Neonatology Flashcards

1
Q

Why do you get ishcaemia in HIE?

A

Hypoxia- causes blood vessles to contrict - ischaemia

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2
Q

What metabolic changes do you get in HIE?

A

Hypoxia- reduced aerobic respiration - increase anaerobic respiration - rise in latctae- metabolic acidosis

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3
Q

Why do you need respiratory support in HIE?

A

HIE management - theraputic hypothermia
Cooled infants are at risk of PPHN
So keep oxyegn sats between 92 and 98%

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4
Q

What anticonvulsants are used in HIE?

A

Phenobarbital remains the standard first-line pharmacotherapy for neonatal seizures resulting from HIE
Phenytoin
Midazolam

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5
Q

Why should you do a CXR of there is a history of meconium aspiration?

A

Meconium aspiration - can cause chemical injury - can result in pneumothorax

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6
Q

What is TTN?

A

Transient tachypnoea of the newborn (TTN)

Caused by delayed clearance/absorption of lung fluid after birth. Presents within 4h of birth. Common after elective CS.

  • CXR: shows streaky perihilar changes and fluid in lung horizontal fissures.
  • Treatment: supplemental O2. Consider nasal CPAP/high flow and antibiotics.
  • Prognosis: spontaneously resolves within 24h.
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7
Q

What is RDS?

A

RDS is a lung disease caused by surfactant deficiency. It is largely seen in preterm infants, being less common after 32wk gestation.

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8
Q

Management of RDS

A
  • Good delivery room resuscitation: this care may involve ETT intubation and administration of surfactant (extremely preterm) or nasal CPAP/high flow.
    • Respiratory support will depend on the severity: may need O2, nasal CPAP/high flow (see graphic Neonatal respiratory support, pp. 140–141), or MV (see graphic Conventional positive pressure ventilation, pp. 142–143).
    • Surfactant (Curosurf® or Survanta®): requires ETT intubation and MV and should be considered in all extremely preterm (<27/40) infants and when FiO2 >0.3–0.4.
    • Antibiotics (e.g. penicillin and gentamicin): until congenital pneumonia has been excluded, as it can mimic or coexist with RDS.
    • Nutrition: use IV fluids until the baby is stable. Then start gastric tube feeds with minimal volumes and slowly increase as tolerated. If unstable, start TPN.
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9
Q

What is old and new Bronchopulmonary dysplasia?

A
  • ‘Old’ BPD was a disease of scarring and repair, and was associated with long periods of MV, often with high PIP and high FiO2.
  • ‘New’ BPD is a condition of impaired alveolar development, with less destruction and scarring. Mechanical, oxidative, and inflammatory factors contribute to lung injury. The CXRs are less dramatic (see Fig. 4.7), but impairment in lung function continue through childhood and is associated with other disorders.
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10
Q

What is the defintion of BPD?

A

‘O2 requirement at 36/40 corrected gestational age (CGA)’

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11
Q

What is the severity classification of BPD?

A
  • Mild: need for supplemental O2 at 28 days, but not at 36/40 CGA.
  • Moderate: need for supplemental O2 <30% at 28 days and 36/40 CGA.
  • Severe: MV or requiring O2 >30% at ≥36/40 CGA.
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12
Q

Risk factors for BPD?

A
  • Gestational immaturity.
  • LBW.
  • ♂.
  • Caucasian heritage.
  • IUGR.
  • Family history of asthma.
  • History of chorioamnionitis.
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13
Q

Prevention of BPD

A

Caffeine citrate for apnoea of prematurity in infants <1250g.
Vitamin A supplementation for infants <1000g.

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14
Q

Management of establish BPD

A

No therapies are known to improve outcome in BPD. However:
* O2 is the most commonly used treatment, and the suggested dose is that needed for SpO2 90–95%
* Other treatments are: diuretics, corticosteroids, sildenafil, and optimizing nutrition.
* Immunization for at-risk infants with monoclonal respiratory syncytial virus (RSV) antibody

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15
Q

What is meconium aspiration syndrome?

A

Aspiration of meconium stained amniotic fluid (MSAF), which can happen either antenatally or during birth
Results in varying degrees of respiratory distress

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16
Q

Why do you get MSAF?

A

** after-effect of in-utero peristalsis**

In term or post term infants, where gastrointestinal maturation is appropriate, this movement leads to meconium passage.

The peristalsis usually is the result of:
- foetal hypoxic stress
- vagal stimulation due to cord compression
- There is also some evidence that chronic hypoxia may lead to it as well.

  • These factors can also lead to fetal gasping which results in MAS.
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17
Q

What happens after aspirating the meconium?

A

Stimulate the release of many vasoactive and cytokine substances thatL:
- activate inflammatory pathways
- triggering vasculature changes
- inhibits the effect of surfactant in the lungs.

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18
Q

Common features seen with MAS-related respiratory distress of the newborn:

A

Partial or Total Airway Obstruction
Foetal Hypoxia
Pulmonary Inflammation
Infection: The inflammation process predisposes the foetal lung to an increased risk of infection and can cause a chemical pneumonitis
Surfactant Inactivation
Persistent Pulmonary Hypertension (PPHN)

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19
Q

RF for MAS

A

Conditions leading to foetal hypoxia and foetal gasping increase the risk of aspirating meconium in a term or post-term baby, they are as follows;

  • Gestational Age > 42 weeks
  • Foetal distress (tachycardia / bradycardia)
  • Intrapartum hypoxia secondary to placental insufficiency
  • Thick meconium particles
  • Apgar Score <7
  • Chorioamnionitis +/- Prolonged pre-rupture
  • Oligohydramnios
  • In utero growth restriction (IUGR)
  • Maternal hypertension, diabetes, pre-eclampsia or eclampsia, smoking and drug abuse
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20
Q
A
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21
Q

Clinical features of MAS

A

clinical diagnosis. A full history of the risk factors, confirmed presence of meconium in the amniotic fluid and aspirated meconium (clinical signs of post-maturity and MSAF staining) are necessary to diagnose MAS in an infant presenting with respiratory distress where no other diagnosis can be confirmed ie. MAS is a diagnosis of exclusion.

On examination the newborn infant will show signs of respiratory distress:

  • Tachypnoea – a respiratory rate of >60 breaths per minute
  • Tachycardia – a heart rate of >160 beats per minute
  • Cyanosis – this requires immediate management
  • Grunting
  • Nasal flaring
  • Recessions – intercostal, supraclavicular, tracheal tug
  • Hypotension – systolic blood pressure of <70 mmHg
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22
Q

Ix for MAS

A
  • CXR
  • Infection markers:
    FBC
    CRP
    Blood cultures

Other neonatal ix:
* Arterial Blood Gas
* Dual Pulse Oximetry – (pre- and post-ductal) to determine hypoxia and assess any potential right-to-left shunts that may be present. A difference of 5-10% between the limbs is clinically significant of neonatal pathology.
* Echocardiography – Used to exclude any congenital heart abnormalities causing pulmonary hypertension e.g. PDA, PFO, tricuspid valve regurgitation
* Cranial Ultrasound – Used to assess for results of any hypoxic damage to the brain

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23
Q

Differentials for MAS

A

Transient tachypnoea of the newborn
* Neither hypoxia nor cyanosis are usually seen
* MSAF may or may not have been seen at delivery
* CXR may show some perihilar markings and/or sail sign
* Blood gases should be within normal values

Surfactant deficiency
* Causes respiratory distress similar to MAS but more often seen in pre-term infants.
* The infant will likely need some ventilator and oxygen support.
* no MSAF was seen at delivery
* Blood gases shows hypoxaemia and acidosis.

Persistent pulmonary hypertension
* This can be present on its own or in combination with MAS.
* The newborn has persistent hypoxaemia causing respiratory distress.
* Causes of PPHN need to be investigated e.g. PDA with pre-ductal and post-ductal oxygen saturations.

24
Q

Management of MAS

A
  • Observations esp o2 sats
  • Routine care: Newborns should be placed under an infant warmer, as hypothermia inhibits surfactant production
    Continuous oxygen saturations should be monitored
    Blood glucose, UE, FBC, CRP and calcium may need to be assessed and corrected if necessary to exclude other treatable pathologies.
    Nutritional support should be commenced on day one in the form of IV fluids. The aim should be to switch to nasogastric and oral feeds when permitting.
  • Ventilation /Oxygen Therapy: Via nasal canula/ CPAP/intubation and ventilation
  • Antibiotics:Antibiotics are usually indicated in infants born who have clinical suspicion of infection. Antibiotics can be stopped if the 48hr cultures and clinical examination findings are negative.
  • Surfactant: A bolus of surfactant may be administered in newborns with moderate MAS or if a pneumothorax is present
  • Inhaled Nitric Oxide (iNO):
    In newborns requiring mechanical ventilation and surfactant there is often pulmonary hypertension also present which requires iNO.
25
Q

Complications of MAS

A
  • Air leak
  • PPHN
  • Cerebral Palsy (CP)
  • Chronic lung disease
26
Q

Why do you get air leak in MAS?

A

Due to thick meconium sometimes causing a “ball-valve” effect, air leaks can occur due to alveolar hyperdistention leading to a pneumothorax or a pneumomediastinum.

Prompt investigation and treatment, such as needle aspiration or continuous drainage, needs to be performed in order to stop further hypoxia and PPHN. Air leaks have a greater incidence when mechanical ventilation is used.

27
Q

Why is CP a complication of MAS?

A

MAS can lead to cerebral hypoxia resulting in cerebral palsy and other neurological conditions.

28
Q

Why do you get CLD with MAS?

A

CLD can develop from barotrauma and oxygen toxicity, amongst other things. Thus, MAS new-borns that have required mechanical ventilation with increased pressures and prolonged oxygen exposure are at high risk. Close monitoring of oxygen saturations and re-assessing the need for oxygen and potential to step down ventilatory measures can help reduce the likelihood of developing CLD.

29
Q

What will a CXR of MAS show?

A

increased lung volumes
asymmetrical patchy pulmonary opacities (figure 1)
pleural effusions
pneumothorax or pneumomediastinum
multifocal consolidation – due to chemical pneumonitis (15)

30
Q

What are the causes of NEC?

A

Multifactorial. Severe intestinal necrosis is the end-result of an exaggerated immune response within the immature bowel, leading to inflammation and tissue injury.

innate immune response to the microbiota of the premature infant’s gut, thereby leading to inflammation and injury

31
Q

What are the predisposing factors to NEC?

A
  • Prematurity.
  • IUGR (causes chronic bowel ischaemia).
  • Hypoxia.
  • Polycythaemia.
  • Exchange transfusion.
  • Hyperosmolar milk feeds.
32
Q

Which week after birth does NEC commonly present?

A

2nd week

33
Q

What are the triple abx used in NEC?

A

IV antibiotics: for 10–14 days (e.g. benzylpenicillin, gentamicin, and metronidazole).

34
Q
A
35
Q

What are the RF for NEC?

A

Prematurity or very low birth weight (VLBW)
Formula feeding
Intrauterine growth restriction (IUGR)
Polycythaemia
Exchange transfusion
Hypoxia

36
Q

What can you see on AXR for NEC?

A

distended bowel loops
thickened bowel wall (bowel oedema) intramural gas (pneumatosis intestinalis)
gas in the portal tract
pneumoperitoneum in the later stages due to bowel perforation

37
Q

What staging system is used for NEC?

A

Bell scoring system based on clinical features and abdominal x-ray features:

38
Q

What prophylactic measures can be taken for NEC?

A
  • administering antenatal steroids if premature delivery is anticipated
  • Breastfeeding is a protective factor
  • probiotics reduce the risk of NEC
39
Q

Describe medical management for NEC

A

Suitable for most infants with Bell Stage I and Stage II NEC and includes the following:

Withhold oral feeds for 10-14 days and replace with parenteral nutrition.
IV antibiotics for 10-14 days based on local protocols.
Systemic support in the form of ventilatory support, fluid resuscitation, inotropic support, correction of acid-base balance coagulopathy and/or thrombocytopenia.1,7

40
Q

What are the indications for surgical management of NEC?

A
  • Intestinal perforation
  • GI obstruction secondary to stricture formation
  • Deterioration despite medical management
41
Q

What is the most common surgical management of NEC?

A

intestinal resection with stoma formation.

42
Q

What is congenital rubella syndrome?

A

caused by maternal infection with the rubella virus during pregnancy. The risk is highest during the first 3 months of pregnancy.

43
Q

What should women planning pregnancy do to prevent congenital rubella syndrome?

A

Ensure they have had the MMR vaccine. If in doubt they can be tested for rubella immunity. If they do not have antibodies to rubella they can be vaccinated with 2 doses of the MMR 3 months apart.

44
Q

Can pregnant women be given the MMR vaccine?

A

Pregnant women should not receive the MMR vaccination, as this is a live vaccine.
Non-immune women should be offered the vaccine after giving birth.

45
Q

What are some features of congenital rubella syndrome?

A
  • Congenital cataracts
  • Congenital heart disease (PDA and pulmonary stenosis)
  • Learning disability
  • Hearing loss
46
Q

Why is chicken pox dangerous in pregnancy?

A
  • More severe cases in the mother, such as varicella pneumonitis, hepatitis or encephalitis
  • Fetal varicella syndrome
  • Severe neonatal varicella infection if mum is infected around delivery
47
Q

Exposure to chicken pox in pregnancy

A
  • If the pregnant women has previously had chickenpox, they are safe
  • If they are not sure about their immunity, test the VZV IgG levels. If positive, they are safe.
  • If they are not immune, they can be treated with IV varicella immunoglobulins as prophylaxis against developing chickenpox. This should be given within 10 days of exposure.

If the chickenpox rash starts in pregnancy, they may be treated with oral aciclovir if they present within 24 hours and are more than 20 weeks gestation.

48
Q

When does congenital varicella syndrome occur?

A

It occurs when there is infection in the first 28 weeks of gestation

49
Q
A
50
Q

What are some typical features of congenital varicella syndrome?

A
  • Fetal growth restriction
  • Microcephaly, hydrocephalus and learning disability
  • Scars and significant skin changes following the dermatomes
  • Limb hypoplasia (underdeveloped limbs)
  • Cataracts and inflammation in the eye (chorioretinitis)
51
Q

When does congenital cytomegalovirus occur?

A

Congenital cytomegalovirus (CMV) infection occurs due to maternal CMV infection during pregnancy. The virus is mostly spread via the infected saliva or urine of asymptomatic children. Most cases of CMV in pregnancy do not cause congenital CMV.

52
Q

What are the features of congenital CMV?

A
  • Fetal growth restriction
  • Microcephaly
  • Hearing loss
  • Vision loss
  • Learning disability
  • Seizures
53
Q

When does congeintal toxoplasmosis occur?

A

When infection occurs during pregnancy it can lead to congenital toxoplasmosis. This risk is higher later in the pregnancy

54
Q

What is the classic triad of sx in congenital toxoplasmosis?

A

Intracranial calcification
Hydrocephalus
Chorioretinitis

55
Q

What are the features of congenital zika syndrome?

A
  • Microcephaly
  • Fetal growth restriction
  • Other intracranial abnormalities, such as ventriculomegaly and cerebellar atrophy
56
Q

What is the management for preganncy women that may have ocntracted the Zika virus?

A

Pregnant women that may have contracted the Zika virus should be tested for the viral PCR and antibodies to the Zika virus. Women with a positive result should be referred to fetal medicine to monitor the pregnancy.
There is no treatment for the virus.

57
Q

How is the zika virus spread? What symptoms does it usually cause?

A

The zika virus is spread by host Aedes mosquitos in areas of the world where the virus is prevalent. It can also be spread by sex with someone infected with the virus. It can cause no symptoms, minimal symptoms or a mild flu like illness. In pregnancy it can lead to congenital Zika syndrome