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D W Bond Department of Child Health
R M Gregson Department of Ophthalmology, Queen's Medical Centre,
University Hospital, Nottingham NG7 2UH
A 13 year old boy with Crohn's disease in remission
presented with a 10 day history of head and back pain. He also
mentioned intermittent blurring of vision and had developed a new
squint four days before admission. He had a history of hay fever and was being treated with fluticasone propionate aqueous nasal spray 50 µg to each nostril once a day (Glaxo Wellcome). This had been taken
infrequently until five days before admission when our colleagues from
the ear, nose, and throat department reviewed him and advised regular treatment.
On examination his optic discs were swollen bilaterally and he had a
right sixth nerve palsy. Investigations showed no evidence of
intercurrent infection. Urea and electrolytes, liver function, and
concentrations of calcium, phosphate, and magnesium were all within
normal limits. Fluorescein angiography showed leakage of dye from the
optic discs, confirming mild bilateral papilloedema (figure). An
unenhanced computed tomogram gave normal results. Cerebrospinal fluid
was clear and colourless with no cells, and the protein concentration
was 0.1 g/l and glucose concentration 4.3 mmol/l (blood glucose 5.2 mmol/l). The opening pressure of the cerebrospinal fluid was not
measured. Magnetic resonance imaging excluded cavernous sinus
thrombosis.

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Disc swelling, vascular nipping, and vessel leakage shown by
fluorescein angiography
The fluticasone propionate was stopped, and over the next few weeks his headaches and back pain disappeared. His sixth nerve palsy resolved, and his disc margins cleared. On review five months later his optic discs had returned to normal and he had remained asymptomatic.
We propose that nasal fluticasone propionate caused this child's benign intracranial hypertension because of the temporal relation between symptoms to its regular administration. After lumbar puncture and the cessation of the drug his symptoms resolved over a few weeks and the papilloedema resolved over several months.
The occurrence of benign intracranial hypertension is well
documented with corticosteroids when given
systemically1-3 or topically,
1 4
together
with their withdrawal.5 We reported this adverse reaction
to the Committee on Safety of Medicines. The Medicines Control Agency
and the manufacturers have confirmed that there have been no previous
reports of benign intracranial hypertension with nasal fluticasone
proprionate. Benign intracranial hypertension should be considered as a
potential cause of headache in children taking nasal steroids.
Footnotes
Competing interests: None declared.
References
| 1. | Grant DN. Benign intracranial hypertension: a review of 79 cases in infancy and childhood. Arch Dis Child 1971; 46: 651-655. |
| 2. | Vyas CK, Talwar KK, Bhatnagar V, Sharma BK. Steroid-induced benign intracranial hypertension. Postgrad Med J 1981; 57: 181-182[Medline]. |
| 3. |
Newton M, Cooper BT.
Benign intracranial hypertension during prednisolone treatment for inflammatory bowel disease.
Gut
1994;
35:
423-425 |
| 4. | Hosking GP, Elliston H. Benign intracranial hypertension in a child with excema treated with topical steroids. BMJ 1978; 1: 550-551. |
| 5. | Neville BGR, Wilson J. Benign intracranial hypertension following corticosteroid withdrawal in childhood. BMJ 1970; 3: 554-556. |
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