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Case Study 4 Papilloedema Faye McDearmid, Redcar A 57-year-old Caucasian male, employed as an ambulance driver, was advised to have an eye examination by his general practitioner after complaining of ‘blurred vision’ for a few weeks. He had not experienced any headaches, nausea, double vision or other symptoms of visual disturbance. His general health was good; he was not taking any medications and was a non-smoker. His father has glaucoma – there was no other relevant personal or family history. This gentleman has been a patient at our family practice since 1986. Previously his visual acuity has averaged R 6/5 and L 6/9 with a Snellen self-illuminated wall chart. Figure 1 Left: The initial visual field plot for the RE with an enlarged blind spot Right: The initial visual field plot for the LE with a slightly enlarged blind spot Clinical signs On this particular day his best corrected visual acuity was reduced to 6/12 (no improvement with pinhole) for the RE and 6/9, as usual, in the LE (Table 1). Corrected near acuity was N5 R&L. Ocular motility testing revealed an incomitant deviation causing diplopia on right gaze. This was identified as under-action of the right lateral rectus muscle. HFAII Central 30-2 threshold visual fields revealed marked enlargement of the RE blind spot, and a slightly enlarged LE blind spot (compared to previous field plots for this patient). Perkins applanation tonometry at 9.38am revealed intraocular pressure (IOP) of 22 and 23mmHg R&L respectively. Pupil reactions were normal with no afferent pupillary defect observed. At this point, the signs and symptoms observed included: • Visual obscurations • Reduced RE visual acuity • Diplopia on right gaze due to right lateral rectus underaction • Blind spot enlargement, particularly RE • Marginally elevated IOP • Normal pupil reactions. Sphere Cylinder Axis VA Near add R +4.75 -1.25 67.5 6/12 +2.00 Near acuity NS L +5.50 -1.00 95 6/9 +2.00 NS Internal eye examination with undilated direct ophthalmoscopy revealed bilateral, asymmetrical optic nerve head hyperaemia, with elevation and blurring of the disc margins. The appearance of the RE was more progressive. There was mild dilatation and tortuosity of the retinal veins, but no haemorrhages, cotton-wool spots or macular oedema. The optomap retinal images enabled me to view the optic nerve heads together and directly compare the degree of laterality and symmetry. I was also able to explain and show this patient, using these and previous images, how and possibly why he was experiencing his symptoms. As this patient was displaying the clinical features of optic nerve swelling, possibly indicative of raised intracranial pressure, prompt referral was warranted with suspected papilloedema. Swollen disc? Papilloedema is defined as disc swelling secondary to increased intracranial pressure. As optometrists we may not be aware of the presence or absence of raised intracranial pressure and therefore the appropriate term to use is ‘disc swelling’ or ‘disc oedema’. Causes of raised intracranial pressure include: space-occupying lesions (brain tumour, intracranial haemorrhage or abscess), cerebral oedema from head trauma, abnormalities in the production and flow of cerebrospinal fluid (increased cerebrospinal fluid (CSF) production, for exam- 9 Case Study 4 Papilloedema Faye McDearmid, Redcar volume due to vascular malformations, obstructions of cranial venous outflow (venous sinus thrombosis) or pseudotumour cerebri (idiopathic intracranial hypertension). Therefore, if papilloedema is suspected, emergency referral is required – not only is it sightthreatening, but raised intracranial pressure may be life-threatening. At present the exact mechanism of papilloedema is not perfectly understood. It has been suggested that raised intracranial pressure is transmitted through the optic nerve sheath which causes compression of the nerve fibres, particularly at the lamina cribrosa, where the optic nerve passes through the sclera. The compression impairs Figure 2a The optomap retinal scan of the right eye, illustrating the swollen disc and tortuous retinal veins Figure 3 The RE optomap retinal scan 19 months after the initial presentation Figure 2b The optomap retinal scan of the left eye illustrating the bilat eral nature but asymmetry of the swollen discs ple due to choroid plexus tumour, decreased CSF production related to, for example, meningitis or subarachnoid haemorrhage, CSF flow obstruction may be congenital or acquired), increased cerebral blood 10 intracellular transport within the nerve axons, leading to axoplasmic stasis, resulting in leakage, swelling, vascular obstruction and dilatation, with eventual retinal and optic nerve ischaemia. Transient visual obscurations are common in the early stages of papilloedema; visual acuity is usually unaffected in the early stages – which helps to differentially diagnose papilloedema from other potential causes of optic nerve swelling such as optic neuritis or anterior ischaemic optic neuropathy. The lateral rectus extraocular muscle is innervated by the sixth cranial nerve (abducens) which passes over the petrous portion of the temporal bone. Raised intracranial pressure may lead Management Typically, this case occurred on a Saturday when the fast-track eye clinic at the local hospital was closed. Consequently we decided to telephone the hospital to try to arrange for a neurologist to see this patient as soon as they saw necessary. Eventually I got to speak to the neurologist on call who was keen to see the patient straight away, although he did ask us to send him in an hour and a half as he wasn’t actually at the hospital and it would take him that long to get thereThat afternoon the patient underwent CT and MRI scans of his brain and optic nerves and had lumbar punctures to confirm elevated intracranial pressure and analyse the cerebrospinal fluid. Initial tests suggested idiopathic intracranial hypertension and this was confirmed after three further lumbar punctures. He was discharged from the neurology department after the final lumbar puncture, 11 months after his presentation to us. Follow-up His most recent eye examination 19 months after the referral showed the RE visual acuity had recovered to 6/9 and he even managed 6/6 with his LE. Motility testing was once again normal and the RE optic nerve appears just slightly paler than the LE (Figure 3). His visual fields show a much less enlarged blind spot area (Figure 4). Due to the family history of glaucoma he is currently being monitored on an annual basis. Figure 4 The RE less enlarged blind spot some months after the initial presentation to compression of this area of the abducent nerve leading to sixth nerve palsy – a non-specific feature of intracranial pathology. Disc swelling can be observed in a number of different ocular conditions, for example: papilloedema, papillitis, anterior ischaemic optic neuropathy, pseudopapilloedema, accelerated/malignant hypertension, intraocular inflammation, central retinal vein occlusion (CRVO), optic nerve compression, optic nerve head infiltration – for example a lymphoma, ocular hypotony, toxic optic neuropathy and diabetic papillopathy to list a few. Optic disc drusen and hypermetropia can also give the appearance of a swollen optic nerve head. These conditions can be differentially diagnosed from true papilloedema using other co-existing signs – for example in a CRVO there will be haemorrhages on the disc but also throughout the affected retina. Further reading Bruce AS, O’Day J, McKay D, Swann PG. Posterior Eye Disease and Glaucoma A-Z. Butterworth Heinemann. Elsevier, 2008;198-201. Jackson TL. Moorfields Manual of Ophthalmology. Mosby. Elsevier, 2008;644-646. Hu K and Hammond C. Differentiating sight threatening from nonsight threatening eye disease: the optic nerve and ophthalmoplegia. Optometry Today, 8 September 2006;30-36. Faye McDearmid is an optometrist in independent practice in Redcar and at James Cook University Hospital. She is also a part-time PhD student at the University of Bradford. 11