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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-
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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
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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.
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