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Phase 3a - Paediactrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What are the key components of paediatric Basic Life Support (BLS)?

A

Ensure the scene is safe.
Check for responsiveness.
Shout for help and call for emergency services.
Open the airway (head tilt-chin lift).
Check for breathing for no more than 10 seconds.
Deliver 5 initial rescue breaths.
Start chest compressions if no signs of life.

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2
Q

What is the compression-to-ventilation ratio in paediatric BLS for a single rescuer?

A

30:2.

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3
Q

What is the compression-to-ventilation ratio in paediatric BLS for two rescuers?

A

15:2

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4
Q

How deep should chest compressions be in paediatrics?

A

One-third of the chest depth or approximately 4 cm for infants and 5 cm for children.

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5
Q

What is the correct rate of chest compressions in paediatrics?

A

100–120 compressions per minute.

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6
Q

The recommended compression depth for a child during CPR is __________ of the chest depth.

A

one-third

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7
Q

The initial number of rescue breaths in paediatric resuscitation is __________.

A

5

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8
Q

The recommended chest compression rate is __________ compressions per minute.

A

100–120

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9
Q

During paediatric BLS, the compression-to-ventilation ratio for two rescuers is __________.

A

0.6263888888888889

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10
Q

Which of the following is the most common cause of cardiac arrest in children?
A. Arrhythmias
B. Trauma
C. Hypoxia and respiratory failure
D. Sepsis

A

C. Hypoxia and respiratory failure

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11
Q

In paediatric advanced life support, what is the first-line drug for cardiac arrest?
A. Amiodarone
B. Atropine
C. Adrenaline
D. Calcium gluconate

A

C. Adrenaline

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12
Q

What is the correct energy dose for defibrillation in paediatrics?
A. 1 J/kg
B. 2 J/kg
C. 4 J/kg
D. 10 J/kg

A

B. 2 J/kg (initial dose, increasing to 4 J/kg if necessary).

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13
Q

T/F: In paediatric CPR, you should perform rescue breaths before starting chest compressions.

A

True.

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14
Q

T/F: Adrenaline is administered every 3–5 minutes during paediatric resuscitation.

A

True.

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15
Q

T/F: The recovery position is contraindicated in an unconscious child who is breathing normally.

A

False (It is recommended to place such a child in the recovery position).

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16
Q

Scenario: A 3-year-old child is found unresponsive, not breathing, but has a pulse of 70 bpm.
Q: What is the next step in resuscitation?

A

Provide rescue breaths at a rate of 1 breath every 2–3 seconds (20–30 breaths per minute) and recheck the pulse every 2 minutes.

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17
Q

Scenario: A 5-year-old child in cardiac arrest requires defibrillation. The child weighs 20 kg.
Q: What energy dose should be used for the first shock?

A

40 Joules (2 J/kg × 20 kg).

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18
Q

Arrange the steps of paediatric BLS in the correct order:
A. Open the airway.
B. Deliver 5 initial rescue breaths.
C. Perform chest compressions.
D. Check for breathing.

A

D → A → B → C

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19
Q

Bag-valve mask →

A

To deliver rescue breaths.

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20
Q

Defibrillator →

A

To administer shocks in ventricular fibrillation or pulseless ventricular tachycardia.

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21
Q

Oropharyngeal airway →

A

To maintain airway patency

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22
Q

Adrenaline →

A

First-line drug in cardiac arrest.

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23
Q

What are the pros and cons of using an oropharyngeal airway in paediatric resuscitation?

A

Pros:

Maintains airway patency.
Prevents tongue obstruction.
Cons:

Can cause gagging if the child is semi-conscious.
Risk of trauma during insertion.

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24
Q

Why is it important to deliver rescue breaths before chest compressions in paediatric BLS?

A

Cardiac arrest in children is commonly caused by hypoxia or respiratory failure. Delivering rescue breaths helps correct hypoxia and improves oxygenation, which is critical for restoring circulation.

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25
Q

What are some key points to remember in paediatric resuscitation?

A

Start CPR if the heart rate is below 60 bpm with poor perfusion.
Always consider reversible causes of cardiac arrest (4 Hs and 4 Ts).
Use age-appropriate equipment, such as smaller bag-valve masks and defibrillator pads.

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26
Q

Respiratory Distress Syndrome

A

Affects premature neonates, before the lungs start producing adequate surfactant, common in below 32 week babies.

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27
Q

Pathophysiology of Respiratory Distress Syndrome

A
  • Inadequate surfactant leads to high surface tension within alveoli leading to atelectasis (lung collapse) as it is more difficult for the alveoli and the lungs to expand leading to inadequate gaseous exchange and hypoxia, hypercapnia and respiratory distress.
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28
Q

Management of Respiratory Distress Syndrome

A

Dexamethasone is given to mothers with suspected or confirmed preterm labour to increase production of surfactant and reduce the incidence and severity of respiratory distress syndrome in the baby - Intubation and ventilation may be needed to fully assist breathing if the distress is severe - Endotracheal surfactant, which is artificial surfactant delivered into the lungs via an endotracheal tube - CPAP via a nasal mask to keep the lungs inflated during breathing - Supplementary oxygen to maintain sats between 91 and 95%

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29
Q

Short term complications of Respiratory Distress Syndrome

A
  • Pneumothorax - Infection - Apnoea - Intraventricular haemorrhage - Pulmonary haemorrhage - Necrotising Enterocolitis
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30
Q

Long term complications of Respiratory Distress Syndrome

A

Chronic lung disease of prematurity - Retinopathy of prematurity - Neurological, hearing and visual impairment

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31
Q

Signs of Respiratory Distress

A

Cyanosis, Nasal flaring, Head bobbing, Tracheal tug, use of accessory muscles, sub/intercostal recessions, grunting/stridor/wheeze, hypoxia, tachypneoa

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32
Q

What is the primary role of surfactant in the lungs?

A

To reduce surface tension within the alveoli, preventing collapse during exhalation and allowing efficient gas exchange.

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33
Q

What gestational age is considered the threshold below which RDS is most common?

A

Below 32 weeks gestation.

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34
Q

What is the typical chest X-ray appearance in neonatal respiratory distress syndrome?

A

Ground-glass appearance with air bronchograms.

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35
Q

What are some risk factors for developing respiratory distress syndrome?

A

Premature birth.
Maternal diabetes.
Male sex of the neonate.
Caesarean delivery without labor.
Sibling history of RDS.

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36
Q

The administration of __________ to mothers at risk of preterm labor significantly reduces the risk of neonatal RDS.

A

dexamethasone

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37
Q

The ground-glass appearance on a chest X-ray in RDS reflects __________ in the alveoli.

A

atelectasis

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38
Q

Scenario: A 28-week neonate is born via emergency caesarean section. Within minutes of birth, the baby exhibits tachypnoea, nasal flaring, and intercostal recession. SpO₂ is 85% on room air.
Q: What is the immediate management?

A

Administer CPAP to keep the alveoli open, provide supplemental oxygen, and consider intubation for surfactant administration if the respiratory distress is severe.

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39
Q

T/F: Retinopathy of prematurity is a short-term complication of RDS.

A

False (It is a long-term complication).

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40
Q

T/F: Nasal CPAP is preferred over intubation for mild-to-moderate respiratory distress in neonates.

A

True.

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41
Q

Why is it essential to maintain oxygen saturations between 91–95% in neonates with RDS?

A

To prevent hypoxia while avoiding hyperoxia, which can increase the risk of complications such as retinopathy of prematurity.

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42
Q

Purpose of Dexamethasone in RDS

A

To stimulate fetal lung maturity and surfactant production.

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43
Q

Purpose of CPAP in RDS

A

To maintain alveolar inflation during breathing.

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44
Q

Purpose of Endotracheal surfactant in RDS

A

To replace deficient surfactant in the neonate’s lungs.

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45
Q

Purpose of Supplemental oxygen in RDS

A

To correct hypoxia and maintain target saturations.

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46
Q

To correct hypoxia and maintain target saturations.

A

Pros:

Non-invasive.
Effective in maintaining alveolar inflation and reducing atelectasis.
Cons:

May cause nasal trauma.
Can be insufficient in severe cases requiring intubation.

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47
Q

Infants who still require oxygen at a postmenstrual age of 36 weeks are described as having ____

A

Bronchopulmomonary Dysplasia (BPD)

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48
Q

Pathophysiology of BPD

A

The lung damage comes from pressure and volume trauma of artificial ventilation, oxygen toxicity and infection with the CXR characteristically showing widespread areas of opacification and sometimes cystic changes, fibrosis and even lung collapse

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49
Q

Managment of BPD

A

These infants are mainly weaned onto CPAP followed by additional oxygen where needed and sometimes given corticosteroids to facilitate weaning from the ventilation however there is a risk of abnormal neurodevelopment with these. - A few infants with severe disease can die from intercurrent infection or pulmonary HTN.

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50
Q

At what postmenstrual age is Bronchopulmonary Dysplasia (BPD) diagnosed in infants still requiring oxygen?

A

36 weeks

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51
Q

The characteristic chest X-ray in BPD shows widespread areas of __________ and sometimes cystic changes, fibrosis, or lung collapse.

A

opacification

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52
Q

What are the primary causes of lung damage in Bronchopulmonary Dysplasia?

A

Pressure and volume trauma from artificial ventilation.
Oxygen toxicity.
Infection.

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53
Q

T/F: Corticosteroids are used in BPD management to facilitate weaning from ventilation, but they carry a risk of abnormal neurodevelopment.

A

True.

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54
Q

What are the key components of managing infants with Bronchopulmonary Dysplasia?

A

Gradual weaning onto CPAP.
Supplemental oxygen as needed.
Corticosteroids for ventilation weaning (with careful consideration of neurodevelopment risks).

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55
Q

Scenario: A premature infant at 28 weeks gestation has been on mechanical ventilation for 6 weeks. The infant’s chest X-ray shows areas of opacification, cystic changes, and fibrosis. Oxygen is still required at 36 weeks postmenstrual age.
Q: What is the likely diagnosis, and what steps can be taken to manage this condition?

A

The likely diagnosis is Bronchopulmonary Dysplasia. Management includes weaning onto CPAP, providing supplemental oxygen as required, and considering corticosteroids to assist in ventilation weaning.

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56
Q

Why might corticosteroids, despite their risks, be necessary in some cases of Bronchopulmonary Dysplasia?

A

Corticosteroids can reduce lung inflammation, facilitate weaning from mechanical ventilation, and improve outcomes in severe cases, but their use must be carefully weighed against the risk of abnormal neurodevelopment.

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57
Q

What are the pros and cons of using corticosteroids in BPD management?

A

Pros:

Reduces inflammation and lung damage.
Facilitates weaning from mechanical ventilation.
Cons:

Risk of neurodevelopmental abnormalities.

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58
Q

What is the pathophysiology of Bronchopulmonary Dysplasia?

A

Lung damage arises from pressure and volume trauma during artificial ventilation, oxygen toxicity, and infection, leading to widespread opacification, cystic changes, fibrosis, and potential lung collapse.

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59
Q

What is Meconium Aspiration Syndrome (MAS)?

A

MAS occurs when a newborn inhales a mixture of meconium (the first stool) and amniotic fluid during or before delivery, leading to respiratory distress and potential complications.

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60
Q

The presence of meconium-stained amniotic fluid in the airways can lead to __________, chemical pneumonitis, and surfactant inactivation.

A

airway obstruction

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61
Q

What is the pathophysiology of Meconium Aspiration Syndrome?

A

Meconium in the airways causes partial or complete airway obstruction.
Trapped air can lead to overdistension and risk of pneumothorax.
Chemical pneumonitis occurs due to inflammation from meconium exposure.
Surfactant inactivation leads to atelectasis and impaired gas exchange.

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62
Q

True/False:
Q: Meconium aspiration is more common in preterm infants than in term or post-term infants

A

False. (It is more common in term and post-term infants.)

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63
Q

What are the risk factors for Meconium Aspiration Syndrome?

A

Post-term pregnancy.
Fetal distress during labor.
Meconium-stained amniotic fluid.
Complicated deliveries.

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64
Q

Scenario: A term newborn is delivered with meconium-stained amniotic fluid. The baby shows signs of respiratory distress with grunting and intercostal recessions.
Q: What steps should be taken to manage this case?

A

Immediate resuscitation if the baby is not breathing effectively.
Suctioning of the airways if thick meconium is obstructing breathing.
Administration of oxygen or ventilation support as needed.
Monitoring for complications like pneumothorax and persistent pulmonary hypertension.

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65
Q

How is MAS diagnosed?

A

Clinical features: Respiratory distress at birth, cyanosis, and grunting.
Chest X-ray findings: Patchy opacities, areas of overdistension, and sometimes pneumothorax.

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66
Q

Why is routine suctioning of the oropharynx and nasopharynx not recommended for all meconium-stained newborns?

A

Routine suctioning can cause harm and is no longer recommended unless the newborn is not breathing effectively or has airway obstruction from thick meconium.

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67
Q

What are the pros and cons of surfactant therapy in MAS?

A

Pros:

Improves lung compliance.
Reduces atelectasis.
Enhances gas exchange.
Cons:

Expensive.
May not be effective in severe cases without addressing other underlying issues like PPHN.

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68
Q

What are the main complications of MAS?

A

Pneumothorax.
Persistent pulmonary hypertension of the newborn (PPHN).
Hypoxia leading to long-term neurodevelopmental issues.

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69
Q

What is Hypoxic-Ischaemic Encephalopathy (HIE)?

A

A condition caused by reduced oxygen or blood flow to the brain and other organs, leading to brain injury, primarily in neonates.

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70
Q

HIE often results from __________ during the perinatal period, such as umbilical cord prolapse or uterine rupture.

A

intrapartum asphyxia

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71
Q

What are the primary causes of HIE?

A

Placental abruption.
Uterine rupture.
Cord prolapse.
Prolonged or obstructed labor.
Severe maternal hypotension or hypoxia.

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72
Q

True/False:
Q: Therapeutic hypothermia is an effective treatment for moderate to severe HIE in neonates.

A

True.

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73
Q

What is the pathophysiology of HIE?

A

Interruption of oxygen or blood supply leads to anaerobic metabolism.
Accumulation of lactic acid causes cellular damage and apoptosis.
Reperfusion injury during resuscitation exacerbates the damage

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74
Q

Mild HIE →

A

Hyperalert, increased tone, normal feeding, no seizures.

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75
Q

Moderate HIE →

A

Lethargic, hypotonia, poor feeding, occasional seizures.

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76
Q

Severe HIE →

A

Comatose, flaccid, absent primitive reflexes, frequent seizures.

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77
Q

Scenario: A term baby is delivered following an emergency C-section due to cord prolapse. The baby has an Apgar score of 3 at 1 minute and requires resuscitation. Post-resuscitation, the baby is lethargic with poor tone.
Q: What are the immediate management steps?

A

Initiate therapeutic hypothermia if criteria are met.
Supportive care in the neonatal intensive care unit (NICU).
Monitor for seizures and treat with antiepileptics if needed.
Monitor oxygenation, ventilation, and fluid balance.

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78
Q

What are the criteria for initiating therapeutic hypothermia in HIE?

A

Gestational age ≥ 36 weeks.
Evidence of perinatal asphyxia: low Apgar scores, severe acidosis (pH < 7.0), or base deficit ≥ 16 mmol/L.
Signs of moderate to severe encephalopathy.

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79
Q

Why is it important to avoid over-oxygenation during resuscitation in HIE?

A

Over-oxygenation can contribute to reperfusion injury by generating reactive oxygen species, exacerbating cellular damage.

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80
Q

What are the potential complications of HIE?

A

Cerebral palsy.
Epilepsy.
Intellectual disability.
Vision and hearing impairment.
Behavioral disorders.

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81
Q

Therapeutic hypothermia aims to reduce the extent of brain injury by slowing __________ and reducing the inflammatory response.

A

cellular metabolism

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82
Q

What investigations are used in the diagnosis and management of HIE?

A

Blood gas analysis (acidosis and base deficit).
Brain imaging: MRI to assess the extent of brain injury.
EEG: To monitor for seizures.
Clinical examination: Grading of encephalopathy.

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83
Q

What are the three main stages of HIE based on clinical presentation?

A

Mild: Hyperalert, increased tone, normal feeding, no seizures.
Moderate: Lethargic, hypotonia, poor feeding, occasional seizures.
Severe: Comatose, flaccid, absent reflexes, frequent seizures.

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84
Q

What are the pros and cons of therapeutic hypothermia in HIE?

A

Pros:

Reduces the extent of brain injury.
Improves long-term neurodevelopmental outcomes in moderate to severe HIE.
Cons:

Must be initiated within 6 hours of birth.
Requires intensive monitoring and NICU care.

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85
Q

What does the acronym “TORCH” stand for in the context of infections?

A

T: Toxoplasmosis
O: Other (e.g., syphilis, varicella-zoster, parvovirus B19)
R: Rubella
C: Cytomegalovirus (CMV)
H: Herpes simplex virus (HSV)

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86
Q

TORCH infections are a group of infections that can cause congenital abnormalities due to __________ transmission.

A

Vertical

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87
Q

What are the common clinical features seen in neonates with TORCH infections?

A

Intrauterine growth restriction (IUGR).
Hepatosplenomegaly.
Jaundice.
Microcephaly.
Rash (petechial or purpuric).
Seizures.

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88
Q

True/False:
Q: Cytomegalovirus (CMV) is the most common cause of congenital infection worldwide.

A

True.

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89
Q

Match each TORCH infection to its characteristic feature:

Toxoplasmosis →
Other (syphilis) →
Rubella →
Cytomegalovirus →
Herpes simplex virus →

A

Toxoplasmosis → Intracranial calcifications, chorioretinitis.
Other (syphilis) → Snuffles, Hutchinson teeth.
Rubella → Cataracts, deafness, congenital heart defects (PDA).
Cytomegalovirus → Periventricular calcifications.
Herpes simplex virus → Vesicular skin lesions, encephaliti

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90
Q

Scenario: A newborn presents with petechial rash, hepatosplenomegaly, microcephaly, and jaundice. The mother had a history of a flu-like illness during pregnancy.
Q: What is the most likely diagnosis, and what investigation confirms it?

A

Likely diagnosis: Cytomegalovirus (CMV) infection.
Investigation: PCR for CMV DNA in urine or saliva.

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91
Q

What investigations are commonly used to diagnose TORCH infections?

A

Maternal serology for specific infections (e.g., Toxoplasma IgM/IgG).
Neonatal PCR for viral DNA (e.g., CMV, HSV).
TORCH screen in neonates (tests for antibodies or pathogens).
Imaging: Cranial ultrasound, MRI, or CT for calcifications and brain abnormalities.

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92
Q

Why is early identification and treatment of TORCH infections crucial in neonates?

A

Early treatment can reduce the severity of complications such as neurodevelopmental delays, hearing loss, and vision impairment.

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93
Q

What are the characteristic congenital abnormalities caused by TORCH infections?

A

Toxoplasmosis: Intracranial calcifications, hydrocephalus, chorioretinitis.
Rubella: Cataracts, deafness, congenital heart defects.
CMV: Periventricular calcifications, microcephaly, hearing loss.
HSV: Skin vesicles, encephalitis, disseminated disease.

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94
Q

The characteristic triad of congenital toxoplasmosis is __________, __________, and __________.

A

intracranial calcifications, hydrocephalus, chorioretinitis

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95
Q

What is the treatment approach for TORCH infections in neonates?

A

Toxoplasmosis: Pyrimethamine, sulfadiazine, and folinic acid.
Syphilis: Penicillin.
Rubella: Supportive (no specific antiviral treatment).
CMV: Ganciclovir or valganciclovir.
HSV: Acyclovir.

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96
Q

Scenario: A neonate is born with cataracts, a PDA, and bilateral sensorineural hearing loss. The mother reports a rash during the first trimester.
Q: What is the likely diagnosis, and how would you confirm it?

A

Likely diagnosis: Congenital rubella syndrome.
Confirmation: Rubella-specific IgM in the neonate.

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97
Q

What are some preventive measures for TORCH infections during pregnancy?

A

Avoid contact with cat litter (toxoplasmosis).
Screen and treat maternal infections (syphilis, rubella immunity).
Vaccination (e.g., rubella vaccine before pregnancy).
Hygienic practices (e.g., handwashing, avoiding exposure to CMV).
Safe sexual practices to prevent herpes and syphilis.

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98
Q

True/False:
Q: Rubella vaccination is contraindicated during pregnancy.

A

True.

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99
Q

What is neonatal jaundice?

A

Neonatal jaundice is the yellow discoloration of the skin and sclera due to elevated bilirubin levels in the blood, commonly seen in neonates.

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100
Q

Neonatal jaundice becomes clinically visible when bilirubin levels exceed __________ µmol/L.

A

85

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101
Q

What are the two main types of neonatal jaundice?

A

Physiological jaundice (common, resolves spontaneously).
Pathological jaundice (may require treatment).

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102
Q

List the common causes of unconjugated hyperbilirubinemia in neonates.

A

Physiological jaundice.
Breastfeeding jaundice.
Hemolysis (e.g., ABO or Rh incompatibility, G6PD deficiency).
Infection (e.g., sepsis).
Polycythemia.
Prematurity.

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103
Q

What are the causes of conjugated hyperbilirubinemia in neonates?

A

Biliary atresia.
Neonatal hepatitis.
Sepsis.
Metabolic disorders (e.g., galactosemia, hypothyroidism).

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104
Q

Match the type of jaundice to its common timeframe:

<24 hours →
2–7 days →
>2 weeks →

A

<24 hours → Pathological jaundice (e.g., hemolysis).
2–7 days → Physiological jaundice.
>2 weeks → Prolonged jaundice (e.g., breast milk jaundice, biliary atresia).

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105
Q

What investigations are performed for neonatal jaundice?

A

Serum bilirubin (total and direct).
Blood group and Coombs test (for ABO/Rh incompatibility).
Full blood count and blood film.
G6PD levels.
Liver function tests.
Infection screen (e.g., CRP, blood culture).

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106
Q

Scenario: A neonate develops jaundice within 24 hours of birth. Blood group testing reveals an ABO incompatibility between mother and baby.
Q: What is the likely diagnosis, and how would you manage it?

A

Likely diagnosis: Hemolytic jaundice due to ABO incompatibility.
Management: Phototherapy, exchange transfusion if severe.

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107
Q

What is the main treatment for neonatal jaundice?

A

Phototherapy.

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108
Q

__________ therapy is used in severe cases of jaundice to remove bilirubin and replace the neonate’s blood.

A

Exchange transfusion

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109
Q

What are the key thresholds for treatment in neonatal jaundice?

A

Treatment thresholds depend on:

Total serum bilirubin level.
Postnatal age in hours.
Gestational age of the neonate.

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110
Q

True/False:
Q: Blue light phototherapy converts unconjugated bilirubin into a water-soluble form that can be excreted in bile and urine.

A

True.

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111
Q

What is kernicterus?

A

Kernicterus is a severe and potentially fatal condition caused by deposition of unconjugated bilirubin in the brain, leading to neurological damage.

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112
Q

Kernicterus primarily affects the __________ nuclei in the brain.

A

basal ganglia

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113
Q

List the clinical features of kernicterus.

A

Lethargy.
Hypotonia or hypertonia.
Poor feeding.
High-pitched cry.
Seizures.
Developmental delay (long-term).

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114
Q

What are the long-term complications of kernicterus?

A

Cerebral palsy.
Hearing loss.
Intellectual disability.
Gaze abnormalities.

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115
Q

Scenario: A premature neonate presents with severe jaundice. Total serum bilirubin is significantly elevated, and the baby shows signs of lethargy and poor feeding.
Q: What is the concern, and how should it be managed?

A

Concern: Risk of kernicterus.
Management: Immediate phototherapy, possible exchange transfusion, close monitoring of bilirubin levels.

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116
Q

Name 3 key differences between physiological and pathological jaundice.

A

Onset: Physiological >24 hours; Pathological <24 hours.
Bilirubin levels: Physiological mild elevation; Pathological significant rise.
Resolution: Physiological resolves by 1–2 weeks; Pathological often persists.

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117
Q

Necrotising Enterocolitis

A

Acute inflammatory disease affecting preterm neonates leading to bowel necrosis and multi system organ failure

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118
Q

Epidemiology of Necrotising Enterocolitis

A

Low birth weight (1500g) - Prematurity
- Abx therapy > 10 days
- Genetic

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119
Q

What is the most common surgical emergency in neonates?

A

Necrotising Enterocolitis

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120
Q

Necrotising Enterocolitis commonly presents when?

A

the first 2 weeks of life

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121
Q

Symptoms of Necrotising Enterocolitis

A

New feed intolerance - Vomiting (+ bile) - Fresh blood in stools

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122
Q

Signs of Necrotising Enterocolitis

A

Abdominal distention - Reduced bowel sounds - Palpable abdominal mass - Visible intestinal loops - Sepsis

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123
Q

Ix for Necrotising Enterocolitis

A

Bloods + Cultures + Blood Gas+ USS + X ray

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124
Q

What may you find on bloods for Necrotising Enterocolitis

A

: thrombocytopenia, neutropenia

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125
Q

What may you find with Blood Gas for Necrotising Enterocolitis

A

: acidotic

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126
Q

What may you find on USS for Necrotising Enterocolitis

A

Air in the portal system, ascites, perforation

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127
Q

What may be seen on X-ray for Necrotising Enterocolitis

A
  1. Rigler’s sign: both sides of the bowel are visible due to gas in the peritoneal cavity 2. Dilated bowel loops 3. Distended bowel 4. Thickened bowel wall 5. Air outlining falciform ligament. Dilated bowel loops, portal venous gas, intramural gas
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128
Q

Managment of Necrotising Enterocolitis

A

Nil by mouth - Bowel decompression by NG tube - IV Cefotaxime - Surgery to remove necrotic bowel

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129
Q

STAIN - Management of Necrotising Enterocolitis

A

-Surgical emergency -Total parenteral nutrition -Antibiotics -IV fluids -Nil by mouth

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130
Q

What is gastroschisis?

A

Gastroschisis is a congenital abdominal wall defect where the bowel herniates outside the abdomen through a defect, usually to the right of the umbilicus, without a protective membrane.

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131
Q

Gastroschisis is an abdominal wall defect that lacks a __________ covering the exposed bowel.

A

peritoneal sac

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132
Q

How does gastroschisis differ from omphalocele?

A

Gastroschisis: No peritoneal sac, bowel exposed directly to amniotic fluid.
Omphalocele: Covered by a peritoneal sac and involves midline herniation through the umbilicus.

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133
Q

What are the risk factors for gastroschisis?

A

Younger maternal age (teenage pregnancies).
Smoking.
Alcohol use.
Recreational drug use.

134
Q

True/False:
Q: Gastroschisis is more common in older mothers and often associated with other congenital anomalies.

A

False. (It is more common in younger mothers and typically isolated.)

135
Q

Describe the pathophysiology of gastroschisis.

A

Failure of the abdominal wall to close during development leads to herniation of bowel through a defect.
Exposure of bowel to amniotic fluid causes inflammation, thickening, and damage.

136
Q

The defect in gastroschisis is usually located __________ to the umbilicus.

A

right

137
Q

What are the clinical features of gastroschisis?

A

Visible herniation of the bowel at birth.
Bowel appears inflamed and thickened.
No covering sac.

138
Q

What prenatal investigation is used to diagnose gastroschisis?

A

Antenatal ultrasound.

139
Q

Elevated __________ on maternal serum screening can indicate gastroschisis prenatally.

A

alpha-fetoprotein (AFP)

140
Q

Scenario: A 19-year-old pregnant woman undergoes an antenatal ultrasound at 20 weeks, showing herniation of bowel loops into the amniotic cavity without a covering sac.
Q: What is the likely diagnosis?

A

Gastroschisis.

141
Q

What are the key steps in the management of gastroschisis after birth?

A

Stabilization: Prevent heat and fluid loss using a plastic covering.
Nasogastric decompression: To prevent aspiration.
Parenteral nutrition: Due to delayed bowel function.
Surgical correction: Primary closure or staged repair depending on severity.

142
Q

The initial step in managing gastroschisis is to cover the exposed bowel with a __________ to minimize heat and fluid loss.

A

sterile plastic wrap

143
Q

What are the two surgical approaches for gastroschisis?

A

Primary closure: Immediate repair of the defect.
Staged repair: Gradual reduction of the bowel using a silo, followed by defect closure.

144
Q

What are the complications associated with gastroschisis?

A

Bowel necrosis.
Short bowel syndrome.
Sepsis.
Feeding difficulties.

145
Q

True/False:
Q: Gastroschisis can result in long-term feeding problems due to bowel damage and dysfunction.

A

True.

146
Q

What factors influence the prognosis of gastroschisis?

A

Extent of bowel damage.
Presence of complications like sepsis or necrosis.
Success of surgical repair.

147
Q

What is oesophageal atresia (OA)?

A

A congenital condition where the oesophagus ends in a blind pouch instead of connecting to the stomach, often associated with a tracheoesophageal fistula (TOF).

148
Q

Oesophageal atresia is often associated with a __________, which is an abnormal connection between the trachea and the oesophagus.

A

tracheoesophageal fistula (TOF)

149
Q

What is the incidence of oesophageal atresia?

A

Approximately 1 in 3,500 live births.

150
Q

What causes oesophageal atresia and tracheoesophageal fistula?

A

A failure in the division of the foregut into the oesophagus and trachea during the 4th and 5th weeks of gestation.

151
Q

What is the most common type of oesophageal atresia?

A

OA with a distal tracheoesophageal fistula (85% of cases)

152
Q

Match the type of oesophageal atresia with its description:

Isolated OA →
OA with distal TOF →
H-type TOF →

A

Isolated OA → No tracheoesophageal fistula.
OA with distal TOF → Blind-ending oesophagus with a connection to the trachea distally.
H-type TOF → Tracheoesophageal fistula without oesophageal atresia.

153
Q

What are the typical symptoms of oesophageal atresia in a neonate?

A

Excessive salivation and drooling.
Coughing and choking during feeding.
Cyanosis.
Inability to pass a nasogastric tube into the stomach.

154
Q

A neonate with oesophageal atresia will often have an inability to pass a __________ tube into the stomach.

A

nasogastric

155
Q

True/False:
Q: Oesophageal atresia is typically diagnosed in the antenatal period.

A

True (often identified on ultrasound showing polyhydramnios and absence of a stomach bubble).

156
Q

What congenital anomalies are commonly associated with oesophageal atresia?

A

VACTERL association: Vertebral defects, Anal atresia, Cardiac defects, Tracheoesophageal fistula, Renal anomalies, Limb abnormalities.

157
Q

The __________ association is a collection of congenital anomalies that may occur alongside oesophageal atresia.

A

VACTERL

158
Q

How is oesophageal atresia diagnosed prenatally?

A

Ultrasound findings: Polyhydramnios, absence of stomach bubble.

159
Q

How is oesophageal atresia confirmed postnatally?

A

Inability to pass a nasogastric tube into the stomach.
X-ray showing the nasogastric tube coiled in the upper oesophagus.

160
Q

True/False:
Q: A contrast swallow study is required to confirm oesophageal atresia in all cases

A

False (Plain X-ray with a coiled NG tube is often sufficient).

161
Q

What are the initial steps in managing oesophageal atresia?

A

Keep the neonate nil by mouth.
Continuous suction of the blind-ending pouch to prevent aspiration.
Provide intravenous fluids.
Initiate antibiotics if a tracheoesophageal fistula is suspected.

162
Q

In oesophageal atresia, __________ suction is used to prevent aspiration of secretions from the blind pouch.

A

continuous

163
Q

What is the definitive treatment for oesophageal atresia?

A

Surgical correction, often involving repair of the oesophagus and closure of the tracheoesophageal fistula.

164
Q

True/False:
Q: Delayed primary anastomosis is sometimes required in oesophageal atresia when the gap between oesophageal ends is too wide.

A

True.

165
Q

What are the complications of oesophageal atresia?

A

Aspiration pneumonia.
Gastroesophageal reflux disease (GERD).
Anastomotic stricture or leak post-surgery.
Recurrent tracheoesophageal fistula.
Feeding difficulties.

166
Q

Match the complication with its description:

GERD →
Anastomotic leak →
Recurrent TOF →

A

GERD → Reflux of stomach contents into the oesophagus.
Anastomotic leak → Failure of the surgical repair to heal properly.
Recurrent TOF → Reformation of the tracheoesophageal fistula after repair.

167
Q

What factors influence the prognosis of oesophageal atresia?

A

Associated anomalies (e.g., VACTERL).
Birth weight.
Presence of complications (e.g., aspiration pneumonia, surgical complications)

168
Q

The __________ classification is used to predict survival in oesophageal atresia based on birth weight and associated anomalies.

A

Waterston

169
Q

What is bowel atresia?

A

A congenital condition where part of the bowel is completely obstructed or absent, leading to an interruption in the continuity of the gastrointestinal tract.

170
Q

What are the types of bowel atresia?

A

The types of bowel atresia include:

Duodenal atresia
Jejunoileal atresia
Colonic atresia

171
Q

What is the most common type of bowel atresia?

A

Duodenal atresia is the most common type of bowel atresia.

172
Q

What are the key clinical features of bowel atresia?

A

Vomiting, often bilious
Abdominal distension
Failure to pass meconium
Jaundice in some cases

173
Q

____ is the most common clinical sign of bowel atresia in neonates.

A

Vomiting

174
Q

How is bowel atresia diagnosed?

A

Diagnosis is confirmed via imaging, typically with:

Abdominal X-ray, showing dilated loops of bowel and absence of gas in the distal bowel
Contrast studies like barium enema or contrast fluoroscopy

175
Q

What other conditions may be associated with bowel atresia?

A

Bowel atresia can be associated with other congenital conditions, including:

Down syndrome
Cardiac defects
Malrotation
Anorectal malformations

176
Q

What is the management of bowel atresia?

A

Management typically involves:

Surgical repair, often within 24 hours of birth
Supportive care including IV fluids, electrolytes, and nutrition
Post-surgery monitoring for complications such as infection or anastomotic leaks

177
Q

____ is a common complication after surgical repair of bowel atresia.

A

Anastomotic leak

178
Q

What is the prognosis for infants with bowel atresia?

A

The prognosis depends on the type and location of the atresia, but with early surgical intervention, many infants can survive and thrive. Long-term complications may include malabsorption and bowel obstruction.

179
Q

True or False: Bowel atresia is typically diagnosed after birth.

A

TRUE.

180
Q

What is the role of prenatal screening in bowel atresia?

A

While bowel atresia can sometimes be detected on prenatal ultrasound, it is often not diagnosed until after birth when the clinical signs appear.

181
Q

What is gestational diabetes?

A

A form of diabetes diagnosed during pregnancy, characterized by hyperglycemia that develops due to insulin resistance and increased insulin demand during pregnancy.

182
Q

Gestational diabetes typically develops during the __________ or __________ trimester of pregnancy.

A

second; third

183
Q

What are the maternal risk factors for developing gestational diabetes?

A

Obesity (BMI >30).
Advanced maternal age (>35 years).
Previous macrosomic baby (>4.5 kg).
Family history of diabetes (first-degree relative).
Previous gestational diabetes.
Ethnic groups at higher risk (South Asian, Black, or Middle Eastern).
Polycystic ovary syndrome (PCOS).

184
Q

True/False:
Q: A history of polycystic ovary syndrome (PCOS) increases the risk of gestational diabetes

A

TRUE.

185
Q

How is gestational diabetes diagnosed?

A

Through an oral glucose tolerance test (OGTT):

Fasting glucose: \u2265 5.6 mmol/L.
2-hour post-75 g glucose load: \u2265 7.8 mmol/L.

186
Q

An oral glucose tolerance test (OGTT) is usually performed between __________ and __________ weeks of pregnancy in at-risk women.

A

24; 28

187
Q

True/False:
Q: Women with a fasting blood glucose \u2265 7.0 mmol/L at any point in pregnancy should be diagnosed with overt diabetes rather than gestational diabetes.

A

True.

188
Q

What are the potential neonatal complications of gestational diabetes?

A

Macrosomia (birth weight >4.5 kg).
Neonatal hypoglycemia.
Shoulder dystocia during delivery.
Premature birth.
Respiratory distress syndrome.
Hyperbilirubinemia (jaundice).
Increased risk of developing obesity or diabetes later in life.

189
Q

Neonatal __________ is a common complication of gestational diabetes due to hyperinsulinemia in the fetus after delivery.

A

hypoglycemia

190
Q

What are the maternal complications of gestational diabetes?

A

Increased risk of cesarean delivery.
Preeclampsia.
Polyhydramnios.
Increased risk of developing type 2 diabetes later in life.

191
Q

True/False:
Q: Women with gestational diabetes have an increased lifetime risk of developing type 2 diabetes.

A

True.

192
Q

What is the initial management for gestational diabetes?

A

Dietary modifications: Low glycemic index diet, portion control.
Regular physical activity: Moderate exercise to improve glucose control.
Blood glucose monitoring: Fasting and postprandial levels.

193
Q

What medications are used if blood glucose targets are not achieved with lifestyle changes?

A

Metformin: First-line medication.
Insulin: Used if metformin is contraindicated or insufficient.

194
Q

The target fasting blood glucose level in gestational diabetes management is <__________ mmol/L.

A

5.3

195
Q

True/False:
Q: Insulin is the first-line treatment for all women with gestational diabetes.

A

False (Diet and metformin are often tried first).

196
Q

When is delivery typically recommended for women with gestational diabetes?

A

At 37–39 weeks, depending on glucose control and the presence of complications.

197
Q

Cesarean delivery may be recommended in women with gestational diabetes if the estimated fetal weight is >__________ kg due to the risk of shoulder dystocia.

A

4.5

198
Q

How is gestational diabetes managed postpartum?

A

Glucose monitoring: Blood glucose levels typically normalize postpartum.
Follow-up testing: OGTT at 6–13 weeks postpartum to check for persistent diabetes or prediabetes.
Lifestyle advice: Weight management, healthy diet, and regular exercise to reduce future diabetes risk.

199
Q

True/False:
Q: Breastfeeding is encouraged for women with gestational diabetes as it reduces the risk of diabetes in both mother and baby.

A

true.

200
Q

What are the long-term risks for mothers with a history of gestational diabetes?

A

50% risk of developing type 2 diabetes within 10 years.
Increased cardiovascular risk.

201
Q

Children of mothers with gestational diabetes are at an increased risk of developing __________ and __________ later in life.

A

obesity; type 2 diabetes

202
Q

What is maternal hyperthyroidism?

A

A condition where an overactive thyroid gland during pregnancy produces excess thyroid hormones, potentially affecting both the mother and fetus.

203
Q

The most common cause of maternal hyperthyroidism is __________ disease, an autoimmune condition characterized by the presence of TSH receptor antibodies (TRAbs).

A

Graves’

204
Q

How does maternal hyperthyroidism affect the fetus?

A

Increased risk of fetal and neonatal hyperthyroidism due to the transfer of maternal TSH receptor antibodies (TRAbs).
Preterm birth.
Low birth weight.
Fetal tachycardia.
Fetal goitre.
Intrauterine growth restriction (IUGR).

205
Q

Fetal hyperthyroidism occurs when maternal __________ cross the placenta and stimulate the fetal thyroid gland.

A

TSH receptor antibodies (TRAbs)

206
Q

True/False:
Q: Fetal tachycardia is a potential sign of fetal hyperthyroidism.

A

true.

207
Q

What are the potential complications of untreated hyperthyroidism in pregnancy?

A

Miscarriage.
Pre-eclampsia.
Placental abruption.
Preterm labor.
Stillbirth.

208
Q

What are the clinical features of neonatal hyperthyroidism?

A

Tachycardia.
Irritability.
Poor feeding.
Failure to thrive.
Goitre.
Exophthalmos (bulging eyes).
Increased stool frequency.

209
Q

Neonatal hyperthyroidism is usually transient and lasts for __________ to __________ months, corresponding to the duration of maternal antibody persistence in the neonate.

A

3; 6

210
Q

How is neonatal hyperthyroidism diagnosed?

A

Elevated free T4 and suppressed TSH in the neonate.
Detection of maternal TRAbs.

211
Q

True/False:
Q: Neonatal hyperthyroidism may present with symptoms of heart failure if untreated

A

True.

212
Q

What investigations are performed to diagnose hyperthyroidism during pregnancy?

A

Thyroid function tests: Elevated free T4/T3 and suppressed TSH.
Detection of TRAbs to assess fetal risk.
Ultrasound for fetal growth and signs of fetal goitre or hyperthyroidism.

213
Q

Suppressed __________ and elevated free __________ are hallmark findings in maternal hyperthyroidism.

A

TSH; T4

214
Q

What are the key principles in managing maternal hyperthyroidism?

A

Use of antithyroid drugs (ATDs):
First trimester: Propylthiouracil (PTU) preferred to reduce the risk of teratogenicity.
After the first trimester: Switch to carbimazole or continue PTU at the lowest effective dose.
Regular monitoring of thyroid function.
Monitoring for side effects of ATDs (e.g., agranulocytosis).
Obstetric monitoring for fetal well-being.

215
Q

True/False:
Q: Antithyroid drugs (ATDs) can cross the placenta and may cause fetal hypothyroidism or goitre.

A

True.

216
Q

Propylthiouracil (PTU) is preferred during the __________ trimester due to its lower risk of teratogenicity.

A

first

217
Q

What are the postpartum considerations for maternal hyperthyroidism?

A

Risk of postpartum thyroiditis.
Neonatal monitoring for thyroid dysfunction.
Continuation of ATDs while breastfeeding if required.

218
Q

_________ can occur postpartum, presenting as a transient hyperthyroid phase followed by hypothyroidism.

A

Postpartum thyroiditis

219
Q

True/False:
Q: ATDs like carbimazole are safe during breastfeeding in controlled doses.

A

True.

220
Q

What are the potential long-term complications for the neonate if maternal hyperthyroidism is untreated?

A

Developmental delay.
Cardiac complications (e.g., tachycardia, heart failure).
Persistent growth restriction.

221
Q

What is the prognosis for neonates with hyperthyroidism?

A

Excellent if appropriately treated, as most cases resolve with the clearance of maternal TRAbs.

222
Q

What is hypoglycaemia in neonates and children?

A

Hypoglycaemia refers to abnormally low blood glucose levels, which can lead to neurological impairment if untreated.

223
Q

In neonates, hypoglycaemia is defined as a blood glucose level <__________ mmol/L.

A

2.6

224
Q

True/False:
Q: Hypoglycaemia in neonates always presents with clear clinical symptoms.

A

False (It can be asymptomatic).

225
Q

What are the main causes of neonatal hypoglycaemia?

A

Inadequate glycogen stores: Prematurity, small for gestational age (SGA), intrauterine growth restriction (IUGR).
Increased glucose utilization: Sepsis, hypothermia, polycythemia.
Endocrine causes: Congenital hyperinsulinism, adrenal insufficiency, hypopituitarism.
Maternal factors: Gestational diabetes, maternal drug use (e.g., beta-blockers).

226
Q

What are the causes of hypoglycaemia in older children?

A

Fasting hypoglycaemia: Glycogen storage disorders, prolonged fasting.
Hyperinsulinism: Insulinoma, accidental insulin overdose.
Hormonal deficiencies: Cortisol or growth hormone deficiency.
Metabolic disorders: Fatty acid oxidation defects, organic acidemias.

227
Q

The most common cause of neonatal hypoglycaemia is __________ due to gestational diabetes.

A

hyperinsulinism

228
Q

What are the signs and symptoms of hypoglycaemia in neonates?

A

Jitteriness.
Poor feeding.
Lethargy.
Apnoea.
Hypotonia.
Seizures (in severe cases).

229
Q

How does hypoglycaemia present in older children?

A

Sweating.
Irritability or confusion.
Tremors.
Dizziness.
Palpitations.
Seizures or loss of consciousness (if severe).

230
Q

Hypoglycaemia can cause __________ symptoms such as sweating, tachycardia, and irritability due to catecholamine release.

A

adrenergic

231
Q

How is hypoglycaemia diagnosed?

A

Blood glucose measurement (<2.6 mmol/L in neonates, <3.0 mmol/L in children).
Critical sample analysis during hypoglycaemia:
Insulin levels.
Cortisol and growth hormone levels.
Ketones and lactate.
Plasma amino acids and acylcarnitine profile (to identify metabolic disorders).

232
Q

The presence of __________ during hypoglycaemia suggests a fatty acid oxidation disorder.

A

hypoketonaemia

233
Q

True/False:
Q: Measuring insulin levels during hypoglycaemia helps differentiate between hyperinsulinism and other causes.

A

true.

234
Q

What is the immediate treatment for hypoglycaemia in neonates?

A

Immediate feeding or glucose gel if asymptomatic and mild hypoglycaemia.
IV dextrose (10%) for symptomatic or severe hypoglycaemia.
Monitor blood glucose closely after treatment.

235
Q

How is hypoglycaemia treated in older children?

A

Oral glucose (e.g., sugary drinks, glucose tablets) if mild and the child can take orally.
IV dextrose (10-25%) for severe cases.
Address underlying cause (e.g., treat infection, adjust insulin dosage).

236
Q

The initial IV glucose bolus for hypoglycaemia in children is __________ mL/kg of 10% dextrose.

A

2

237
Q

True/False:
Q: Glucagon can be used in cases of hypoglycaemia when IV access is unavailable.

A

true.

238
Q

What are the potential complications of untreated hypoglycaemia?

A

Seizures.
Permanent brain injury.
Developmental delays.

239
Q

Prolonged untreated hypoglycaemia can lead to irreversible __________ damage.

A

neurological

240
Q

How is neonatal hypoglycaemia monitored and prevented in at-risk neonates?

A

Early and frequent feeding.
Blood glucose monitoring in at-risk infants (e.g., SGA, LGA, preterm).
IV glucose if feeding is inadequate to maintain glucose levels.

241
Q

How can recurrent hypoglycaemia in children be prevented?

A

Treat underlying causes (e.g., endocrine or metabolic disorders).
Frequent small meals with complex carbohydrates.
Avoid prolonged fasting

242
Q

True/False:
Q: Neonates born to mothers with diabetes require routine glucose monitoring in the first 24 hours of life.

A

true.

243
Q

What is Group B Streptococcus (GBS)?

A

A gram-positive bacterium that is part of the normal flora in the gastrointestinal and genitourinary tracts but can cause severe infections in neonates, pregnant women, and immunocompromised individuals.

244
Q

Group B Streptococcus (GBS) is also known as __________.

A

Streptococcus agalactiae

245
Q

True/False:
Q: GBS is the most common cause of neonatal sepsis and meningitis.

A

true.

246
Q

What are the two types of GBS infections in neonates?

A

Early-onset GBS infection (EOGBS):
Occurs within the first 7 days of life (commonly within 24 hours).
Acquired during delivery from colonized maternal genital tract.
Late-onset GBS infection (LOGBS):
Occurs between 7–90 days of life.
Acquired from the environment or colonized caregivers.

247
Q

Early-onset GBS infection (EOGBS) typically presents within the first __________ days of life.

A

7

248
Q

What are the main clinical features of EOGBS?

A

Sepsis (e.g., temperature instability, lethargy, poor feeding).
Respiratory distress (e.g., grunting, tachypnoea).
Pneumonia.
Meningitis (rare but possible).

249
Q

What are the main clinical features of LOGBS?

A

Meningitis.
Bacteraemia.
Osteomyelitis or septic arthritis.

250
Q

What are the risk factors for neonatal GBS infection?

A

Maternal GBS colonization.
Premature delivery (<37 weeks).
Prolonged rupture of membranes (>18 hours).
Maternal fever during labor (>38\u00b0C).
Previous baby with GBS infection.
Use of intrapartum antibiotics.

251
Q

True/False:
Q: Premature rupture of membranes is a significant risk factor for early-onset GBS infection.

A

true.

252
Q

How is GBS infection diagnosed in neonates?

A

Blood cultures: Confirm bacteraemia.
Lumbar puncture: Confirm meningitis if CNS infection is suspected.
Chest X-ray: Assess for pneumonia.
CRP and full blood count: Supportive evidence of infection.

253
Q

A __________ puncture is performed in suspected cases of GBS meningitis to confirm the diagnosis.

A

lumbar

254
Q

What is the treatment for neonatal GBS infection?

A

Empirical antibiotics: Start with benzylpenicillin and gentamicin.
Adjust antibiotics based on culture results.
Supportive care for complications (e.g., respiratory support, fluid management).

255
Q

The first-line antibiotics for suspected neonatal GBS infection are __________ and __________.

A

benzylpenicillin; gentamicin

256
Q

True/False:
Q: Antibiotics should be started immediately in neonates with suspected GBS infection, even before culture results.

A

true.

257
Q

What are the strategies to prevent neonatal GBS infection?

A

Maternal screening: Vaginal and rectal swabs at 35–37 weeks gestation.
Intrapartum antibiotic prophylaxis (IAP):
Indicated for GBS colonization, prolonged rupture of membranes, or maternal fever.
First-line antibiotic: Benzylpenicillin.

258
Q

Intrapartum antibiotic prophylaxis (IAP) with __________ is the standard approach to prevent early-onset GBS infection.

A

benzylpenicillin

259
Q

True/False:
Q: Intrapartum antibiotic prophylaxis eliminates the risk of late-onset GBS infection.

A

False (It reduces early-onset GBS infection but does not prevent late-onset infection).

260
Q

What are the complications of neonatal GBS infection?

A

Meningitis leading to long-term neurological sequelae (e.g., hearing loss, developmental delay).
Septic shock.
Death in severe cases

261
Q

Long-term complications of GBS meningitis include __________ impairment and developmental delay

A

hearing

262
Q

True/False:
Q: Mortality rates for early-onset GBS infection are higher in preterm neonates.

A

true.

263
Q

What factors influence the prognosis of neonatal GBS infection?

A

Gestational age (worse in preterm infants).
Timeliness of diagnosis and treatment.
Presence of complications such as meningitis or septic shock.

264
Q

What is Listeria infection?

A

An infection caused by Listeria monocytogenes, a gram-positive, facultative intracellular bacterium that can cause severe infections in neonates, pregnant women, and immunocompromised individuals.

265
Q

Listeria monocytogenes is a __________-positive bacterium that can survive and multiply at refrigeration temperatures.

A

gram

266
Q

True/False:
Q: Listeria infection is a zoonotic disease transmitted primarily through contaminated food.

A

true.

267
Q

How is Listeria transmitted?

A

Ingestion of contaminated food (e.g., unpasteurized dairy, soft cheeses, deli meats, raw vegetables).
Vertical transmission from mother to fetus during pregnancy.
Postnatal exposure through contaminated hospital environments

268
Q

Vertical transmission of Listeria monocytogenes occurs transplacentally or during __________.

A

delivery

269
Q

What are the clinical features of Listeria infection in neonates?

A

Early-onset (within 7 days of birth):
Sepsis.
Pneumonia.
Meningitis.
Disseminated granulomatosis infantiseptica (a severe form with abscesses and granulomas).
Late-onset (7–90 days):
Meningitis.
Sepsis.

270
Q

Early-onset neonatal Listeria infection typically presents as __________ and pneumonia.

A

sepsis

271
Q

What are the maternal symptoms of Listeria infection during pregnancy?

A

Flu-like symptoms (fever, chills, myalgia).
Gastrointestinal symptoms (nausea, vomiting, diarrhea).
In severe cases, preterm labor, miscarriage, or stillbirth.

272
Q

True/False:
Q: Maternal Listeria infection during pregnancy is often asymptomatic.

A

true.

273
Q

How is Listeria infection diagnosed?

A

Blood cultures: To confirm bacteraemia.
CSF analysis: Elevated WBCs, low glucose, and positive cultures in meningitis.
Placental cultures: Useful in maternal infections.
PCR: For rapid detection of Listeria monocytogenes.

274
Q

__________ cultures are the gold standard for diagnosing neonatal Listeria infection.

A

blood.

275
Q

True/False:
Q: PCR testing can rapidly confirm the presence of Listeria monocytogenes in blood or CSF samples.

A

true.

276
Q

What is the treatment for Listeria infection in neonates?

A

Empirical antibiotics:
Ampicillin and gentamicin are the first-line treatment.
Adjust antibiotics based on culture and sensitivity results.

277
Q

The first-line antibiotics for neonatal Listeria infection are __________ and __________.

A

ampicillin; gentamicin

278
Q

True/False:
Q: Gentamicin is often used synergistically with ampicillin to treat Listeria infection.

A

true.

279
Q

What are the complications of Listeria infection in neonates?

A

Meningitis leading to long-term neurological sequelae.
Septicemia.
Respiratory failure.
Death in severe cases.

280
Q

Long-term complications of Listeria meningitis include __________ impairment and developmental delay.

A

hearing

281
Q

True/False:
Q: Mortality rates are higher in early-onset Listeria infection compared to late-onset.

A

True.

282
Q

How can Listeria infection be prevented in pregnancy?

A

Avoid high-risk foods (e.g., unpasteurized dairy, deli meats, raw vegetables).
Practice good food hygiene (e.g., washing vegetables, cooking meat thoroughly).
Maintain aseptic techniques during delivery and neonatal care

283
Q

Pregnant women should avoid __________ cheeses to reduce the risk of Listeria infection.

A

soft

284
Q

True/False:
Q: Pasteurization of dairy products eliminates the risk of Listeria infection.

A

true.

285
Q

What factors influence the prognosis of neonatal Listeria infection?

A

Timing of diagnosis and treatment.
Gestational age (worse in preterm infants).
Severity of infection (e.g., meningitis, septic shock).

286
Q

Neonatal survival improves significantly with early __________ therapy

A

antibiotic

287
Q

What is HSV encephalitis?

A

A severe, potentially fatal inflammation of the brain caused by the herpes simplex virus (HSV), primarily HSV-1 in older children and HSV-2 in neonates.

288
Q

HSV encephalitis in neonates is typically caused by __________, while in older children it is more commonly caused by __________.

A

HSV-2; HSV-1

289
Q

True/False:
Q: HSV encephalitis is the most common cause of sporadic viral encephalitis in children.

A

true.

290
Q

How does HSV cause encephalitis?

A

The virus enters the central nervous system (CNS) via hematogenous spread or reactivation in the trigeminal or olfactory nerve.
It leads to inflammation, necrosis, and hemorrhage, particularly in the temporal and frontal lobes.

291
Q

HSV encephalitis predominantly affects the __________ and __________ lobes of the brain.

A

temporal; frontal

292
Q

What are the common clinical features of HSV encephalitis in neonates?

A

Seizures.
Lethargy or irritability.
Poor feeding.
Fever or hypothermia.
Apnoea or respiratory distress.

293
Q

How does HSV encephalitis present in older children?

A

Fever.
Headache.
Altered mental status (confusion, drowsiness, or coma).
Focal neurological signs (e.g., hemiparesis).
Seizures.
Speech disturbances (aphasia).

294
Q

True/False:
Q: Seizures are a common presenting feature of HSV encephalitis in both neonates and older children.

A

true.

295
Q

What investigations are used to diagnose HSV encephalitis?

A

Lumbar puncture:
Elevated white cell count, protein, and normal or low glucose in CSF.
PCR to detect HSV DNA in CSF (gold standard).
Neuroimaging:
MRI showing temporal lobe hyperintensities.
EEG:
May show focal abnormalities or periodic lateralized epileptiform discharges (PLEDs).

296
Q

The gold standard for diagnosing HSV encephalitis is the detection of __________ in CSF by PCR.

A

HSV DNA

297
Q

True/False:
Q: A normal MRI excludes the diagnosis of HSV encephalitis.

A

False (Early disease may not show changes on imaging).

298
Q

What is the first-line treatment for HSV encephalitis?

A

Intravenous acyclovir.

299
Q

Acyclovir is typically administered at a dose of __________ mg/kg IV every 8 hours for HSV encephalitis.

A

20

300
Q

What supportive care measures are important in HSV encephalitis?

A

Seizure control with antiepileptic drugs (e.g., phenobarbital, levetiracetam).
Management of cerebral edema (e.g., head elevation, hypertonic saline, or mannitol).
Monitoring and treatment of complications like respiratory failure or shock.

301
Q

True/False:
Q: Treatment with acyclovir should begin immediately if HSV encephalitis is suspected, even before confirmation.

A

true.

302
Q

What are the potential complications of HSV encephalitis?

A

Persistent neurological deficits (e.g., hemiparesis, aphasia).
Developmental delay.
Epilepsy.
Hearing loss.
Death if untreated.

303
Q

Untreated HSV encephalitis has a mortality rate of up to __________%.

A

70

304
Q

True/False:
Q: Early treatment with acyclovir significantly reduces the risk of long-term complications and mortality.

A

TRUE.

305
Q

What factors influence the prognosis of HSV encephalitis?

A

Timing of treatment initiation (earlier treatment improves outcomes).
Severity of neurological symptoms at presentation.
Presence of complications like seizures or cerebral edema.

306
Q

Long-term outcomes of HSV encephalitis depend on __________ diagnosis and treatment.

A

early

307
Q

How can neonatal HSV encephalitis be prevented?

A

Screening and treatment of maternal genital HSV during pregnancy.
Cesarean delivery if active genital lesions are present.
Antiviral prophylaxis for at-risk neonates.

308
Q

True/False:
Q: Cesarean delivery is recommended for women with active genital HSV lesions at the time of labor to prevent neonatal HSV infection.

A

TRUE.

309
Q

What are cleft lip and palate?

A

Congenital deformities caused by incomplete fusion of the lip and/or palate during embryonic development.

310
Q

A __________ occurs when the tissue that forms the lip does not join properly during development, while a __________ occurs when the roof of the mouth fails to close.

A

cleft lip; cleft palate

311
Q

True/False:
Q: Cleft lip and palate are the most common craniofacial abnormalities.

A

true.

312
Q

What is the prevalence of cleft lip and/or palate?

A

Approximately 1 in 700 live births worldwide.

313
Q

Which populations are more affected by cleft lip and palate?

A

Higher prevalence in Asian and Native American populations; lower prevalence in African populations.

314
Q

When does the formation of the lip and palate occur during gestation?

A

Lip: Between 4th and 7th weeks of gestation.
Palate: Between 6th and 9th weeks of gestation.

315
Q

Cleft lip and palate occur due to failure of fusion of the __________ and __________ processes during embryogenesis.

A

maxillary; medial nasal

316
Q

True/False:
Q: Cleft lip and palate may occur in isolation or as part of a syndrome.

A

true.

317
Q

What are the risk factors for cleft lip and palate?

A

Genetic predisposition.
Maternal smoking or alcohol use.
Maternal folate deficiency.
Maternal medications (e.g., anticonvulsants like phenytoin).
Syndromes (e.g., Pierre Robin sequence, trisomy 13).

318
Q

Maternal __________ deficiency is a modifiable risk factor for cleft lip and palate.

A

folate

319
Q

What are the primary clinical features of cleft lip and palate?

A

Cleft lip: Visible gap or opening in the upper lip, which may be unilateral, bilateral, or midline.
Cleft palate: Opening in the roof of the mouth, which may involve the hard palate, soft palate, or both.

320
Q

What are the potential complications associated with cleft lip and palate?

A

Feeding difficulties.
Speech and language delays.
Recurrent otitis media.
Hearing impairment.
Dental malformations.

321
Q

Recurrent __________ is common in cleft palate due to dysfunction of the eustachian tube.

A

otitis media

322
Q

How are cleft lip and palate diagnosed?

A

Antenatal diagnosis: Detected on routine ultrasound after 20 weeks of gestation.
Postnatal diagnosis: Visual inspection at birth or failure to feed effectively.

323
Q

True/False:
Q: Cleft palate is always detected antenatally.

A

False (It may not be identified until feeding difficulties arise).

324
Q

What is the general approach to managing cleft lip and palate?

A

Multidisciplinary care involving:

Surgeons: For surgical repair.
Speech therapists: To address speech delays.
Audiologists: For hearing assessment and management.
Dentists/Orthodontists: For dental malformations.

325
Q

Surgical repair of cleft lip is typically performed around __________ months of age, while cleft palate repair is performed around __________ months

A

3–6; 9–12

326
Q

What are the feeding interventions for neonates with cleft palate?

A

Specialized bottles and nipples.
Upright feeding position to reduce nasal regurgitation.
Referral to a lactation consultant or feeding specialist.

327
Q

What are the long-term complications of cleft lip and palate?

A

Speech and language difficulties.
Malocclusion requiring orthodontic treatment.
Psychosocial issues due to cosmetic appearance.

328
Q

What role does speech therapy play in long-term care?

A

Improves articulation and phonation.
Addresses nasality caused by velopharyngeal insufficiency.

329
Q

True/False:
Q: Most children with cleft palate require multiple surgeries throughout childhood.

A

True.

330
Q

What syndromes are commonly associated with cleft lip and palate?

A

Pierre Robin sequence.
Trisomy 13 (Patau syndrome).
DiGeorge syndrome.
Van der Woude syndrome.

331
Q

Match the syndrome with its associated features:
Pierre Robin sequence →
Trisomy 13 →
DiGeorge syndrome →

A

Pierre Robin sequence → Micrognathia, cleft palate, glossoptosis.
Trisomy 13 → Midline facial defects, cleft lip/palate.
DiGeorge syndrome → Cardiac defects, hypocalcemia, cleft palate.

Phase 3a - Paediactrics (17 decks)

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