CP, developmental delay, learning disability, epilepsy.
How is neonatal hypoglycaemia managed?
Aim to feed immediately after birth then every 3 hours.
Test pre-feed blood sugar before the 2nd feed.
If pre-feed <2.7, retest 1 hour post feed, if still <2.7, feed again and retest 1 hour post feed, if still <2.7, consider admission and IV dextrose.
If pre-feed >2.7, retest BEFORE the next feed.
Good feeding usually sufficient (formula top ups or NG), but IV dextrose infusion (10% –> 20%) may be needed, and rarely diazoxide may be used to suppress insulin secretion.
What gut / surgical problems can affect term infants?
Bilious vomiting
Gastroschisis
Exomphalos
Oesphogeal atresia + tracheo-oesophageal fistula
What is Oesphogeal atresia + tracheo-oesophageal fistula?
Management?
Failure of division of oesophagus + trachea from their common tube.
Presentation: failure to swallow saliva (‘mucousy’), lung irritation from acid reflux into trachea, gastric distention with air from trachea, cyanosis & choking with aspiration.
Management: NBM, start IVI, pass large bore NG tube then X-ray, continuous suction & lavage of oesophagus with replogle tube, primary surgical repair
What is bilious vomiting? How is it managed?
Green vomit (not yellow): always taken seriously.
Caused by intestinal obstruction:
- Malrotation > volvulus
- Intestinal atresia
Management: NBM, NG on free drainage, IV fluids, IV Abx, upper GI contrast study, Ladd’s procedure
What is Gastroschisis? management?
Bowel protruding from anterior abdominal wall adjacent to umbilicus.
Management: immediately place in cling film, manage fluids & electrolytes, ensure bowel does not become necrotic, surgeons put bowel in silo & then close defect
What is exomphalos?
Abdominal contents herniate into cord surrounded by a sac.
Associated with: chromosomal abnormalities (T21, 13 & 18, Turner’s, Klinefelter’s), Beckwith-Weidemann, Pentalogy of Cantrell, cardiac anomalies, renal tract anomalies, lethal exomphalos-cleft palate syndrome.
Management: operative.
What is cleft palate + lip?
Diagnosis?
Cleft palate: failure of fusion of the palatine processes and the nasal septum
Cleft lip: failure of fusion of the fronto-nasal & maxillary processes.
During routine baby check, hard + soft palate should be felt and visualised to ensure subtle cleft is not missed. Abnormally shaped or absent uvula may be indicative of a sub-mucous cleft that may not otherwise be visible.
Cleft palate + lip usually occur in isolation, but may be part a chromosomal abnormality or sequence + may also occur secondary to anticonvulsant therapy.
Large abnormalities often picked up on antenatal USS, however, small defects may be missed.
How is cleft lip / palate managed?
Management: multidisciplinary: paediatric surgeons (ENT, maxillofacial, plastic), orthodontists, audiologists & speech therapists.
Biggest immediate concern is feeding – most can breast feed normally but special teats may be helpful, particularly in more severe cases. Surgery for cleft lip can take place early, although repair of the palate is usually delayed until the infant is several months old.
What is Pierre-Robin Sequence?
Congenital disorder comprising micrognathia, posterior tongue displacement, cleft palate
Clinical diagnosis: may present with feeding difficulty or difficulty breathing (particularly when supine), management involves airway mgmt + optimising nutrition – supine position and a nasopharyngeal airway may help.
In some cases, feeding assistance with NG tube may be required – cleft palate can later be repaired with surgery.
What is napkin rash?
Perineal erythema - predominantly irritant aetiology: may have painful scaling papules or erosions in severe cases.
Lactose intolerance = rare cause of severe napkin rash (frothy, explosive diarrhoea).
If complicated by secondary Candida albicans infection – red plaques, satellite papules + superficial pustules.
Fungal infection more common following broad-spectrum Abx. Bacterial less common but can be due to Staph. aureus, (fragile pustules + crusting).
Treatment: exposure of the affected area + topical barrier creams to prevent irritation form urine + faeces. Secondary fungal / bacterial infections require topical or oral anti-fungals / Abx.
What is Erythema Toxicum Neonatorum?
Occurs in ~50%!
Migratory raised erythematous rash with overlying papules or pustules – (central yellow plaque with halo of erthyema).
Normally appears on day 2 or 3 of life.
Exact pathogenesis unclear but resolves spontaneously after 3-5 days + asymptomatic.
