A histological review of dura mater taken from a post-mortem series of 50 paediatric cases aged up to 5 months revealed fresh bleeding in the dura in 36/50, the bleeding ranging from small perivascular haemorrhages to extensive haemorrhage which had ruptured onto the surface of the dura. Severe hypoxia had been documented clinically in 27 of the 36 cases (75%). In a similar review of three infants presenting with classical 'shaken baby syndrome', intradural haemorrhage was also found, in addition to subdural bleeding, and we believe that our findings may have relevance to the pathogenesis of some infantile subdural haemorrhage. Recent work has shown that, in a proportion of infants with fatal head injury, there is little traumatic brain damage and that the significant finding is craniocervical injury, which causes respiratory abnormalities, severe global hypoxia and brain swelling, with raised intracranial pressure. We propose that, in such infants, a combination of severe hypoxia, brain swelling and raised central venous pressure causes blood to leak from intracranial veins into the subdural space, and that the cause of the subdural bleeding in some cases of infant head injury is therefore not traumatic rupture of bridging veins, but a phenomenon of immaturity. Hypoxia with brain swelling would also account for retinal haemorrhages, and so provide a unified hypothesis for the clinical and neuropathological findings in cases of infant head injury, without impact or considerable force being necessary.

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The results of orbital decompression for thyroid eye disease are presented in a cohort of 33 patients. It was performed by an external Patterson approach in 21 individuals and in 13 by an endonasal endoscopic approach. The endoscopic approach was entirely comparable in respect of improvement in axial proptosis, giving a mean improvement of 4.4 mm as compared with a mean of 3.8 mm for the external approach, and produced a demonstrable improvement in visual acuity and perception of colour in three individuals, where this was compromised, and was associated with fewer complications.

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ObjectivesTo estimate the incidence of severe retinopathy of prematurity (ROP) requiring treatment and describe current treatment patterns in the UK.DesignNationwide population-based case ascertainment study via the British Ophthalmic Surveillance Unit and a national collaborative ROP special interest group. Practitioners completed a standardised case report form (CRF).SettingAll paediatric ophthalmologists providing screening and/or treatment for retinopathy in the UK were invited to take part.ParticipantsAny baby with ROP treated or referred for treatment between 1 December 2013 and 30 November 2014, treated with laser, cryotherapy, vascular endothelial growth factor (VEGF) inhibitor or vitrectomy/scleral buckling, or a combination.Main outcome measureIncidence of ROP requiring treatment.ResultsWe received 370 CRFs; 327 were included. Denominator from epidemiological data: 8112 infants with birth weight of <1500 g. The incidence of ROP requiring treatment was 4% (327/8112, 95% CI 3.6% to 4.5%). Median gestational age was 25 weeks (IQR 24.3–26.1), and median birth weight 706 g (IQR 620–821). Median age at first treatment was 80 days (IQR 71–96). 204 right eyes (62.39%) had type 1 ROP, and 27 (8.26%) had aggressive posterior ROP. Infants were also treated for milder disease: 9 (2.75%) right eyes were treated for type 2 ROP, and 74 (22.63%) for disease milder than type 1 with plus or preplus, which we defined here as ‘type 2 plus’ disease. First-line treatment was diode laser photoablation of the avascular retina in 90.5% and injection of VEGF inhibitor in 8%.ConclusionsROP treatment incidence in the UK is 2.5 times higher than previously estimated. 8% of treated infants receive intravitreal VEGF inhibitor, currently unlicensed. Research is needed urgently to establish safety and efficacy of this approach. Earlier treatment and increasing numbers of surviving premature infants require an increase in appropriate eye care facilities and staff.Trial registration numberNCT02484989.

Botulinum Toxin A injected into the levator palpebrae superioris produces a flaccid ptosis of the upper lid and provides a safe and effective protection for the cornea to aid healing in indolent ulceration or as prophylaxis when there is fifth or seventh cranial nerve damage. Fifteen patients have received this treatment. Levator paresis, producing ptosis for a mean of 2-3 weeks and recovering in a mean of 8.1 weeks was successfully produced in all patients and complete corneal healing was produced in 80% of patients. The major side effect was weakness of the superior rectus muscle which occurred in 80% of cases and lasted a mean of 6 weeks.

Background: To determine the rate of glaucoma following congenital cataract surgery at Moorfields Eye Hospital (MEH), and to investigate potential risk factors for glaucoma in our case series.