Prematurity Flashcards

1
Q

Define prematurity and what proportion of babies in the UK are premature

A

Birth from 24-37+0 weeks
7.7%

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2
Q

What are the physical/clinical features of extremely premature babies that differ from term babies

A

Lower birthweight
Very thin, dark red colouration
Ear pinnas are soft with no recoil
Genitalia: no testes in scrotum, labia major widely separated and prominent clitoris
Often requires respiratory support
No coordinated sucking → requires parenteral nutrition
Faint cry
eyelids may be fused

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3
Q

What are the management steps in stabilising a preterm infant

A

1.Airway and breathing: check for respiratory distress and apnoea, consider LOW CONCENTRATION O2 support/CPAP/nasal cannula ± surfactant ± mechanical ventilation
2. Delayed cord clamping if resus not requred, monitor obs
3. <32w →Place in a plastic bag (wrap) to keep warm, stabilisation under a radiant warmer ± heated mattress or humidified incubator
4. Place a venous and arterial line ± PICC for parenteral nutrition
5. CXR ± AXR
5. Investigaitons
5. Consider Abx

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4
Q

What is the purpose of delayed cord clamping

A

Better physiological transition if lungs are aerated before clamping
Increased peak Hb
Reduction in need for transfusion
Reduced necrotising enterocolitis and intraventricular haemorrhage

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5
Q

What are the considerations for oxygen therapy in preterm infants

A

Excessive oxygen may cause tissue damage to the brain, lungs, and eyes from free radicals - avoid a pre-ductal saturation of 95%

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6
Q

What are the possible complications of premature delivery

A

Circulatory: hypotension, PDA
Respiratory: RDS, pneumothorax, apnoea, bronchopulmonary dysplasia
Temperature: hypothermia
Infection
Brain: haemorrhage, ventricular dilatation, periventricular leukomalacia
GI: necrotising enterocolitis
Metabolic: hypoglycaemia, electrolyte disturbance, osteopenia
Eyes: retinopathy of prematurity
Jaundice
Anaemia

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7
Q

What are the causes of premature delivery

A

Idiopathic
Uterine stretch: multiple gestation, polyhydramnios, uterine anomalies
Bleeding: abruption, APH
Infection: chorio, BV, PPROM
Foetal: IUGR, chromosomal/congenital anomalies
Maternal: PET, HTN, UTI, maternal infection, cervical weakness

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8
Q

Describe respiratory distress syndrome

A

Aka hyaline membrane disease
Deficiency of surfactant (mixture of phospholipids and proteins excreted by type II pneumocytes of the alveolar epithelium), which lowers surface tension.
Risk increases with earlier age of gestation, being very common in infants <28w
More severe in boys than girls

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9
Q

What are the signs of respiratory distress syndrome

A

Usually within 4 hours of birth:
Tachypnoea >60
Increased work of breathing
Chest wall recession (Sternal and subcostal)
Nasal flaring
Expiratory grunting (creates a positive airway pressure during expiration)
Cyanosis (severe)

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10
Q

What are the management steps for respiratory distress syndrome and how can it be prevented

A
  1. CXR (ground class apperance)
  2. Supplemental oxygen (21-30% to avoid damage from excess free radicals)
    - Aim for sats 91-95%
  3. CPAP or high flow nasal cannula
  4. Surfactant therapy - instilling directly into the lungs via tracheal tube or catheter
  5. Mechanical ventilation

Prevention is via antenatal steroid

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11
Q

What is the complications of respiratory distress syndrome and what are the signs

A

Air from the overdistended alveoli (RDS) may track into the interstitium → pulmonary interstitial emphysema
Air may leak into the pleural cavity and cause a pneumothorax

Breath sounds and chest movement on the affected side are reduced
Transillumination with a bright fibre-optic light source applied to the chest

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12
Q

What investigations and management should be done for pneumothorax in premature neonates and how could it be prevented

A

CXR: shows pneumothorax
Tension pneumothorax: decompression by needle aspiration + chest drain

Prevention: ventilate with the lowest pressures possible

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13
Q

What are the causes of apnoea/bradycardia/desaturation

A

Immaturity of central respiratory control
Hypoxia
Infection
Anaemia
Electrolyte disturbance
Hypoglycaemia
Seizures
Heart failure
Aspiration due to reflux

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14
Q

How should apnoea, bradycardia and desaturation be managed

A

Gentle physical stimulation
Caffeine (resp. stimulation)
Frequent: CPAP or mechanical ventilation

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15
Q

Why are premature infants vulnerable to hypothermia

A

Large surface area:mass ratio - greater heat loss than generation
Skin is thin and heat permeable - transepidermal water loss is significant in the first week
Little SC fat for insulation
Nursed naked and cannot conserve heat by curling up or shivering

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16
Q

How should heat be maintained in premature neonates

A

Wrapping in a plastic bag without drying
Placing under a radiant heater
Warmed humidified respiratory gases
Incubator (allows ambient humidity)
Cover the head
Nurse on a heated mattress

17
Q

What are the common brain lesions that may occur in premature neonates and how are they detected

A

Haemorrhage (IVH)
White matter injury
Abnormal cerebral development
Periventricular leukomalacia

Detection: cranial ultrasound

18
Q

Describe haemorrhage in preterm neonates

A

25% of very LBW infants
Typically in the germinal matrix above the caudate nucleus
Large haemorrhage → extends to ventricles → intraventricular haemorrhage (IVH) → infarction of brain parenchyma → hemiplegia
Large IVH → impairs drainage and reabsorption of CSF → accumulates under pressure → hydrocephalus → separation of cranial sutures → rapid increase in head circumference and tense fontanelle
Associated with cerebral palsy

19
Q

What is the management for Intraventricular haemorrhage

A
  1. LP to relieve pressure
  2. ventriculoperitoneal or subgaleal shunt
20
Q

Describe white matter injuries in premature infants

A

Usually follows ischaemia and inflammation
Cranial ultrasound: Cystic white matter lesions visible

21
Q

Describe periventricular leukomalacia in premature infants

A

Bilateral multiple cysts
80-90% risk of spastic diplegia + cognitive impairment if posteriorly sited

22
Q

What is retinopathy of prematurity

A

Vascular proliferation of blood vessels at the junction of the vascularised and non-vascularised retina → retinal detachment → fibrosis → blindness
Bilateral blindness in 1% of VLBW infants (<28w)

23
Q

What are the risk factors for retinopathy of prematurity

A

Uncontrolled use of high oxygen concentrations
Very low birth weight infants (35% prevalence)

24
Q

What is the sign of retinopathy of prematurity, how is it screened for and what is the management

A

S/S: loss of red reflex
Screening: for preterm infants <1500g or <32 by opthalmologist
Management: laser therapy (± intravitreal anti-VEGF)

25
Q

What is bronchopulmonary dysplasia

A

Infants who still have an oxygen requirement at 36 weeks
→ recurrent infection or pulmonary hypertension → mortality
→ pertussis and RTI → respiratory failure

26
Q

What investigations should be done for bronchopulmonary dysplasia and what is the management

A

CXR: widespread areas of opacification ± cystic changes
Management:
- Prolonged artificial ventilation
- CPAP or high flow nasal cannula therapy + supplemental oxygen
- Steroids may be used to facilitate weaning, but there is concern about risk of neurodevelopment e.g. cerebral palsy

27
Q

How does premature birth impact nutrition

A

Preterm infants have a high nutritional requirement as they grow rapidly.
Infants born at 35-36 weeks gestational age are mature enough to suck and swallow milk
Less mature infants will need feeding through an orogastric or nasogastric tube

Requires supplementation with phosphate, protein, calories, calcium, iron
(Cow’s milk based formula → risk of NEC)

28
Q

What is necrotising enterocolitis

A

Surgical emergency where a combination of insults (vascular, mucosal, toxic, other) damages an immature gut
3 in 10,000 (7% of those premature get NEC)

29
Q

What are the risk factors for NEC

A

Prematurity
Patient ductus arteriosus

30
Q

What are the signs and symptoms of necrotising enterocolitis

A

Early signs = biliary vomiting, feed intolerance
Abdomen distension
Blood-stained stool
Rapid deterioration and shock

31
Q

What are the investigations for necrotising enterocolitis

A

AXR – ‘gas cysts’ in bowel wall
Blood cultures

32
Q

What is the management for necrotising enterocolitis

A

Bowel rest (NPO (stop oral feed) and switch to parenteral nutrition)
Broad-spectrum antibiotics (cefotaxime/tazocin and vancomycin)
- Stage IA/IB (3 days), stage IIA (7-10 days), stage IIB, III (14 days)
Laparotomy (if perforated as seen on AXR)