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Editor,—Haemorrhage into the various spaces and potential spaces of the eye is a not uncommon finding in idiopathic intracranial hypertension (IIH), especially nerve fibre layer haemorrhages, a nearly constant feature of fully developed papilloedema. Less frequently reported are vitreous, subhyaloid, and subretinal haemorrhages. We present a patient with bilateral peripapillary subretinal haemorrhages as the prominent manifestation of IIH, whose haemorrhages resolved as her IIH improved.
A 41 year old obese woman was evaluated because of an unusual optic disc appearance bilaterally. One year before evaluation, she developed severe, diffuse headaches which would wake her from sleep. There were no associated visual symptoms. Brain computed tomography (CT) was normal. The headaches resolved spontaneously, only to recur months later, this time accompanied by blurred vision. She was seen by an optometrist, who noted “retinal bleeding”.
On examination she was obese but appeared well with a blood pressure of 130/90. Corrected visual acuity was 20/20 in both eyes, and colour vision was normal. Pupils were briskly reactive with no relative afferent pupillary defect. Ocular motility was normal. Automated perimetry revealed enlarged blind spots. There was minimal bilateral disc oedema with prominent surrounding subretinal haemorrhages (Fig 1). The haemorrhages spared the inferotemporal disc in the right eye and the temporal disc in the left. The maculas, periphery, and vessels were normal.
B-scan ultrasonography revealed no evidence of optic nerve drusen. Fluorescein angiogram did not demonstrate neovascularisation. Magnetic resonance image (MRI) of the brain and orbits, with and without gadolinium, was normal. Lumbar puncture demonstrated an opening pressure of 280 mm CSF with normal contents. A diagnosis of IIH was made.
Over the next 2 years, the patient lost a total of 54 lb (24.5 kg), and took no new medications. On follow up examination, she reported normal vision and no further headaches. Her visual function was stable, and fundus examination showed near complete resolution of the subretinal haemorrhages (Fig 2).
The differential diagnosis of subretinal haemorrhage is extensive. Among the more frequently cited aetiologies are trauma, choroidal tumour, aneurysmal subarachnoid haemorrhage, and retinal vascular disease such as diabetic or hypertensive retinopathy. Infrequently, subretinal haemorrhages have been reported in association with IIH.1 2 All of these reports noted the additional features of either small anomalous discs or peripapillary subretinal neovascular membranes, the latter usually associated with chronic papilloedema. In our patient, there was no evidence of neovascular membranes, and the papilloedema itself was not prominent.
Ocular haemorrhages are common in cases of aneurysmal subarachnoid haemorrhage, occurring in 17% of cases.3 The haemorrhages may be subretinal, retinal, preretinal, or intravitreal. When subretinal, the haemorrhages are frequently peripapillary. It is now well accepted that the ocular haemorrhages seen in patients with aneurysmal subarachnoid haemorrhage are caused by acute elevations in the intracranial pressure with subsequent retinal venous hypertension. Acute increases in intracranial pressure induce a venous stasis retinopathy, which may result in intraocular bleeding.4
Given that the mechanism of disc oedema in IIH is raised intracranial pressure, it would follow that retinal haemorrhages should be common in this disorder. Large vitreous bleeds, however, are very rare in IIH, as are subretinal haemorrhages, probably because of the chronicity and lack of sudden pressure elevation in IIH. Pre-existing communicating vessels between the retinal and choroidal circulations probably dilate in response to long standing papilloedema, creating optociliary shunt vessels of varying sizes.5 Perhaps these shunts unload the increased venous pressure on the retinal circulation, reducing the incidence of large intraocular haemorrhages from venous stasis retinopathy. An acute elevation in intracranial pressure in a patient with IIH may occur with coughing or other variants of the Valsalva manoeuvre. Such a precipitous rise in pressure could produce ocular haemorrhages of the type seen in our patient.
We believe our patient’s elevated intracranial pressure probably caused prominent peripapillary subretinal haemorrhages with only mild disc oedema. Subsequent weight loss probably resulted in normalisation of her intracranial pressure, as it paralleled the resolution of her disc oedema as well as her headaches and visual complaints. Near complete resolution of the peripapillary haemorrhages accompanied the improvement in her symptoms. This case serves as yet another confirmation of the proposed mechanism of peripapillary subretinal haemorrhage as occurring secondary to raised intracranial pressure.
This work was supported in part by a departmental grant (ophthalmology) from Research to Prevent Blindness, Inc (NY) and ophthalmology department, National Institutes of health CORE grant no P30-EY0 6360.
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