Neonatology Flashcards
average weight of children at different ages
birth: 3.3kg M 3.2kg F (7 pounds 6, 7 pounds 2 respectively)
1: 9-10kg
2: ~12kg
3: ~14kg
4: 15.5-16.5kg
5: ~18kg
6: ~20kg
7: ~22kg
8: ~26kg
9: ~28kg
10: 32kg
11: ~36kg
12: ~40kg
13: ~45-46kg
14: 50kg boys 48kg girls
15: 56M 52F
16: 60M 54F
WHO growth charts
have been developed to show normal patterns of growth - exist for different genders and conditions
there is a low birth weight chart for infants born <32 weeks
WHO standard does not include data for
preterm babies born and so the preterm section to the left of the A4 chart and the preterm PCHR chart have been compiled
using UK 1990 reference data
Once a preterm baby has reached an age of EDD plus two weeks measurements can no longer be plotted on the “preterm” section of the chart. Any subsequent measurements must be plotted on the 0-1 chart, using
gestationally corrected age
Gestational correction simply adjusts the plot for the number of weeks a baby was born early.
Number of weeks early = 40 weeks
minus gestational age at birth
You should never gestationally correct for babies born after 36 weeks and 6 days. All such babies are considered “term”.
Gestational correction should be continued until:
1 year for infants born 32-36 weeks
2 years for infants born before 32 weeks
to plot these adjustments:
First work out how many weeks early this infant was, which is 40 minus the gestation at birth. For example a child born at 34 weeks is 40-34 = 6 weeks early. Then work out the actual (calendar) age the child is now and
plot this. Draw a line back the number of weeks the baby was early (in this case 6 weeks). Mark this with an arrow.
The point of the arrow shows the baby’s centile with adjustment for preterm birth.
The WHO did a worldwide study using six different countries including Brazil, Norway, Oman, United States, Ghana and India. So a very diverse population and took millions of children and measured and weighed them and did head circumference, and then produced their growth charts. However the growth charts were not designed by following people over time and then creating lines. They just basically measure tons of kids at certain times and different ages. We assume by making those lines that that’s how kids grow. That is not how kids grow. They grow fast, they grow slow. Some slipping around centiles isn’t necessarily a bad thing and the charts can overestimate failure to thrive, particularly in certain population subsets like east asian
development weeks and teratogenesis
weeks 1-3: all or nothing, kill fetus or no effect
3-10: organogenesis
10-40: growth or physiological function of normally formed tissues/organs
You are the paediatric SHO and you have been called to the delivery suite to see baby Chen who was born 5 min ago weighing 1700 g.
how would you describe this weight? what is your immediate mx? what dd will you consider?
<2500g is lo birth weight, <1500g is v low,
<1000 is extremely low
immediate mx: first ensure has patent airway and breathing normally - if not spont breathing after birth then immediately resus (begun by drying baby)
then check APGAR score, then use A-E approach; if not breathing spontaneously or HR falls <100 then mask ventilation or intubation, start chest compressions if HR <60
do history and examination; if seems likely constitutional then encourage breastfeeding and to keep baby warm, keep baby and mum in for 24 hours while testing for complications of low birth weight or IUGR
dd for low birth weight baby: constitutionally small, preterm deliv, iugr, genetic syndrome
breastfeeding
the most consistent association of infant formula is increased childhood infections, including hospitalisations
breastfeeding for at least 2 months is associated with half the risk of SIDS
Lower rates of post-natal depression and later maternal breast cancer
Every breastfeeding problem should first of all trigger an expert face-to-face assessment of positioning and attachment. Obviously this is not you, but actually it’s not a midwife or health visitor either – make sure that you are referring or advising mothers to self-refer to your local infant feeding lead, breastfeeding clinic or specific community breastfeeding support groups – they should have a list in their discharge pack or red book. If it’s out of hours, they can always ring a breastfeeding telephone helpline
how to assess if feeding well:
Day 0-1 should have at least 4 feeds
Day2+ Should have at least 8 (time between feeds less important than number in 24 hours)
Day 1-2 should have at least 2 wet nappies a day, day 3-4 at least 3, and day 5+ at least 6
Day 1-2 should have 1 poo a day, day 3 at least 2; by week 5-6 may reduce to once a week
Baby should wake for feed, have audible rhythmic sucking, comfortable breast and nipples, and baby spontaneously ends feed and is content, with feeds lasting 5-40 minutes (if consistently >45 mins may not be feeding effectively)
amount of milk a mother produces in the 1-2 weeks postnatally is directly correlated to long-term milk supply, because firstly, breast stimulation is needed to activate milk producing cells and hormone receptor sites. Secondly, if milk doesn’t get expressed from a full breast, an inhibitory feedback loop is activated that reduces supply. Therefore if baby isn’t frequently stimulating and draining the breast in the first few weeks, a mother may be left with a low milk supply and baby will struggle to gain weight without supplementation later on. If there is any concern in the first few weeks, mothers should be advised to express milk to secure their supply. That means expressing at least 8 times per 24 hours, including once at night
normal things to see: frequent feeds, may be irregularly timed, crying, fussing, not sleeping for long periods -> advice is to feed responsively
breastfeeding problems and trouble shooting
pain, consider:
engorgement - typically starts in the first few days after birth, is often bilateral and worse before a feed. seen in up to 2/3 of mums
Infant attachment may be difficult due to breast fullness and milk flow may be reduced.
The whole breast is typically swollen and oedematous and may be shiny, diffusely erythematous and may leak excessively.
The nipple may be stretched and look flat in appearance.
The infant may cough and pull off the breast on feeding or clamp down on the nipple during feeding to control flow.
Lasts 24-48 hours and resolves. Warm compresses in mean time, wear well fitting bra
blocked ducts - May present with a localized, tender cord of tissue in one breast (usually a few centimetres in diameter), which may be relieved by expression of milk — overlying skin may be erythematous.
A small white spot (bleb) about 1 mm in diameter may be present at the end of the nipple.
Warm compress before feed, keep feeding and massage during will help to unblock it
Ductal infection may present with deep burning, aching, or shooting breast pain that occurs during and between feeds. There may be erythematous, flaky or shiny skin of the nipple, or a nipple fissure.
Purulent exudate or crust may suggest associated bacterial infection.
galactocoele - may result from a blocked duct, and typically presents as a smooth, round, painless breast swelling which causes milky nipple discharge when pressed
mastitis - woman often has a fever and is systemically unwell — mastitis may present with a hard painful swelling in a wedge-shaped distribution in one breast, with erythema of the overlying skin.
A breast abscess may present with a worsening painful breast lump, which may be fluctuant, and the overlying skin is often erythematous and warm; warm compress, simple analgesia, keep breast feeding, and send milk culture (if positive, if nipple fissure, or not improving in 24 hours then for fluclox for 10-14 days)
low milk supply, consider:
short or infrequent feeds, and/or no night feeds.
Use of a dummy; or giving supplementary feeds other than breast milk may also contribute.
Maternal depression, stress, and/or anxiety may result in a reduced response to infant feeding cues and a reduced frequency of feeds,
suboptimal positioning - Suggested by nipple pain/trauma; frequent feeding more than every 2 hours; no long intervals between feeds; feeding for less than five minutes or longer than 40 minutes duration
true low milk supply due to maternal prolactin deficiency may include drugs, thyroid disorders, retained placenta, alcohol use, and eating disorders
sore nipples:
often short lived — within a few weeks, your nipples often “toughen up.” But if the uncomfortable sensation persists, the most likely cause is a poor latch; alternate sides, use cool compresses, get a qualified person to do a feeding assessment
leaking:
normal to leak in first few weeks, especially if think about/see/hear baby; wear nursing pads; will resolve by 6 weeks or so; don’t pump to prevent as this only stimulates to make more milk
nipple thrush:
Candida infection may cause bilateral burning nipple pain, itching, and hypersensitivity of the nipple, especially during and soon after feeds.
The nipple may be red, shiny, swollen, or fissured.
Typically the pain does not resolve despite improved positioning and attachment, or follows a period of pain-free breastfeeding.
Clinical signs of candida infection may also be present in the breast fed infants mouth.
Topical or oral antifungal
Viral infection (such as herpes simplex, herpes zoster or varicella zoster) may present with vesicular rash affecting the breast.
Eczema typically causes a bilateral red, dry, scaly rash which may have lichenified (thickened) areas, which tend to spare the base of the nipple.
Psoriasis typically causes red plaques with clearly demarcated borders, which may have a fine overlying scale.
Irritant dermatitis may occur due to soaps, nipple creams and other substances in direct contact with the breast.
Paget’s disease of the nipple may mimic eczema, but is usually unilateral, persistent, and unresponsive to treatment for eczema. In addition, there may be skin ulceration or erosions. Needs 2WW.
Nipple vasospasm:
More common if has raynauds but anyone can get; Nipple pain (may be described as shooting, throbbing or burning) is typically intermittent, and present during and immediately after breastfeeds, and in between feeds if exposed to cold temperatures.
Blanching of the nipple may be followed by cyanosis and/or erythema.
Nipple pain resolves when the nipple returns to its normal colour.
milk oversupply:
suboptimal positioning, so sucks more stimulating more milk production; excessive expression; infant may:
Choke and splutter when let-down occurs.
Clamp down on the nipple or pull off the breast during feeds
mother may describe:
Breast fullness and possible engorgement or blocked ducts.
A painful, forceful milk let-down reflex.
Milk leakage and/or milk spraying from the opposite breast when feeding
For all women with breastfeeding problems:
Ensure that a person with appropriate training and expertise (such as a health visitor or breastfeeding specialist) observes the woman breastfeeding and expressing milk to check and give advice
Offer information on local and national breastfeeding support groups and organisations, such as:
The National Childbirth Trust
and give leaflet (NHS A-Z has many relevant to different problems)
vomiting baby
Most babies vomit small amounts from time to time and bring up some milk when they burp. This is known as posseting and is usually nothing to worry about. You can tell when your baby is vomiting rather than posseting because there will be a lot more coming out.
Vomiting is also very common (up to half of all babies) and in most cases will improve with time; However, vomiting can occasionally be a sign of an underlying problem such as severe reflux, milk allergy, pyloric stenosis, or gastroenteritis
Milky or mucous vomit suggests a cause above the duodenum e.g. overfeeding,
gastric reflux, pyloric stenosis.
Bilious or faeculent vomiting implies bowel obstruction
True projectile vomiting (other side of the room) implies pyloric stenosis
check onset and pattern
Started after milk feeds initiated? Always post feeds?
Associated symptoms
Fever, abdominal pain / distension, diarrhoea, irritability etc.
Feed volumes
Standard volumes = 150 ml/kg/day or 8 – 12 breastfeeds a day
Weigh and measure head circumference and plot on growth chart
urine dip if well
if unwell:
- Bloods: FBC, CRP, U+E, blood gas with blood sugar, blood cultures
- Urine: dip and culture, metabolic screen, toxicology screen
- Lumbar puncture
- CXR
- abdo USS
- CTH if indicated
if well and gaining weight likely overfeeding or physiological reflux: check amount given adn advise parents on correct amount, advise on anti-reflux measures, if not effective then CMP free diet and dietician referral
if well but faltering growth/losing weight then consider GORD, pyloric stenosis, CMPA; get urine dip and blood gas
if unwell then ix as above, resus inc broad spectrum abx; if bilious vomiting, distended abdo, abnormal imaging then likely surgery so refer, keep NBM, insert NGT
if fever, hyponat, metabolic acidosis or otherwise thinking medical cause then ix as above (detailed version) and monitor
for GORD:
Clinical features may include feed refusal, back arching / irritability temporarily
related to feeds or reflux episodes, faltering growth
1 - advise on feed volume/freq and anti-reflux position
2 - In formula fed infants, offer thickened feeds; In breast fed infants, offer a 2 week trial of Gaviscon infant sachets (). If successful, continue with it, but try stopping at
intervals to see if infant has recovered); In formula-fed infants, if thickeners are not effective, stop the thickened feeds
and start a 2 week trial of Gaviscon infant sachets. If successful, continue
with it, but try stopping at intervals to see if there is recovery.
3 - if no response, start a 2 week trial of cow’s milk-free formula in formula-fed infants / maternal cow’s milk-free diet in breast fed infants if suspicion of CMPA or intolerance and refer to dietician
4 - If all above measures are unsuccessful, start a 4 week trial of an acid
suppressing drug. If improvement seen, continue for 3 months; omeprazole and ranitidine favoured
formula
Most infant formulas are made from cow’s milk which has been processed to make it
“suitable” for babies. (They may also contain, among other things, soya protein, structured vegetable oils, inositol, antioxidants and fish oils). They have to meet regulations for composition.
no evidence that one company’s milk is better for a baby than any other, and no need for the parents to stick to one brand: if parents find that one brand seems to disagree with their baby, they could try
switching brands
3 main types of formula:
first milks: for newborns, based on the whey of cow’s milk (ratio of proteins in the formula approximates to the ratio of whey to casein found in human milk (60:40)) and are more easily digested than the other milks; first milk is the only food baby needs for the first six months, then continue as add solid foods and switch to cow’s milk at 1 year
second milks: not recommended
follow on milks: not nutritionally suitable for <6mo old, marketed as for babies over 6mo but no need, can continue the first milk
feed responsively as long as not regurgitating significant amounts -> if he is try smaller, more frequent feeds
if baby is constipated: can try changing brand of milk, or mx per constipation guidelines; no evidence to offer baby extra water to produce softer/more frequent stools; if baby seems dehydrated may need more milk
hold baby close, make eye contact, hold fairly upright, support head in neutral position, bottle almost horizontal with slight tilt, give breaks during feeding and burp if required, keep number of ppl feeding baby small and make sure everyone uses the same technique
start solid foods around 6mo but continue first milk too (can try in cups); continue first milk until 12mo; if given solid foods before 6mo risk of D&V that may require hospital; developmentally ready for solids when: can co–ordinate his eyes, hand and mouth and look at food, grab it and put it in his
mouth all by himself, can swallow, can hold head steady when in a sitting position
The belief that babies need burping after feedings, or help “bringing up the wind,” originated with the spread of bottle–feeding. The faster flow of milk from bottle nipples forces babies to gulp air in between closely–spaced swallow; if the baby shows signs of distress during the feed, parents should be encouraged to help him let go of the teat and sit up. Alternatively he can be put over his parent’s shoulder, to see if he needs to burp. The feed can be resumed when he seems more comfortable; they should be re–assured that if the baby does not burp after being upright for a minute or two after the end of the feed, or if he goes to sleep – he doesn’t need to burp!
GORD ix/mx
Suspect GORD in an infant (up to 1 year of age) or child if they present with regurgitation and one or more of the following:
Distressed behaviour shown, for example, by excessive crying, crying while feeding, and adopting unusual neck postures.
Hoarseness and/or chronic cough.
A single episode of pneumonia.
Unexplained feeding difficulties, for example, refusing to feed, gagging, or choking.
Faltering growth.
Note that:
Children over 1 year of age may present with heartburn, retrosternal pain, and epigastric pain.
Additional features such as episodic torticollis with neck extension and rotation may indicate the presence of Sandifer’s syndrome.
red flags: projectile <2mo (pyloric stenosis), bilious (obstruction/intuss), distended abdo (obstruction), blood in vomit (mallory weiss tear), bulging fontanelle (raised ICP, meningitis), vomit worse in morning or enlarging head circ (raised ICP), blood in stool (bacterial gastroent or CMPA), chronic diarrhoea or has atopy or strong FH of atopy (CMPA), unwell or with fever or onset after 6mo or lasting over 12mo (UTI or other infection, or metabolic disorder)
Do not offer an upper gastrointestinal (GI) contrast study to diagnose or assess the severity of GORD in infants, children and young people.
Perform an urgent (same day) upper GI contrast study for infants with
unexplained bile-stained vomiting. Explain to the parents and carers that this is
needed to rule out serious disorders such as intestinal obstruction due to mid-gut
volvulus.
Consider an upper GI contrast study for children and young people with a history
of bile-stained vomiting, particularly if it is persistent or recurrent.
Offer an upper GI contrast study for children and young people with a history of
GORD presenting with dysphagia.
Arrange an urgent specialist hospital assessment to take place on the same day
for infants younger than 2 months with progressively worsening or forceful
vomiting of feeds, to assess them for possible hypertrophic pyloric stenosis. - note babies with pyloric stenosis still seem hungry even after their meals
Consider performing an oesophageal pH study (or combined oesophageal pH and
impedance monitoring if available) in infants, children and young people with:
* suspected recurrent aspiration pneumonia
* unexplained apnoeas
* unexplained non-epileptic seizure-like events
* unexplained upper airway inflammation
* dental erosion associated with a neurodisability
* frequent otitis media
* a possible need for fundoplication or suspected sandifers
Investigate the possibility of a urinary tract infection in infants with regurgitation if
there is:
* faltering growth
* late onset (after the infant is 8 weeks old)
* frequent regurgitation and marked distress
stepped mx approach:
review the feeding history, then
* reduce the feed volumes only if excessive for the infant’s weight, then
* offer a trial of smaller, more frequent feeds (while maintaining an appropriate
total daily amount of milk) unless the feeds are already small and frequent,
then
* offer a trial of thickened formula (for example, containing rice starch,
cornstarch, locust bean gum or carob bean gum)
If this stepped care approach is not successful, stop the thickened formula and offer a 1–2 week trial of alginate therapy (Gaviscon® Infant) added to formula.
If symptoms improve after a 1–2 week trial of alginate therapy:
Continue with the treatment.
Advise the parents or carers to stop treatment at regular intervals (for example every 2 weeks) in order to see if symptoms have improved
In breast-fed infants with frequent regurgitation associated with marked distress
that continues despite a breastfeeding assessment and advice, consider alginate
therapy for a trial period of 1 to 2 weeks
If symptoms improve after a 1–2 week trial of alginate therapy:
Continue with the treatment.
Advise the parents or carers to stop treatment at regular intervals (for example every 2 weeks) in order to see if symptoms have improved
if symptoms remain troublesome despite a 1–2 week trial of alginate therapy in both breastfed and formula-fed infants:
Consider prescribing a 4-week trial of a proton pump inhibitor (PPI, such as omeprazole suspension or a histamine-2 receptor antagonist (H2RA).
Assess the response to the 4‑week trial of the PPI or H2RA, and consider referral to a specialist for possible endoscopy if the symptoms do not resolve or recur after stopping treatment.
Consider a 4-week trial of a PPI or H2RA for those who are unable to tell you
about their symptoms (for example, infants and young children, and those with a
neurodisability associated with expressive communication difficulties) who have
overt regurgitation with 1 or more of the following:
* unexplained feeding difficulties (for example, refusing feeds, gagging or
choking)
* distressed behaviour
* faltering growth.
Consider a 4-week trial of a PPI or H2RA for children and young people with
persistent heartburn, retrosternal or epigastric pain
For children aged 1–2 years who have persistent heartburn, retrosternal pain, or epigastric pain:
Consider a 4-week trial of a PPI (such as oral omeprazole) or an H2RA.
If symptoms do not resolve or recur after stopping treatment, consider referral to a paediatrician or paediatric gastroenterologist
Specialist assessment by a paediatrician or paediatric gastroenterologist should be arranged if there is:
* An uncertain diagnosis or ‘red flag’ symptoms which suggest a more serious condition.
* Persistent faltering growth associated with regurgitation.
* Suspected complications, such as recurrent aspiration pneumonia, or unexplained
apnoea.
sandifer syndrome
classical symptoms of the syndrome are spasmodic torticollis and dystonia with nodding and rotation of the head, neck extension, gurgling, writhing movements of the limbs, and severe hypotonia also noted
Spasms may last for 1–3 minutes and may occur up to 10 times a day. Ingestion of food is often associated with occurrence of symptoms; this may result in reluctance to feed. Associated symptoms, such as epigastric discomfort, vomiting (which may involve blood) and abnormal eye movements have been reported.
peak prevalence at 18–36 months, but in rare cases, particularly where the child is severely mentally impaired or has eg cerebral palsy, onset may extend to adolescence
Diagnosis is made on the basis of the association of gastro-oesophageal reflux with the characteristic movement disorder. Neurological examination is usually normal. Misdiagnosis as benign infantile spasms or epileptic seizures is common, particularly where clear signs or symptoms of gastro-oesophageal reflux are not apparent. no dev delay
Most of the time, Sandifer syndrome goes away within the first two years of a baby’s life. Given the link to gastroesophageal reflux disease, treatment revolves around treating the reflux itself
When Sandifer syndrome is suspected, 24-h oesophageal pH monitoring is usually diagnostic; however, an empirical trial of pharmacological management (e.g., prescribing a PPI) is also appropriate without prior invasive investigation - both may be preferable to extensive neuro workups, and if negative can always do the neuro work ups afterwards
Once diagnosed, it can be successfully managed by treating the underlying GERD/hiatus hernia which typically leads to a complete resolution of all associated symptoms
milk ladder
ONLY FOR CHILDREN WHO ARE BEING MANAGED AS MILD-TO-MODERATE
NON-IgE COW’S MILK ALLERGY
the practical concept of this Ladder is the recognised fact that the more ‘baked’ cow’s milk protein is, usually the less allergenic it is
normally start between 1 and 3 years as this is when children tend to outgrow CMPA - normally need to be on milk free diet for at least 6 mo first, and be well and allergy sx free
start on whatever step the child is currently on; generally spend a week on each step
1: cookie/biscuit, start with 1 and build up to three
2: muffin, start with 1/2 then build to 1
3: pancake, as above
4: cheese (15g hard, then once tolerates can do baked cheese on eg pizza)
5: yoghurt
6: milk
weaning infants
babies don’t need anything but breastmilk or
infant formula for the first six months of life.
This is because babies’ digestive systems and kidneys are still developing (even large/small babies dev at same rate).
Introducing solids too soon may increase the risk of asthma, eczema, digestive problems, allergies and obesity in later life.
Every baby is different but there are three clear signs that together show your
baby is ready for some solid foods alongside breastmilk or infant formula:
1. Baby can stay in a sitting position and hold his head steady.
2. Baby can coordinate his eyes, hands and mouth so that he can look at
the food, pick it up and put it in his mouth all by himself.
3. Baby can swallow food (a baby who is not ready will push food back out
of his mouth)
You can wean before 6months but should never wean before 4 months (17 weeks).
idea of weaning is to introduce your baby gradually to a wider range of foods
and textures, so that by the age of 1 year your baby will be joining in family meals. Offer a small amount of food before or after a milk feed, or in the middle of the feed if that works better - just a few spoonfuls a day to start with; do yogurt, well mashed fruit or cooked veggies; don’t add salt or sugar, avoid honey before 12mo due to infant botulism risk
after first couple of weeks add mashed/minced meat, dahl, hummous, mashed egg or fish, nut butters, cereals breads and pastas; good to introduce soft lumps (better speech development) eg mashed beans or meat, and give finger foods like toast, carrot and cheese sticks, peeled fruits
by 7mo have 3 meals a day of mashed and finger foods with a cup of water to sip from; continue to breastfeed on demand or offer 500-600ml milk a day
by 9mo move on to chopped foods with water or 1 in 10 fruit juice and continue milk as above
Whole cows’ milk should not be used as the main drink until 1 year.
If your child is eating a varied diet, semi-skimmed milk may be given from 2
years. Skimmed milk should not be given to children under 5 years. However,
remember that cows’ milk can be added to foods, for example breakfast
cereals, from 6 months.
tips for fussy eaters: avoid frequent snacks and drinking throughout the day, keep small portions at regular meal times, make sure there are no distractions, don’t force them to eat, if baby refuses food clear away and then wait until next meal time to offer more; normally a passing phase and no concern if not losing weight
From birth, all babies, including breastfed babies, should be given a vitamin
supplement containing 8.5–10 micrograms of vitamin D daily as babies’ bones are growing and developing very rapidly in these early years.
From 6 months of age it is recommended that all babies should be given a supplement containing vitamins A, C and D.
Babies fed infant formula will only need vitamin supplements if they are receiving less than 500mls (about a pint) of infant formula a day (usually around 1 year) because infant formula has vitamins added during processing.
It is recommended that vitamin supplements are continued until the child is 5 years old.
B12 and riboflavin supplements must be given to all children being weaned onto a vegan diet
iron stores and supplementation in infants
babies born with good stores of iron that last until around 6mo, and breast milk/formula will provide enough iron during this period only if they have these good stores; after 6mo iron rich foods need to be included while weaning; haem iron in red meat and non-haem iron in grains, veg, legumes, eggs; vit C helps with absorption of non-haem iron so get that in at same time
all infants born <37 weeks gestation should be considered for iron supplementation from 4 weeks of age according to the following criteria:
Where infants are breastfed exclusively or tube fed with expressed breast milk (EBM) or donor breast milk (DBM)
Iron supplementation IS recommended.
Iron supplementation IS recommended where Nutriprem Human Milk Fortifier is used.
Iron supplementation IS NOT recommended where SMA Breast Milk fortifier is used.
for pre-term formulas:
Nutriprem 1/ Nutriprem Hydrolysed / SMA Gold Prem 1 - supplementation not recommended
for nutrient enriched post discharge formulas:
Iron supplementation IS recommended where SMA Gold Prem 2 is used.
Iron supplementation IS NOT recommended where Nutriprem 2 is used.
If on standard term infant formula fe supplementation is recommended
9 Infants ≥37 weeks who are born weighing less than 2.5kg should also be considered for iron supplements especially if exclusively breastfed.
As many will have been discharged prior to 4 weeks of age the GP should be asked to prescribe until 6 months of age.
various formulations acceptable, sytron commonly used
bear in mind that loss due to eg excess phlebotomy might increase iron need and transfusion might decrease iron need - some centres in europe will monitor weekly ferritin for their inpatient babies to guide iron supplementation
You are the paediatric SHO and you have been called to the delivery suite to see baby Chen who was born 5 min ago weighing 1700 g.
what history and examination to do?
history - is she well?what were her Apgar scores? symmetricalor disprop small body compared to head?
what is gestational age? what type of delivery? any difficulties during pregnancy or labour? check mothers booking bloods
did scans suggestpoor fetal growth? any maternal illnesses? including any longstanding ones? was mother well nourished during pregnancy? did she use alcohol, tobacco, or illicit drugs?
how tall are mother and father? do they know what they weighed at birth? any FH of small babies or genetic disorders? any geneti relation between parents?
exam - any fever or resp distress? any jaundice or plethoric signs? does she seem thin or have subcut fat? plot height, weight, head circ on growth chart; any dysmorphic features (check ears, palms, feet)
how big was placenta, was it complete, did cord appear normal w 2 a’s 1v?
The nurse on the special baby unit calls you to review Sam, an infant born at 28 weeks, now 10 days old, who was being weaned off ventilation. He has now become unwell, desaturating on handling and with temperature instability.
what are your dd and what to look for in history and examination? what ix to order?
dd - sepsis, meningitis, pneumonira, nec ent, IVH, apnoea of prematurity, resp distress, PDA
how and when did babys condition change? what feeding regimen and is he tolerating? how is urine production? any blood or melaena in nappies? any abdo distension? any neuro sx?
obstetric history, how was labout, was sam small at birth, did his mum recieve steroids before birth?
examination - colour, chest movements and sounds, fluid balance, feel all pulses, auscultate for murmurs, any abdo distension? any peritonitis? any bowel sounds? any abdo transillum (suggest perf), examine contents of nappy, feel fontanelle
ix - fbc for haem/plats, U&Es, clotting for DIC, G&S as blood products may be needed for anaem/DIC/surg, blood cultures, stool cultures, AXR
4 leading causes of neonatal deaths? 4 most common diseases seen in neonatal unit? most common surgical emerg in neonates?
prematurity, conge malform, intrapartum complications, infection
NEC, sepsis, resp distress, chronic lung disease of prematurity
NEC (may perf)
You are called to the delivery suite to review a newborn. The midwife has reported the boy is having difficulty breathing
what 9 dd? what initial mx?
transient tachyp of newborn
meconium or milk aspiration
resp distress syndrome, congen pneumo
birth asphyxia, diaphragm hernia
trach-oesoph fistula, sepsis, laryngomalacia
A-E assessment, APGAR scores; doesnt need resus but give O2 due to desaturating, freq review as may deteriorate rapidly; keep warm
You are called to the delivery suite to review a newborn. The midwife has reported the boy is having difficulty breathing
history, examination, ix, mx
how old is child? how and when did difficulty come on? was resus needed? any meconium staining of liquor? has fed yet? any froth in mouth? obstetric and labour hist inc were steroids given predelivery; any FH of congen or resp problems?
place in incubator w high ambient O2, gain iv access and take FBC, culture, LFT, U&Es, glucose, VBG or ABG
insert NG tube to exclude trachoesoph fistula
CXR
consider broad spectrum abx
principles of managing resp distress syndrome
ventilators - careful as too much oxygenation <32 weeks -> retinopathy of prem
surfactant - directly into airway
prevent hypotherm and acidosis
by doing the above allow the time needed for RDS to abate, normally taking 3-7 days
what are the complications of RDS?
ptx in 20% of cases due to ventilation - trauma can also lead to bronchopulm dysplasia
lobar collapse
pulm htn leading to cor pulmonale
IVH due to fluctuating BP/blood pH
You are performing an initial baby check in the delivery suite. This baby has ambiguous-looking genitalia. The parents are eager to know if everything is ok - intro explanation, dd, hist, exam, ix
Explain the issue – there is a problem with the development of the genitalia and, at this stage, the details are unclear. * Explain that tests will be able to determine what the baby’s sex is and what has gone wrong. * Use terms like ‘your baby’ rather than ‘it’, which could seem dehumanizing and impair parent–child bonding. * Do not guess the sex. You may have to change your mind later on. * Encourage the parents not to name the baby until they know the sex
dd - female virilization from CAH, maternal androgen ingestion; male inadequate virilization from cryptorchidism, CAH, androgen insens; or true hermaphroditism
history - obstetric inc any acne/hirsutism of mum in preg, what meds did she take and how was her health/PMH
examine - hydration (salt wasting crisis), hypoglyc (inadequate steroids), try to identify scrotum or labia and any hyperpigmentation, look for urethral opening (to tell small penis from cliteromegaly, and to spot hypospadias), palpate inguinal canals for testes (if not theyre either in abdo or female), and plot on growth chart
ix - chromosomal analysis, urine for steroid metabs and 17-OH prog, U&Es, glucose, serum LH and testos, USS of pelvis/inguinal areas/scrotum looking for testes and uterus
MDT will be needed inc neonatalogist, endocrinologist, geneticist, psychiatrist, social worker
fludro can treat salt wasting if present and stop pitu overstim; surgical correction of ext genitalia within 1yr
structure and function of mature placenta
devs from start of pregnancy, persists for 9 months, delivered as afterbirth with other extraembryonic structures; does gas transfer, excretion, water balance, pH reg, catabolism/resoprtion, synthetic/secretory functions, metabolism, haematopoiesis, and immunological protection; is discoid, 20-25cm diameter and 400-600g
side that faces foetus is chorionic plate and is where umbilical cord attaches; basal plate attaches to decidua basalis and is structure through which maternal blood enters placenta; functional unit is foetal villus tree which arises from chorionic plate as 2 layers (syncytiotrophoblast and cytotrophoblast) surrounding foetal caps; maternal blood circulates in intervillus space and bathes the villi; due to this, human placenta classified as haemochorial; maternal/foetal circulations never mix with nutrients/gases diffusing or being transported across trophoblast into foetal caps; 10-14m^2 surface area for fast exchange; caps in tips of terminal villi dilate and form tortuous loops which helps slow flow to facilitate metabolite exchange
histiotrophic vs haemotrophic nutrition
maternal arterial circulation not fully established until weeks 10-12, so prior to this foetus relies on oviductal/uterine secretions taken up by trophoblast and yolk sac (histiotrophic) with principle source being carb/lipid rich secretions from endometrial glands, glandular secretion being stimulated by progesterone and signals from trophoblast; this also ensures low O2 environment - good as at this point foetus sensitive to ROS and teratogenesis, and this also favour stem cells; once placental villi established, relies on haemotrophic nutrition which causes clear increase in intraplacental O2 tension; note old textbooks wrong when say maternal circulation starts day 9 - it’s not till weeks 10/12
embryonic vs foetal dev period
embryonic 0-8 weeks, approx first trimester, when major organ systems dev; embryo at highest risk of congenital problems and most sensitive to external factors (O2, alcohol, mutagens) with each organ having period of peak sensitivity; most deaths occur within this period; foetal period then 9-38 weeks with most organs differentiated, and undergoing maturation and growth; note dates of clinical pregnancy from first day of last menstrual period so 2 weeks longer than dates corresponding to post fertilisation; 3 trimesters of 12-13 weeks each; timing of switch from ebryo to foetus corresponds to histio to haemo switch, thus pO2 rises in placenta at end of embryogenesis; (dates in this card are postfertilisation ie add 2 for pregnancy dates)
placental villi maturation and foetal health
low/high birth weights at higher risk of mortality and poor placental dev correlates with intrauterine growth restriction; in early placenta, villi have low SA:V ratio (yet to undergo branching) with outer syncytiotrophoblast layer and inner cytotrophoblast layer, within stroma are some foetal caps; intervillous space has uterine gland secretions and some maternal blood with histiotrophic nutrition relied on; during latter half of pregnancy, nuclei of SCT cells cluster so rest of cell is thin diffusional barrier, absolute number of CT cells increases but morphological changes in villous means layer no longer consistent; terminal villi formed and highly vascularised (placenta major site of angiogenesis); foetal caps no longer in core of villi but directly abut trophoblast cells to reduce diff distance; defects in these processes affect nutrient/gas exchange, causing IUGR; may be small weight if: preterm, multiple pregnancies, IUGR if born full term; growth until ~week32 from inc cell number, after from inc cell size
foetal material in maternal circulation
trophoblast cells slough off from placenta during dev, and if they have functional role in maternal circulation is unknown; foetal cells in maternal tissue can give microchimerism ie male cells in mother thyroid is mother has male child and a thyroid disorder, and unknown if the cells trying to repair or contributing to the disease; foetal DNA/RNA from placenta in maternal circulation from early pregnancy onwards, making up 10% of circulating DNA and in shorter fragments than that of the mother; can be sued to test for paternally inherited traits (sex, rhesus D group status, aneuploidies like ts21), can also sequence foetal genome to detect not just down syndrome but other possible disease causing mutations, with fewer risks doing this than amniocentesis or CVS
foetal DNA prenatal testing
foetal DNA in blood can be collected easily, no extra risk of miscarriage, earlier diagnoses (from 7 weeks); this DNA comes from placenta and represents whole foetal genome, is detectable from 4 weeks and levels increase with gestation, and is cleared from circulation within 30 mins of delivery; it is shorter than free maternal DNA: 143bp vs 166bp; noninvasive prenatal diagnosis NIPD is done in high risk patients for sex determination and single gene disorders; NIPT/NIPS (testing/screening) in low risk groups for aneuploidy, requires invasive testing for confirmation; with x-linked recessive disorders, if mother carrier, father normal, then male baby needs invasive testing as 50% chance has it, females dont as can only be normal or carrier; paternally inherited disorders will show up in free DNA
factors affecting foetal growth
maternal: uterine size (reciprocal crosses between shire horses, shetland ponies, with differences in growth persisting after birth - indicating long term programming); nutrition (undernutrition commonest cause of FGR with birthweight affected by famine during third trimester); parity, with first babies usually smaller (uterus expansion, artery remodelling easier in future ones); socioeconomic status, smoking, drugs (up to 300g reduction, dose dependent), teenage mothers (last one more nutrients to themselves, less to baby, as still growing); maternal CVD (inc hypertension) reduce birthweight and hyperglycaemia leads to increased birthweight; hypobaric hypoxia reduces brithweight by 100g per 1000m altitude, indigenous populations protected due to adaptive mutations which increase uterine blood flow
placental: placental insufficiency major cause of FGR in developed countries, often due to problems remodelling spiral a’s: US assessment of uterine a waveform where it crosses internal iliac a, high resistance suggesting FGR and preeclampsia (shown by absent/reversed end diastolic flow), reduced expression of transporter proteins precedes evidence of FGR and may be induced by placental oxidative stress due to malperfusion - also loss of surface area for exchange due to infarction; if barrier compromised then xenobiotics or maternal cortisol could cross, influencing foetal growth; stress can raise maternal cortisol, treatment in 3rd trimester with glucocorticoids can also reduce foetal weight, as can decreased activity of 11beta-HSD2 (in placenta maternal cortisol to cortisone, activity dep on hypoxia and other stressors)
foetal: sex (males larger, longer, bigger head), genome (<10% cases FGR caused by genes though), infection (toxoplasmosis, HCMV, rubella, herpes can all occur, in first trimester so cause symmetric growth reduction and <10% cases); endocrine, as maternal hormones dont cross placenta so foetal endocrine environment drives growth with IGF-I/II important (usually only expressed from paternal allele, uniparental disomy or loss of imprinting resulting in double dose and hypertrophic beckwith-weidemann syndrome; levels of IGF-1 sensitive to O2/nutrient availability; foetal insulin may be important in late pregnancy with increased glucose uptake and body weight
initiation of parturition
decrease in progesterone:oestrogen ratio leading to increase in prostaglandin synthesis: oestrogen up but little evidence for prepartum progesterone decrease in humans (though seen in other animals); growth and activation of foetal adrenals means more foetal cortisol and dehydroepiandrosterone sulphate DHEAS with former causing organ maturation, latter causing rapid rise in maternal oestrogen levels; this leads to prostaglandin production resulting in cervical ripening and increased uterine contractility; oestrogen upregs oxytocin receptors and distension of uterine cervix during 2nd phase of labour causes reflexive rapid pulsatile release of oxytocin from post pitu, causing increased contraction, which incs pressure on cervix so +ve feedback until expulsion (ferguson reflex)
no evidence of removal of progesterone block to uterine contraction but may be local ratio changes and changes in progesterone r isoform; CRH in foetal and maternal blood, rises towards term and in labour and if early/late then early/late labour; CRH increases DHEAS production directly and indirectly (via pituitary), acts on uteroplacental tissues to increase PG availability and on myometrium to inhib contractions via raised cAMP; in culture progesterone inhibs CRH production, catecholamines/glucocorticoids stimulate; stretch of uterus as baby grows causes increasing GAP junction protein which activates myometrium; thus initiating labour has mechanical, foetal, maternal, and local factors
CRH causes increased PGHS-II (prostaglandin endoperoxide synthase 2 makes PG) and decreased PGDH (metabolises PG) so PG levels up; PG inhibits 11betaHSDII (cortisol to cortisone) and stims 11betaHSDI (cortisone to cortisol) giving cortisol up; cortisol increases CRH release and PGHS-II and decreases PGHS-I (COX1); stress like hypoxia/trauma alter cortisol and PG to trigger this positive feedback cycle and thus cause labour
cervical ripening and myometrial changes
cervical canal closed in pregnancy to stop ascending infections, prolapse of membranes; must soften and dilate; ECM matrix changes: high water content, few fibrous elements, increased hyaluronic acid, decreased chondroitin and dematen sulphates; oestogen activates collagenase, progesterone allows collagen breakdown, PGE2 increases distensibility and is given therapeutically, causing WBCs to migrate in and release cytokines; softening begins in first trimester, ripening in weeks or days before birth causing loss of tissue complicance/integrity; suggested NO may be involved, inhib of iNOS in animal studies stopped ripening
most of pregnancy, myometrium relaxed with parts uncoupled and isolated electrically/mechanically; progesterone induces degeneration of uterine nerve endings and decreases resting potential; at term, rp increases (becomes less negative) due to oestrogen, which also increases oxytocin/PG r concs as well as coupling via gap junctions and increased PGF2-alpha and oxytocin to cause contraction; oestrogen stims inc myometrial bulk by increasing cell size from 50-500 microns
change in O:P ratio causes actin/myosin increase, contraction requires MLCK activity; Ca activates calmodulin which activates MLCK; influx of Ca from outside and SR with uterotonins inc [Ca]i; cAMP and cGMP act to reduce Ca flux or MLCK activity and so reduce contractility, tocolytics affect them to do this; steroids and mechanical stress cause connexin expression tof form gap junctions and allow coupled contraction; oxytocin/PG both via receptors inc Ca, NO via cGMP and adr, relaxin, CRH via cAMP decrease contraction
labour
preceded by painless braxton-hicks contractions; is onset of regular, painful uterine contractions, giving intrauterine pressures of 50-100mmHg, 10mmHg between contractions, and these contractions retract lower uterine upwards to allow vagina/uterusto become continuous birth canal, as this part doesnt take part in contractions and res tof myometrial cells shorten with each contraction; stage 1 has increasing uterine activity and cervical dilation (to 10cm) with blood/mucous and babies head forced into birth canal, triggering neuroendocrine reflexes to cause positive feedback to maintain labour, lasts 10-12hrs in primagravida and 6-8 in multigravida, and has mild maternal hyperventilation
stage 2 is expulsion of foetus which requires voluntary effort and baby must engage, flex, and rotate; lasts 45-120mins in prima and 15-45mins in multi, maternal breath holding and most dangerous stage for baby; stage 3 is expulsion of placenta (uterus contracts till this happens) which usually takes 10 mins, and women with retained bits of placenta at risk of post-partum haemorrhage; light-dark cycle, food supply, and infection influence timing of delivery
strong uterine contractions prevent postpartum H+ with oxytocin to mother once shoulders through to stimulate this, or induce endogenous release through suckling/nipple stimulation; 500ml blood lost in normal delivery, 1000ml in caesarean; uterus takes 6 weeks to regress to non-pregnant size and vasculature may not fully return to normal, explaining why subsequent pregnancies usually have higher birthweights
maternal: increased CO/mABP with danger of rupture of berry aneurysms (at eg circle of willis), mostly this comes from pain/anxiety with epidural helping to minimise rise; foetal: periods of hypoxaemia as placental bloodflow cut off during contraction, deceleration in HR during contraction is autonomic response to raised intracranial pressure
the booking visit
should be prior to 10 weeks, can be w midwife
height, weight, and baseline blood pressure should be obtained as early in pregnancy as poss
record all previous pregnancies inc duration of gestation + miscarriages and terminations as well as antenatal complications, duration and onset of labour, presentation and method of delivery, birth weight and gender of each infant; also condition of each infant at birth and if eg special care needed; any complications of puerperium inc vte, h+, trauma, infection, difficulty breastfeeding
FBC at first visit and repeated at 28 and 34-36 weeks, give fe supplements if deficient; determine blood group and screen for anti rbc antibodies, and rh antibodies in rh- women; also standard to give anti-d Ig proph at 28 and 34 weeks to rh- women
screening for syphillis, hep b&c, HIV should be done; thalassaemia and sickle cell if hish risk ethnicity; group b strep swab form vagina/rectal oft done but not universal; asymp bacteriuria also oft done to treat early before uti/asc pye devs
glucose tolerance test can be used to screen for gestational DM and is either done universally or only for those with inc’d risk depending on jurisdiction
