Neonatology Flashcards

1
Q

PHYSIOLOGY
i) which type of cells produce surfactant? between which weeks gestation do these produce surfactant? what do premature babies therefore have?
ii) which two hormones are released in the baby in response to the stress of labour and contribute to stim respiratory effort?
iii) what causes the closure of foramen ovale? what is it called when its closed?
iv) what are required to keep ductus arteriosus open? what causes a drop in these? what is DA called when it closes?

A

i) type II alvelolar cells > surfactant aat 24-34 weeks gestation
prematuure - problems assoc with reduced pulm surfactant
ii) adrenaline and cortisol
iii) first breath expands alveoli > dec pulm vasc resis > drop in pressure in RA (LA pressure > RA) which squashes septum > closure of FO and becomes fossa ovalis
iv) prostaglandins keep DA open > increase in O2 blood causes drop in PGs > closure of DA
becomes ligamentum arteriosum

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2
Q

BIRTH INJURIES
i) what is caput succedaneum? does it cross suture lines? does it require treatment?
ii) what is a cephalohaematoma? what causses it? does it cross suture lines? how may skin appear? does it usually req tx? which two complications should baby be monitored for?
iii) what is facial nerve injury typically associated with? how long does it usually take for function to return?

A

i) caput > oedema collects on the scalp outside the periosteum (due to pressure to a spec are of scalp during prolonged/traumatic/instrumentaal delivery)
crosses the suture lines asa it lies outside the periosteum
doesnt req tx and resolves in a few days
ii) cephalohaematoma = collection of blood between skull and periosteum (damage to bv in delivery)
does not cross suture lines as below the periosteum > may caause discolouration of skin
usually resolves in a few months without tx
risk of anaemia and jaundice due to bdown of blood that collects > release bilirubin
iii) facial nerve injury often assoc with forceps delivery
weakness of facial nerve on one side > spont resolves in a few months

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3
Q

BIRTH INJURIES CONTINUED
i) which nerves are affected in erbs palsy? name three things it can be associated with?
ii) what appearance of the arm does this lead to? does it need tx?
iii) name three things a fractured clavicle can be assoc with? name three things that may be seen on newborn exam?
iv) how can it be confirmed? how is it managed? what is the main complication?

A

I) injury to C5/C6 nerves in the brachial plexus during birth
assoc with shoulder dystocia. traumatic/instrument delivery, large birth weight (macrosomia)
ii) leads to waiters tip appearance of arm - internal rotated shoulder, ext elbow, flexed wrist facing back, lack of movement in affected arm
function usually returns spont in a few months (may need neurosurgical input if it does not)
iii) assoc with shoulder dystocia, traumatic/instrumental delivery/large birth weight
newborn exam: lack of move/assym of movement in affected arm, assym shoulders with affected lower thaan normal, pain/distress on movememnt of arm
iv) confirm with US or xray
mx by immobilising the arm (may not need to do anything)
complication - injury to brachial plexus > nerve palsy

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4
Q

HYPOXIC ISCHAEMIC ENCEPHALOPATHY
i) what is it caused by? what can it lead to?
ii) name four things in the perinatal/intrapartum period that can lead to suspicion of HIE?
iii) name three causes? what staging system is used?
iv) what % of mild/mod/severe dev ceb palsy?how is it managed?
v) when by therapeutic hypothermia be used? what does it inovolve? how long does it occur for? what is the benefit?

A

i) occurs in neonates as a result of hypoxia during birth
can lead to permanent change eg ceb palsy
ii) acidosis (<7) on umbilical artery blood gaas, poor apgar score, evidence of multi organ failure
iii) anything that leads to asphyxia (depriv of oxygen) eg maternal shock, intrapartum haemmorhage, prolapsed cord (cord compression during birth), nuchal cord (cord wrapped around baby neck)
sarnat staging system (mild/mod/severe)
iv) mild - normal prognosis
mod - 40% ceb palsy
severe - 90% ceb palsy
manage w supportive care - resuss, vent, circ support, nutrition, acid base balance
v) actively cooling core temp in ICU using cooling blanket and cooling hat
temp target of 33-34 degrees for 72 hours then gradually warm baby overr 6 hours
benefit is to reduce inflammation and neuron loss after acute hypoxic injury
reduces risk of ceb paalsy, dev delay, learning disability, blind, death

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5
Q

PREMATURITY
i) what is it defined as? name four associations with prematurity?
ii) name two ways birth can be delayed?
iii) which calcium channel blocker can be given to delay labour? when can corticosteroids can be given and what do they do?
iv) what is IV Mg sulphate for and what can it help protect? what is the benefit of cord clamping/cord milking?
v) name four issues that may arise in early life and three long term effects of prematurity?

A

i) birth before 37 weeks
assoc with social deprivation, smoking, alcohol, drugs, over or underweight, maternal co-morbid, twins, FH
ii) prophylactic vaginal progesterone (suppository in vagina discourage labour)
prophylactic cervical cerclage (suture in cervix to hold it closed)
iii) tocolysis with nifedipine
maternal CS caan be offered before 35 weeks to reduce neonate morbid and mortal
iv) Mg sulphate before 34 weeks to protect baby brain
delayed cord clamping - increases circ blood vol/Hb to baby
v) early - resp distress synd, hypothermia, poor feeding, hypogly, apnoeaa, jaundice, retinopathy of premat, nec enterocolitis
late - chronic lung disease of premat, leaarning difficulties, suscep to infections, hearing/visual impair/ceb palsy

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6
Q

APNOEA OF PREMATURITY
i) what is apnoea? what is it often accompanied by?
ii) what does it occur due to? what may apnoea be a sign of? (4)
iii) how is apnoea monitored in premature babies? what is used to prompt the baby to restart breathing?
iv) what may be given IV to prevent apnoea in babies with recurrent episodes

A

i) periods where breathing stops spontaneously for >20s
or shorter periods with oxygen desat or bradycardia
often accompanied by periods of bradycardia
ii) occ due to immaturity of the ANS that controls resp and HR
sign of - infection, anaemia, airway obstruc, CNS pathol eg seizure, GORD, neonatal abstinence synd
iii) apnoea monitors that beep when it is occuring
can use tactile stim to restart breathing
iv) can give IV caffiene to prevent apnoea and brady in babies with recurrent episodes

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7
Q

RETINOPATHY OF PREMATURITY
i) who does it affect? (2) what causes it? name three things it can cause
ii) when does retinal bv dev start? when does it end? where to bv grow out from and what are they stimulated by? what removes the stim for normal blood vessel dev?
iii) whaat causes excessive blood vessel production (neovasc) in the retina? what may then happen to these vessels?
iv) what is contained in zone 1 of retina? in zone 2? in zone 3?

A

i) preterm (pre 32 weeks) and low birth weight babies
caused by abnormal blood vessel development in the retina > scarring, retinal detachment and blindness
ii) bv dev startss at 16 weeks aand complete by 37-40 weeks
bv grow from middle of retina outwards and is stimulated by hypoxia (normal in pregnancy)
when retina is exposed to high oxygen conc - normal bv dev stops
iii) when the hypoxic environment recurs the retina responds by maaking excess bv (neovasc) as well as scar tissue
vessels may then regress and leave the retina with no blood supp
scar tissue can lead to retinaal detachment
iv) zone 1 - optic nerve and macula
zone 2 - edge of zone 1 to ora serrate (pigmented border between retina and cilliry body)
zone 3 - outside ora serrata

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8
Q

RETINOPATHY OF PREMATURITY SCREENING AND MX
i) what is stage 1 disease? what is stage 5? name two things that may be found in ‘plus disease’
ii) who is screened? (2) when is screening done (gestational age) for babies born before 27 weeks and when is it done for babies born after 27 weeks?
iii) how often is screening done? when does screening end?
iv) what is looked at on examination? (2)
v) what does treatment aim for? what is first line? name two other things that can be done? what can be done if retinal detachment occurs

A

i) stage 1 (slight abnormal vessel growth)
stage 5 (complete retinal detachment)
plus diseasae - tortuous vessels or hazy vitreous humour
ii) babies born before 32 weeks or under 1.5kg screened by opthalmologist
pre 27 weeks - screen at 30-31 weeks gestational age
post 27 weeks - screen 4-5 weeks of age
iii) screen every 2 weeks - stop once retinal vessels enter zone 3 (usually around 36 weeks ges)
iv) O/E - look at all retinal areas - monitor all retinal vessels and look for plus diseaase
v) tx aaims to target aareas of the retina to stop new bv developing
1st line - transpupillary laser photocoagulation to halt/reverse neovasc
may also do cryotherapy or inject VEGF inhibitors
surgery if retinal detachment occurs

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8
Q

NECROTISING ENTEROCOLITIS
i) who does it affect? what happens? how quickly does it need to be treated? name three complications that can happen if left untreated?
ii) name four factors that increase the risk of developing it?
iii) name four ways it may present? name three bloods that should be done? what will blood gas show
iv) what is the investigation of choice for dx? name three things this may show

A

i) affects premature neonates > part of the bowel becomes necrotic
life threatening emergency > death of bowel leads to perforation, peritonitis and shock
ii) very low BW or very premature, formula feeding, resp distress/assisted ventilation, sepsis, patent ductus arteriosis
iii) px with intolerance to feeds, vomiting (green bile), generally unwell, distended/tender abdo, absent bowel sounds, blood in stool
bloods - FBC (low plats and WCC), CRP (inflam), blood culture for sepsis
cap blood gas - metabolic acidosis
iv) abdo xray > dilated loops of bowel, bowel wall oedma
pneumatosis intestinalis - gas in bowel wall
pneumoperitoneuum - free gaas in peritoneal cavity (indicates perf)

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9
Q

NEC MX
i) what should all neonates with suspected NEC be? name three things that need to be given
ii) what can be done to drain fluid and gas from stomach/intestines
iii) what needs to be done immediately?
iv) name four complications

A

i) nil by mouth
need IV fluid, TPN and antibiotics
ii) NG tube insertion
iii) refer to neonatal surgical team (some will recover with medical tx but some may need sx to remove dead bowel)
iv) perf/peritonitis, sepsis, death, strictures, abscess, long term stoma, short bowel syndrome post surgery

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10
Q

NEONATAL ABSTINENCE SYNDROME
i) what is it? name four substances that can cause it?
ii) withdrawal from which substances occ between 3-72hrs after birth? (4) withdrawal from which substances occ 24hrs to 21d after birth? (2)
iii) name three CNS symptoms? name three vasomotor/resp symptoms? name three metab/gastro symptoms?

A

i) withdrawal symptoms that happen in neonates of mothers that used substances in pregnancy
opiates, methadone, benzos, cocaine, amphetamines, nicotine/cannabis, alcohol, SSRIs
ii) opiates/diazepam/SSRIs/ETOH 3-72hrs
other benzos and methadone 24hrs to 21d
iii) CNS - irritable, increased tone, high pitched cry, not settled, tremors, seizures
VM/resp- yawning, sweating, unstable temp/pyrexia, tachypnoea
metab/gastro - poor feeding, vomiting, hypogly, loose stools with sore nappy area

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11
Q

NEONATAL ABSTINENCE SYNDROME MX
i) how are babies monitored? for how long? how long are they monitored for SSRIs?
ii) how can substance levels be tested in neonate? in what environment should they be supported?
iii) name a medical tx for mod-severe symptoms in opiate withdraw? for non opiate withdraw? does SSRI withdrawal benefit from medical tx?
iv) name three other things that should be tested for?

A

i) NAS chart for at least 3 days (48hrs for SSRIs) for withdrawal symptoms
ii) urine sample
supoort in a quiet dim environment with gentle handling and comforting
iii) opiates - oral morphine sulphate
non opiates - oral phenobarbitone
SSRI withdraw - dont get medical tx
iv) also test for hep B, hep C and HIV

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12
Q

FETAL ALCOHOL SYNDROME
i) when are effects of alcohol the greatest?
ii) name three things it can lead to?
iii) what is FAS? name four principle features seen?

A

i) first 3 months of pregnancy
ii) miscarriage, small for dates, preterm delivery
iii) FAS = effects and characs that are found in children of mothers with significant alcohol intake
microcephaly, thin upper lip, smooth/flat philtrum, short palpebral fissure (short width of eyes)

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13
Q

CONGENTIAL CONDITIONS
i) what causes congenital rubella? when is the highest risk? what should be done if a women does not have antibodies to rubella when tested? name three signs
ii) do most cases of CMV in pregnancy cause congenital CMV? name four features of congenital CMV
iii) what are the classic triad of symptoms for congenital toxoplasmosis?
iv) how is zika virus spread? (2) name three features of congenital zika syndrome?

A

i) caused by maternal infection with rubella during pregnancy - highest risk at first 3 months
planning to be preg > MMR
during preg - cant have MMR as live so wait til after birth
congenital cataracts, congen heart disease, learning disability, hearing loss
ii) most cases dont lead to C CMV
fetal growth restriction, microcephaly, hearing loss, vision loss, learning disability, seizure
iii) intracranial calcification, hydrocephalus, chorioretinitis
iv) spread via aedes mosquitos and sexually
microcephaly, fetal growth restriction, intracranial abnorms eg ventriculomegaly or cerebellar atrophy

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14
Q

CONGENITAL VARICELLA SYNDROME
i) name three things VZV can lead to in pregnancy? which Ig levels can be tested if unsure whether mum has has chickenpix?
ii) how should a woman exposed to chickenpox in pregnancy who is not immune be treated? how quickly should this be given?
iii) how may a pregnant woman be treated if chickenpox rash starts in pregnancy?
iv) when does congential varicella syndrome occur? name four typical features

A

i) VZV > severe case in mother eg pneumonitis/hepatitis/encephalitis
fetal varicella syndrome, severe neonatal varicella infection
check IgG levels > if positive then safe
ii) exposure and not immune > IV varicella immunoglobilin within 10 days of exposure
iii) rash > treat with oral aciclovir if they px within 24 hours and >20 weeks
iv) CVS occ when there is infection in first 28 weeks of preg (1% of chickenpox cases dev it)
fetal GR, microcephaly/hydrocephalus, scars/skin change assoc with dermatomes, limb hypoplasia (underdev), cataracts and inflam (chrioretinitis)

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15
Q

SUDDEN INFANT DEATH SYNDROME
i) when does it usually occur?
name four RFs
ii) name four things that can reduce the risk
iii) which charity helps support affected families?
iv) what is the CONI team?

A

i) in first six months of life
RFs - prematurity, low birth weight, smoking during pregnant, male
ii) baby on back when unsupervised, head uncovered, feet at foot of bed to prevent sliding, clear cot of toys and blankets, avoid smoking, comfortable room temp 16-20 degrees
iii) lullaby trust helps support families
iv) CONI team is care of next infant after SIDS - extra support/home visits/resus training

16
Q

NEONATAL JAUNDICE
i) what is it caused by in the blood? between which time is ir normal for babies to be jaundiced? when is jaundice always pathological?
ii) name four causes related to increased production? name four causes related to decreased clearance?
iii) what exaggerates jaundice in premature babies? what complication is there increased risk of?
iv) are breastfed babies more or less likely to be jaundiced? why?

A

i) high levels of bilirubin (dec bdwon or inc production)
normal between 2-7 days of age
pathological in first 24hours - often caused by neonatal sepsis
ii) inc prod - haemolytic disease if newborn, ABO incompat, haemmorhage, cephalohaematoma, polycythaemia, sepsis/DIC, G6PD defic
dec bdown - premature, breast milk jaundice, neonatal cholestasis, extrahep biliary atresia, endocrine, gilbert syndrome
iii) premature - immature liver > inc risk of complications eg kernicterus = brain damage due to high bilirubin
iv) more likely - components of breast milk can inhibit bilirubin processing, more likely to be dehydrated > slow passage of stools > more bili absorbed by intestines

17
Q

HAEMOLYTIC DISEASE OF THE NEWBORN
i) what is it caused by? what may be seen in the skin of the neonate?
ii) what initiates the disease? (antibody production)
iii) what Hb levels will be seen? what bilirubin levels will be seen?

A

i) caused by haemolysis due to incompatibility of rhesus antigens on RBC surface between mum and baby > jaundice
ii) mother who is rhesus negative and baby is positive > mum produces ABs (stay in system)
in subsequent pregnancies antibodies can cross placenta and attack baby RBC if positive > haemolysis
iii) low Hb and high bilirubin

18
Q

JAUNDICE CONTINUED
i) what is classed as prolonged jaundice in full term babies? in premature babies? name three conditions that can cause this
ii) name three bloods that should be done? what special tests? (2) what deficiency should be tested for?
iii) what decides whether treatment should be started? what is done if there are exremely high bilirubin levels?
iv) what is the usual first line treatment? how does it work? what is rebound bilirubin?
v) what is kernicterus? what is it caused by? how does it present? (3) name three permanent damages?

A

i) >14d in full term babies
>21d in premature babies
can be caused by billiary atresia, hypothyroid oe G6PD deficiency
ii) do FBC, conjugated bilirubin, blood type testing (ABO incompat), direct coombs test (haemolysis), thyroid function
blood and urine cultures if infection is suspected
test for G6PD deficiency
iii) plot total bilirubin on threshold charts specific for gestational age of the baby
decides whether phototherapy should be started or exchange transfusion in extreme cases
iv) first line is phototherapy - converts unconj bili to isomers that can be excreted in bile/urine without conj by the liver
shine blue light on the babys skin
measure rebound bilirubin 12-18 hours post therapy to make sure levels have not risen up again
v) kernicterus is brain damage caused by excessive bili levels
bili > BBB > damage to CNS
presents with less responsive, floppy, drowsy, poor feeding
permanent damge - ceb palsy, learning disability, deafness
(rare as jaundice is usually treated effectively)