Learn — Growth, development & behaviour

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Weech formula — birth weight and height

Weech's formulae are the bedside arithmetic that turn a child's age into an expected weight and height when no scale, no stadiometer and no growth chart are within reach. They matter twice over: in the resuscitation room every emergency drug, every fluid bolus and every joule of defibrillation energy is prescribed per kilogram, and in the exam the three age-band weight equations and the height equations are asked as direct calculation items.

Weech weight for 3 to 12 months: weight in kg = (age in months + 9) divided by 2, so a 9-month-old is expected to weigh 9 kg.
Weech weight for 1 to 6 years: weight in kg = age in years multiplied by 2, plus 8, so a 5-year-old is expected to weigh 18 kg.
Weech weight for 7 to 12 years: weight in kg = (age in years multiplied by 7, minus 5) divided by 2, so a 10-year-old is expected to weigh 32.5 kg.
Weech height beyond 2 years: height in cm = age in years multiplied by 6, plus 77; length gain runs at about 2.5 cm per month from 0 to 6 months and about 1.25 cm per month from 6 to 12 months.
Weight milestones anchor the formulae: birth weight doubles by 5 months, triples by 1 year and quadruples by 2 years, with a gain of 25 to 30 g per day in the first three months.
Length milestones: about 50 cm at birth, 75 cm at 1 year, 87 to 88 cm at 2 years, and double the birth length (about 100 cm) by 4 years.
A physiological weight loss of up to 10 percent of birth weight in the first week is normal and must be regained by day 10 to 14; loss beyond 10 percent or failure to regain by day 14 is pathological and needs a feeding assessment.
The formulae give an expected weight, not the child's weight — in a malnourished or oedematous child the calculated figure will overshoot badly, so weigh the child the moment a scale is available and recalculate the doses.

Fetal weight — Johnson, Shepard, Hadlock formulas

Estimated fetal weight is the birth weight predicted before delivery, either clinically from the symphysio-fundal height or sonographically from fetal biometry. It matters because the number decides the place and mode of birth, warns of macrosomia and shoulder dystocia at one end and of growth restriction and low birth weight at the other, and it tells the labour room what size of resuscitation equipment and which level of newborn care to have ready.

Johnson's formula is the clinical one: estimated fetal weight in grams = (symphysio-fundal height in cm minus n) multiplied by 155, where n is 12 when the vertex is above the ischial spines and 11 when it is at or below the spines.
Worked example: a fundal height of 36 cm with the vertex at station minus 2 gives (36 minus 12) multiplied by 155, which is 3720 g.
Johnson's formula is unreliable in obesity, polyhydramnios, oligohydramnios, uterine fibroids, multiple pregnancy and any malpresentation, because the tape is no longer measuring the fetus.
Hadlock's formula is the most accurate ultrasound estimate because it combines four biometric parameters — biparietal diameter, head circumference, abdominal circumference and femur length.
Shepard's formula uses only biparietal diameter and abdominal circumference and is therefore less accurate than Hadlock's; abdominal circumference alone is the single parameter most sensitive to fetal growth restriction.
Dare's formula multiplies symphysio-fundal height in cm by abdominal girth in cm to give the weight in grams, and is the usual alternative clinical method quoted alongside Johnson's.
Even the best ultrasound estimate carries an error of about 10 percent either way near term, so estimated fetal weight is never used alone to decide a caesarean section.
Birth weight bands the estimate is aiming at: low birth weight below 2500 g, very low below 1500 g, extremely low below 1000 g, and macrosomia at 4000 g and above.
Small for gestational age is a birth weight below the 10th centile for gestation, which is not the same as prematurity — a term baby can be small and a preterm baby can be appropriately grown.

Teeth eruption timeline

Tooth eruption is the orderly appearance of the 20 deciduous and later the 32 permanent teeth, and its timing is one of the standard markers of somatic maturation used alongside weight, length and head circumference. Nurses are asked about it because the order and the ages are directly examinable, because delayed eruption points to rickets, hypothyroidism and Down syndrome, and because feeding and oral-hygiene advice at the first tooth prevents early childhood caries.

The lower central incisors erupt first, at about 6 to 10 months; the upper central incisors follow at about 8 to 12 months.
The deciduous sequence after the incisors is first molars at 13 to 19 months, canines at 16 to 22 months and second molars at 23 to 33 months.
All 20 deciduous teeth are present by about 2.5 to 3 years — 8 incisors, 4 canines and 8 molars, with no premolars in the primary set.
A working rule for the first two years is that the number of teeth is roughly the age in months minus 6, so a 12-month-old has about 6 teeth.
Shedding of the deciduous teeth begins at about 6 years, and the first permanent molar erupts at about 6 years behind the last milk molar without any tooth being shed for it.
The permanent set is completed by the third molars at 17 to 21 years, giving 32 teeth in all.
No tooth by 13 months is delayed eruption and needs evaluation; the classic causes are rickets, hypothyroidism, Down syndrome, malnutrition, prematurity and a familial pattern.
Natal teeth are present at birth and neonatal teeth erupt within the first 30 days; they are usually poorly rooted lower incisors and are extracted if mobile because of the risk of aspiration or a Riga-Fede ulcer on the underside of the tongue.
Teething causes drooling, gum discomfort and irritability but never high fever, convulsions or diarrhoea — attributing those to teething and delaying assessment is a well-recognised and dangerous error.

Fontanel closure

The fontanels are the membrane-covered gaps where the skull bones have not yet met, and they exist so that the head can mould through the birth canal and the brain can triple in size in the first two years. They are read at every infant examination because a bulging fontanel is a window on raised intracranial pressure, a sunken one on dehydration, and a large or late-closing one on rickets, hypothyroidism and hydrocephalus.

The anterior fontanel, or bregma, is diamond-shaped at the meeting of the coronal, sagittal and frontal sutures, measures about 2.5 by 2.5 cm at birth and closes between 9 and 18 months.
The posterior fontanel, or lambda, is triangular at the meeting of the sagittal and lambdoid sutures, measures about 0.5 to 1 cm and closes by 6 to 8 weeks.
Palpate with the infant upright, quiet and not feeding; lying flat or crying makes a normal fontanel feel full and produces a false alarm.
A tense or bulging fontanel at rest means raised intracranial pressure — meningitis, encephalitis, hydrocephalus, intracranial bleed or vitamin A toxicity.
A depressed or sunken fontanel is a sign of dehydration and is one of the features looked for alongside sunken eyes and a slow skin pinch.
Delayed closure or an abnormally large anterior fontanel occurs in rickets, congenital hypothyroidism, hydrocephalus, Down syndrome, achondroplasia, osteogenesis imperfecta and intrauterine growth restriction.
Premature closure of sutures is craniosynostosis, which gives an abnormally shaped head and a ridged suture line and needs surgical referral; a small head with early closure also raises microcephaly.
A persistent third fontanel between the anterior and posterior fontanels along the sagittal suture is associated with Down syndrome and congenital rubella.
Head circumference is measured with the fontanels: about 33 to 35 cm at birth, growing roughly 2 cm per month for the first 3 months, 1 cm per month from 4 to 6 months and 0.5 cm per month from 7 to 12 months to reach about 47 cm at 1 year.

Integrated Child Development Services (ICDS)

The Integrated Child Development Services scheme is India's national programme for early childhood, launched on 2 October 1975 and now run by the Ministry of Women and Child Development under the Saksham Anganwadi and Poshan 2.0 umbrella. It delivers six services from a single village-level point, the anganwadi centre, to children under 6 years and to pregnant and lactating women, on the reasoning that nutrition, immunisation, health care and pre-school education fail when they are offered separately.

The six services are supplementary nutrition, immunisation, health check-up, referral services, non-formal pre-school education, and nutrition and health education.
Three of the six — immunisation, health check-up and referral — are delivered by the health system through the ANM and the medical officer, which is why the anganwadi worker and the ANM must work as a pair.
Beneficiaries are children from 0 to 6 years, pregnant women, lactating mothers and adolescent girls; nutrition and health education targets women aged 15 to 45 years.
The anganwadi worker is the functionary, chosen from the local community and paid an honorarium rather than a salary, and she is helped by an anganwadi helper and supervised by the mukhya sevika or supervisor.
Coverage norm is one anganwadi centre per 400 to 800 population in rural and urban areas and per 300 to 800 in tribal areas, with a mini-anganwadi for smaller habitations.
Supplementary nutrition is provided for 300 days in the year, bridging the gap between the recommended dietary allowance and the average intake rather than replacing the home diet.
Growth monitoring is the core nursing activity at the centre — children under 3 years are weighed every month and children 3 to 6 years quarterly, and each weight is plotted on the growth chart in the mother and child protection card.
The anganwadi worker refers upward: a child in grade III or IV undernutrition, or with severe acute malnutrition, goes to the primary health centre or the nutrition rehabilitation centre, and a child with a birth defect or developmental delay goes to the RBSK mobile health team.
Village Health, Sanitation and Nutrition Day is held at the anganwadi centre, usually monthly, where the ANM gives immunisation, antenatal checks and iron and folic acid alongside the anganwadi worker's weighing and counselling.

Height measurement technique

Linear growth is measured as recumbent length in a child under 2 years and as standing height from 2 years onward, because a young child cannot stand straight and because the two measurements are not interchangeable. The technique matters as much as the instrument: a badly positioned head or a bent knee produces an error of a centimetre or more, and stunting is defined by a height-for-age below minus 2 standard deviations, so a sloppy measurement can create or hide a diagnosis.

Under 2 years, measure recumbent length on an infantometer with two people — one holding the head against the fixed board with the eyes looking straight up, the other straightening the knees and bringing the movable footboard against the soles.
From 2 years onward, measure standing height on a stadiometer with the child barefoot, feet together and flat, and the heels, calves, buttocks, shoulder blades and back of the head touching the vertical board.
The head is positioned in the Frankfort horizontal plane — the lower border of the eye socket level with the upper margin of the external auditory meatus, so that the line of sight is horizontal.
Ask the child to stand tall and take a deep breath while the headpiece is lowered to compress the hair, and read to the nearest 0.1 cm at eye level.
Recumbent length reads about 0.7 to 1 cm more than standing height in the same child, so if a child under 2 has to be measured standing, add about 0.7 cm before plotting, and if a child over 2 has to be measured lying down, subtract it.
Plot length-for-age on the WHO growth standards under 2 years and height-for-age from 2 years, and use the same chart type at every visit so that the trend line is real.
Expected linear gain: about 25 cm in the first year, 12 cm in the second, 8 cm in the third, and then about 5 to 6 cm a year until the pubertal growth spurt.
Remove shoes, socks, hair clips, buns and turbans before measuring, and measure at about the same time of day, since height is a few millimetres less in the evening.
A single height is almost useless — it is the height velocity across two measurements at least three to six months apart that separates a constitutionally short child from one whose growth has stopped.

Developmental milestones

Developmental milestones are the age-linked skills a child acquires in four streams — gross motor, fine motor, language, and personal and social — that together map the maturation of the nervous system. They matter because the sequence is fixed even when the pace varies, so a child who has missed a milestone or lost one that was already gained is flagged early, when physiotherapy, hearing aids and stimulation still change the outcome.

Gross motor spine: social smile at about 2 months, head holding at 3 months, rolls over at 5 months, sits with support at 6 months and without support at 8 months, stands holding on at 9 months, walks holding furniture at 11 to 12 months, and walks alone by 13 to 15 months.
After the first year: runs and climbs stairs with help at 18 months, goes up and down stairs two feet to a step and jumps at 2 years, pedals a tricycle and climbs stairs with alternate feet at 3 years, hops on one foot at 4 years and skips at 5 years.
Fine motor: the grasp reflex disappears by 3 months, the child reaches for objects at 4 months, transfers hand to hand at 6 months, has an immature pincer grip at 9 months and a mature pincer at 12 months.
Fine motor construction: a tower of 3 cubes at 18 months, 6 cubes at 2 years and 9 cubes at 3 years; copies a circle at 3 years, a cross at 4 years and a triangle at 5 years.
Language: cooing at 2 to 3 months, monosyllabic babble at 6 months, bisyllables such as mama and dada without meaning at 9 months, the first word with meaning at about 12 months, two-word sentences at 18 to 24 months and three-word sentences at 3 years.
Speech intelligibility to a stranger is about half at 2 years, three-quarters at 3 years and complete by 4 years — a useful discriminator when a parent says the child talks but nobody understands.
Personal and social: stranger anxiety appears at 6 to 9 months, waves bye-bye at 9 to 10 months, drinks from a cup at 12 to 15 months, feeds itself with a spoon at 18 months, and daytime toilet control is usual by 2 to 3 years.
In a preterm baby, correct the age for prematurity until 2 years — a baby born at 32 weeks is assessed at 8 months chronological age as a 6-month-old.
Denver II is a screening test, not a diagnostic one, and covers personal-social, fine motor-adaptive, language and gross motor domains; the Trivandrum Development Screening Chart is the short Indian field tool, and RBSK screens for developmental delay as one of its four Ds along with defects at birth, deficiencies and diseases.

Moro reflex, creeping, parachute

Primitive reflexes are brainstem-level motor patterns present at birth that must disappear as the cortex matures, while postural reflexes such as the parachute appear later and stay for life. Their timing is a developmental clock: a primitive reflex that persists beyond its age, or a postural reflex that never appears, points to an upper motor neurone lesion such as cerebral palsy, and asymmetry of any reflex points to a focal lesion such as Erb palsy or a fractured clavicle.

The Moro reflex is elicited by letting the head drop back a few centimetres into the examiner's hand: the arms abduct and extend with the fingers fanned, then adduct in an embrace, usually with a cry. It is present at birth in every normal term baby and disappears by about 5 to 6 months.
An absent Moro at birth suggests severe central depression, sedation or a cervical cord lesion; an asymmetrical Moro suggests a fractured clavicle, a brachial plexus (Erb) palsy or a hemiparesis on the weaker side; and a Moro persisting beyond 6 months is a cerebral palsy red flag.
Palmar grasp is present from birth and fades by about 3 to 4 months — it must go before the child can voluntarily release an object; plantar grasp persists longer, to about 9 to 10 months, and must go before the child can stand and walk.
Rooting and sucking are present at birth, rooting disappearing at about 3 to 4 months while awake; the asymmetrical tonic neck (fencing) reflex appears in the first weeks and disappears by about 6 months, and an obligatory or persistent fencing posture is abnormal.
The parachute reflex is the odd one out: it APPEARS at about 8 to 9 months, when the child is suspended prone and lowered head-first and throws the arms out to protect the fall, and it never disappears. Its absence after 12 months, or its asymmetry, is abnormal.
The extensor plantar (Babinski) response is normal in infancy and may persist until about 1 to 2 years, so it cannot be used as a sign of an upper motor neurone lesion in a baby the way it is used in an adult.
Gross motor milestones sit alongside the reflexes: head holding by 3 months, rolling over by about 5 months, sitting without support by about 8 months, creeping and crawling on hands and knees at about 9 to 10 months, standing holding furniture at about 9 months, walking with one hand held at about 12 months and walking alone by about 15 months.
Not walking by 18 months, not sitting without support by 9 months, no head control by 4 months, persistent fisting beyond 3 months and any loss of an already acquired milestone are referral-level warnings under RBSK developmental screening.

Pulse rate of a child (chronologic)

The normal pulse rate of a child falls steadily from birth to adolescence, because a small heart with a fixed stroke volume can only raise its output by beating faster. Knowing the age band is what turns a number into a decision: the same rate of 150 a minute is normal in a newborn, a warning in a 5-year-old and a probable arrhythmia in an adolescent.

Awake resting heart rate by age: newborn and infant under 1 year 100 to 160 a minute, toddler 1 to 3 years about 90 to 150, preschool 3 to 5 years about 80 to 140, school age 6 to 12 years about 70 to 120, and adolescent 13 to 18 years 60 to 100.
Respiratory rate falls in parallel and is the other half of the same question: newborn 30 to 60 a minute, infant about 30 to 50, toddler about 24 to 40, preschool about 22 to 34, school age about 18 to 30 and adolescent about 12 to 20.
The pulse is counted for a full minute in any child under 2 years and in any child with an irregular rhythm, and it is counted apically with a stethoscope in infants and young children because the radial pulse is unreliable at those rates.
Fever raises the heart rate by roughly 10 beats a minute for every 1 degree Celsius rise, so a febrile child is expected to be tachycardic; the rate that does not settle as the temperature falls is the one that needs explaining.
The discriminator between sinus tachycardia and supraventricular tachycardia is rate, variability and history: sinus tachycardia in an infant is usually under 220 a minute and in a child under 180, varies with activity, crying and treatment, and has an explanation such as fever, pain, anaemia, dehydration or fear; supraventricular tachycardia is faster than those cut-offs, starts and stops abruptly, is monotonously regular with no beat-to-beat variation, and has absent or abnormal P waves.
Bradycardia in a child is almost always due to hypoxia, and the paediatric rule is that a heart rate under 60 a minute with signs of poor perfusion, despite effective oxygenation and ventilation, is an indication to begin chest compressions.
The pulse is described by rate, rhythm, volume and symmetry, not by rate alone — bounding pulses with a wide pulse pressure suggest a patent ductus arteriosus or an aortic run-off lesion, a thready pulse suggests shock, and weak or absent femoral pulses with normal brachial pulses suggest coarctation of the aorta.
Sinus arrhythmia, in which the rate speeds up on inspiration and slows on expiration, is a normal finding in children and adolescents and is not a disease.

Babinski sign

The plantar reflex is elicited by stroking the lateral border of the sole firmly from the heel towards the ball of the foot and then medially across the metatarsal heads with a blunt object. The normal response beyond infancy is plantar flexion of the great toe; the Babinski sign is the abnormal response of dorsiflexion of the great toe with fanning of the other toes, and it is the single most reliable bedside marker of an upper motor neuron, pyramidal tract lesion.

An extensor plantar response is physiological in infancy because the corticospinal tract is not yet myelinated; it is normal through the first year, may persist to about 2 years, and after 2 years an extensor response is pathological.
The reflex arc runs through the tibial nerve to the L5 and S1 segments, so it can also be lost altogether when that arc is interrupted by a peripheral neuropathy or a cauda equina lesion.
Use a blunt object such as a key, an orange stick or the handle of the reflex hammer, stroke once and firmly but not painfully, and watch the FIRST movement of the great toe; a sharp point produces a voluntary withdrawal that is easily misread as a positive sign.
Equivalents that confirm a doubtful or ticklish response: Chaddock (stroke below the lateral malleolus), Oppenheim (run the knuckles down the shin), Gordon (squeeze the calf), Schaefer (squeeze the Achilles tendon) and Gonda (flex and release the fourth toe).
An extensor plantar with brisk reflexes, spasticity, clonus and no wasting is a pure upper motor neuron picture; an extensor plantar with ABSENT ankle jerks is the mixed picture of subacute combined degeneration of the cord, Friedreich ataxia, taboparesis or a conus lesion, and that combination is a favourite examination question.
In children the commonest causes of a genuinely abnormal Babinski sign are cerebral palsy, hydrocephalus and other causes of raised intracranial pressure, spinal cord compression or tumour, transverse myelitis, and a post-ictal or post-anoxic state.
It is transiently extensor after a generalised seizure, in deep sleep, under anaesthesia and after hypoglycaemia, so a single extensor response in a drowsy child is repeated when the child is awake and settled.

ADHD

Attention-deficit hyperactivity disorder is a neurodevelopmental disorder of persistent inattention and/or hyperactivity-impulsivity that is out of keeping with the child's developmental level and interferes with functioning at home, at school and with friends. The DSM-5-TR criteria require at least six symptoms from a domain (five from the age of 17), lasting at least 6 months, with several symptoms present before the age of 12, in TWO OR MORE settings, and not better explained by another condition - and it is the requirement for two settings that separates it from a child who is simply unhappy in one classroom.

Three presentations are recognised: predominantly inattentive, predominantly hyperactive-impulsive, and combined. Hyperactivity tends to fade with age while inattention, disorganisation and impulsivity persist, and a substantial proportion of children remain impaired as adults.
Boys are diagnosed considerably more often than girls, largely because girls more often have the inattentive presentation - quiet, dreamy, disorganised and underachieving rather than disruptive - and are therefore missed or labelled as slow.
There is no blood test and no scan. The diagnosis is made from a developmental and school history plus standardised rating scales completed by BOTH parent and teacher, such as the Vanderbilt, Conners or SNAP-IV scales, and a physical examination that includes vision and hearing.
The mimics must be excluded before the label is applied: hearing loss, absence seizures (brief blank staring that stops the child mid-sentence, provoked by hyperventilation, with 3 Hz spike-and-wave on the EEG), specific learning disability, iron deficiency anaemia, thyroid disease, obstructive sleep apnoea from adenotonsillar hypertrophy, chronic sleep deprivation, anxiety, depression, abuse or neglect, and simple age-appropriate liveliness in a child placed in an unsuitable class.
Comorbidity is the rule rather than the exception: oppositional defiant disorder, conduct disorder, specific learning disorder (especially of reading), anxiety, depression, tic disorders, autism spectrum disorder and sleep disorders. Treating the ADHD without treating the comorbidity leaves the child failing.
For a preschool child under 6 years, parent training in behaviour management is FIRST-line treatment and medication is reserved for severe or refractory cases; from 6 years onwards, medication combined with behavioural therapy and school accommodations gives the best result.
Methylphenidate is the first-line and most effective medication. Atomoxetine, a noradrenaline reuptake inhibitor which takes 4 to 6 weeks to show benefit, and the alpha-2 agonists clonidine and guanfacine are the alternatives when stimulants fail, are not tolerated, or where there is a tic disorder or a risk of stimulant misuse.
Monitoring on a stimulant is a nursing responsibility at every visit: appetite and weight (give the dose with or after food and offer a calorie-dense snack in the evening when the drug has worn off), sleep (avoid late-afternoon doses), height plotted every 3 to 6 months, heart rate and blood pressure, and a personal and family cardiac history including sudden death taken BEFORE the first prescription.
School and home strategies that the nurse teaches: seat the child at the front away from windows and doors, break work into short tasks with movement breaks, give one instruction at a time with eye contact, use written checklists and a visual timetable, keep routines predictable, give immediate and specific praise and a token reward system, build in daily physical activity, protect sleep, limit screen time in the evening, and keep a daily home-school diary. The symptoms are not punished.
In India, developmental and behavioural problems in school-age children are picked up through Rashtriya Bal Swasthya Karyakram school screening and referred to District Early Intervention Centres, and the school must be brought into the plan for the treatment to work.

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