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Year 4 PAEDS > Neonates/Newborn > Flashcards

Neonates/Newborn Flashcards

1
Q

What is the APGAR tool?

A

The assessment tool used to assess all babies (1, 5 and 10 mins)

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2
Q

What does APGAR consist of?

A
  1. Activity (muscle tone)
  2. Pulse
  3. Grimace (reflex irritability, response to stimuli)
  4. Appearance (skin colour)
  5. Respiration
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3
Q

Physical characteristics of a newborn?

A
  • 2 fontanelles (anterior + posterior)
  • Laguna body hair
  • Skin: milia, neonatal acne, erythema toxicum (resolves within a week)
  • Urinary: 1st urine within 24hrs.
  • Genitalia: maternal hormones can cause large scrotum/breasts or discharge.
  • Stool: meconium within 24-48hrs (black/tarry/sticky to green-brown/mustard yellow). Pale grey stool is worrying, suggest liver dysfunction.
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4
Q

How common is Neonatal jaundice?

A

Common (50% term).

5-10% are still jaundiced at >2wks- ‘prolonged neonatal jaundice’

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5
Q

What if a baby is jaundiced within the first 24hrs of life?

A

NEVER physiological + needs investigation!!

nb: not sickle cell, as foetal Hb is formed by FHb not SHb (sickle Hb)

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6
Q

Some causes for Unconjugated and Conjugated Jaundice within 24hrs of birth?

A

Unconjugated:

  • Haemolytic disease
  • Neonatal sepsis

Conjugated:

  • Neonatal Hepatitis
  • Congenital infections (rubella, CMV, syphilis)
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7
Q

Some causes for Unconjugated and Conjugated Jaundice between 24hrs-2wks?

A

Unconjugated:

  • Physiological !!!
  • Hypothyroidism
  • Haemolysis/Sepsis

Conjugated:

  • Neonatal Hepatitis
  • Congenital infections (rubella, CMV, syphilis)
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8
Q

Some causes for Unconjugated and Conjugated Jaundice after 2wks?

A

Unconjugated:

  • Breast milk jaundice
  • Haemolysis/Sepsis
  • Hypothyroidism

Conjugated:

  • Biliary Atresia!
  • Choledochal Cyst
  • Neonatal Hepatitis
  • α1-Antitrypsin Deficiency
  • Galactosaemia
  • CF
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9
Q

What is jaundice of prematurity?

A

Caused by immaturity of liver + failure of hepatocytes to conjugate bilirubin adequately.
The babies are well + it is self-limiting.
Moderately high levels of bilirubin may require phototherapy.

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10
Q

What are the two causes of Haemolytic disease of the newborn?

A
  • Rhesus incompatibility: mother Rh-ve, fetus Rh+ve. Mother’s anti-Rh Abs cross placenta and haemolyse fetal RBC.
  • ABO incompatibility: mother commonly group O, baby group A. Mother’s anti-A react with fetal cells.
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11
Q

Presentation of Haemolytic disease of the newborn?

A

Initial anaemia, then severe oedema (hydrops) occur.

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12
Q

What is breast-milk jaundice?

A

Benign condition, requires no treatment just reassurance.

Most common cause of prolonged unconjugated hyperbilirubinaemia.

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13
Q

What is neonatal hepatitis caused by?

A
  • Virus (hep B, CMV), CF or a metabolic cause.

- Hep B caught in 3rd tri: baby needs immunizing at birth + 6months.

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14
Q

What is the presentation of Biliary Atresia?

A
  • Atresia of intrahepatic/ extrahepatic bile ducts.
  • Babies present with increasing conjugated hyperbilirubinaemia from 4wks.
  • If undiagnosed: liver failure. If diagnosed <3months, surgery may restore liver function.
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15
Q

How can the Coomb’s test be used in neonatal jaundice?

A

It determines whether there are antibodies on the RBC membrane- looking for any autoimmune/immune-mediated haemolysis, so it is +ve in Rhesus incompatibility.

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16
Q

What is the mx of neonatal jaundice mainly aimed at?

A

Avoiding Kernicterus (bilirubin encephalopathy).
(more haem –> more bilirubin –> more unconjugated bilirubin –> can lead to kernicterus).
Kernicterus can cause nerve deafness, choreoathetoid cerebral palsy + mental retardation.

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17
Q

What is the initial treatment of unconjugated jaundice?

A

Phototherapy (degrades the unconjugated bilirubin to non-toxic soluble compounds that are excreted in the urine).
Next you would do an exchange transfusion.

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18
Q

How do you manage conjugated jaundice (conjugated hyperbilirbinaemia)?

A

Management of underlying cause.

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19
Q

(Birth trauma)

What is a Cephalohaematoma?

A
  • Haematoma due to bleeding below peri-osteum, confined within the margins of the skull sutures.
  • Commonly involves the PARIETAL BONE.
  • Not concerning, self-resolves in weeks.
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20
Q

(Birth trauma)

What is a Caput Succedaneum?

A
  • Bruising/oedema of the presenting part, extending beyond the margins of the skull bone.
  • Common following ventouse delivery.
  • Will resolve within few days.
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21
Q

(Birth trauma)

What is intraventricula haemorrhage?

A
  • One of commonest forms of head trauma in newborn.
  • Traumatic delivery can lead to bleeding in brain’s ventricles –> clots can develop which block CSF drainage –> hydrocephalus.
  • Increases risk of seizures.
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22
Q

(Birth trauma)

What is the most common palsy of the brachial plexus at birth?

A

ERB’s PALSY! (C5-6 nerve routes)

  • Common after shoulder dystocia
  • Arm is flaccid w/pronated forearm + flexed wrist (waiter’s tip)
  • In 2/3 cases complete recovery within 6wks
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23
Q

(Birth trauma)

How does a Facial Nerve Palsy occur?

A
  • Follows pressure on face either from maternal ischial spines/ forceps.
  • Will present as facial asymmetry worse on crying.
  • Majority recover within 1-2wks.
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24
Q

What fractures occur as a result of birth trauma?

A
  • Clavicle (most common)
  • Long bones (usually avulsion fractures of femoral/tibial epiphyses)
  • Skull fracture (a/w forceps)
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25
Q

What is Hypoxic Ischaemic Encephalopathy a result of?

A

Perinatal asphyxia –> either the gas exchange in pulmonary system of neonate/mother’s placenta is compromised –> hypoxia + hypercabia + metabolic acidosis.

It is often a/w intra-ventricular haemorrhage.

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26
Q

What are some risk factors for Hypoxic Ischaemic Encephalopathy?

A
  • Failure of gaseous exchange across placenta: placental abruption, ruptured uterus.
  • Disrupted umbilical blood flow: excessive/prolonged uterine contractions, cord compression/prolapse, shoulder dystocia.
  • Inadequate maternal placental perfusion: maternal hypo/hyper-tension.
  • Compromised foetus: anaemia, IUGR.
  • Delay in establishing spontaneous respiration (>10mins)
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27
Q

How does Hypoxic Ischaemic Encephalopathy present?

A

(immediately- up to 48hrs)
Mild: irritable, hyperventilation, staring eyes, ^response to stimulation.
Moderate: abnormalities in tone/movement, cant feed, seizures.
Severe: no spontaneous movements/ responses to pain, fluctuating hyper/hypo-tonia, prolonged seizures, multi-organ failure.

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28
Q

Management of Hypoxic Ischaemic Encephalopathy?

A
  • Rapid resus
  • EEF monitoring
  • Fluid restriction
  • If encephalopathy, may benefit from therapeutic cooling (slows cerebral metabolism to limit release of neurotransmitters + oxygen free radicals)
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29
Q

What may indicate a high risk of cerebral palsy as a result of hypoxic ischaemic encephalopathy?

A

MRI 4-14days shows: B/L abnormalities in basal ganglia, thalamus + lack of myelin in posterior limb of internal capsule)

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30
Q

What is Developmental Hip Dysplasia?

A
  • When femoral head hasnt formed correctly, meaning doesn’t fit properly in acetabulum + can dislocate easily.
  • Main reasons: shallow acetabulum.
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31
Q

Risk factors for Developmental Hip Dysplasia?

A

Female, breech, oligohydramnios, first born, +ve FHx, high birth wt.

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32
Q

What are the investigations for developmental hip dysplasia?

A
  • USS @6wks for early detection (look for position of femoral head).
  • Newborn assessment: Barlow’s (apply downward pressure) + Ortolani’s (trying to relocate). Tests repeated @8wks.
  • Asymmetric skin folds around hip- help detect.
33
Q

What are the main causes of haemolytic anaemia in the neonate?

A
  • Immune (most common: haemolytic disease of the newborn)
  • Red cell enzyme disorders (G6PD deficiency)
  • Red cell membrane disorders (hereditary spherocytosis)
  • Abnormal haemoglobin (thalassaemia major)
34
Q

How do you diagnose haemolytic anaemia?

A
  • Increased reticulocyte count (^release of immature RBCs into systemic circulation, to try + overcome the relative lack of RBCs)
  • Increased unconjugated bilirubin (RBCs broken down faster than liver can metabolise)
35
Q

(Birthmarks)

What are Cafe-au-lait spots?

A

Common light brown coloured, flat + painless spots on skin.

If 6 have developed by 5yrs, may indicate - neurofibromatosis!

36
Q

What are neurofibromatomas (type 1)?

A
  • Multiple Cafe-au-lait spots
  • Autosomal dominant
  • Non-cancerous tumours on/under the skin (a/w peripheral nerve sheath tumours)
  • Problems w/ bone, eyes, nervous system.
37
Q

What are Salmon patches/ Stork marks?

A
  • V common
  • Red/pink patched often on baby’s eyelids, head or neck
  • Usually fade by 2yrs
38
Q

What are Port Wine stains?

A
  • Red/purple/dark marks usually on face/neck.
  • Can be a sign of Sturge-Weber syndrome
  • Faded using laser treatment
39
Q

What are Mongolian blue spots?

A
  • Blue/grey birthmarks on lower back/bottom
  • Commonly on darker-skinned babies
  • Usually disappear by 4yrs, dont need treatment
40
Q

What is a Haemangioma (‘Strawberry naevus’)

A
  • Benign overgrowth of blood vessels, usually self-limiting.
  • More common in girls/prems/low birth wt babies.
  • Need careful looking after (can bleed): avoid sun, apply vaseline.
  • A/w PHACE syndrome
41
Q

What are the different phases of Haemangioma?

A
  • Most appear during first few weeks + grow rapidly for 6-12months (proliferative phase)
  • Then begin a process of shrinking (involuting phase), can take 1-7yrs
42
Q

What are the components of PHACE syndrome? (9:1 F:M)

A

P- posterior fossa/ structural brain abnormalities.
H- haemangiomas (of cervical facial regions).
A- arterial cerebrovascular anomalies.
C- cardiac defects (aortic coarctation etc).
E- eye anomalies

43
Q

(problems of the small baby- prems or IUGR)

Why do smaller babies get hypothermia more easily + how is it managed?

A
  • Larger SA:V
  • Less waterproofing keratin layer, water lost more easily through skin.
  • Causes ^energy consumption (hypoxia + hypoglycaemia)
  • Mx: high humidity, under Perspex heat shield.
44
Q

(problems of the small baby- prems or IUGR)
What glucose conc. are small babies hypoglycaemic?
Why is it a particular problem in IUGR babies?

A

<2.4mmol/L

IUGR have fewer fat stores

45
Q

(problems of the small baby- prems or IUGR)

What is the prognosis for small babies with hypoglycaemia?

A

Depends on whether symptomatic/assymptomatic.

50% infants w/sustained neonatal convulsions due to a hypo will develop severe neurological disability.

46
Q

(problems of the small baby- prems or IUGR)

Why are small babies at ^risk of bronchopulmonary dysplasia (chronic lung disease)?

A
  • Lung damage from pressure + volume trauma from artificial ventilation, O2 toxicity + infection.
  • Most infants are weaned onto CPAP (corticosteroid therapy may help this earlier).
47
Q

(problems of the small baby- prems or IUGR)

What feeding problems do small babies have?

A
  • Sucking reflex doesnt develop until 35wks.

- NG tube- may be C/I in ill prems due to ^risk of necrotizing enterocolitis.

48
Q

(problems of the small baby- prems or IUGR)

What is Necrotizing Enterocolitis caused by?

A

It is caused by impaired blood flow through bowel which predisposes the mucosa to invasion of enteric organisms.
Long-term complications= development of strictures + malabsorption.

49
Q

(problems of the small baby- prems or IUGR)

How does Nec. Enterocolitis present? How is it mx?

A
  • Acute deterioration, apnoea, abdo distention + bloody diarrhoea.
  • In 20% bowel perf occurs.
  • Abdo Xray: gas in bowel.
  • Enteral feeds stopped for 10days.
  • Broad-spec Abx.
50
Q

What feeding/ supplements are given to premature babies? (<37wks)

A
  • Enteral feeds (breast milk) introduced asap.
  • Phosphate, protein, calories, calcium.
  • Iron supplements t few weeks of age (iron mostly transferred to foetus in last trimester so prems have low iron stores).
51
Q

What is the pathophysiology behind a Patent Ductus Arteriosus?

A

In a foetus, the ductus arteriosus shunts blood from right to left away from the unexpanded lungs.
In prems with RDS, the ^pulmonary resistance + hypoxia makes it more likely the ductus will reopen.
This increases work of breathing + makes it more difficult to wean off ventilator.

52
Q

What is the presentation of patent ductus arteriosus in a baby?

A

Systolic murmur + collapsing pulse.
CXR: plethoric lung fields if shunt large.
Diagnosis confirmed on ECHO.

53
Q

Management of Patent Ductus Arteriosus?

A
  • Fluid restriction + diuretics.

- Indomethacin (prostaglandin sythetase inhibitor)

54
Q

Why are premature babies at increased risk of infection?

A

IgG mostly transferred across placenta in last trimester, + no IgA/IgM transferred.
Most infections in prems are nosocomial (hospital-derived).
Major cause of death (contributes to pulmonary dysplasia, white matter injury in brain + disability)

55
Q

What causes Retinopathy of Prematurity in prems?

A
  • Iatrogenic oxygen toxicity is a factor, retina becomes ischaemic which may progress to retinal detachment, fibrosis + blindness.
  • Mx: most need no treatment + prognosis is good. Weekly screening by ophthalmologists.
56
Q

(problems of IUGR)

What does Symmetrical Growth Restriction suggest?

A

Suggests an insult causing impaired growth of both body + head occurred EARLY in gestation.

57
Q

(Problems of IUGR)

What are some causes of symmetrical growth restriction?

A
  • Prenatal infection (commonest): TORCH
  • Chromosomal abnormalities
  • Maternal disease
  • Maternal alcoholism
58
Q

What are the long-term sequelae of TORCH infections? (toxoplasma, other (syphillis), rubella, CMV, herpes)

A

Microcephaly, cerebral palsy, mental retardation, blindness/deafness.

59
Q

(Problems of IUGR)

What is asymmetrical growth restriction and what does it suggest?

A

Baby’s weight is most affected, followed by length, with head growth LEAST impaired.

Suggests the cause of growth restriction has occurred relatively late in foetal development, most likely due to placental insifficiency.

60
Q

(Problems of IUGR)

What are some causes of Asymmetrical growth restriction?

A
  • Toxaemia of pregnancy
  • Multiple pregnancy
  • Placental insufficiency
  • Maternal smoking
61
Q

Why does IUGR result in a REDUCED risk of RDS?

A

The prenatal stress causes endogenous corticosteroid release with the effect of maturing the foetal lung + enhancing surfactant production.

62
Q

What increases the risk of Respiratory Distress Syndrome? (hyaline membrane disease)

A

(the commonest cause of death in the prem, + disability in those who survive).

  • Prematurity
  • Diabetic mothers (as hyperinsulinaemia inhibits surfactant development)
63
Q

How may RDS present on a chest Xray?

A
  • Air bronchogram (radiolucent air in the bronchi seen against the airless lung)
  • Widespread GROUND GLASS appearance of lung fields (due to alveolar collapse)
64
Q

Management of RDS?

A

Prevention: administer CORTICOSTEROIDS for 48hrs before prem delivery.

  • Titration of inspired O2 level against ppO2 in arterial blood.
  • CPAP (prevents alveolar collapse on expiration)
  • Administer exogenous surfactant.
65
Q

What is the difference between the two types of Talipes?

A
  1. Talipes Equinovarus: feet are hyper-introverted.

2. Talipes Calcaenovalgus: ankles are hyper-flexed.

66
Q

What is Talipes Equinovarus associated with?

A

Oligohydramnios
Spina bifida
DDH

67
Q

What must Talipes Equinovarus be differentiated from?

A

Vertical talus (congenital condition, foot is much stiffer + rocker-bottom in shape).

68
Q

Mx of Talipes Equinovarus?

A
  • PONSETTI method (immediate plaster casting + bracing).

- Foot position is fixed + cannot be corrected by manipulation.

69
Q

What is Talipes Calcaneovalgus associated with and how is it managed?

A

A/w: DDH.

Less concerning as usually arisen from shape of uterus + normally self-resolves.

70
Q

What is Spina Bifida?

A

Failure of the neural tube to close normally in early pregnancy.
(reduced by peri-conceptual folic acid supplementation).

71
Q

Briefly summarise the different severities of Spina Bifida:

  1. Anencephaly
  2. Myelomeningocoele
  3. Meningocoele
A
  1. Anencephaly: most severe, brain doesnt develop.
  2. Myelomeningocoele: open lesion with exposed spinal cord (myelocoele) covered with thin layer of meninges (meningoecoele)
  3. Meningocoele: spinal cord intact, but exposed bag of meningeal membranes.
72
Q

What is Spina Bifida occulta?

A

‘Hidden’ + can later cause serious neuro disability (bladder dysfunction, pyramidal tract signs in lower limbs as child grows).
Subtle abnormality of midline: deep pit over lower back, tuft of hair, naevus, lipoma.

73
Q

What is apnoea defined as in a baby + what may it mean?

A
  • Pause in respiration >20secs.
  • Non-specific sx + needs Ix to discover underlying cause.
  • V common in neonatal period, particularly in prems.
74
Q

What is Obstructive apnoea?

A

Continues to make respiratory efforts despite increasing cyanosis/bradycardia.

75
Q

What is obstructive apnoea caused by?

A
  • Small jaw
  • Thick oropharyngeal secretions
  • Congenital blockage of posterior nares
76
Q

What is central apnoea + what is it caused by?

A

Slowing of RR until apnoea.

  • Prematurity
  • Hypoglycaemia
  • Infection (no IgG if prems)
  • Intracranial haemorrhage
  • Nec enterocolitis
77
Q

Management of apnoea in a baby?

A
  • Xanthine-based drugs to stimulate resp system (aminophylline, theophylline, caffeine)
  • CPAP/ mechanical ventilation if severe.
78
Q

Organisms of nerborn infections?

a) Perinatal
b) Nosocomial

A

a) Group B beta-haemolytic strep, E coli

b) Staph epidermidis, Pseudomonas

Year 4 PAEDS (5 decks)

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