L17 Prematurity

Question 1

At what point does the possibility of survival outside of the womb begin?

Answer 1

• 22 weeks
• Note that deadline is gradually progressing with improvement in care
• Will inform parental counselling; decision to resuscitate bearing in mind the likelihood of disability

Question 2

Problems associated with small babies:

Answer 2

• Surface area: volume -> fluid and heat regulation issues -> struggle to keep warm following birth
• Organ maturation (e.g. lungs) -> lacking life support mechanisms
• Suckling capabilities develop after 35 weeks -> unable to feed

Question 3

List the 7 key pathologies in preterm infants:

Answer 3

• RDS
• Chronic lung disease
• Injury to intestines
• Compromised immune system
• Cardiovascular disorders
• Hearing and vision disorders
• Neurological insults

Question 4

How is artificial feeding administered in preterm babies?

Answer 4

• Nasogastric tube -> bypass mouth
• Unable to coordinate sucking, swallowing and breathing

Question 5

Rates of admission for neonatal care:

Answer 5

• 10% of newborns -> 6% of these are preterm
• Approximately 3% of newborn infants require full intensive care

Question 6

What is the threshold for extreme prematurity?

Answer 6

• Less than 28 weeks
• Beyond 25 weeks, babies are nearing threshold of viability (22 weeks)

Question 7

Thresholds of low birth weight:

Answer 7

• Low: 2.5kg
• Very low: 1.5kg
• Extremely low: 1kg

Question 8

Give 3 mechanisms for preterm birth:

Answer 8

• Maternal illness e.g. hypertension
• Placental failure (poor growth, abruption)
• Preterm Labour (mechanical, inflammation/infection)

Question 9

Lung inflation: How does this occur after birth and how may we intervene?

Answer 9

• First cry -> generating large negative pressure in first breath
• Weak small babies unable to generate enough -> resuscitation by enforcing large positive pressure from outside via breathing tube

Question 10

Stages of management of high risk neonates:

Answer 10

• Antenatal: Antibiotics in case baby comes out infected, steroids (lung maturation)
• Intensive care: nasogastric tube, plastic bag with radiant heater, breathing support
• High dependency care
• Special care (gastric tube transitioning to feeding)
• Transitional care (training with specialist)
• Follow up (development monitoring)

Question 11

What is respiratory distress syndrome?

Answer 11

• Premature babies who don’t have sufficiently matured lungs for breathing (e.g. fragility or insufficient surfactant production)
• Can give medications to stimulate breathing (caffeine)

Question 12

How do steroids stimulate lung development?

Answer 12

• During canalicular phase of lung development (16 - 26 weeks), pulmonary capillaries are coming closer to branching airways with mesenchyme regressing to facilitate this (and increase SA as gaseous exchange begins)
• Steroids stimulate this regression -> making gaseous exchange feasible

Question 13

Phases of lung development:

Answer 13

• Pseudoglandular (6 -16w): fairly solid mass, rigid; airways starting to branch out from mesenchyme
• Canalicular phase (16 - 26w): pulmonary capillaries aligning with airways, gaseous exchange beginning and mesenchyme regressing
• Saccular phase 26 - 32w): further loss of mesenchyme, end of airways developing into saccules; further mesenchyme regression needed to increase SA:vol and increase elasticity
• Alveolar phase: saccules -> alveoli

Question 14

What are the mechanisms behind RDS in preterm infants (<26 weeks)?

Answer 14

• Overdistension due to high pressure ventilation -> tissue damage of underdeveloped saccules -> hypoxic toxic conditions -> apoptosis -> increased permeability -> plasma influx, white cell invasion -> organisation of plasma exudate
• Contributed to by collapse of alveoli (then reinflation) due to lack of surfactant protein and fragility of underdeveloped lung
• Overall, gas exchange becomes increasingly difficult as fluid and then plasma exudate blocks up the alveoli

Question 15

What are the complications of RDS?

Answer 15

• Pneumothorax -> lung collapses (chest drain required)
• Emphysema
• In severe cases, tension can impact other lung (tension pneumothorax)
• Long term oxygen support -> not always tolerated
• Chronic lung disease can arise due to RDS; CLS -> hyperexpansion, atelectasis, fibrosis

Question 16

Current approaches to management of RDS:

Answer 16

• Conservative approach; less is more
• Intubation and ventilation
• CPAP therapy
• High flow O2

Question 16

Potential future intervention for RDS:

Answer 16

LISA therapy

Question 17

Why may a left to right shunt arise in preterm babies?

Answer 17

• Failure of ductous to close -> oxygenated blood flowing from aorta through to major pulmonary artery (called left to right shunt) -> harder to replenish oxygen in lungs as blood is already saturated
• Should close when breathing starts after birth; an open (i.e. patient) ductous arteriosus can lead to heart failure and reduced blood flow to vital organs -> also at higher risk of other conditions such as NEC

Question 18

Effect of preterm birth on immature brain:

Answer 18

• Episodes of hypoxia, hypercarbia, acidosis, hypo/hypertension due to poor cerebral autoregulation
• Leads to cerebral perfusion (bleeding of vessels due to dysregulation of pressure) -> severity and location in brain determines outcome -> intracranial haemorrhage
• Baby must undergo regular USS to monitor for evidence of bleeds
• Ultimately, neonates are predisposed to white matter injury

Question 19

Retinopathy of prematurity: (ROP)

Answer 19

• Disease of the eye as a result of hyperoxic insult
• VEGF produces by tissues in hypoxic conditions -> induces blood vessel growth
• Excess oxygen -> VEGF inhibited, blood vessels regress into avascular fibrous ridges
• Abnormal eye development -> associated with blindness

Question 20

What are the risks to GI tract in preterm babies?

Answer 20

• Slow development of intrinsic activity (delayed feed tolerance and delayed passage of stool) -> results in GI reflux
• Also contributed to by fragility and inadequate length of underdeveloped tract
• Can lead to necrotising enterocolitis -> probiotics are now routine in preventing NEC
• NEC can also arise due to overstress of tract via feeding tube -> introduction of fluid must be gradual and carefully monitored
• NEC can lead to ischaemic reperfusion injury

Question 21

Pathology of NEC:

Answer 21

• Many proposed mechanisms
• Thought to involved hypoxia, hypertension, acidosis (contributed to by early feeds, infection, plasticisers, activated T cells) -> IRI
• Leads to ischaemic damage of mucosal barrier
• ->Secondary bacterial invasion -> NEC

Question 22

How does IRI arise>

Answer 22

• Ischaemia of small intestine
• Blood flow returns (due to feeds, oxygenation, other substances) -> mural oedema
• Intramural gas
• Perforation

Question 23

Therapy option for NEC:

Answer 23

Probiotic therapy

Question 24

Results of Epicure 1995 11 year followup:

Answer 24

• Looked at impact of prematurity on IQ, mobility, vision and hearing
• Overall, 45% moderate/severe disability
• More behavioural and emotional difficulties
• Maths a particular problem
• Concession: Follow up assessment on quality of life added context (disability not a direct cause of poor quality of life)

Question 25

Morbidity in low birth weight children:

Answer 25

• Increased need for special schooling in low and very low birth weight (up to 15%)
• Increased need for learning support
• Further follow-up required on predisposition to depressive and psychotic illness later in life

Question 26

Skin issues in premature infants:

Answer 26

• If on border of viability -> gelatinous tissue
• Easily injured when touched
• Lots of fluid loss
• Inadequate protection from pathogens

Question 27

Nutrition in the NICU:

Answer 27

• Total parenteral nutrition (CHO, protein, lipid, vitamins, electrolytes)
• Milk (ideally breast)
• Conservative approach in beginning -> avoiding excess fluid