Respiratory adaptation and pathologies Flashcards

1
Q

What are the 3 common transition disorders that cause respiratory distress?

A

Transient tachypnea of the newborn (TTN)

Respiratory Distress Syndrome (RDS) / hyaline membrane disease

Persistent pulmonary hypertension of the newborn (as a result of meconium aspiration, lung hypoplasia, hyaline membrane disease, TTN, pneumonia)

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2
Q

What are the risk factors for respiratory distress at term?

A
  • Infants born to diabetic mothers
  • Congenital anomlaies
  • IUGR
  • Fetal distress
  • Meconium liquor
  • Elective LSCS
  • PROM
  • Untreated GBS
  • Maternal fever
  • Maternal chorioamnionitis
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3
Q

List clinical findings of neonatal respiratory distress.

A
•	Nasal flaring
•	Mild intercostal and subcostal retractions
•	Expiratory grunting
•	Audible wheeze
•	Stridor
•	Cyanosis
•	Poor feeding
•	Lethargy
•	Tachypnoea (RR>60)
<br>•	Tachycardia (HR >160)
<br>•	Rales or rhonchi on auscultation
<br>•	Cardiac murmur<p></p>
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4
Q

What are the differential causes of neonatal respiratory distress at term?

A

• Common:
- transient tachypnoea of the newborn

• Less common:

  • pneumonia/sepsis
  • mec aspiration (Causes mechanical obstruction, chemical pneumonitis and reduced surfactant)
  • pneumothorax (spont or mechanical vent/CPAP),
  • congenital heart disease.
  • Persistant pulmonary HTN,
  • HIE

• Rare e.g. ;lung obstruction, severe anaemia

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5
Q

What is the pathogenesis of meconium aspiration syndrome?

A

Pathogenesis:

1) Passage of meconium into amniotic fluid; may be caused by
- increased vagal outflow associated with umbilical cord compression
- increased sympathetic inflow during hypoxia
- infection (e.g. listeriosis)

2)Aspirated during fetal gasping or in the initial breaths after delivery (more likely to occur in depressed infant)

  • Causes mechanical obstruction and air trapping
  • Causes a chemical pneumonitis
  • Rarely causes infection, unless already infected neonate
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6
Q

What is Transient tachypnea of the newborn (TTN)

A
  • A lung disorder presenting in the first few hours after birth, with marked tachypnoea and respiratory distress
  • Results in decreased pulmonary compliance and increased airway resistance
  • It is a self-limited condition (usually resolves in 48-72 hours), management is supportive

Caused by:

  • pulmonary oedema due to delayed resorption of lung fluid
  • Delivery by CS is a risk factor as it contributes to pathophysiology - passage through the birth canal exerts ‘squeeze’ which increases intrathroacic pressure and aids reabsorption of fluid through alveoli walls and pushes fluid out of the upper airways and pharynx. If elective then lack of catecholamines can also reduce resorption of fluid.
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7
Q

What is Respiratory Distress Syndrome (RDS)

A

AKA hyaline membrane disease

  • Largely a disease of prematurity - Incidence and severity of RDS decreases with increasing gestational age
  • Caused by reduced number and function of type II pneumocytes, causing a deficiency of pulmonary surfactant leading to decreased lung compliance
  • Hypoxemia results primarily from V/Q mismatching due to collapse of large portions of the lung
  • Administration of surfactant to infants with RDS improves survival
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8
Q

What is the pathophysiology and causes of Persistent pulmonary hypertension of the newborn?

A

• PPHN occurs primarily in term or late preterm infants ≥34 weeks gestation

Pathogenesis:

  • Pulmonary vasoconstriction is exacerbated by hypoxia and acidosis.
  • leads to right-to-left shunting through the foramen ovale and the ductus arteriosus
  • Exacerbating hypoxemia and presenting with cyanosis

Causes:

  • underdevelopment, maldevelopment, or maladaptation of pulmonary vasculature
  • Meconium may trigger a vasoactive process to exacerbate this.
  • Structural lung abnormalities (e.g. Congenital Diaphragmatic Hernia, Congenital Pulmonary Airway Malformations, Alveolar Capillary Dysplasia) are frequently associated with PPHN.
  • Group B streptococcal sepsis via Strep polysaccharide toxins.
  • Polycythaemia, hyaline membrane disease, hypocalcaemia and hypoglycaemia may contribute similarly.
  • Some maternal medications e.g. NSAIDs, SSRIs²- persistently elevated pulmonary vascular resistance
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9
Q

Meconium aspiration syndrome:

  • Incidence
  • Which babies are most at risk?
A
  • Incidence from 0.1-0.4% of all deliveries
  • MAS occurs in 5-10% of newborns delivered with mec liquor
  • Most at risk: infants who are post-mature, SGA, acute hypoxic event/fetal distress
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10
Q

Cause, Sx and Rx of RDS:

A

Due to a deficiency of surfactant leading to atelectasis, VQ mismatch and hypoventilation
Sx: tachypnoea, desaturation, respiratory distress, apnoea

Treatment: antenatal steroids, CPAP, surfactant, good neonatal care

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11
Q

What is the presentation and management of persistent pulmonary hypertension of the neonate (PPHN)?

A

Features:
- severe cyanosis and tachypnoea

Treatment:
- strategies for PPHN are directed at reducing pulmonary vascular resistance, reverse right-to-left shunting, minimise barotrauma as result of ventilation, treating acidemia and improving hypoxia and maintaining stable blood pressure

  • Mechanical ventilation typically is needed early in the course
  • 100% oxygen
  • Pulmonary vasodilators: inhaled nitric oxide, MgSO4 if refractory
  • Fluids +/- inotropes
  • Alkalosis: hyperventilation +/- bicarbonate
  • ECMO for severe and refractory cases
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12
Q

How do steroids reduce the risk of pulmonary morbidity in preterm babies?

A
  • Promote lung maturation - alveoli growth, differentiation and thinning of the alveoli walls to promote gas exchange
  • Promotes development of type II pneumocytes and thus surfactant production, to reduce the surface tension of alveoli and reduce the negative pressure required to take inspiratory breaths
  • Increases nitric oxide in the pulmonary vasculature to increase pulmonary blood flow for gas exchange
  • Increased sodium channels in the epithelium of lung, to increase sodium and water transport out of the alveolar space
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13
Q

What is bronchopulmonary dysplasia?

A

A chronic lung disease of newborns. Typically a complication of prematurity and those requiring oxygen supplementation after birth.

Characterised by irreversible damage to fragile airways and alveoli resulting in dysplasia.

Diagnosed if ongoing oxygen requirement at 36/40 gestation or >28 days from birth.

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14
Q

What is apnoea of prematurity?

A

cessation of breathing that lasts for more than 15 seconds and is accompanied by desaturation (SpO₂≤80%) or bradycardia (HR ≤2/3 of baseline HR) lasting ≥ 4 seconds in infants born under 37 weeks’ gestation

Causes:

  • Immaturity of central respiratory drive
  • Decreased peripheral reflex pathways (e.g. inactivity of carotid body or laryngeal chemoreceptor reflex)
  • Increased bradycardia to hypoxia

Treat with caffeine and ventilatory support

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15
Q

What were the outcomes of the Cochrane 2020 review of antenatal steroids?

A

Looked at steroids for suspected delivery prior to 37 weeks

Outcomes:
Perinatal mortality RR 0.85
RDS RR 0.71
IVH RR 0.58
Childhood developmental delay RR 0.51
Little to no effect on birthweight (-14g, wide CIs),
Maternal outcomes, chorioamnionitis, endometritis - no effect

Subgroup analyses key points:
No difference in outcomes between the 2 overlapping subgroups 1) gestation <35+0, and 2) gestation 34-36+6
No difference in outcome when single course antenatal steroids vs weekly steroids as long as perceived risk of preterm birth continues

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16
Q

What are the potential adverse effects of steroids?

A

Impaired fetal growth
Suggested in large retrospective study, but not borne out in recent cochrane review

Hypoglycemia
ALPS study (large RCT) looking at ACS in later preterm showed increased risk hypoglycaemia 

Poorer school performance
LANDMARK - follow-up to ASTECS study looking at steroids prior to ElCS after 37 weeks showed steroids associated with lower school performance - NB theses are term babies

Longterm health
Some evidence babies more likely to have higher BPs in adolescence and increased risk of T2DM in adulthood

17
Q

LANDMARK TRIAL - Antenatal betamethasone for women at risk for late preterm delivery (ALPS). Gyamfi-Bannerman et al. 2016

A

Methodology:
Multicentre randomised placebo-controlled trial
Inclusion: singelton pregnancy 34-36+6 pregnant with likely delivery by 36+6 weeks
Randomised to 2 doses betamethasone 24hr apart or placebo

1st outcome:
composite of neonatal treatment in first 72 hours (incl CPAP, high flow oxygen, ventilation, ECMO)
stillbirth
neonatal death within 72 hours

Findings:
Respiratory support in first 72 hours significantly reduced in betamethsone treatment group RR 0.80
NB. sub group analysis showed majority of difference was noted for babies with TTN and bronchopulmonary dysplasia
Severe respiratory complications, TTN, bronchopulmonary dysplasia, resuscitation, surfactant use and duration of NICU stay also significantly reduced
No difference in chorioamnionitis, maternal or neonatal sepsis
significant increase in neonatal hypoglycaemia in betamethasone group RR1.60; but no serious adverse outcomes, but on average 2 day longer inpatient stay

18
Q

LANDMARK TRIAL - Neonatal respiratory distress syndrome after repeat exposure to antenatal corticosteroids: a randomised controlled trial (ACTORDS). 2006

A

Methodology:
Multicentre randomised placebo controlled trial
Inclusion: Women <32 weeks with ongoing risk of preterm birth, and > 7 days after initial course steroid
Either given weekly steroid or placebo after initial steroid course, if ongoing risk PTB <32 wks
Outcome: neonatal RDS, severity RDS, weight and length at birth and discharge home

Findings:
RDS RR = 0.82
Severe RDS RR = 0.6
No effect on weight
significant effect on duration and oxygen requirement
19
Q

LANDMARK TRIAL - Antenatal betamethasone and incidence of neonatal respiratory distress after elective caesarean section: pragmatic randomised trial. (ASTECS). 2005

A

Methodology:
Multicentre pragmatic randomised trial
1000 women
Randomised to 2 x betamethasone in 48hrs prior to CS, vs usual treatment
Inclusion: ElCS at term
1st outcome: admission to SCBU with respiratory distress
2nd: severity respiratory distress and level of care given in response

Findings:
steroids significantly reduced SCBU/NICU admissions for respiratory distress RR=0.46
Reduction in RDS and TTN though not statistically significant
the benefits reduce with increasing gestation - recommendation to delay ELCS to >39wk if possible

ASTECS follow-up study (2013):
Following ACS administration children twice as likely to be assessed as in the lowest quartile of academic performance

—> Because of transient benefits and concerns re. possible long-term implications of steroids use, RANZCOG only supports steroids prior to ELCS at term if there is “evidence of lung immaturity” (???!)