Paediatric Neonatology Flashcards

1
Q

Main Issue in neonatal Resuscitation

A

hypoxia

baby has large sa: weight ratio= get cold very easy

baby born wet, lose heat rapid

baby born through meconium = in mouth/airway

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2
Q

explain hypoxia in neonates at birth

issues etc

A

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

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3
Q

principles of neonatal resuscitation

A
  1. dry baby and maintain temp
  2. assess tone , resp rate, hr
  3. 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.
  4. reassess -chest movements
  5. 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)

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4
Q

ways to get baby warm

how does this help

neonatal resus

A

vigorous drying stimulates breathing

warm delivery rooms
heat lamp

if under 28 weeks place in plastic bag while still wet - manage under heat lamp

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5
Q

what is the APGAR score and when is it calculated

score total out of?

findings?

A

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

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6
Q

when performing inflation breaths, what should be used in term, pre term babies

aim of ox sat

A

air - near term

air and oxygen - pre-term babies.

aim for gradual rise, not exceed 95%

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7
Q

what is delayed umbilical cord clamping

benefits

drawbacks

how much should you delay in uncompromised neonate.

A

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

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8
Q

What is respiratory distress syndrome?
caused by?

affects who

when?

cxr sign

A

premature neonates

born before lungs start producing enough surfactant.

below 32 weeks

ground glass appearance

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9
Q

pathophysiology of respiratory distress syndrome

A

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

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10
Q

how would you manage respiratory distress syndrome?

mother

premature neonate

A

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
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11
Q

comps of resp distress syndrome

short term

long term

A

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

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12
Q

What is bronchopulmonary dysplasia?

affects who

what other condition do they have

diagnosis made how?

tx?

A

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

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13
Q

features of bronchopulmonary dysplasia?

A

low ox sats

increased work of breathing

poor feeding and weight gain

crackles and wheezes on chest auscultation

increased susceptibility to infection

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14
Q

how to prevent bronchopulmonary dysplasia?

A

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

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15
Q

how would you manage bronchopulmonary dysplasia?

what do you have to protect against?
how to treat?

A

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.

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16
Q

risk factors of respiratory distress syndrome

A

male
diabetic mother
c section
second born of premature twins

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17
Q

clinical features of resp distress syndrome pt

A

tachynpnoea
intercostal recession
expiratory grunting
cyanosis

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18
Q

what is meconium aspiration syndrome?

more common in?

can cause?

higher rates if hx of ?

A

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

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19
Q

causes of HIE

A

anything that leads to asphyxia - deprivation of oxygen

20
Q

What is gastroschisis and exomphalos

A

examples of congenital visceral malformations

21
Q

what is gastroschisis and how would you manage

A

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

22
Q

what is exomphalos

give 3 associations

give mx

A

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.

23
Q

How do the TORCH infections present

A

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

24
Q

How can TORCH infections be investigated?

A

Serology on maternal and infant blood (IgM, IgG)
PCR testing for viral DNA
USS (Fetal abnormalities - hydrocephalus, calcifications)
Amniocentesis

25
Q

What is necrotising enterocolitis?

A

Bowel disorder affecting premature neonates. Part of the bowel becomes necrotic and can lead to perforation, peritonitis, shock and sepsis

26
Q

RF for necrotising enterocolitis

A

Premature or very low birth weight
Formula feeds
Respiratory distress/assisted ventilation
Sepsis
Patent ductus arteriosus

27
Q

How does necrotising enterocolitis present

A

Feeding intolerance
Green bilious vomit
Distended tender abdomen
Absent bowel sounds
Blood in stools

28
Q

How is necrotising enterocolitis investigated?

A

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

29
Q

Mx of necrotising entercolitis and complications of short bowel syndrome

A

NBM
IV fluids
TPN
ABx

Surgical emergency - short bowel syndrome is a complication.

30
Q

complications of necrotising enterocolitis

A

Perforation and peritonitis
Sepsis
Strictures
Abscess
Recurrence

31
Q

What is group b strep

A

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)

32
Q

How is GBS prevented and what are its complications?

A

Recto-vaginal swab for GBS at 35-37 weeks

Intrapartum antibiotics for at risk or confirmed

Neurodevelopmental impairment (esp meningitis)
High mortality (10-20%)

33
Q

rf for listeria infection

A

Listeria monocytogenes (Gram positive rod)

Maternal consumption of contaminated food (Unpasteurised dairy, deli meat, smoked seafood)
Immunocompromised
Preterm birth

34
Q

Ix of listeria infection

A

Blood culture
CSF culture
Placental/cord culture

CSF analysis shows elevated protein, low glucose, increased WBC (pleocytosis)

35
Q

Effect of listeria on child

A

Sepsis, meningitis, pneumonia

36
Q

Mx of listeria

A

IV Amoxicillin or ampicillin

+ Gentamicin

37
Q

What is a cleft lip and palate

A

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

38
Q

Problems caused by cleft lip and palate

A

Feeding: Orthodontic devices
Speech: speech therapy
Increased risk of otitis media

39
Q

Management of cleft lip and palate

A

Lip repaired first first week-3 months
Palate repaired 6-12 months

40
Q

What are the types of bowel atresia and oesophageal atresia

A

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

41
Q

Presentation of bowel vs oesophageal atresia

A

Bowel
- Bilious vomiting
- Abdominal distension
- Failure to pass meconium

Oesophageal
- Drooling/choking post birth
- Difficulty swallowing
- Coughing, gagging, cyanosis
- Abdo distension

42
Q

Ix in bowel and oesophageal atresia

A

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

43
Q

What atresia is polyhydramnios most common in

A

Oesophageal - impaired swallowing of amniotic fluid.

Also seen in duodenal atresia, less frequently in other bowel atresias.

44
Q

Associations with bowel atresia

A

Downs (duodenal)
CF (jejunal/ileal atresia)

45
Q

Association with oesophageal atresia

A

VACTERL abnormalities
- Vertebral
- Anorectal
- Cardiac
- Transoesophageal
- Renal
- Limb

Downs, Trisomy 18

46
Q

Immediate management of the atresias + Long term complications

A

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

47
Q
A