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3a > Paed:Neonates > Flashcards

Paed:Neonates Flashcards

1
Q

How does the heart adapt to ex-utero life?

A
  • closure of foetal shunts
  • perfusion of lungs
  • decrease in pulmonary artery pressure
  • increase in systemic BP
  • increase in CO
  • foetal lung fluid removed
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2
Q

How does the resp system adapt to ex-utero life?

A
  • lungs filled with air
  • surfactant released
  • gas exchange
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3
Q

What is the implantation phase?

A

Weeks 1-2 following missed period

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4
Q

What is the embryo stage?

A

up to 8-9 weeks (by end of this stage you are fully formed)

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5
Q

What is the foetus stage?

A

from 12-16 weeks movements felt by mother, all systems present + functioning to varying degrees, lasts 4-6 weeks and is mainly all growth (mostly fat.)

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6
Q

What are the low birth weight categories?

A

Very low: <1500g
Extremely low: <1000g
Incredibly low: <750g

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7
Q

What are the infant benefits of breast feeding?

A

less infection, decreased gastroreflux, less immune drives/alergic disease, decreased risk of : NEC, SIDS, inguinal hernia, higher IQ

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8
Q

What are the maternal benefits of breast feeding?

A

Reduces cancer: breast, uterine, ovarian, endometrial
Improved health: less PPH, depression, osteoporosis
Promotes postpartum weight loss
Delays fertility
Less medical + food expense

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9
Q

How do premature babies feed and why?

A

IV fluids/parental nutrition because they cannot yet suckle

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10
Q

What is necrotising enterocolitis (NEC)?

A

A bacteria invasion of ischaemic bowel wall, usually preterm infants who are fed cow’s milk formula.

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11
Q

What are the clinical signs of NEC?

A

Stops tolerating feeds, bile-stained vomiting, distended abdomen + pain, stools with fresh blood, shock

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12
Q

What would you see on X-ray for NEC?

A

Distended loops of bowel + thickening of bowel wall with intramural gas + may be gas in portal tract.

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13
Q

What is the treatment of NEC?

A 
Stop oral feeding
Broad spec Abs
Parenteral nutrition
Artificial ventilation + circulatory support
Surgery if perforated bowel
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14
Q

Complications of NEC

A

Bowel perforation
Strictures
Malabsorption

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15
Q

What is retinopathy of prematurity?

What causes it?

What to do if there are high risk changes?

A

Arrest of normal vascular growth of the developing blood vessels at the junction of the vascular + non-vascularised retina. Vascular proliferation > retinal detachment, fibrosis + blindness.

Caused by hyperopic insult.
Laser therapy for high risk changes.

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16
Q

Why do >50% of all newborn infants become jaundiced?

A
  • marked physiological release of Hb from RBC breakdown because of high Hb conc at birth
  • red cell life Spain of newborn infants is 70 days compared to 120 in adults
  • hepatic bilirubin metabolism is less efficient in first few days of life
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17
Q

Why is neonatal jaundice important?

A

May be a sign of another disorder (e.g. infection, liver disease or haemolytic anaemia.)
Unconjugated bilirubin can deposit in basal ganglia and cause kernicterus.

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18
Q

Causes of unconjugated bilirubin?

A

Haemolysis, prematurity, sepsis, dehydration, hypothyroid, metabolic disease

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19
Q

What can high levels of unconjugated bilirubin cause? Explain it

A

Kernicterus

  • encephalopathy due to deposition of unconjugated bilirubin in basal ganglia + brainstem nuclei .
  • there is excess albumin-binding capacity so it passes by itself through BBB
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20
Q

Where does unconjugaed bilirubin deposit?

A

Basal ganglia + brainstem nuclei

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21
Q

How does kernicterus present?

A

Lethargy, poor feeding, irritability, increased muscle tone (opsithotonos), seizures and coma

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22
Q

What may develop after kernicterus?

A

LD sensorineural deafness, cerebral palsy

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23
Q

How do you treat kernicterus?

A
  • Phototherapy (blue light, 450nm) which converts unconjugated bilirubin into harmless, was-soluble pigment that is excreted in the urine.
  • Exchange transfusion (remove blood + replace with donor)
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24
Q

What causes high levels of conjugated bilirubin?

A

Prolonged parenteral nutrition, NEC, sepsis

high levels not a worry

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25
Q

What bilirubin measurement is classified as clinically jaundiced?

A

80umol/L

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26
Q

What is respiratory distress syndrome? (RDS)

A

Deficiency of surfactant which lowers surface tension. This leads to widespread alveolar collapse and inadequate gas exchange.

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27
Q

Where is surfactant retained?

A

In type 2 pneumocytes of alveolar epithelium

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28
Q

When do alveoli start increasing in number?

A

From 24 weeks (therefore RDS common in premature babies born before 28 weeks)

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29
Q

What are clinical signs of RDS?

A

Tachypnoea >60b/m
Laboured breathing with chest wall recession + nasal flaring
Expiratory grunting
Cyanosis

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30
Q

Why is there expiratory grunting in rds?

A

to create positive airway pressure + maintain functional residual capacity

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31
Q

What is seen on CXR in RDS?

A
  • diffuse granular or ‘ground glass’ appearance of lungs + air on bronchogram
  • indistinct heart border
  • tracheal tube + umbilical artery catheter present
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32
Q

What is the treatment for RDS?

A

Surfactant therapy

Raised ambient O2 (CPAP via nasal cannula) or artificial ventilation via tracheal tube

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33
Q

What are the complications of RDS?

A

Pulmonary interstitial emphysema (PIE)
> if air from over distended alveoli track into the interstitium

Pneumothorax

34
Q

What is chronic lung disease of prematurity?

A

Officially needing O2 at 36 weeks corrected age

  • reduced lung volume
  • reduced alveolar surface are
  • diffusion defect

Increase mortatiliy and recurrent admissions

35
Q

What is apnoea of prematurity?

A

Baby ‘forgets’ to breathe because the brainstem is not fully myelinated until 32-34 weeks.
Often accompanied by bradycardia if they stop breathing for 20-30secs or if breathing continues against a closed glottis.

36
Q

How do you treat apnoea of prematurity?

A

Gentle physical stimulation
NCPAP
Caffeine

37
Q

Where does a haemorrhage usually occur?

A

Germinal matrix above the caudate nucleus

38
Q

What are the risk factors for a haemorrhage?

A

Perinatal asphyxia, RDS, pneumothorax

39
Q

What is oesophageal atresia usually assoc with?

A

Polyhramnios during pregnancy

Tracheo-oesphageal fistula

40
Q

What is the clinical presentation of oesophageal atresia?

A 
Persistent salivation
Drooling from mouth after birth
Cough + choke on feeds
Cyanotic episodes
Aspiration of saliva/milk into lungs
41
Q

How is oesophageal atresia diagnosed (if not at birth)?

A

Pass a wide-calibre feeding tube to see if it reaches stomach (checked on X-ray)

42
Q

What other congenital malformations do babies with oseophgeal atresia often have?

A 
Vertebral
Anorectal
Cardiac
Tracheo-o
Eoesophageal
Renal + radial
Limb (radial limb)
43
Q

What causes small bowel obstruction?

A
  • Atresia or stenosis of duodenum (1/3rd have Down’s: ‘double bubble’)
  • atresia or stenosis of jejunum or ileum
  • malrotatino with volvulus
  • meconium ileum
  • meconium plug
44
Q

What is the complication of malrotation with volvulus?

A

Infarction of entire midgut

45
Q

What are the symptoms of small bowel obstruction?

A

Persistent, bile-stained vomiting

Abdominal distension

46
Q

How do you investigate and treat SBO?

A

Abdo x-ray
Surgical
Dislodge meconium ileum with gastrografin contrast medium (laparotomy needed)

47
Q

What can cause large bowel obstruction?

A

Hirschprung disease

48
Q

What is gastroschsis?

A

When the bowel protrudes through a defect in the anterior abdominal wall, adjacent to umbilicus

  • bowel exposed with no sac
  • less congenital anomalies
  • reduce surgically or silo (wrap sling film to reduce risk of dehydration and protein loss and heat loss)
49
Q

What is exomphalos?

A

Abdo content protrude through umbilical ring, covered with a transparent sac formed by amniotic membrane and peritoneum.
More congenital anomalies. (e.g. Beckwith Wide Mann)
Can be so big they are inoperable

50
Q

What can cause meconium aspiration?

A

Hypoxia can result in meconium passage in utero and associated gasping leads to aspiration.

51
Q

What are the consequences of meconium aspiration?

A

inhibits surfactant, obstructs resp tract and induced pneumonitis

52
Q

How does meconium aspiration present?

A

Respiratory distress soon after birth

53
Q

What is seen on CXR for meconium aspiration?

A

Generalised overinflation with patchy collapse/consolidation +/- air leaks

54
Q

How can meconium aspiration be prevented?

A

If liquor is meconium-stained: delivery should be expedited to prevent further hypoxia and gasping

Apnoeic baby at birth: suck out meconium from larynx/trachea using bore suction tube

55
Q

How do you treat meconium aspiration?

A

O2, surfactant, Abx

56
Q

What is hypoxic-ischaemic encephalopathy?

A

Results from perinatal cerebral hypoxia

57
Q

What causes hypoxic-ischaemic encephalopathy?

A
  • Decreased umbilical blood flow (eg. cord prolapse)
  • Decreased placental gas exchange (e.g. placental abruption)
  • Decreased maternal placental perfusion
  • Maternal hypoxia
  • Inadequate postnatal cardiopulmonary circulation
58
Q

How does hypoxic-ischaemic encephalopathy present?

A

Depends on grade but affects:

- LOC, muscle tone, posture, reflexes, suck, moro, autonomic dysfunction, heart rate and seizures

59
Q

How is hypoxic-ischaemic encephalopathy managed?

A

Resuscitate at birth, exclude other causes

60
Q

What complications can hypoxic-ischaemic encephalopathy cause in the future?

A 
Spastic quadriplegia
Dyskinetic cerebral palsy
Severely reduced IQ
Cortical blindess
Hearing loss
Epilepsy
61
Q

What is bronchopulmonary dysplasia? (BPD)

A

Persistent respiratory distress usually after prolonged intubation with high o2 conc.

62
Q

What are the clinical features of BPD?

A

Hypoxamiea, hypercapnia, apnea, bradycardia, congestive heart failure

63
Q

How do you treat BPD?

A

Gradual warning from ventilator, feed and grow, dexamethasone to decrease inflammation and help weaning

64
Q

When should intrapartum IV penicllin or clindamycin be offered to women?

A
  • previous baby with neonatal GBS disease
  • GBS bacteria in current pregnancy

GBS sx

65
Q

What could indicate group b strep infection?

A
  • intrapartum fever >38
  • preterm
  • PROM >18hr
  • GBS maternal carriage detected on vaginal swab culture
66
Q

What are the TORCH infections?

A 
Toxoplasmosis
Other: syphilis, varicella-zoster, parvovirus
Rubella
CMV
Herpes simplex
67
Q

What are the clinical features of torch infections?

A
  • SGA, jaundice, hepatitis, hepatosplenomegaly, pupura, hydrocephalus

Rubella + CMV: deafness, cataracts, congenital heart disease
Parvo: rubella-like rash, haemolytic anaemia +/- hydrops

68
Q

What is bowel atresia?

A

A birth defect affecting a part of the small intestine (the tube that connects stomach to intestine to digest food)

69
Q

What can cause bowel atresia?

A

Inadequate blood supply to baby’s intestine during fetal development.

70
Q

What is assoc with small bowel atresia?

A

Polyhydramnios - may be suggested during pregnancy from USS

71
Q

How can small bowel atresia be diagnosed?

A

Clinically identified from sx such as vomiting, green bile and swollen abdo indicating need for Xray or contrast scan. Always requires surgical treatment.

72
Q

What is the most common cause of viral encephalitis in children?

A

Herpes simplex encephalitis

73
Q

How is HSV transmitted?

A

During delivery through an infected maternal genital tract

74
Q

Symptoms of HSV

A

Skin or mucosal vesicles
CNS disease
Neonates with disseminated disease and visceral organ involvement have hepatitis, pneumonitis, disseminated intravascular coagulation, or a combination, with or without encephalitis or skin disease.

Other signs, which can occur singly or in combination, include temperature instability, lethargy, hypotonia, respiratory distress, apnea, and seizures.

75
Q

How is HSV diagnosed?

A

HSV culture or PCR

76
Q

Treatment of HSV?

A

Parenteral acyclovir + supportive therapy

77
Q

How do orofacial clefts happen?

A

failure of fusion of maxillary and premaxillary processes.

78
Q

Causes of orofacial clefts?

A

Genetic, associated syndromes eg Pierre-Robin syndrome

maternal medications: phenytoin

79
Q

Treatment of orofacial clefts?

A

Surgical repair lip at 3 months
Repair palate at 6-12 months
Dental plate used if cleft palate too large to allow adewuate suck/feeding

80
Q

Complications of cleft?

A 
Secretory otitis media
Speech defect
Hindered parentaral bonding
Aspiration pneumonia
Psychological morbidity

3a (25 decks)

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