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Zero to finals Paediatrics Marina > Neonatology > Flashcards

Neonatology Flashcards

1
Q

Which cells produce surfactant?

A

Type 2 alveolar cells

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2
Q

What are the 5 parts of neonatal resus?

A
  1. Warm baby
  2. Calculate APGAR
  3. Stimulate breathing
  4. Inflation breaths
  5. Chest compressions
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3
Q

What is used for inflation breaths?

A

Term babies - Air

Preterm babies - Air + oxygen

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4
Q

What are the five parts of APGAR?

A

Appearance = Blue centrally, blue peripheries, pink

Pulse = Absent, <100, >100

Grimace = Absent, little response, good response

Activity = None, flexed arms/legs, active.

Respiration = Absent, weak, good/crying

The components of the Apgar score include pulse, respiratory effort, colour, muscle tone and reflex irritability.

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5
Q

What is caput succudaneum?

A

Present at birth

Oedema of the scalp at the presenting part - typically the vertex (eg patient sitting upside down)

No discolouration associated

Lump crosses suture lines

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6
Q

What is cephalohaematoma?

A

Develops several hours after birth

Collection of blood between the skull and the periosteum

Lump does not cross suture lines

Jaundice may be apparent due to blood breakdown

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7
Q

What is Erb’s palsy?

A

A result of injury to C5/C6

Internally rotated shoulder

Extended elbow

Pronated wrist

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8
Q

What is the most organism responsible for neonatal sepsis?

A

GBS

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9
Q

What are features of neonatal sepsis?

A

Respiratory distress - grunting, nasal flaring, tachypnoea

Apnoeas

Fever

Reduced tone

Jaundice

Seizures

Poor feeding

Vomiting

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10
Q

How is neonatal sepsis managed?

A

IV Benzylpenicillin + Gentamicin (suspected or confirmed neonatal sepsis)

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11
Q

What are some RFs for neonatal sepsis?

A

-prolonged rupture of membranes (>18 hours)
-previous GBS infection mother /previous birth with GBS
-low birth weight
-prematurity
-intrapartum temperature ≥38ºC/evidence of maternal chorioamnionitis

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12
Q

What are causes of persistent or severe neonatal hypoglycaemia?

A

Preterm birth

Maternal DM

IUGR

Hypothermia

Neonatal sepsis

Inborn errors of metabolism

Nesidioblastosis

Beckwith-Wiedemann syndrome

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13
Q

How can neonatal hypoglycaemia present?

A

Irritability

Tachypnoea

Pallor

Poor feedng

Drowsiness

Hypotonia

Seizures

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14
Q

How is neonatal hypoglycaemia treated?

A

Encourage normal feeding

If severe (less than 1) IV 10% dextrose

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15
Q

What is hypoxic ischaemic encephalopathy? What are the causes?

A

Damage to brain due to hypoxia during birth

Maternal shock

Intrapartum haemorrhage

Prolapsed cord

Nuchal cord (cord wrapped around neck of baby)

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16
Q

How can the risk of hypoxic ischaemic encephalopathy be reduced?

A

Therapeutic hypothermia after birth

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17
Q

When is jaundice pathological in neonates?

A

If it presents in first 24 hours of life

If it is prolonged (more than 14 days in term babies, more than 21 days in preterm babies)

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18
Q

What are causes of neonatal jaundice?

A

Can be split into causes which cause increased bilirubin production, and causes which cause decreased clearance of bilirubin

Increased production = haemolytic disease, ABO incompatibility, haemorrhage, cephalohaematoma, polycythaemia, G6PD

Decreased clearance = prematurity, breast milk jaundice, neonatal cholestasis, biliary atresia, hypothyroidism, Gilbert syndrome

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19
Q

What is classed as prolonged jaundice?

A

> 14 days in term neonates

> 21 days in preterm neonates

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20
Q

What is kernicterus? How can it present?

A

Brain damage due to excessive bilirubin - Bilirubin can cross the BBB

Floppy, drowsy baby

Poor feeding

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21
Q

What are risk factors for necrotising enterocolitis?

A

VLBW // very preterm

Formula fed

Respiratory distress

Sepsis

PDA

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22
Q

How does necrotising enterocolitis present?

A

Intolerance to feeds

Green bilious vomiting

Distended, tender abdomen

Absent bowel sounds

Blood in stools

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23
Q

What is seen on Abdominal XR in necrotising enterocolitis?

A

Dilated loops of bowel

Bowel wall oedema

Pneumatosis intestinalis (gas in bowel wall)

Pneumoperitoneum (free gas in peritoneal cavity)

Football sign = air outlining the falciform ligament

Rigler sign = air both inside and outside of the bowel

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24
Q

How is NEC managed?

A

NBM

IV Fluids

TPN

Surgery

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25
Q

What are causes of bilious vomiting in neonates?

A

Necrotising enterocolitis

Duodenal atresia

Meconium ileus

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26
Q

Neonate will double bubble sign on abdominal XR?

A

Duodenal atresia

Double bubble sign = dilation of both the duodenum and the stomach.

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27
Q

Bilious vomiting in a neonate with CF?

A

Meconium ileus

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28
Q

Neonate with persistent salivation/drooling?

A

Oesophageal atresia

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29
Q

What are features of fetal alcohol syndrome?

A

Microcephaly

Thin upper lip

Smooth, flat philtre

Short palpebral fissure

Learning disability

Behavioural difficulties

Hearing + vision problems

Cerebral palsy

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30
Q

What are features of congenital rubella syndrome?

A

Congenital cataracts

Congenital heart disease

Learning disability

Hearing loss

31
Q

What are features of congenital varicella syndrome?

A

Fetal growth restriction

Microcephaly

Hydrocephalus

Learning difficulty

Limb hypoplasia

Scarring/skin changes in the dematomes

Cataracts

32
Q

What is Exomphalos/Omphalocele and Gastroschisis?

A

Exomphalos/Omphacele = abdominal contents protrude through the umbilical ring - covered with a transparent sac

Gastoschisis = abdomianl contents protrude through defect in anterior abdominal wall - no covering sac

33
Q

What are causes of jaundice presenting within the first 24 hours of life? How should it be investigated?

A

Investigate with a blood film analysis

Rhesus haemolytic disease (RHD)

ABO incompatibility

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

hereditary spherocytosis

34
Q

How does malrotation present?

A

Bilious vomiting

Haemodynamic instability

35
Q

An infant born at 41 weeks gestation has respiratory distress shortly after birth. The amniotic fluid during labour is noted to be darkly stained. Shortly after the infant develops significant respiratory distress and desaturates rapidly. Given the most likely diagnosis, what complication has occurred?

A. Transient tachypnoea of the newborn

B. Persistent pulmonary hypertension

C.Pneumothorax

D. Respiratory tract infection

E. Tracheo-oesophageal fistula

A

C. Pneumothorax

The baby has meconium aspiration syndrome, which is associated with high rates of air leak, pneumothorax and pneumomediastinum. The sudden development of profound respiratory distress suggests a pneumothorax.

Not B:
This is the failure of the foetal circulation to adapt to extra-uterine conditions. Meconium aspiration causes hypoxia and pulmonary vasoconstriction, maintaining higher pulmonary pressures

36
Q

What is seen on abdominal XR in meconium ileus?

A

Air-fluid levels

37
Q

How does meconium ileus present?

A

Failure to pass meconium within 48hrs

Billous vomiting

Abdominal distension

38
Q

What is transient tachypnoea of the newborn and how does it present?

A

Most common cause of respiratory distress in the newborn period
Delayed resorption of fluid in the lungs
Low oxygen sats at birth
Resolves within a couple of days

39
Q

What is seen on CXR in transient tachypnoea of the newborn?

A

Hyperinflation of the lungs

Fluid in the horizontal fissure

40
Q

Duodenal atresia vs. Malrotation

A

Both present with billous vomiting

Duodenal atresia = few hours after birth
Malrotation = 3-7 days after birth + signs of haemodynamical instability

41
Q

How is malrotation managed?

A

Ladd’s procedure

42
Q

How does the abdomen feel in duodenal atresia?

A

Soft, distended

43
Q

How does meconium aspiration syndrome present?

A

Respiratory distress

Patchy infiltrates on CXR

44
Q

What is transient tachypnoea of the newborn and how does it present?

A

Most common cause of respiratory distress in the newborn period
Delayed resorption of fluid in the lungs
Low oxygen sats at birth
Resolves within a couple of days

45
Q

What is seen on CXR in transient tachypnoea of the newborn?

A

Hyperinflation of the lungs

Fluid in the horizontal fissure

46
Q

Congenital infection: Sensorineural deafness + congenital cataracts + congenital heart disease (E.g. PDA)?

A

Rubella

47
Q

Congenital infection: Cerebral calcification + Chorioretinitis + Hydrocephalus

A

Toxoplasmosis

48
Q

Congenital infection: Growth retardation. + Purpuric skin lesions

A

Cytomegalovirus

49
Q

What does neonatal resp distress + fluid in the horizontal fissure suggest?

A

Transient tachypnoea of the newborn

50
Q

What’s the chest compression rate/ratio for infants?

A

Chest compressions rate of 100-120/min, ratio of 15:2

51
Q

You are working with the paediatrics team who are called to an emergency C-section at 37 weeks’ gestation. Immediately after birth, the baby lets out a strong cry. As you towel the baby dry, the arms and legs resist extension, and the baby cries with stimulation. The hands and feet look a little blue, but the face and trunk are pink. The baby’s heart rate is 140 beats per minute.

What is the APGAR score of the baby?

A. 9

B. 3

C. 1

D. 5

E. 7

A

A. 9: One point is lost for blue extremities, which is very common immediately postpartum

52
Q

How long after birth is APGAR calculated?

A

at 1, 5 and 10 minutes.

53
Q

How long after birth is APGAR calculated?

A

at 1, 5 and 10 minutes.

54
Q

what are the apgar score cutoffs and meanings?

A

-Apgar score of 7–10 as reassuring
-a score of 4–6 as moderately abnormal
- a score of 0–3 as low

55
Q

Difference between caput succedanum and cephalohaematoma:

A
56
Q

You are attending labour for an emergency Caesarean section for failure to progress. The operation goes on without any complications. The baby cries immediately after birth and there is 30 seconds of delayed cord clamping. On examination, baby is centrally pink with blueish hands and feet. Saturation probes are attached to the baby and show an oxygen saturation of 73% at 1 minute. What is the most appropriate next step in management?

A. Intubation

B. Urgent chest x-ray

C. Ventilation breaths

D. Observe and reassess at next interval

E. No further assessment required

A

D. Observe and reassess at next interval

In first 10 minutes of life, suboptimal SpO2 readings can be expected from a healthy neonate.

Transient cyanosis is very common initially after birth. It does not require any further management as it usually self-resolves.

APGAR scores, including appearance/colour, should be assessed at 1 min, then reassessed at 5 and 10 minutes.

57
Q

paediatric BLS algorithm

A

The 2015 Resuscitation Council guidelines made the following changes to paediatric basic life support
compression:ventilation ratio:
1. lay rescuers should use a ratio of 30:2

  1. If there are two or more rescuers with a duty to respond then a ratio of 15:2 should be used

-age definitions: an infant is a child under 1 year, a child is between 1 year and puberty

Key points of algorithm (please see link attached for more details)
1. unresponsive?
2. shout for help
3. open airway
4. look, listen, feel for breathing
5. give 5 rescue breaths
6. check for signs of circulation
-infants use brachial or femoral pulse, children use femoral pulse
7. 15 chest compressions:2 rescue breaths (see above)
-chest compressions should be 100-120/min for both infants and children
-depth: depress the lower half of the sternum by at least one-third of the anterior–posterior dimension of the chest (which is approximately 4 cm for an infant and 5 cm for a child)
-in children: compress the lower half of the sternum
-in infants: use a two-thumb encircling technique for chest compression

58
Q

difference between caput succedaneum & subaponeurotic haemorrhage or subgaleal haemorrhage:

A

A subaponeurotic haemorrhage or subgaleal haemorrhage is a rare condition seen in newborns caused by rupturing of the emissary veins that connect the dural sinuses and the scalp veins. This leads to blood accumulating in the aponeurosis of the scalp and periosteum (can cause widespread bleeding–> shock)

-These can occur secondary to ventouse delivery and are an important differential to caput succedaneum.

-They cross cranial sutures (like caput succedaneum) but run deep to the galeal aponeurosis and are bloody rather than serosanguinous or oedematous fluid in nature.

59
Q

A baby born at 35 weeks gestations via normal vaginal delivery is found to be irritable 48 hours after birth and suffers a convulsion. There is no obvious head trauma or swellings. Which one of the following cranial injuries is most likely to have occurred?

A. Caput succedaneum

B. Cephalohaematoma

C. Subaponeurotic haemorrhage

D. Intraventricular haemorrhage

E. Extradural haemorrhage

A

D. Intraventricular haemorrhage

In neonatal practice the vast majority of IVH occur in the first 72 hours after birth, the aetiology is not well understood and it is suggested to occur as a result of birth trauma combined with cellular hypoxia, together the with the delicate neonatal CNS.

60
Q

You are asked to speak to a family who have just received a diagnosis of pulmonary hypoplasia on fetal MRI. Which of the following conditions is the most common cause of pulmonary hypoplasia?

A. Polyhydramnios

B. Congenital diaphragmatic hernia

C. Diaphragm agenesis

D. Tetralogy of Fallot

E. Osteogenesis imperfecta

A

B. Congenital diaphragmatic hernia

Pulmonary hypoplasia in CDH occurs alongside the hernial development rather than as a direct result of it, as part of a sequence

Pulmonary hypoplasia is a term used for newborn infants with underdeveloped lungs

Causes include
oligohydramnios
congenital diaphragmatic hernia

61
Q

how is retinopathy of prematurity screened for?

A

Undertaken by opthalmologists

  1. 30 – 31 weeks gestational age in babies born before 27 weeks
  2. 4 – 5 weeks of age in babies born after 27 weeks

Screening should happen at least every 2 weeks and can cease once the retinal vessels enter zone 3, usually at around 36 weeks gestation.

62
Q

how is retinopathy of prematurity managed?

A
  1. First line is transpupillary laser photocoagulation to halt and reverse neovascularisation.
  2. Other options are cryotherapy and injections of intravitreal VEGF inhibitors (very low dose avastin)
  3. Surgery may be required if retinal detachment occurs
63
Q

how is the retina divided (zones)

A

The retina is divided into three zones:

  1. Zone 1 includes the optic nerve and the macula
  2. Zone 2 is from the edge of zone 1 to the ora serrata, the pigmented border between the retina and ciliary body
  3. Zone 3 is outside the ora serrata
    The retinal areas are described as a clock face, for example “there is disease from 3 to 5 o’clock”. The areas of disease are described from stage 1 (slightly abnormal vessel growth) to stage 5 (complete retinal detachment).

“Plus disease” describes additional findings, such as tortuous vessels and hazy vitreous humour.

64
Q

what happens when retina is exposed to oxygen (pathophysiology):

A

Retinal blood vessel development starts at around 16 weeks (same time as foetal movements) and is complete by 37 – 40 weeks gestation. The blood vessels grow from the middle of the retina to the outer area. This vessel formation is stimulated by hypoxia, which is a normal condition in the retina during pregnancy.

When the retina is exposed to higher oxygen concentrations in a preterm baby, particularly with supplementary oxygen during medical care, the stimulant for normal blood vessel development is removed.

When the hypoxic environment recurs, the retina responds by producing excessive blood vessels (neovascularisation), as well as scar tissue. These abnormal blood vessels may regress and leave the retina without a blood supply. The scar tissue may cause retinal detachment.

65
Q

family history questions:

A

eyes, heart, hip problems in family

66
Q

questions to ask for DDH screening:

A

breech presentation (>34 weeks), when did they turn?

67
Q

what is Pierre Robin sequence? mnemonic

A

A set of abnormalities affecting the head and face, consisting of a small lower jaw (micrognathia ), a tongue that is placed further back than normal (glossoptosis), and blockage (obstruction) of the airways.

68
Q

what is microtia?

A

when the external ear is small and not formed properly

69
Q

describe anatomical pathology in Erb’s palsy:

A

An Erbs palsy is the result of injury to the C5/C6 nerves in the brachial plexus during birth. It is associated with shoulder dystocia, traumatic or instrumental delivery and large birth weight.

Damaged to the C5/C6 nerves leads to weakness of shoulder abduction and external rotation, arm flexion and finger extension. This leads to the affected arm having a “waiters tip” appearance:

  1. Internally rotated shoulder
  2. Extended elbow
  3. Flexed wrist facing backwards (pronated)
  4. Lack of movement in the affected arm
  5. Function normally returns spontaneously within a few months. If function does not return then they may required neurosurgical input.
70
Q

2 biggest causes of bilious vomiting in neonatal unit

A

volvulus/malroation (admit, NBM, IV fluids), xray and upper GI contrast)

71
Q

what is hypospadius? management?

A

Hypospadias is a birth defect in boys in which the opening of the urethra is not located at the tip of the penis
-referral to urology for followup (contraindication to circumscision)

72
Q

what is this?

A

Slate gray nevi (Mongolian blue spots)

73
Q

what is port wine stain associated with?

A

Sturge-Weber syndrome

74
Q

sturge weber syndrome mnemonic:

A

STURGE. S – Seizures. T – Tram track calcifications. U – U/L port wine stain and weakness (usually opposite side) R – Retardation.v

Zero to finals Paediatrics Marina (18 decks)

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