Neonatal + infant Flashcards
Feeding, IUGR, infection, jaundice, prematurity, NIPE, RDS, blood group incompatibility, birth marks, birth trauma, biliary atresia, congenital abnormalities, congenital infection, HIE, meconium delay, hypoglycaemia, IEM, HIV, talipes
What are the benefits of breast feeding?
- 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
Properties of breast milk?
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
Complications of breast feeding?
- 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
How long should women ideally BF for?
6m ebf, then alongside foods until 2y
Physiology of breast feeding?
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
Know a bit about formula feeding too
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
Group B Streptococcus infection
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
What are the types of IUGR?
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
What issues are more likely in a baby born with IUGR?
Intrauterine hypoxia, IUD, asphyxia during birth + delivery, hypothermia (as large SA), hypoglycaemia (less fat + glycogen stores), hypocalcaema, polycythaemia
Early onset sepsis <48h old
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
Late onset sepsis >48h old
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
What specific infections are neonates at risk of?
- 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)
What is neonatal jaundice?
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
What are the causes of neonatal jaundice>
- 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
What is kernicterus?
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
How do you assess neonatal jaundice?
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
How is neonatal jaundice managed?
- 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
How do babies born at 23-27w differ to term neonates?
- 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
Long term problems of prematurity?
- LD, cerebral palsy
- Difficulties with other areas of development
- Hearing and vision impairments
Medical complications of prematurity?
- 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
Respiratory distress syndrome?
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
Apnoea + bradycardia
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
Patent ductus arteriosus
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)
Nutritional problems in premature babies
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
Intraventricular haemorrhage + periventricular leukomalacia
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
Necrotising enterocolitis
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
Retinopathy of prematurity
Developing bv damaged - retinal detachment - fibrosis - blindness
Screen eyes of susceptible infants
Laser therapy + intra-vitreal VEGF can help
Bronchopulmonary dysplasia (prev name chronic lung disease)
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
What is the Apgar score?
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)
Outline the newborn physical examination
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:
- Brief history: maternal + newborn, parental concerns
- Weight
- General inspection: pallor, cyanosis, jaundice, rashes etc
- Tone: gently passively move limbs
- Head: microcephaly, sutures, shape (moulding to birth canal common), injuries, anterior fontanelle
- Skin: document any birth marks of lacerations in case of future child protection concerns
- Face: dysmorphic features, asymmetry like CNVII palsy, nose patency
- Eyes: signs of conjunctivitis, sclera for jaundice, position + shape, epicanthic folds, red reflex, subconjunctival haemorrhage (common from delivery)
- Ears: pinna symmetry, accessory auricles, hearing screen test before discharged
- Mouth: visualise whole palate + central uvula, look for tongue-tie (ankyloglossia)
- Neck: appearance e.g. Turner’s, swellings e.g. cystic hygroma, clavicular# from delivery
- Upper limb symmetry, digits, palms (2 palmar creases per hand), brachial pulses
- ChesT: deformities, air entry, murmurs, pulse oximetry
- 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
- 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)
- Lower limbs symmetry, tone, movement, femoral pulses (CoA), ankle deformity (talipes), digits
- Hips: examine individually with nappy off, Barlow’s + Ortolani’s tests
- Back for scoliosis, hair tufts, sacral pits
- Anus patency
- Reflexes
What are the main conditions screened for on the NIPE?
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
Signs of respiratory distress at term
Tachypnoea, laboured breathing (sternal + subcostal indrawing, nasal flaring), expiratory grunting, cyanosis
Causes of respiratory distress at term
- 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
Transient tachypnoea of the newborn
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
Meconium aspiration
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
Persistent pulmonary hypertension of the newborn
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
Outline neonatal resuscitation
- 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
Neonatal seizures
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
Blood group incompatibility
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
Biliary atresia
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
What are the common types of birth mark?
- 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
What are the possible traumatic injuries a baby can acquire from birth?
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
Cleft lip + palate
- 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
Pierre Robin sequence
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)
Oesophageal atresia
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
Exomphalos (omphalocele) vs gastroschisis
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
What are the typical features of congenital infections?
Growth restriction, intracerebral calcification, hydrocephalus, microcephaly, deafness, eye problems, pneumonitis, cardiomegaly, PDA< hepatomegaly, jaundice, rashes e.g. blueberry muffin, bone abnormalities, BM suppression
What are the major congenital infections?
- 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
Hypoxic-ischaemic encephalopathy
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
Meconium delay
- 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
Neonatal hypoglycaemia risk factors
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
CF of neonatal hypoglycaemia
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)
How would you manage neonatal hypoglycaemia?
M: dextrose, promote feeding
May need ix if suspect a rare cause like CAH
Ambiguous genitalia
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
Inborn errors of metabolism
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)
What is screened for on the newborn blood spot test at day 5-7?
- 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)
HIV infection in the neonate diagnosis
- > 18m anti-HIV antibodies
* <18m: DNA PCR (as they will have maternal HIV antibodies confirming exposure but not infection)
CF of HIV infection
Varies with degree of immunosuppression
Suspect in persistent lymphadenopathy, parotid swelling, recurrent fever, recurrent bacterial/candidal/unusual infections, hepatosplenomegaly, chronic diarrhoea, lymphocytic interstitial pneumonitis
Management of HIV
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
How is vertical transmission of HIV prevented?
*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
Talipes
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
Sticky eyes
Common from day 3 onwards, clean with water/saline
Discharge + redness may be conjunctivitis
neonatal conjunctivitis
- 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)
Skull problems?
- 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
What are the tests for DDH?
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
Neonatal reflexes
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
After delivery involving meconium what signs would prompt the need for neonatal medics to review?
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
