L17 Prematurity Flashcards
1
Q
At what point does the possibility of survival outside of the womb begin?
A
- 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
2
Q
Problems associated with small babies:
A
- 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
3
Q
List the 7 key pathologies in preterm infants:
A
- RDS
- Chronic lung disease
- Injury to intestines
- Compromised immune system
- Cardiovascular disorders
- Hearing and vision disorders
- Neurological insults
4
Q
How is artificial feeding administered in preterm babies?
A
- Nasogastric tube -> bypass mouth
- Unable to coordinate sucking, swallowing and breathing
5
Q
Rates of admission for neonatal care:
A
- 10% of newborns -> 6% of these are preterm
- Approximately 3% of newborn infants require full intensive care
6
Q
What is the threshold for extreme prematurity?
A
- Less than 28 weeks
- Beyond 25 weeks, babies are nearing threshold of viability (22 weeks)
7
Q
Thresholds of low birth weight:
A
- Low: 2.5kg
- Very low: 1.5kg
- Extremely low: 1kg
8
Q
Give 3 mechanisms for preterm birth:
A
- Maternal illness e.g. hypertension
- Placental failure (poor growth, abruption)
- Preterm Labour (mechanical, inflammation/infection)
9
Q
Lung inflation: How does this occur after birth and how may we intervene?
A
- 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
10
Q
Stages of management of high risk neonates:
A
- 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)
11
Q
What is respiratory distress syndrome?
A
- 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)
12
Q
How do steroids stimulate lung development?
A
- 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
13
Q
Phases of lung development:
A
- 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
14
Q
What are the mechanisms behind RDS in preterm infants (<26 weeks)?
A
- 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
15
Q
What are the complications of RDS?
A
- 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
16
Q
Current approaches to management of RDS:
A
- Conservative approach; less is more
- Intubation and ventilation
- CPAP therapy
- High flow O2
16
Q
Potential future intervention for RDS:
A
LISA therapy
17
Q
Why may a left to right shunt arise in preterm babies?
A
- 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
18
Q
Effect of preterm birth on immature brain:
A
- 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
19
Q
Retinopathy of prematurity: (ROP)
A
- 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
20
Q
What are the risks to GI tract in preterm babies?
A
- 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
21
Q
Pathology of NEC:
A
- 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
22
Q
How does IRI arise>
A
- Ischaemia of small intestine
- Blood flow returns (due to feeds, oxygenation, other substances) -> mural oedema
- Intramural gas
- Perforation
23
Q
Therapy option for NEC:
A
Probiotic therapy
24
Results of Epicure 1995 11 year followup:
* 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)
25
Morbidity in low birth weight children:
* 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
26
Skin issues in premature infants:
* If on border of viability -> gelatinous tissue
* Easily injured when touched
* Lots of fluid loss
* Inadequate protection from pathogens
27
Nutrition in the NICU:
* Total parenteral nutrition (CHO, protein, lipid, vitamins, electrolytes)
* Milk (ideally breast)
* Conservative approach in beginning -> avoiding excess fluid
