Delayed milestones

Delayed milestones are failure to reach expected developmental skills by the age at which nearly all children achieve them. It is a presenting concern of parents, health workers and nurseries in primary care and paediatric clinics.

It can reflect normal variation, or an environmental cause (lack of stimulation, neglect, hearing or vision loss). It can also reflect a pathological condition of the brain, muscles, nerves, senses or genes (cerebral palsy, intellectual disability, autism spectrum disorder, hearing impairment, genetic and metabolic disease, hypothyroidism, neuromuscular disease).

Definitions

• Developmental delay: performance significantly lower than expected in one or more domains in a child under 5 years (usually a z score under minus 2, or 25% or more behind chronological age).
• Global developmental delay: significant delay in two or more domains (gross and fine motor, speech and language, cognitive, social and personal, and activities of daily living), usually in children under 5 years.
• Intellectual disability: replaces the term global developmental delay once the child is old enough for standardised testing (usually 5 years and over). It is defined by an intelligence quotient under 70 with deficits in adaptive function.
• Developmental regression: loss of previously acquired skills. It has its own assessment.
• Developmental dissociation: marked difference between domains (for example good motor skills with poor language).
• Developmental disorder: a persistent pattern of delay or atypical development.
• Corrected age: chronological age minus the number of weeks born before 40 weeks, used up to 2 years for infants born before 37 weeks.

Developmental milestones (the age by which 90% to 95% of children have achieved the skill)

• Gross motor: head control 4 months, rolls over 6 months, sits without support 9 months, pulls to stand 12 months.
• Gross motor, later: walks independently 18 months (red flag if not walking by 18 months, or by 15 months in some tools), runs 24 months, jumps with both feet 30 months, rides a tricycle 3 years, hops on one foot 4 to 5 years.
• Fine motor and vision: follows an object 2 months, reaches for objects 5 months, transfers objects and raking grasp 7 months, pincer grasp 12 months.
• Fine motor and vision, later: scribbles 15 to 18 months, tower of 4 to 6 blocks 24 months, copies a circle 3 years, a cross 4 years and a square 5 years, draws a person with 6 parts at 5 years.
• Speech and language: cooing 3 months, babbling with consonants (mama, dada nonspecific) 9 months, first words with meaning 12 to 15 months.
• Speech red flags: no babble by 12 months, no single words by 16 months, no two word phrases by 24 months.
• Speech and language, later: 50 words and two word phrases 24 months, three word sentences 3 years, understood by strangers 75% at 3 years and 100% at 4 years, complete sentences 5 years.
• Social, emotional and play: social smile 6 to 8 weeks, laughs aloud 4 months, stranger anxiety 8 to 9 months, waves goodbye and plays peek-a-boo 10 to 12 months, points to show 12 to 14 months.
• Social, emotional and play, later: symbolic play 18 to 24 months, parallel play 2 years, cooperative play 3 to 4 years, understands turn taking 4 years.
• Self care: finger feeding 9 months, spoon use 15 to 18 months, dresses partly 3 years, toilet trained by day 2 to 3 years, dresses fully 5 years.
• Hearing: startle to loud sounds in the neonatal period, turns to sound by 4 to 6 months, responds to name by 9 months.

Classification by cause

• Prenatal and genetic: chromosomal disorders (Down syndrome, fragile X syndrome, Williams syndrome, 22q11.2 deletion, Angelman and Prader-Willi syndromes), single gene disorders, brain malformations, congenital infection (cytomegalovirus, toxoplasmosis, rubella, syphilis, Zika, HIV), foetal alcohol spectrum disorder, maternal diabetes and thyroid disease, and intrauterine growth restriction.
• Perinatal: prematurity, hypoxic ischaemic encephalopathy, neonatal hypoglycaemia, kernicterus, intraventricular haemorrhage, periventricular leukomalacia, neonatal sepsis and meningitis, and neonatal stroke.
• Postnatal: meningitis and encephalitis, cerebral malaria, head injury (including abusive head trauma), severe malnutrition, lead poisoning, hypothyroidism, iron deficiency, hearing and visual loss, epilepsy and infantile spasms, hydrocephalus, tumour, and stroke.
• Metabolic: phenylketonuria, galactosaemia, mitochondrial disease, lysosomal storage disorders, creatine disorders, biotinidase deficiency, and glucose transporter deficiency.
• Neuromuscular: spinal muscular atrophy, muscular dystrophy (Duchenne), congenital myopathies, hypotonia, and peripheral neuropathy.
• Neurodevelopmental disorders: cerebral palsy, intellectual disability, autism spectrum disorder, developmental language disorder, developmental coordination disorder, and attention deficit hyperactivity disorder.
• Psychosocial and environmental: understimulation, neglect, abuse, institutional care, maternal depression, poverty, and multiple adverse childhood experiences.
• Sensory: sensorineural and conductive hearing loss, visual impairment, and cortical visual impairment.
• Normal variants: bottom shuffling (late walking), late talking with normal comprehension (late talker), familial pattern, and prematurity (corrected age).

Epidemiology

• Developmental delay affects 10% to 15% of children under 5 years, global developmental delay 1% to 3%, and intellectual disability about 1% to 2% of the population.
• Cerebral palsy affects 2 to 3 in each 1,000 live births (higher in low income countries and in preterm infants).
• Autism spectrum disorder affects about 1 in 50 to 100 children. Permanent childhood hearing loss affects 1 to 3 in each 1,000.
• Over 250 million children under 5 years in low and middle income countries do not reach their developmental potential. Causes are poverty, stunting, inadequate stimulation, iron and iodine deficiency, and infection.
• In about half of children with global developmental delay, a cause is found.
• Genetic disorders (chromosomal microarray, exome sequencing) give the highest yield (15% to 40%). Structural brain abnormalities on magnetic resonance imaging follow (30% to 40% abnormal).

Mechanisms. Development reflects maturation of the nervous system under genetic, nutritional, hormonal, environmental and experience driven influences. The first 1,000 days are a sensitive period. Brain injury, abnormal brain structure or neuronal function, sensory deprivation, toxic stress, and lack of responsive caregiving each interrupt normal progress.

Key distinctions

• Delay in all domains from early infancy points to global developmental delay or intellectual disability.
• Isolated motor delay with hypotonia or hypertonia points to cerebral palsy, myopathy or neuromuscular disease.
• Delay with spasticity, abnormal tone and early handedness (before 12 months) points to cerebral palsy.
• Isolated speech delay with normal other domains points to hearing loss, a language disorder, or autism.
• Delay in language and social interaction with restricted, repetitive behaviour and lack of pointing points to autism.
• Speech delay with frequent ear infections and poor response to sound points to hearing loss.
• Loss of previously acquired skills points to regression, a neurological emergency or neurodegenerative condition.
• Delay with growth failure, coarse features, constipation and prolonged jaundice points to hypothyroidism.
• Delay with microcephaly points to congenital infection, genetic disease or perinatal injury.
• Delay with macrocephaly points to hydrocephalus, metabolic disease, or genetic syndrome.
• Delay with seizures points to epileptic encephalopathy, brain malformation, or metabolic disease.

History

• Parental concern: which skills, when first noted, whether skills are static, slowly progressing or lost, and how the child compares with siblings. Parental concern is a sensitive indicator.
• Developmental history by domain: age of each milestone (use records, video, photographs), current abilities, play, communication (babble, words, understanding, pointing, gesture, eye contact), social interaction, behaviour, sleep, feeding, and self care.
• Regression: any loss of skills, and its timing (needs a separate urgent assessment).
• Pregnancy: infections, rash, fever, drugs, alcohol, tobacco, seizures, diabetes, thyroid disease, foetal movement, and scan abnormalities.
• Birth: gestation, birth weight, mode of delivery, Apgar scores, resuscitation, neonatal unit stay, hypoglycaemia, seizures, jaundice (phototherapy, exchange), infection, ventilation, cranial ultrasound, and head growth.
• Postnatal: feeding, growth, head size, serious illnesses, meningitis, seizures, head injury, hospital admissions, surgery, vision and hearing screening, and lead exposure.
• Family history: developmental delay, intellectual disability, autism, hearing loss, epilepsy, neuromuscular disease, early deaths, consanguinity, metabolic disease, and genetic conditions. Draw a three generation pedigree.
• Social history: caregivers, stimulation (reading, play, talking), screen time, nursery, maternal mental health, neglect or abuse concerns, domestic violence, substance use, food security, and cultural expectations.
• Medicines and allergies, immunisation status, and history of exposure to toxins (lead, mercury).
• School and functional impact in older children.

Examination

• Growth: weight, length or height, head circumference (microcephaly: z score under minus 2; macrocephaly: z score over plus 2), and plot on charts, with attention to growth failure or obesity.
• Dysmorphic features: facial shape, ears, eyes, palate, hands, feet, palmar creases, skin (neurocutaneous stigmata: café au lait macules, ash leaf macules, shagreen patch, facial angiofibromas, port wine stain), hair, nails, and genitalia. Compare with parents.
• Vision: fixation, tracking, red reflex, strabismus, nystagmus, cataracts, and fundus (retinal disease, optic atrophy, chorioretinitis).
• Hearing: observe responses to sound, and arrange formal testing in every child with delay.
• Neurological: tone (axial hypotonia, peripheral hypertonia), power, reflexes (increased, persistent primitive reflexes after expected age), clonus, plantar responses, posture (asymmetry, hand preference before 12 months), involuntary movements, cranial nerves, gait, coordination, and fasciculations.
• Cardiac, respiratory and abdominal examination (organomegaly in storage disorders, murmur in congenital syndromes), spine, and hips.
• Developmental assessment: use structured tools to examine each domain, and observe play and interaction.
• Behaviour and social communication: eye contact, joint attention, response to name, imitation, stereotypies, and emotional regulation.
• Screening tools: Ages and Stages Questionnaire (3rd edition), Parents' Evaluation of Developmental Status, Denver Developmental Screening Test (II), Survey of Well-being of Young Children.
• Diagnostic tools: Griffiths Scales or Bayley Scales of Infant and Toddler Development.
• Autism and adaptive tools: the Modified Checklist for Autism in Toddlers (revised, with follow up; age 16 to 30 months), and the adaptive behaviour scales.
• Look for signs of abuse or neglect: bruises, poor hygiene, poor growth, withdrawn behaviour.

Red flags

• Loss of skills (regression) at any age.
• No social smile by 3 months, no head control by 4 to 5 months, not sitting by 9 months, no babbling by 12 months, not walking by 18 months, no single words by 16 months, no two word phrases by 24 months, no pointing or waving by 12 to 14 months.
• Persistent primitive reflexes beyond 6 months, hand preference before 12 months (suggesting hemiplegia), toe walking, stiffness or floppiness, asymmetry of movement or posture.
• Concerns about hearing or vision at any age, or no response to sound.
• Head circumference z score under minus 2 or over plus 2, rapid head growth, or crossing centiles.
• Seizures, infantile spasms (clusters of flexor or extensor jerks, often at waking, with hypsarrhythmia), or abnormal movements.
• Dysmorphic features, congenital anomalies, or neurocutaneous signs.
• Failure to thrive, vomiting, poor feeding, hypoglycaemia, or acidosis suggesting metabolic disease.
• Hepatosplenomegaly, coarse features, corneal clouding, or skeletal changes (storage disorder).
• Prolonged jaundice, constipation, hoarse cry, or large tongue (hypothyroidism).
• Neglect, abuse, parental mental illness, institutional care, or severe poverty.
• Parental concern about development (highly predictive).
• Difficulty feeding with choking or aspiration.
• Delay in a child with a history of meningitis, hypoxia, kernicterus, head injury, lead poisoning, or HIV.
• Failure to attain a milestone by the 95th centile age for the skill.

Special groups

• Preterm infants: use corrected age until 2 years. Delay beyond corrected expectations needs evaluation for cerebral palsy, hearing loss and vision loss (retinopathy of prematurity).
• Children with Down syndrome and other recognised syndromes: use condition specific growth charts and developmental expectations.
• Children with HIV or exposed to HIV: neurodevelopmental screening at each visit.
• Children from adverse environments: assess stimulation and parental support.
• Children with sickle cell disease: silent infarcts and cognitive effects.
• Children in conflict zones or who are displaced: trauma and deprivation.
• Region specific: cerebral malaria, congenital infection, neonatal jaundice and kernicterus, iodine deficiency, anaemia and iron deficiency, severe acute malnutrition, lead poisoning, perinatal asphyxia, meningitis, HIV, and limited access to early intervention.

Global developmental delay and intellectual disability

• Chromosomal and genetic disorders: Down syndrome, fragile X, Rett syndrome (girls, regression after normal early development), Angelman syndrome, Prader-Willi syndrome, Williams syndrome, Smith-Magenis syndrome, 22q11.2 deletion, tuberous sclerosis complex, neurofibromatosis, and many others including single gene disorders.
• Brain malformations: lissencephaly, polymicrogyria, corpus callosum agenesis, holoprosencephaly, Dandy-Walker malformation, and cerebral palsy of prenatal origin.
• Acquired brain injury: hypoxic ischaemic encephalopathy, intraventricular haemorrhage, meningitis, encephalitis, head injury, kernicterus, and stroke.
• Congenital infection and teratogens: cytomegalovirus, rubella, toxoplasmosis, syphilis, Zika, HIV, foetal alcohol spectrum disorder, and anticonvulsant embryopathy (valproate).
• Metabolic and endocrine: congenital hypothyroidism, phenylketonuria and other aminoacidopathies, organic acidaemias, mitochondrial disease, galactosaemia, Menkes disease, Wilson disease (older children), and storage disorders.
• Nutritional and environmental: iron deficiency, iodine deficiency, vitamin B12 deficiency, severe malnutrition, lead poisoning, and understimulation or deprivation.

Motor delay

• Cerebral palsy (spastic, dyskinetic, ataxic, mixed).
• Neuromuscular: spinal muscular atrophy, congenital myopathy, congenital muscular dystrophy, Duchenne muscular dystrophy (late walking, calf hypertrophy, Gowers sign), peripheral neuropathy.
• Benign hypotonia and variants: bottom shuffling, late walking with normal examination, familial.
• Developmental coordination disorder, joint hypermobility, rickets, hip dysplasia, and spinal cord lesions.

Speech and language delay

• Hearing impairment (conductive: otitis media with effusion; sensorineural).
• Developmental language disorder, late talker, autism spectrum disorder, intellectual disability, selective mutism, childhood apraxia of speech, and neurological conditions (Landau-Kleffner syndrome, epileptic encephalopathy with regression).
• Bilingual exposure alone does not cause delay.
• Psychosocial deprivation and neglect.

Social communication delay

• Autism spectrum disorder, intellectual disability, attachment disorders, language disorder, hearing loss, visual impairment, and trauma.

Other

• Visual impairment (cataract, retinopathy of prematurity, cortical visual impairment, optic nerve hypoplasia).
• Epilepsy and epileptic encephalopathy, sleep disorders, and chronic illness (heart disease, renal disease, coeliac disease).
• Medication effects (phenobarbital, benzodiazepines).

Step 1. Confirm delay and exclude regression. Perform or obtain a validated developmental assessment. Document each domain with the age equivalent, correct for prematurity, and decide whether the pattern is global, isolated, or dissociated. Ask explicitly about lost skills. Delay with regression needs urgent evaluation.

Step 2. Identify treatable and urgent causes. Check vision and hearing in every child, and growth, head size, and neurological examination. Screen for neglect or abuse, and exclude acute illness, hypoglycaemia and seizures.

Step 3. First line tests (directed by history and examination; tests are chosen from this list, not given as a routine panel)

• Formal audiology in every child with delay: newborn screening results, otoacoustic emissions, tympanometry, auditory brainstem response, and behavioural audiometry by age.
• Vision assessment: ophthalmology or orthoptic review (visual acuity, refraction, fundus).
• Thyroid function (thyroid stimulating hormone and free thyroxine) if not part of newborn screening or if features of hypothyroidism.
• Full blood count and ferritin (iron deficiency), blood lead level where risk exists, and electrolytes, calcium, glucose, urea, creatinine, liver tests, creatine kinase (markedly elevated in muscular dystrophy), and venous gas.
• Chromosomal microarray is the first line genetic test in unexplained global developmental delay and intellectual disability (diagnostic yield 10% to 15%).
• Fragile X testing (FMR1 repeats) in boys and in girls with suggestive features.
• Rett syndrome testing (MECP2) in girls with regression, microcephaly or stereotypic hand movements.
• Newborn screening results, and review of birth records.

Step 4. Targeted tests

• Magnetic resonance imaging of the brain (preferred over CT) in global developmental delay with abnormal head size, abnormal neurology, seizures, regression, dysmorphism, or no cause found.
• Look for malformation, white matter injury, hypomyelination, basal ganglia disease, and atrophy. MRI spectroscopy for suspected metabolic disease.
• Electroencephalogram for seizures, regression, speech regression, or suspected epileptic encephalopathy (including sleep recording for suspected electrical status epilepticus).
• Metabolic screening in selected children (when suggestive features, regression, family history, consanguinity or abnormal neurology): ammonia, lactate, plasma amino acids, urine organic acids, acylcarnitine profile, very long chain fatty acids.
• Further metabolic tests: transferrin isoforms (congenital disorders of glycosylation), copper and caeruloplasmin, biotinidase, creatine metabolites, 7-dehydrocholesterol, lysosomal enzymes, purine and pyrimidine metabolites.
• Cerebrospinal fluid studies: glucose with paired blood glucose, lactate, neurotransmitters, folate.
• Exome or genome sequencing (second tier after microarray, or first line in some settings), gene panels (epilepsy, intellectual disability, neuromuscular), and mitochondrial DNA tests, with genetic counselling.
• Congenital infection tests: cytomegalovirus polymerase chain reaction on dried blood spot or urine in the first 3 weeks of life (later retrospective testing on newborn screening card), syphilis serology, toxoplasma IgG and IgM, HIV test.
• Muscle disease: creatine kinase, nerve conduction, electromyography, and genetic tests (survival motor neuron 1 gene deletion, dystrophin).
• Skeletal survey if abuse is suspected, and radiographs for rickets.
• Cranial ultrasound for infants with an open fontanelle.
• Autism-specific assessment (Autism Diagnostic Observation Schedule, Autism Diagnostic Interview) by a multidisciplinary team.
• Speech and language therapy, occupational therapy and physiotherapy assessment, and psychological testing (age 5 years and over for intelligence quotient).

Step 5. Interpretation.

• History and examination guide testing. The most valuable first tests are formal hearing and vision tests, thyroid function and chromosomal microarray.
• Aetiological yield is highest in children with dysmorphism, microcephaly, seizures, abnormal tone, and consanguinity.
• A treatable condition needs to be found early: hypothyroidism, phenylketonuria, biotinidase deficiency, creatine transporter defects, glucose transporter deficiency, Wilson disease, cerebral folate deficiency.
• A normal screening result does not exclude later problems, so repeat assessments.

Limits. Developmental tests are affected by language, culture, illness, tiredness, and examiner. A single assessment is not enough, so repeat after 3 to 6 months. Some children catch up. A cause is never found in many children, and treatment and support should not wait for a diagnosis.

Immediate

• Treat acute or reversible problems: seizures, infantile spasms, hypoglycaemia, hydrocephalus, hypothyroidism, and metabolic crises.
• Infantile spasms need urgent paediatric neurology review. First line is prednisolone 40 to 60 mg daily for 14 days (or high dose 8 mg/kg daily in some settings).
• Alternatively give vigabatrin 50 mg/kg daily increased over 3 days to 100 to 150 mg/kg daily in two doses, especially in tuberous sclerosis, with visual field monitoring.
• Congenital hypothyroidism: levothyroxine 10 to 15 micrograms/kg daily orally (starting within 2 weeks of birth; about 37.5 to 50 micrograms daily in a term infant), crushed in water or breast milk.
• Check thyroid stimulating hormone and free thyroxine at 2 and 4 weeks, then every 1 to 3 months in the first year. Aim for free thyroxine in the upper half of the reference range and thyroid stimulating hormone under 5 milliunits/L.
• Phenylketonuria: low phenylalanine diet (target blood phenylalanine 120 to 360 micromoles/L), phenylalanine free amino acid formula, and sapropterin 5 to 20 mg/kg daily in responsive patients, from the specialist metabolic team.
• Biotinidase deficiency: biotin 5 to 20 mg daily; galactosaemia: galactose free diet; Wilson disease: penicillamine or zinc; glucose transporter 1 deficiency: ketogenic diet.
• Hearing loss: hearing aids within weeks of diagnosis, and cochlear implants for severe to profound loss (by 12 months where possible).
• Treat otitis media with effusion with watchful waiting for 3 months, then grommets if persistent hearing loss over 25 to 30 dB.
• Visual impairment: glasses, patching and surgery for amblyopia, cataract surgery, and low vision services.
• Iron deficiency: ferrous sulphate 3 to 6 mg/kg of elemental iron daily in 2 to 3 divided doses for 3 months, with dietary advice.
• Lead exposure: remove the source. Use chelation (succimer 10 mg/kg three times daily for 5 days, then twice daily for 14 days) for blood lead over 45 micrograms/dL (2.2 micromoles/L), with specialist advice.
• Safeguarding: protect children where neglect or abuse is suspected.

Early intervention and developmental support (start without waiting for a diagnosis)

• Refer to a multidisciplinary child development team. Start physiotherapy (motor delay, hypotonia, cerebral palsy), occupational therapy (fine motor, sensory, feeding, self care), speech and language therapy (communication, feeding, alternative communication such as signs and symbols), special educator and early stimulation programmes, and psychology.
• Parent centred programmes: responsive caregiving, play, reading, singing and talking (at least 15 minutes daily of structured interaction), parent coaching, and community based rehabilitation in low resource settings.
• Early educational placement (nursery, special education), individual education plans, and school readiness support.
• Family support: explain findings honestly, the uncertainty of the diagnosis, and the importance of early intervention. Offer counselling, peer parent groups, respite care, and benefits and social care assessments. Screen parents for depression.
• Nutritional support and feeding advice, growth monitoring, and treatment of reflux and constipation.
• Orthopaedic care for spasticity: botulinum toxin A injections, orthoses, positioning, and hip surveillance with radiographs every 6 to 12 months for cerebral palsy.
• Baclofen 0.3 mg/kg daily in three divided doses, increased every week to 2 mg/kg daily (maximum 40 mg daily at 2 to 7 years, 60 mg daily over 8 years), or intrathecal baclofen under specialist care.
• Management of cerebral palsy is multidisciplinary. It includes treatment of drooling (glycopyrronium 40 to 100 micrograms/kg three times daily), sleep (melatonin 2 to 5 mg at night), epilepsy, pain, and gastrostomy for unsafe swallow.
• Autism spectrum disorder: early behavioural and communication intervention (Early Start Denver Model and parent mediated programmes), speech and language therapy, special education, treatment of sleep (melatonin 1 to 5 mg 30 to 60 minutes before bed), and co-existing conditions.
• Use risperidone 0.25 mg daily (maximum 3 mg for children over 20 kg) or aripiprazole 2 mg daily increased to 5 to 10 mg (maximum 15 mg) only for severe irritability and aggression, with metabolic monitoring.
• Attention deficit hyperactivity disorder (age 6 years and over): parent training first.
• Then give methylphenidate 5 mg twice daily increasing weekly to 1 mg/kg daily (maximum 60 mg daily), or atomoxetine 0.5 mg/kg daily increasing to 1.2 mg/kg daily (maximum 100 mg).
• Vaccination as usual, vitamin D, and dental care.

Counselling and genetics

• Give the family a clear explanation, and review the diagnosis as the child grows.
• Offer genetic counselling and recurrence risk for families with a diagnosed condition (for example 25% for autosomal recessive conditions), prenatal and preimplantation options, and carrier testing.

Special populations

• Preterm infants: developmental follow up to at least 2 years corrected age, with cranial imaging, vision and hearing monitoring, and early physiotherapy.
• Children with Down syndrome: annual thyroid function, hearing and vision screening, echocardiography at birth, and coeliac screening.
• Children with HIV: antiretroviral therapy, which improves neurodevelopment.
• Malnourished children: nutritional rehabilitation with psychosocial stimulation (together they improve outcomes).
• Low resource settings: caregiver training, community health worker home visits and the use of locally available toys.

Monitoring. Developmental surveillance at every contact (9, 18 and 30 months and at school entry at minimum), repeat formal assessment every 3 to 6 months, growth and head circumference, hearing and vision, behaviour, sleep, seizure control, and family wellbeing. Reassess diagnosis as new features appear.

Referral and escalation.

• Developmental paediatrician or child development centre for all children with confirmed delay.
• Paediatric neurology for regression, seizures, abnormal tone, microcephaly and structural abnormalities.
• Clinical genetics for dysmorphism, family history, and unexplained global delay.
• Audiology and ophthalmology for all.
• Metabolic medicine for suspected metabolic disease.
• Child and adolescent mental health services for autism, attention deficit hyperactivity disorder, and behaviour.
• Orthopaedics and rehabilitation for cerebral palsy.
• Social services and child protection for neglect.

Admission criteria. Regression, uncontrolled seizures, infantile spasms needing urgent treatment, metabolic crisis, feeding failure with weight loss, aspiration, suspected abuse, and need for urgent diagnostic work up that cannot be done as an outpatient.

Discharge and follow up. Provide a written plan with therapy goals, a named contact, and a follow up date (within 3 months). For children with normal screening, repeat the screening at the next scheduled visit.

Safety netting. Advise return at once if the child loses skills, has a seizure, stops responding to sound or sight, has a fall in alertness, develops vomiting with a rapidly enlarging head, or becomes ill.