Ocular Prescribing in Children and Pregnancy
A drop on the eye feels like the most local thing in medicine — a milligram of drug touching a surface the size of a fingernail. But that surface drains straight into the nose and the bloodstream, and it delivers the same dose whether the patient weighs 70 kilograms or 3. In an infant, a routine dilating drop can raise the blood pressure; a glaucoma drop can stop the breathing. In pregnancy, the same molecule that lowers eye pressure can reach a developing fetus. The whole discipline of prescribing eye drops in these two populations comes down to one habit of mind: never ask only what the drop does to the eye — ask what dose it delivers to the body.
A 5-week-old infant is brought to the eye clinic before surgery for a squint assessment, and the resident instils a standard drop to dilate the pupils. Twenty minutes later the baby is drowsy, flushed and warm, the heart racing — the atropine-type drop, given at adult strength to a 4-kilogram body, has produced systemic anticholinergic toxicity. In the next cubicle a premature infant in the neonatal unit is being screened for retinopathy of prematurity, the ophthalmologist weighing an intravitreal anti-VEGF injection against laser. And in the waiting room a woman with glaucoma, newly pregnant, asks whether the drops she has taken every morning for three years are safe for her baby. None of these patients has a rare disease. What they share is that the ordinary eye-drop rules — written for an average adult — do not apply to them, and treating them as if they did is exactly how harm happens.
Why a drop is never "just local"
The eye is not a sealed compartment — it drains into the body. As the Eyedrop-pharmacology chapter sets out, most of a drop never enters the eye at all. It rolls over the conjunctiva, spills through the puncta into the nasolacrimal duct, and pours onto the highly vascular nasal mucosa — from where it is absorbed straight into the systemic circulation, bypassing the first-pass metabolism of the liver. A topical drug therefore behaves partly like an intravenous one. This is the mechanism behind the Systemic-effects chapter, where timolol drops cause bronchospasm and bradycardia. It is also why the single most useful safety manoeuvre in every population is the same: punctal occlusion — pressing on the inner corner of the eye for a minute after instilling the drop — which blocks that drainage route and can cut systemic absorption dramatically.
Now add the arithmetic of size. The drop that leaves the bottle is a fixed volume — roughly 30 to 50 microlitres — designed for an adult. Give that same drop to an infant and you deliver the same milligrams into a body a twentieth of the mass, with a smaller blood volume to dilute it and immature liver and kidney pathways to clear it. As the Principles of Pharmacology teaches with weight-based dosing, an adult dose in a small child is a relative overdose. The eye does not scale the drop to the patient; the prescriber must.
Think of a drop of dye added to water. A drop into a full bathtub barely tints it; the same drop into a teacup turns it deep colour. The eye dispenses one fixed "drop of dye" regardless of the vessel — a large adult is the bathtub, a newborn is the teacup. The molecule is identical; only the volume it disperses into has changed. That is the entire reason a routine adult drop can be a toxic dose in an infant, and why the same drop can reach across the placenta to a fetus that measures its blood in millilitres.
Children: the drops that punch above their weight
Some agents cross into an infant's brain and circulation with frightening ease. The starkest example is brimonidine, the alpha-2 agonist covered in the Autonomic and Glaucoma chapters. In adults it lowers eye pressure safely. In young children and infants it is contraindicated, because it crosses the immature blood–brain barrier and switches off the central nervous system — producing somnolence, apnoea, bradycardia, hypotension, hypothermia and, in reported cases, coma. A drop meant for the eye can put a small child into a stupor. The anticholinergic cycloplegics — atropine and cyclopentolate — are the next danger: systemic absorption produces the classic "dry as a bone, red as a beet, hot as a hare, mad as a hatter" picture — flushing, fever, dry mouth, tachycardia and delirium. The defences are to use lower concentrations (atropine 0.5% or 0.1% rather than 1% in infants; cyclopentolate 0.5%), to use the smallest effective drop, and to apply punctal occlusion afterwards.
Phenylephrine, the alpha-1 agonist used to dilate the pupil, tells the same story. The 10% strength routinely used in adults can trigger a hypertensive surge in a small child — so paediatric practice uses the 2.5% concentration, which dilates adequately at a fraction of the systemic pressor load. Topical corticosteroids close the list: as the Glaucoma chapters warn, steroids raise eye pressure and cloud the lens, and children are disproportionately strong steroid responders — a child on prolonged topical steroids can develop steroid-induced glaucoma or cataract faster and more severely than an adult, which is why paediatric steroid courses are kept short and closely monitored.
Two low-cost habits neutralise most of this risk, and both are worth saying out loud to every parent. First, punctal occlusion: press gently on the inner corner of the child's closed eye for a minute after the drop — it keeps the drug on the eye and off the nasal mucosa. Second, the right strength: reach for the paediatric concentration by default — phenylephrine 2.5% not 10%, dilute atropine not 1%, cyclopentolate 0.5% — and give one drop, not two. The order of magnitude that separates a safe dilation from a systemic toxicity is decided at the point of prescribing, not at the point of rescue.
Paediatric eye conditions and their drugs
Beyond drop safety, a handful of paediatric conditions have their own pharmacology. Ophthalmia neonatorum — conjunctivitis in the first month of life — is treated systemically, not just topically, because the culprits are serious: gonococcal infection needs systemic ceftriaxone, and chlamydial infection needs systemic oral erythromycin (topical alone fails to clear the nasopharyngeal reservoir), with credé/antibiotic prophylaxis given at birth in many settings. Retinopathy of prematurity (ROP), abnormal retinal vessel growth in premature infants, is where the Anti-VEGF chapter meets neonatology: intravitreal anti-VEGF (such as bevacizumab or ranibizumab) can regress the disease, but injecting a VEGF blocker into a developing infant raises the concern of suppressing systemic VEGF needed for brain, lung and organ development — so it is weighed carefully against laser photocoagulation, which is destructive but stays confined to the eye.
Amblyopia ("lazy eye") — atropine penalisation: a drop of atropine in the good eye blurs it, forcing the brain to use the weaker eye, an alternative to patching. Cycloplegic refraction — cyclopentolate, or atropine for a strong accommodative squint, to paralyse focusing and reveal the true refractive error. Congenital glaucoma — surgery (goniotomy/trabeculotomy) is definitive, with topical agents as a bridge; brimonidine is avoided in the young. ROP — intravitreal anti-VEGF vs laser. Ophthalmia neonatorum — systemic ceftriaxone (gonococcus) or oral erythromycin (chlamydia), not topical alone.
- A fixed-volume drop delivers an adult dose to an infant's tiny body — a relative overdose.
- Brimonidine (alpha-2 agonist) is contraindicated in infants/young children — apnoea, bradycardia, CNS depression, coma.
- Atropine/cyclopentolate can cause anticholinergic toxicity — use dilute strengths and punctal occlusion.
- Phenylephrine 2.5% (not 10%) in children to avoid a hypertensive surge; children are strong steroid responders.
- Ophthalmia neonatorum needs systemic antibiotics; amblyopia can be treated by atropine penalisation of the good eye.
- ROP: intravitreal anti-VEGF works but risks suppressing systemic VEGF a developing infant needs — laser is the alternative.
Pregnancy and breastfeeding: minimise systemic exposure
The guiding principle is the lowest systemic dose that controls the eye. In pregnancy the second patient is invisible but always present. The general rule mirrors the paediatric one — every drop reaches the mother's circulation and, potentially, the fetus, so the aim is the lowest effective concentration, the fewest agents, and punctal occlusion with every instillation to blunt systemic uptake. Specific cautions follow the drug classes taught in the Glaucoma chapters. Carbonic anhydrase inhibitors are treated warily: oral acetazolamide has been associated with teratogenicity concerns and metabolic effects and is generally avoided, especially in the first trimester, and topical CAIs (dorzolamide, brinzolamide) are used cautiously. Brimonidine is avoided near term and during breastfeeding for the same CNS-depressant reason it is banned in infants — it can reach the baby. Beta-blockers such as timolol are used cautiously: systemic absorption can cause fetal bradycardia and has been linked to growth concerns, so they are minimised and punctal occlusion is emphasised. In practice, glaucoma management in pregnancy often shifts toward laser trabeculoplasty precisely to reduce the drug burden on the fetus.
The antimicrobials carry their own pregnancy rules, drawn from the Antimicrobials chapter. Systemic tetracyclines (including doxycycline, used long-term for meibomian and ocular surface disease) are avoided in pregnancy and young children because they bind growing bone and staining teeth. Systemic fluoroquinolones are avoided where a safer option exists, on the classic cartilage-toxicity caution. And the Anti-VEGF agents — bevacizumab, ranibizumab, aflibercept — are generally avoided in pregnancy: VEGF is essential for placental development and fetal blood-vessel growth, so a systemic anti-VEGF signal is theoretically hazardous, and any intravitreal injection carries some systemic spill. The recurring logic is identical to the paediatric section: the eye may be the target, but the fetus shares the dose.
- In pregnancy every drop reaches the mother and potentially the fetus — use lowest strength, fewest agents, punctal occlusion.
- Avoid/limit oral acetazolamide and topical CAIs (teratogenicity concerns), and brimonidine near term and in breastfeeding.
- Use beta-blockers (timolol) cautiously — fetal bradycardia and growth concerns; glaucoma often shifts to laser in pregnancy.
- Avoid systemic tetracyclines (teeth/bone) and, where possible, fluoroquinolones (cartilage caution).
- Anti-VEGF is generally avoided in pregnancy — systemic VEGF is needed for placental and fetal development.
- The unifying message: think about the systemic dose of every drop, and blunt it with punctal occlusion and the lowest concentration.
- Prescribing brimonidine to a young child or infant — it crosses into the CNS and can cause apnoea, bradycardia and coma; it is contraindicated.
- Reaching for adult-strength drops in children — phenylephrine 10% or atropine 1% — instead of the paediatric concentration plus punctal occlusion.
- Assuming a topical drug is "safe because it's just an eye drop" in pregnancy — oral acetazolamide, brimonidine, anti-VEGF and systemic tetracyclines all reach the fetus.
A 3-month-old infant with congenital glaucoma is referred for medical management while awaiting surgery. A trainee suggests starting brimonidine drops. What is the most appropriate response?
- A fixed-volume drop delivers the same dose to a 3 kg infant as to a 70 kg adult — a relative overdose with immature clearance — so systemic toxicity is the special-population danger.
- In children: brimonidine is contraindicated (apnoea/coma); atropine/cyclopentolate risk anticholinergic toxicity; use phenylephrine 2.5% not 10%; steroids cause glaucoma/cataract more readily.
- In pregnancy: minimise systemic exposure; avoid/limit oral acetazolamide, topical CAIs, brimonidine and anti-VEGF; use beta-blockers cautiously; glaucoma often shifts to laser; avoid tetracyclines and fluoroquinolones.
- The unifying rule: think about the systemic dose of every eye drop, and blunt it with punctal occlusion and the lowest effective concentration.
- Kanski's Clinical Ophthalmology: A Systematic Approach — Paediatric ophthalmology; retinopathy of prematurity; ophthalmia neonatorum.
- Bartlett & Jaanus, Clinical Ocular Pharmacology — Ocular drugs in children and in pregnancy; systemic absorption and punctal occlusion.
- American Academy of Ophthalmology, Basic and Clinical Science Course (BCSC) — Pediatric Ophthalmology and Strabismus; Glaucoma.
- BNF for Children and BNF — Eye preparations; brimonidine, cyclopentolate, atropine, phenylephrine, and drugs in pregnancy/breastfeeding.
- Royal College of Ophthalmologists / NICE — Guidance on retinopathy of prematurity screening and treatment, and glaucoma management.
- Rang & Dale's Pharmacology / Katzung Basic & Clinical Pharmacology — Autonomic agents, carbonic anhydrase inhibitors, teratogenicity and weight-based dosing.
