26. Problem of the Low Birthweight Infant and Pathology of Prematurity Flashcards Preview

Year 1 - Term 3: Human Development > 26. Problem of the Low Birthweight Infant and Pathology of Prematurity > Flashcards

Flashcards in 26. Problem of the Low Birthweight Infant and Pathology of Prematurity Deck (10)
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1
Q

What is the median UK birthweight at term (40w)?

What classifies low birthweight, very low birthweigh, and extremely low birthweight individuals?

Define the following:

a) Prematurity
b) Small for gestational age
c) Fetal growth restriction (FGR/IYGR)

A

3.5kg NB: 37-42w = term

LBW: <2500g, VLBW: <1500g, ELBW: <1000g

a) birth before 37 completed weeks of gestation
b) birth weight below the 10th centile for gestation
c) failure to acheive normal rate of foetal growth (e.g. from uteroplacental insufficiency or foetal infection)

2
Q

Why might a baby be low birth weight, and why does this matter?

At what week does premature survival odds increase?

Give some reasons for an SGA (small-gestational-age) baby.

A

Born too small (SGA - complications of foetal growth restriction, v. long term health problems), or born too soon (premature - prematurity problems, neurodevelopmental sequelae), or both.

24 weeks.

Genetic: normal small baby, chromosomal disorders, inherited disorders

Acquired: utero-placental insufficiency, congenital infection, smoking, maternal chronic illness (renal, sickle cell), multiple pregnancy (monozygotic twins).

3
Q

What signs might you see on a brain scan of a child with cogenital CMV?

What is trisomy 18?

How can utero-placental insufficiency can cause IUGR?

A

Hydrocephalus and calcification.

Edwards sydrome: SGA with congenital abnormalities e.g. fingers and facial abnormalities.

Failure of syncytiotrophoblast invasion of high resistance spiral arteries. Poor placental development with raised resistance in placental vascular bed. Can be detected using Doppler ultrasound of uterine arteries and foetal ciruclation - may see early diastolic notching.

4
Q

How does the hypoxic foetus redistribute its circulation?

List some neonatal problems of the SGA baby.

What adult diseases is low birth weight associated with?

A

Prioritising blood flow distribution to deliver O2 to brain and cardiac muscle, at expense of kidneys, gut, liver, skin etc. Detect and follow with Doppler ultrasound.

Temperature control (increased SA:V, reduced adipose tissues and capacity for thermogenesis), polycythemia (response to foetal hypoxia -> thicker blood -> strokes, thrombosis etc.), poor nutritional status (-> hypoglycaemia (<2.6mmol/l), low BG treated with feeds/IV dextrose), symptomatic hypoglycaemia (lethargy, fits -> risk of adverse neuro-developmental outcome), increased risk of necrotising enterocolitis.

Diabetes, hypertension, CHD, stroke, chronic bronchitis. Foetal environment affects celluar growth, gene expression and hormonal axes.

5
Q

What are some causes of prematurity?

What are some problems of prematurity?

The preterm baby is at high risk of heat loss - why and how can this be avoided?

A

Spontaneous preterm labour: infection/ruptured membranes, cervical incompetence, polyhydraminos. Delivered by obstetrician: to save mum (hypertension, haemorrhage), to save foetus (placental insufficiency).

Temperature control, respiratory, CDV, nutritional, infection, neurological, long term sequelae.

Large SA:V, thin skin, less adipose, wet at birth, can’t shiver, poor metabolic reserve. Avoidence: modern incubators, deliver baby into polythene bag up to the shoulders to prevent evaporative heat loss.

6
Q

What are some respiratory problems of prematurity?

What are some short term and long term conditions?

What does surfactant do?

A

Structural (primitive alveolar development, susceptibility to oxygen toxicity and barotrauma), functional (surfactant deficiency, lack of respiratory drive), infection susceptibility (immature immune system).

Short term: respiratory distress syndrome (lack of surfactant mainly in premature, tachynea, expiratory grunting, recession, cyanosis, CXR), structural lung immaturity, pneumonia, apnoea. Long term: chronic lung disease of infancy.

Monolayer of phospholipid molecules in alveoli that reduces surface tension at air-fluid interface.

7
Q

What might you see in histology of hyaline membrane disease (fatal RDS)?

How is RDS prevented and treated?

A

Collapsed airspaces, necrotic material, dilation of septal lymphatics, oedema and focal haemorrhage, capillary thrombi. HMD: damaged vascular integrity allows fluid to leak into air spaces. Partial reabsorption leaves proteinaceous material. Acute complications include pneumothorax and pulmonary interstitial emphysema.

Prevent: antenatal steroids, avoidance of intrauterine hypoxia, prophylactic surfactant treatment, keep warm and avoid acidosis. Treatment: surfactant, resp support.

8
Q

What is brochopulmonary dysplasia a.k.a. chronic lung disease?

What are some CDV problems of prematurity?

Roughly how many calories does a preterm baby need to grow?

What are some nutritional challenges in utero/preterm?

A

Oxygen dependancy at 28 days. Lung inflammataion, fibrosis, emphysema.

Failure to maintain BP, patent ductus arteriosus, PPHN (persistant pulm hypertnesion of newborn).

110-135kcals/kg/d

In utero: swallow amniotic fluid. Preterm: immature sucking, poor gut motility, may not tolerate enteral feeds. If baby not fed, gut mucosa atrophies.

9
Q

What is necrotising enterocolitis?

What bacteria most commonly cause infection in the first 48hrs/after 48hrs (hospital acquired)?

How are term babies protected against infection?

A

Acute bacterial invasion/inflammation/necrosis of bowel with gas formation in bowel wall. Risks = prematurity, hypoxia, infection, enteral feeding. Need abx +/- surgery.

<48hrs: group B strep (common in vaginal tract, causes septicemia, pneumonia and menigitis), E.coli. >48hrs: coagulase -ve staph, G- that colonise intestine (preterm baby with leaky gut).

Transplacental IgG in 3rd trimester, IgA and immunologically active cells in colostrum, skin barrier, normal flora from mum and family. Preterm: given broad spectrum abx and invasive procedures breach host defences

10
Q

How can we protect the preterm baby from episodes of infection?

The preterm baby has poor control of brain perfusion and may contract periventricular hemorrhage. What are some potentially modifiable risk factors?

What is periventricular leucomalacia?

What is retinopathy of prematurity?

A

Disinfect hands and objects! Limit abx useage.

Prematurity (rare >34w), RDS, pneumothorax, hypercapnia, acidosis, hypotension, instability and handling, severe bruising at birth. PVH -> collapse and death. loss of brain parenchymal tissue with cyst development, blockage of CSF circulation = hydrocephalus.

Necrosis of white matter, anoxic-ischemic damage in border zones between arterial territories, mainly in preterm. Associated with cerebral palsy. Cognitive and behaviour problems.

Retina vascularisation incomplete before 36w gestation, risks hemorrhage, fibrosis and retinal detachment.

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