Paediatric Neonatology Flashcards
Main Issue in neonatal Resuscitation
hypoxia
baby has large sa: weight ratio= get cold very easy
baby born wet, lose heat rapid
baby born through meconium = in mouth/airway
explain hypoxia in neonates at birth
issues etc
normal labour and birth leads to hypoxia
when contractions happen placenta cant carry out normal gas exchange= hypoxia.
extended hypoxia , leads to anaerobic rep = drop in fetal hr = bradycardia
further hypoxia= reduced gcs = drop in resp effort. if to the brain = hypoxic-ischaemic encephalopathy = can lead to cerebral palsy
principles of neonatal resuscitation
- dry baby and maintain temp
- assess tone , resp rate, hr
- if gasing or not breathing give 5 inflation breaths. ( 2 cycles of 5 breaths 3 seconds each to stimulate breathing and hr) if not 30secs ventilation breaths. if no then chest compressions.
- reassess -chest movements
- if hr not improving and less than 60bpm start compressions and ventilation breaths at a rate of 3:1.
iv drugs and intubation - if risk of hypoxic-ischaemic encephalopathy
(inflation breaths different from ventilation breaths. its for keeping pressure to open lungs)
ways to get baby warm
how does this help
neonatal resus
vigorous drying stimulates breathing
warm delivery rooms
heat lamp
if under 28 weeks place in plastic bag while still wet - manage under heat lamp
what is the APGAR score and when is it calculated
score total out of?
findings?
neonatal resus
1,5,10 mins whilst resus continues.
indicator for progress
/10
each topic 0,1,2
appearance - blue/pale centrall, blue extremeties, pink
pulse - absent, under 100, over 100
grimace - no response, little, good
activity - floppy, flexed arms/legs, active
respiration - absent, slow/irregular, strong/crying
when performing inflation breaths, what should be used in term, pre term babies
aim of ox sat
air - near term
air and oxygen - pre-term babies.
aim for gradual rise, not exceed 95%
what is delayed umbilical cord clamping
benefits
drawbacks
how much should you delay in uncompromised neonate.
a lot of fetal blood vol in placenta after birth. if delayed it can enter baby circulation. - placental transfusion
improved haemoglobin, iron, bp and reduced intraventricular haemorrhage and necrotising enterocolitis.
neonatal jaundice- need more photo therapy
at least 1 minute
What is respiratory distress syndrome?
caused by?
affects who
when?
cxr sign
premature neonates
born before lungs start producing enough surfactant.
below 32 weeks
ground glass appearance
pathophysiology of respiratory distress syndrome
inadequate surfactant = high surface tension within alveoli.
leads to atelactasis - lung collapse because its harder for alveoli and lungs to expand. =
inadequate gas exchange = hypoxia, hypercapnia, resp distress
how would you manage respiratory distress syndrome?
mother
premature neonate
antenatal steroids - dexamethasone - give to mother with suspected/confirm preterm labour so you get more surfactant production.
reduces incidence of severe resp distress syndrome.
premature neonate:
- intubation and ventilation - assist breathing
- endotracheal surfactant - artificial delivered into lungs via endotracheal tube.
- continuous positive airway pressure (cpap) - via nasal mask helps keep lungs inflated whilst breathing
- supplementary ox - 91-91% in preterm neonates
comps of resp distress syndrome
short term
long term
pneumothorax
infection
anpoea
intraventricular haemorrhage
pulmonary haemorrhage
necrotising entercolitis
chronic lung disease of prematurity
retinopathy of prematurity - more often more severly in neonates with rds
neurological hearing and visual impairment
What is bronchopulmonary dysplasia?
affects who
what other condition do they have
diagnosis made how?
tx?
chronic lung disease of prematurity.
premature babies - before 28 weeks gestation
these babies have respiratory distress syndrome and need oxygen therapy or intubation and ventilation at birth.
diagnosis : cxr changes
they require ox therapy after they reach 36 weeks gestation
features of bronchopulmonary dysplasia?
low ox sats
increased work of breathing
poor feeding and weight gain
crackles and wheezes on chest auscultation
increased susceptibility to infection
how to prevent bronchopulmonary dysplasia?
give corticosteroids – betamethasone to mothers that show sign of premature labour at less than 36 weeks gestation.
neonate born:
- using CPAP rather than intubation and ventilation
- use caffeine to stimulate resp effort
- not over oxygenating with supplementary oxgyen
how would you manage bronchopulmonary dysplasia?
what do you have to protect against?
how to treat?
do formal sleep study and assess ox saturations during sleep.
can discharge baby on low dose ox at home - 0.01 litres per min via nasal canula. follow up to wean ox level over 1st yr of life
protect against respiratory syncytial virus -RSV : reduce risk of severity of bronchiolitis.
monthly injections of monoclonal antibody against virus - palivizumab.
risk factors of respiratory distress syndrome
male
diabetic mother
c section
second born of premature twins
clinical features of resp distress syndrome pt
tachynpnoea
intercostal recession
expiratory grunting
cyanosis
what is meconium aspiration syndrome?
more common in?
can cause?
higher rates if hx of ?
resp distress in newborn due to meconium in trachea.
occurs in immediate neonatal period.
more common in post term deliveries.
can cause severe respiratory distress.
maternal htn , pre-eclampsia, chorioamnionitis, smoking or substance abuse
causes of HIE
anything that leads to asphyxia - deprivation of oxygen
What is gastroschisis and exomphalos
examples of congenital visceral malformations
what is gastroschisis and how would you manage
congenital defect in anterior abdominal wall just lateral to umbilical cord
vaginal delivery - attempt
newborns : theratre asap after delivery : within 4 hrs
requires urgent correction
what is exomphalos
give 3 associations
give mx
omphalocoele
abdo contents protrude through anterior abdo wall but covered in amniotic sac formed by amniotic membrane and peritoneum.
beckwithe-wiedemann
downs
cardiac/kidney malformations
c-section- reduce risk of sac rupture
staged repair - lack of space/high intra-abdo pressure so hard to do straight away. you get resp comps if you do straight away.
sac granulates and epithelialise over weeks/months. forms shell. infant grows to point where sac contents fit abdo cavity. - shell removed and abdo closed.
How do the TORCH infections present
T: Chorioretinitis, hydrocephalus, intracranial calcifications
R: Cataracts, Congenital Heart defects, sensorineural hearing loss, developmental delays
CMV: Sensorineural hearing loss, microcephaly, jaundice, hepatosplenomegaly
HSV: Vesicular skin lesions, encephalitis
How can TORCH infections be investigated?
Serology on maternal and infant blood (IgM, IgG)
PCR testing for viral DNA
USS (Fetal abnormalities - hydrocephalus, calcifications)
Amniocentesis
What is necrotising enterocolitis?
Bowel disorder affecting premature neonates. Part of the bowel becomes necrotic and can lead to perforation, peritonitis, shock and sepsis
RF for necrotising enterocolitis
Premature or very low birth weight
Formula feeds
Respiratory distress/assisted ventilation
Sepsis
Patent ductus arteriosus
How does necrotising enterocolitis present
Feeding intolerance
Green bilious vomit
Distended tender abdomen
Absent bowel sounds
Blood in stools
How is necrotising enterocolitis investigated?
X ray
- Dilated bowel loops
- Bowel wall oedema
- Pneumatosis intestinalis (intramural gas)
- Pneumoperitoneum (free gas in peritoneal cavity - implies perforation)
- Air both inside and outside bowel wall
Mx of necrotising entercolitis and complications of short bowel syndrome
NBM
IV fluids
TPN
ABx
Surgical emergency - short bowel syndrome is a complication.
complications of necrotising enterocolitis
Perforation and peritonitis
Sepsis
Strictures
Abscess
Recurrence
What is group b strep
Strep agalctiae. Transferred from mother to baby during labour. Harmless in maternal vagina but can cause serious infection; Sepsis, pneumonia, respiratory distress, meningitis
Late onset (7-89 days): Meningitis, bacteraemia, focal infections (bone joint tissue)
How is GBS prevented and what are its complications?
Recto-vaginal swab for GBS at 35-37 weeks
Intrapartum antibiotics for at risk or confirmed
Neurodevelopmental impairment (esp meningitis)
High mortality (10-20%)
rf for listeria infection
Listeria monocytogenes (Gram positive rod)
Maternal consumption of contaminated food (Unpasteurised dairy, deli meat, smoked seafood)
Immunocompromised
Preterm birth
Ix of listeria infection
Blood culture
CSF culture
Placental/cord culture
CSF analysis shows elevated protein, low glucose, increased WBC (pleocytosis)
Effect of listeria on child
Sepsis, meningitis, pneumonia
Mx of listeria
IV Amoxicillin or ampicillin
+ Gentamicin
What is a cleft lip and palate
1in1000. Most common congenital abnormality affecting orofacial.
Polygenic inheritance
Maternal antiepileptic use increases risk
Lip results from failure of fronto-nasal and maxillary processes to fuse
Cleft palate from failure of palatine processes and nasal septum to fuse
Problems caused by cleft lip and palate
Feeding: Orthodontic devices
Speech: speech therapy
Increased risk of otitis media
Management of cleft lip and palate
Lip repaired first first week-3 months
Palate repaired 6-12 months
What are the types of bowel atresia and oesophageal atresia
Bowel (usually small bowel)
- Duodenal, Jejunal, Colonic
Oesophageal
- Oesophageal atresia with tracheosophageal fistula (TEF) most common
- Can be isolated atresia
- Results in a blind pouch or disconnected oesophagus
Presentation of bowel vs oesophageal atresia
Bowel
- Bilious vomiting
- Abdominal distension
- Failure to pass meconium
Oesophageal
- Drooling/choking post birth
- Difficulty swallowing
- Coughing, gagging, cyanosis
- Abdo distension
Ix in bowel and oesophageal atresia
Prenatal USS
- Bowel: Polyhydramnios and bowel loops.
- Oesophageal: Polyhydramnios
X ray:
- Bowel: Dilated bowel loops. Double bubble sign in duodenal.
- Oesophageal: Confirm diagnosis - blind ending oesophagus. Air in stomach if TEF
OA will block NG tube being passed to stomach
What atresia is polyhydramnios most common in
Oesophageal - impaired swallowing of amniotic fluid.
Also seen in duodenal atresia, less frequently in other bowel atresias.
Associations with bowel atresia
Downs (duodenal)
CF (jejunal/ileal atresia)
Association with oesophageal atresia
VACTERL abnormalities
- Vertebral
- Anorectal
- Cardiac
- Transoesophageal
- Renal
- Limb
Downs, Trisomy 18
Immediate management of the atresias + Long term complications
Nasogastric decompression and fluid resuscitation (+prevention of aspiration in oesophageal)
Oesophageal: GORD, Oesophageal strictures, TEF
Bowel: Short bowel syndrome (if resected), malabsorption, need for nutritional support
