Congestive optic disc

Congestive optic disc swelling is a non-inflammatory swelling that is a sign of increased intracranial pressure.

A congestive disk is swelling of the optic disc secondary to increased intracranial pressure. It is almost always bilateral, although it may be unilateral. All other causes of disc swelling in the absence of increased intracranial pressure involve the edema itself and usually cause visual disturbances. In all patients with a congestive disk, an intracranial neoplasm should be suspected until another cause is proven. However, not all patients with increased intracranial pressure develop a congestive disk. Hemispheric tumors tend to cause congestive disk later than posterior fossa tumors. Patients with a history of congestive disk may have significantly increased intracranial pressure without developing congestive disk again because of glial scarring of the optic disc.

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What causes papilledema?

There are many processes that lead to increased intracranial pressure. The first place among them is occupied by intracranial tumors: they are the cause of the occurrence of congestive optic nerve disks in 2/3 of cases. Among other, less significant, causes of increased intracranial pressure, and consequently the development of congestive optic nerve disks, it is necessary to name craniocerebral trauma, post-traumatic subdural hematoma, inflammatory lesions of the brain and its membranes, non-tumor masses, lesions of the vessels and sinuses of the brain, hydrocephalus, intracranial hypertension of unknown genesis, and spinal cord tumor. The severity of congestive optic nerve disks reflects the degree of increased intracranial pressure, but does not depend on the size of the mass formation in the cranial cavity. The rate of development of a congestive disc is largely determined by the localization of the neoplasm in relation to the cerebrospinal fluid system of the brain and venous collectors, in particular to the sinuses of the brain: the closer the tumor is located to the cerebrospinal fluid outflow pathways and sinuses, the faster the congestive disc of the optic nerve develops.

Symptoms of optic nerve congestion

Clinically, congestive disc is manifested by its edema, which causes blurring of the disc pattern and borders, as well as hyperemia of its tissue. As a rule, the process is bilateral, but in rare cases, congestive disc can develop in only one eye. Sometimes, unilateral congestive disc of the optic nerve is combined with disc atrophy and low visual functions in the other eye (Foster-Kennedy symptom).

Edema occurs first along the lower border of the disc, then along the upper, then the nasal and temporal halves of the disc swell successively. There is an initial stage of development of a stagnant disc, a stage of maximum edema, and a stage of reverse development of edema.

As the swelling increases, the optic disc begins to protrude into the vitreous body, and the swelling spreads to the surrounding peripapillary retina. The disc increases in size, and the blind spot widens, which is revealed by examining the visual field.

Visual functions may remain normal for a fairly long period of time, which is a characteristic symptom of optic nerve congestion and an important differential diagnostic sign. Such patients are referred to an ophthalmologist by therapists and neurologists for an eye fundus examination due to complaints of headache.

Another symptom of a stagnant disc is a sudden, short-term, sharp deterioration in vision, even to the point of blindness. This symptom is associated with a transient spasm of the arteries that feed the optic nerve. The frequency of such attacks depends on several factors, including the degree of disc edema, and can be up to several attacks within 1 hour.

As the congestive disc develops, the caliber of the retinal veins increases, indicating difficulty in venous outflow. In certain cases, hemorrhages occur, the typical localization of which is the area of the disc and the retina surrounding it. Hemorrhages may appear with pronounced edema of the disc and indicate a significant violation of venous outflow. However, hemorrhages are also possible with initial or mild edema. The cause of their development in such cases may be the rapid, sometimes lightning-fast, development of intracranial hypertension, for example, with a ruptured arterial aneurysm and subarachnoid hemorrhage, as well as with a malignant tumor and toxic effects on the vascular wall.

In the stage of developed edema, in addition to the symptoms described above, cotton-like whitish foci and small hemorrhages may appear in the paramacular region against the background of edematous tissue, which can cause a decrease in visual acuity.

A marked decrease in visual acuity is observed in the case of the development of an atrophic process in the optic nerve and the transition of the congestive optic nerve disk to secondary (post-congestive) atrophy of the optic nerve, in which the ophthalmoscopic picture is characterized by a pale optic nerve disk with an unclear pattern and borders, without edema or with traces of edema. The veins retain their plethora and tortuosity, the arteries are narrowed. Hemorrhages and whitish foci at this stage of the process, as a rule, no longer occur. Like any atrophic process, secondary atrophy of the optic nerve is accompanied by the loss of visual functions. In addition to a decrease in visual acuity, defects in the visual field of various natures are detected, which can be caused directly by the intracranial lesion, but more often begin in the inferior nasal quadrant.

Since optic nerve congestion is a sign of intracranial hypertension, its timely recognition and differential diagnostics with other similar processes in the eye are very important. First of all, it is necessary to distinguish between true optic nerve edema and pseudo-optic nerve congestion, in which the ophthalmoscopic picture resembles that of optic nerve congestion, but this pathology is caused by a congenital anomaly of the disc structure, the presence of disc drusen, is often combined with a refractive error and is detected already in childhood. One cannot fully rely on such a symptom as the presence or absence of venous pulse, especially in cases of abnormal disc development. One of the main symptoms facilitating differential diagnostics is a stable ophthalmoscopic picture during dynamic observation of a patient with pseudo-optic nerve congestion. Fluorescein angiography of the fundus also helps to clarify the diagnosis.

However, in some cases it is very difficult to differentiate optic nerve congestion from such diseases as optic neuritis, incipient thrombosis of the central retinal vein, anterior ischemic neuropathy, optic nerve meningioma. These diseases also cause optic nerve edema, but its nature is different. It is caused by pathological processes developing directly in the optic nerve, and is accompanied by a decrease in visual functions of varying degrees of severity.

In some cases, due to difficulties in establishing a diagnosis, it is inevitable to perform a spinal puncture with measurement of the pressure of the cerebrospinal fluid and examination of its composition.

If signs of optic nerve congestion are detected, the patient should be immediately referred to a neurosurgeon or neurologist for consultation. To clarify the cause of intracranial hypertension, computed tomography (CT) or magnetic resonance imaging (MRI) of the brain is performed.

Clinical features of optic nerve congestion

Initial stagnation of the disc can be difficult to diagnose. Its main features are:

• There are no subjective visual disturbances, visual acuity is normal.
• The discs are hyperemic and slightly protruding.
• The edges of the discs (first nasal, then superior, inferior and temporal) appear unclear, and parapapillary edema of the retinal nerve fiber layer develops.
• Disappearance of spontaneous venous pulse. However, 20% of healthy people do not have a spontaneous venous pulse, so its absence does not necessarily imply increased intracranial pressure. Preserved venous pulsation makes the diagnosis of congestive disc disease unlikely.

Advanced stagnant disc

• Transient visual disturbances may occur in one or both eyes, often upon standing, and last for a few seconds.
• Visual acuity is normal or reduced.
• The optic discs are severely hyperemic and moderately protruding, with unclear boundaries, and may initially appear asymmetrical.
• The excavation and small vessels on the disc are invisible.
• Venous congestion, paranasal hemorrhages in the form of “flame tongues”, often reveal cotton-wool-like foci.
• As the swelling increases, the optic disc appears enlarged; circular folds may appear at the temporal margin.
• Deposits of hard exudate can form a "macular fan" radiating from the center of the fovea: an incomplete "star figure" with a missing temporal portion.
• The blind spot is enlarged.

Chronic stagnation of the disc

• Visual acuity varies, and visual fields begin to narrow.
• The discs are mined like a "champagne cork".
• There are no cotton wool spots or hemorrhages.
• Opticiliary shunts and drusen-like crystal deposits (corpora amylacea) may be present on the disc surface.

Atrophic stagnation of the disc (secondary optic atrophy)

• Visual acuity is sharply reduced.
• The discs are dirty gray in color, slightly protruding, with several vessels and unclear boundaries.

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Differential diagnosis of optic nerve congestion

Deep drusen may be mistaken for incipient stasis disc.

Bilateral disc swelling can be caused by:

• Malignant hypertension.
• Bilateral papillitis.
• Bilateral compressive endocrine ophthalmopathy.
• Bilateral simultaneous anterior ischemic optic neuropathy.
• Bilateral venous outflow obstruction in the central retinal vein or carotid-cavernous fistula.

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Treatment of optic nerve congestion

Treatment for a stagnant disc is mainly aimed at the underlying disease, because a stagnant papilla is only a symptom of the disease. In case of neoplasms in the cranial cavity, surgery is indicated - tumor removal. Stagnant papillae in meningitis are treated conservatively depending on the underlying disease. Late diagnosis and long-term existence of a stagnant papilla lead to atrophy of the optic nerve fibers.

After eliminating the cause of optic nerve congestion, if disc atrophy has not yet developed, the fundus picture normalizes within 2-3 weeks to 1-2 months.