Paediatric idiopathic intracranial hypertension (IIH), is a rare but important differential diagnosis in children presenting with papilloedema. It is characterised by raised intracranial pressure in the absence of an identifiable secondary structural or systemic cause and is, therefore, a diagnosis of exclusion. In the adult population, there is a strong predilection for the disease to occur in female patients who are obese. This association is also seen in paediatric patients with IIH but primarily in the post-pubertal cohort. In younger pre-pubertal children, this is not the case, possibly reflecting a different underlying disease aetiology and pathogenesis. Untreated IIH in children can cause significant morbidity from sight loss, chronic headaches, and the psychological effects of ongoing regular hospital monitoring, interventions, and medication. The ultimate goal in the management of paediatric IIH is to protect the optic nerve from papilloedema-induced optic neuropathy and thus preserve vision, whilst reducing the morbidity from other symptoms of IIH, in particular chronic headaches. In this review, we will outline the typical work-up and diagnostic process for paediatric patients with suspected IIH and how we manage these patients.

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Purpose To report a case series involving two cases of acute retinal necrosis (ARN) presenting after treatment and resolution of herpes simplex virus (HSV) encephalitis. In neither case was antiviral prophylaxis after initial episode of encephalitis used. Literature review is presented to evaluate the benefit of prophylaxis in such cases. Methods Two case reports are described and fundus photos presented of patients presenting to the Ophthalmology Department of Queen Alexandra Hospital, Portsmouth, UK within the last 3 years. PubMed was used to conduct the literature review. Results A 67‐year‐old female presented with rapid painful unilateral visual loss. She had had a history of HSV encephalitis 6 years before, treated successfully with no recurrences. Clinical assessment was in keeping with ARN. She was admitted for intravenous acyclovir for 8 days followed by long‐term oral antiviral treatment. Her vision remained poor with a best‐corrected visual acuity (BCVA) of 6/60 in the affected eye. A 66 year‐old male presented with a 10‐day history of painful unilateral visual loss. He had had a history of HSV encephalitis 6 months before and a relapse 2 months later treated successfully with acyclovir. Clinical assessment demonstrated a panuveitis and retinitis in keeping with ARN. He was admitted for intravenous acyclovir then kept on long‐term oral treatment of 400 mg twice‐daily. The BCVA in his affected eye has remained at 5/60. Conclusions HSV encephalitis has been widely documented as a risk factor for ARN and has been reported to occur up to 20 years after initial illness. The virus may reach the eye via a trans‐axonal route and reside in a reservoir awaiting re‐activation within retinal neurons. We propose that prophylaxis with long‐term low‐dose antivirals is necessary after all cases of HSV encephalitis to reduce the risk of ARN.