"¡5 g The pathogenesis of papilledema is not one of leakage of a c fluid into the interstitial spaces of the optic disc. It is actually caused by intrinsic swelling of the ganglion cell axons because of stasis of axoplasmic flow in the prelaminar optic nerve (see Chap. 3, ■ Fig. 3.3). This explains why atrophic optic discs cannot swell when intracranial pressure is elevated. If the disc swelling is present in one eye only, it still could be papilledema. Well-documented cases of unilateral papilledema have been described (see Huna Baron et al. 2001, in "Further Reading" below), and it is thought that the mechanism is one of sheltering the uninvolved eye from the elevated pressure due to an absence of the perineural subarachnoid space around the anterior portion of the optic nerve. This could be either developmental or acquired because of inflammatory scarring. The unilateral finding is rare, however, and when it is encountered, MRI scanning of the optic nerves is necessary to rule out other causes.
Initially, visual function is not disturbed by papillede-ma, although there is an enlargement of the physiologic blind spot. This is thought to be caused by a refractive sco-toma, produced by elevation of the peripapillary retina, since the apparent enlargement can be reversed by using a hyperopic lens correction during the visual field testing (see Corbett et al. 1988, in "Further Reading" below).
Visual function is not initially harmed, but chronic papilledema (over months) can lead to a progressive gliosis and optic atrophy with loss of all useful vision.
Stage 1. Early stage of papilledema (■ Fig. 8.11): There is blurring of the disc margin and elevation of the disc in the nasal half. Capillary ectasias are visible on the surface of the disc, and the peripapillary nerve fiber layer has lost
Fig. 8.11. Early papilledema in a patient with intracranial lymphoma. The signs are very subtle. They show only a mild loss of sharpness at the disc margin and early features of obscuration of the vessels by swollen neural tissue near the disc margin. When seen stereoscopically, the elevation of the disc was readily apparent. The diagnosis of early papilledema was later confirmed by the patient's clinical course
Fig. 8.12. Fully developed, acute papilledema in a 62-year-old man with an intracranial tumor; the appearance is asymmetrical, the swelling more easily seen in the left image, which is not uncommon for acute papilledema. Striking are the hyperemia and capillary ectasias on the surface of the disc and the obscuration of even the largest retinal vessels at the disc margin, again more apparent in the left image
Fig. 8.12. Fully developed, acute papilledema in a 62-year-old man with an intracranial tumor; the appearance is asymmetrical, the swelling more easily seen in the left image, which is not uncommon for acute papilledema. Striking are the hyperemia and capillary ectasias on the surface of the disc and the obscuration of even the largest retinal vessels at the disc margin, again more apparent in the left image its clarity, consistent with the fact that the "edema" is intrinsic to the nerve fibers themselves. Small hemorrhages can be present.
Stage 2. Fully developed papilledema (■ Fig. 8.12): Elevation, blurring, and hemorrhages have worsened, and exudates are now visible. The physiologic cup is usually preserved.
Stage 3. Chronic papilledema (■ Fig. 8.13): The hemorrhages and exudates have subsided, being replaced by small glistening deposits. The physiologic cup has disappeared. Cilioretinal collateral vessels can appear at this stage. Small, concentric, retinal folds can appear in the peripapillary fundus (Paton's lines).
Fig. 8.14. Disc atrophy in chronic papilledema. The prominent blurring of the disc border and the vascular sheathing indicate that the problem is not one of primary optic atrophy
Stage 4. Atrophic papilledema (■ Fig. 8.14): The disc has become pale, although the margin remains more or less blurred, and the retinal vessels show sheathing.
Spontaneous venous pulses are an important diagnostic criterion. It is always absent in the presence of papilledema. If it is visible, it is a reliable sign that intracranial pressure (ICP) is normal. The presence of venous pulses is a good sign, since it rules out elevated pressure at the time of the examination, but it does not exclude the possibility of there being intermittent elevations in ICP. The absence of spontaneous venous pulses is of no help, since at least 20% of healthy people do not show venous pulsations.
Visual function in the first two stages is unaffected, aside from the reversible enlargement of the blind spot. Loss of function is common in chronic papilledema and is often complicated by a maculopathy in addition to the optic neuropathy (see below). The macular changes are thought to be the result of traction of the retina, caused by the elevation and scarring of the peripapillary retina. Atrophic papill-edema, by definition, is associated with severe and irreversible damage to the nerve.
Causes of Papilledema
Any elevation of intracranial pressure can result in papill-edema whether by:
■ Intracranial mass lesions
■ Obstruction of the path of cerebrospinal fluid (CSF) flow by a mass, stenosis, or other cause
■ Limitation of intracranial space by deformities of the skull
■ Cerebral edema caused by tumors, inflammation or toxic disorders
■ Increased rates of CSF production associated with tumors or inflammatory disorders
■ Impaired outflow of CSF, e.g., caused by increased viscosity of the CSF, due to protein formation by a tumor or inflammation
■ Elevated pressure in the venous sinuses that drain the CSF
In this connection, it should be clear that spinal tumors can be the primary cause of papilledema.
Advanced stages of hypertensive retinopathy often produce optic disc edema. Marked narrowing of the arterial vessels should be a clue that the disc swelling could be caused by severely elevated levels of blood pressure. For this reason alone, a sphygmomanometer should be kept in every ophthalmic practice.
Newly diagnosed papilledema should be considered an emergency. An imaging procedure should be done immediately (on the same day as discovery). Ideally, this should be done with MRI. Documentation of the pupillary findings, oculomotor function, and visual field examination should be completed as soon as possible.
The use of long-acting mydriatics is contraindicated, so that intensive neurological monitoring of the patient's findings will not be impaired.
When a mydriatic must be used for adequate visualization of the optic disc, one should use short-acting drugs, such as tropicamide, while documenting the time of administration. Additional measures depend on the results of MRI scanning. If the scan appears normal, the next step is to do a lumbar puncture for collection of CSF and determination of the ICP. Lumbar punctures in the presence of papillede-ma are contraindicated when there is a pressure gradient between the intracranial and spinal subarachnoid spaces.
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