Prematurity (Preterm Birth) – Overview

Article Last Updated:11/09/2026

Prematurity (Preterm Birth) – Overview

Preterm birth = live birth <37 weeks of gestation

Preterm severity classification: ^[Ref]

Classification	Gestational age
Moderate to late preterm	32 – 36+6 weeks
Very preterm	28 – 31+6 weeks
Extremely preterm	<28 weeks

Note: This article covers prematurity from a neonatal / paediatric perspective.

For obstetric assessment and management of preterm labour and birth, see the separate PROM, P-PROM, and Preterm Labour article.

Complications of prematurity (preterm birth) by body system.

Respiratory

Respiratory complications are particularly important in preterm infants and are covered in greater detail in the separate Respiratory Complications of Prematurity article.

Complication	Pathophysiology	Recognition	Management principle
Neonatal respiratory distress syndrome (NRDS) ^[Ref]	Surfactant deficiency → alveolar collapse and reduced lung compliance	Respiratory distress soon after birth (e.g. tachypnoea, grunting, recession and increasing oxygen requirement)	Respiratory support +/- exogenous surfactant
Apnoea of prematurity ^[Ref]	Immature brainstem respiratory centre → apnoea	Recurrent apnoea +/- bradycardia, hypoxia	Caffeine citrate +/- respiratory support
Bronchopulmonary dysplasia (BPD) (chronic lung disease of prematurity) ^[Ref1]^[Ref2]	Immature lungs exposed to ventilation / oxygen / inflammation → chronic lung disease	Persistent oxygen and/or respiratory-support requirement	Minimise ongoing lung injury + respiratory support as needed

For infants requiring oxygen therapy after initial stabilisation, target SpO₂ 91-95% to balance the risks of hyperoxia and hypoxia. ^{[NICE NG124]}

Excess oxygen exposure is associated with increased risk of retinopathy of prematurity and bronchopulmonary dysplasia.

Cardiovascular

Key cardiovascular complication of prematurity is patent ductus arteriosus (PDA)

Pathophysiology ^[Ref]	Normal role of ductus arteriosus: In fetal life, the ductus arteriosus connects the pulmonary artery to the aorta This allows blood to bypass the high-resistance, non-functioning fetal lungs and enter the systemic circulation After birth, the ductus arteriosus closes due to ↑ oxygen tension and ↓ prostaglandin levels In preterm infants, the ductus arteriosus is more likely to remain patent due to the following factors: The preterm ductus is structurally and functionally immature It has a weaker response to oxygen It remains relatively more sensitive to vasodilatory mediators such as prostaglandins and nitric oxide If the ductus arteriosus remains patent in an infant → left to right shunt which results in: Pulmonary oedema Left heart overloading Reduced systemic perfusion may occur in significant shunts
Clinical features ^[Ref1][Ref2]	Typical features of PDA in a preterm infant Murmur Classic PDA murmur: continuous “machinery” murmur, best heard at the left infraclavicular area In preterm infants, however, the murmur may be systolic or occasionally absent Bounding pulses + wide pulse pressure Hyperdynamic precordium Hypotension ↑ Oxygen requirement
Investigation and diagnosis ^[Ref]	Confirmatory test: echocardiography Echo is also used to determine whether PDA is haemodynamically significant, to guide management
Management ^[Ref1][Ref2]	Do NOT routinely treat all PDA in preterm infants. Routine early closure has not clearly improved important long-term outcomes. Active management should only be considered if there is a haemodynamically significant PDA, indicated by: Difficulty weaning from a ventilator ^{[NICE NG124]} Evidence of pulmonary overcirculation Systemic hypoperfusion (e.g. hypoperfusion, oliguria) Significant shunting on echo Choice of management: 1st line: NSAIDs (ibuprofen preferred, alternative: indomethacin) 2nd line (if PDA persists despite 2 courses of pharmacological therapy): transcatheter closure or surgical ligation

Metabolic

Key metabolic complications in a preterm infant: ^[Ref]

Complication	Pathophysiology	Recognition / key points
Hypoglycaemia	↓ Glycogen and fat stores Glycogen synthesis and fat deposition occur primarily during the 3rd trimester. Preterm infants are born before these stores build up	May be asymptomatic If symptomatic: Jitteriness Lethargy Poor feeding Seizures Also see the Neonatal Hypoglycaemia article
Hyperbilirubinaemia / neonatal jaundice	Immature hepatic conjugation and excretion	Jaundice may develop earlier or be more significant Preterm infants are more vulnerable to bilirubin neurotoxicity Also see the Neonatal Jaundice article
Hypothermia	Preterm infants have ↑ heat loss due to Large surface-area-to-volume ratio Low subcutaneous fat storage Immature thermogenesis	Possible features: Cold skin Pale / mottled / cyanotic skin Behavioural changes (e.g. lethargy, irritability, weak cry) Hypotonia (floppy) Poor feeding Shallow breathing, apnoea, bradycardia

Complication

Pathophysiology

Recognition / key points

Hypoglycaemia

↓ Glycogen and fat stores

Glycogen synthesis and fat deposition occur primarily during the 3rd trimester. Preterm infants are born before these stores build up

May be asymptomatic

If symptomatic:

Jitteriness
Lethargy
Poor feeding
Seizures

Also see the Neonatal Hypoglycaemia article

Hyperbilirubinaemia / neonatal jaundice

Immature hepatic conjugation and excretion

Jaundice may develop earlier or be more significant

Preterm infants are more vulnerable to bilirubin neurotoxicity

Also see the Neonatal Jaundice article

Hypothermia

Preterm infants have ↑ heat loss due to

Large surface-area-to-volume ratio
Low subcutaneous fat storage
Immature thermogenesis

Possible features:

Cold skin
Pale / mottled / cyanotic skin
Behavioural changes (e.g. lethargy, irritability, weak cry)
Hypotonia (floppy)
Poor feeding
Shallow breathing, apnoea, bradycardia

Gastrointestinal (GI)

Key GI complications in preterm infants:

Complication	Pathophysiology	Recognition	Management principles
Necrotising enterocolitis (NEC) ^[Ref] NEC is covered in more details in a separate article	Immature intestinal barrier + dysregulated inflammatory response and abnormal microbial colonisation → intestinal inflammation and injury May progress to necrosis and perforation	Feeding intolerance Abdominal distension Vomiting Bloody stools Possible systemic deterioration and sepsis	Stop enteral feed Antibiotics and supportive care Surgery may be required for severe disease / perforation Antenatal corticosteroids in pre-term delivery reduces risk of NEC, beyond its benefit in reducing NRDS and IVH. ^[Ref]
Feeding intolerance ^[Ref]	Immature sucking + small stomach + immature gastrointestinal motility	Vomiting Regurgitation Poor tolerance of feeds	Adjust feeding Close monitoring Note that worsening feeding intolerance may be an early sign of necrotising enterocolitis

Complication

Pathophysiology

Recognition

Management principles

Necrotising enterocolitis (NEC) ^[Ref]

NEC is covered in more details in a separate article

Immature intestinal barrier + dysregulated inflammatory response and abnormal microbial colonisation → intestinal inflammation and injury

May progress to necrosis and perforation

Feeding intolerance
Abdominal distension
Vomiting
Bloody stools
Possible systemic deterioration and sepsis

Stop enteral feed
Antibiotics and supportive care
Surgery may be required for severe disease / perforation

Antenatal corticosteroids in pre-term delivery reduces risk of NEC, beyond its benefit in reducing NRDS and IVH. ^[Ref]

Feeding intolerance ^[Ref]

Immature sucking + small stomach + immature gastrointestinal motility

Vomiting
Regurgitation
Poor tolerance of feeds

Adjust feeding
Close monitoring

Note that worsening feeding intolerance may be an early sign of necrotising enterocolitis

Ophthalmological

Key complication is retinopathy of prematurity (ROP):

Pathophysiology ^[Ref]	Premature birth interrupts normal retinal vascularisation After preterm birth, relative hyperoxia suppresses normal vessel growth (→ retina remains incompletely vascularised) In utero, the fetus normally develops in a relatively low-oxygen environment After premature birth, arterial oxygen exposure rises even in room air (even more with supplemental oxygen) As the retina continues to develop, the incompletely vascularised retina becomes hypoxic Hypoxia drives VEGF production → pathological neovascularisation Fibrosis of abnormal vessels +/- retinal detachment
Clinical features ^[Ref]	Usually asymptomatic initially Severe / progressive ROP may ultimately cause visual impairment Advanced disease can progress to retinal detachment and loss of vision
Screening ^[RCPCH]	Indications for screening: ALL infants born <31 weeks of gestation, OR ≤1,500 g birth weight Screening technique: Binocular indirect ophthalmoscopy with pupillary dilatation or Digital retinal imaging
Prevention	Preventive measures: ^{[NICE NG124]} Careful oxygen titration SpO₂ target: 91-95% for those receiving respiratory support after initial stabilisation Caffeine citrate to be given routinely to preterm infants born at ≤30 weeks (evidence of reduce blindness, alongside reducing BPD and cerebral palsy) Screening for ROP: ^[RCPCH] Indications for screening ALL infant born <31 weeks of gestation, OR ≤1,500 g birth weight Screening method Binocular indirect ophthalmoscopy with pupillary dilatation or Digital retinal imaging
Management ^[RCOphth]	Active management options for established ROP: Intravitreal anti-VEGF therapy Laser photocoagulation Vitreoretinal surgery – reserved for advanced ROP with retinal traction / detachment

Neurological

2 most important preterm related brain injuries:

Complication	Pathophysiology	Clinical manifestation
Intraventricular haemorrhage (IVH) ^[Ref]	Fragile vessels in the germinal matrix of the premature brain are prone to rupture Bleeding may remain within the germinal matrix or extend into the ventricles	Mostly asymptomatic (esp. with low-grade haemorrhage) If symptomatic: Apnoea Seizures Bulging fontanelle Pallor More severe IVH can cause post-haemorrhagic hydrocephalus → raised ICP
Periventricular leukomalacia (PVL) ^[Ref]	Hypoxic-ischaemic and inflammatory injury to vulnerable periventricular white matter Results in white matter necrosis and impaired myelination	PVL typically contributes to later, long-term neurodevelopmental complications (instead of acute complications)

Complication

Pathophysiology

Clinical manifestation

Intraventricular haemorrhage (IVH) ^[Ref]

Fragile vessels in the germinal matrix of the premature brain are prone to rupture

Bleeding may remain within the germinal matrix or extend into the ventricles

Mostly asymptomatic (esp. with low-grade haemorrhage)

If symptomatic:

Apnoea
Seizures
Bulging fontanelle
Pallor

More severe IVH can cause post-haemorrhagic hydrocephalus → raised ICP

Periventricular leukomalacia (PVL) ^[Ref]

Hypoxic-ischaemic and inflammatory injury to vulnerable periventricular white matter

Results in white matter necrosis and impaired myelination

PVL typically contributes to later, long-term neurodevelopmental complications (instead of acute complications)

Shared information: ^[Ref]

Imaging:
- 1st line: cranial ultrasound
- 2nd line: MRI
Routine cranial ultrasound surveillance is standard practice in very preterm infants (<32 weeks) ^{[NHS GGC]}
- Early scans (day 1, 3 7) are used to detect IVH
- Later scans (day 28) are used to detect PVL
There is no specific curative treatment for IVH and PVL, management is largely supportive + monitoring for complications

Antenatal corticosteroids in pre-term delivery reduces risk of IVH, beyond its benefit in reducing NRDS and NEC. ^[Ref]

Long-term neurodevelopmental consequences (IVH and PVL are major independent risk factors): ^{[NICE NG72]}

Cerebral palsy and motor impairment
Cognitive and learning difficulties (including global developmental delay, intellectual disability, special education needs, lower education attainment)
Speech, language and executive-function problems
Behavioural and neurodevelopmental disorders (including ADHD, ASD)
Sensory impairment (including visual and hearing impairment)

In preterm birth, antenatal IV magnesium sulfate is recommended to reduce the risk of cerebral palsy.

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Prematurity (Preterm Birth) – Overview

Prematurity (Preterm Birth) – Overview

Respiratory

Cardiovascular

Metabolic

Gastrointestinal (GI)

Ophthalmological

Neurological

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