Common Causes and Treatment of Optic Disc Swelling

Introduction

Swollen optic discs are often found during optometric examination. Common causes of optic disc swelling include vasculitis, demyelination, elevated cerebrospinal fluid pressure, and abnormal hemodynamics. The differential diagnosis can be challenging because the underlying systemic causes of swollen optic discs are varied and complicated. The appropriate treatment regimens for the common differential diagnoses range from simple monitoring to emergent hospitalization and intravenous steroids. Because of this, it is imperative that an accurate diagnosis is reached when optic disc swelling presents so that appropriate treatment may be instituted.

Optic Disc Anatomy

It is important to understand optic disc anatomy very well when evaluating a swollen disc. The optic disc is susceptible to many systemic diseases because of the tissue types that comprise the nerve head. Present at the discs are nervous, vascular, and connective tissues as well as the meninges and cerebrospinal fluid. It is also important to be aware of normal disc variations that may give the appearance of disc elevation without true swelling.

The Swollen Disc

Characteristics of the swollen disc include a blurry margin, hyperemia, intraretinal hemorrhages, nerve fiber layer infarction (cotton wool spots), loss of physiological cup, and no spontaneous venous pulsation. It is important to recognize the appearance of these findings even in subtle forms as the presentation can be varied. Swollen discs may manifest any or all of the following main functional deficiencies: a decrease in visual acuity, afferent pupillary defects, visual field loss, color vision loss, and reduced contrast sensitivity.

Figure 1: Swollen optic disc

Vasculitis

The most common vasculitis responsible for optic disc swelling is cranial arteritis. This is also known as giant cell arteritis (GCA). Giant cell arteritis is a multi-system inflammatory disease affecting the medium and large arteries of the body. It shows a predilection for the cranial arteries and frequently effects the posterior ciliary arteries. An immunologic mechanism is suspected as the underlying pathophysiology. Making the diagnosis of GCA begins with case history, signs, and symptoms. The current American College of Rheumatology criteria for the diagnosis of giant cell arteritis includes (a) age at onset of symptoms over 50 years; (b) new onset or new type of localized headache; (c) temporal artery tenderness or diminished pulse; (d) ESR above 50mm/h by the Westergren method; (e) temporal artery biopsy specimen showing mononuclear infiltration or granulomatous infiltration with giant cells. The presence of any three criteria constitutes evidence for the diagnosis of GCA with a sensitivity of 93.5% and a specificity of 91.2%(1). The clinical presentation is even more characteristic when associated with polymyalgia rheumatica, a syndrome of bilateral shoulder and hip girdle pain and stiffness occurring in about 50% of GCA patients. Other symptoms of focal large and medium sized vessel ischemia include transient ischemic attacks, strokes, and extremity claudication. Involvement of the thoracic or abdominal aorta may lead to aortic aneurysm. Giant cell arteritis typically occurs in individuals 50-85 years of age, with the average being 70. It occurs in males three times more frequently than females predominantly in Caucasians. Other common symptoms include jaw claudication, neck pain and scalp tenderness secondary to involvement of the facial, occipital, and temporal arteries respectively(2).

In GCA, Westergren erythrocyte sedimentation rate (ESR) is typically elevated to 80-100mm/hr. C-Reactive protein (CRP) is typically above 5.0mg/dL. C-reactive protein is an acute phase reactant that is found in human serum in a variety of conditions including GCA. Some authors advocate measuring the concentration of CRP and pursuing the diagnosis further if CRP is elevated, even if the ESR is not. Some authors quote a combined sensitivity of diagnosing GCA of 97% when both the ESR and CRP are used as screening tools. Other authors are not impressed with CRP in diagnosing GCA(3).

Temporal artery biopsy remains the gold standard for the diagnosis of GCA. Although a positive biopsy generally confirms the diagnosis with certainty, false negative biopsies do occur. Failure to find characteristic histopathologic features may be due to inadequate sample size and the patchy nature of the vasculitic process. Careful sectioning of a substantial biopsy specimen (greater than 5 cm) optimizes the diagnostic yield of the procedure(2).

Giant cell arteritis affects the disc as arteritic anterior ischemic optic neuropathy (AAION) and is considered a true ocular emergency. Arteritic AION is caused by inflammation of the short posterior ciliary arteries that supply the immediate retrolaminar and laminar portions of the optic disc.(3) Sudden complete monocular loss of vision occurs in 50% of cases with 70-80% developing inferior altitudinal visual field loss. Finger counting and no light perception vision is not an uncommon sequella. Transient monocular blindness precedes vision loss in 2-19% of cases. The fellow eye becomes involved in 50-75% of cases usually within 1-10 days if there is no therapeutic intervention(4).

Figure 2: Arteritic anterior ischemic optic neuropathy

The treatment for AAION is the same as treatment for GCA. If the duration of AAION is less than 36 hours, immediate methylprednisolone 1g IV bid x 5 days followed by 60-100mg prednisone orally per day is indicated. The steroid dose is titrated against symptoms and ESR. Rapid tapering of prednisone to less than 20mg/day over the first 1-2 months is associated with a 30% relapse rate. A more reasonable tapering schedule is to a daily dose of 20-30 mg/day within the first 2 months and more slowly thereafter. The goal is a maintenance dose of less than 10mg/day, but it may take more than a year to achieve it(1). Although recovery of vision is considered rare, some instances have been reported. These recovery rates range from 15% to 34%. Although there seems to be some increased recovery with intensive intravenous therapy as opposed to smaller oral dose schedules,(5) it is difficult to be exacting about route of administration or steroid dosage as no strictly controlled trials are available.

Demyelination

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system, affecting approximately 2.5 million young adults world wide. Multiple sclerosis has a poorly understood etiology, but the suspected course is an immune reaction against self-myelin agents possibly triggered by a viral infection. Other possible factors include genetic susceptibility linked to major histocompatability genes. The onset of MS is usually during the 3rd and 4th decade of life. It occurs more frequently in latitudes above the 37th parallel. Risk for developing MS is established around puberty. The symptoms of MS include an acute onset of focal neurological signs and symptoms. Ataxia and intention tremor are manifestations of cerebellar involvement. Motor deficits tend to occur acutely in younger patients and insidiously in older patients. Legs are more likely to be involved than arms. Urinary difficulties are a consequence of upper motor nerve injury in the spinal cord(6).

The diagnosis of MS is made based on neurological history, physical exam, and laboratory testing. Younger patients typically manifest a relapsing-remitting course where symptoms evolve over 24 to 72 hours, stabilize, then resolve. A secondary progressive course may occur in later years with a steady gradual worsening of symptoms. About 10% of patients who present with MS at 40-60 years of age suffer a primary progressive course manifesting as prominent spinal cord involvement. Laboratory testing for MS helps support the diagnosis and may include cerebrospinal fluid analysis looking for increased IgG, myelin basic protein, and pleocytosis. The most sensitive test form is magnetic resonance imaging (MRI), which shows multiple periventricular white matter plaques in 90% of patients with known MS(ibid).

Current therapies for MS are designed to prevent relapses and retard worsening of the disease. The difficult task is to improve the long-term course of the illness. Efforts to treat MS have focused on suppressing the immunologically induced inflammatory response. The U.S Food and Drug Administration has approved three drugs for patients with relapsing-remitting MS. These drugs are Avonex (Interferon beta 1a), Betaseron (Interferon beta 1b), and Copaxone (glatiramer acetate). They have all been tested in separate placebo controlled, double-blinded multi-center trials. Reductions in relapse rates of 37%, 33%, and 29% respectively were demonstrated(ibid).

Optic neuritis is found clinically at some time in 75% of patients with MS and is one of the presenting signs of MS in about 35% of cases. It is second only to glaucoma in frequency of optic nerve disorders in persons younger than 50. Optic neuritis is characterized by an acute loss of vision, often associated with retrobulbar pain with eye movement. Generally the presentation is unilateral with loss of acuity, decreased color vision, and afferent pupillary defect. Although optic disc swelling is common, the disc may appear normal in retrobulbar optic neuritis. Prognosis for visual recovery is generally very good, but, optic neuritis resolution is almost never complete. Patients typically show some signs of optic nerve damage and mild dysfunction. Even when acuity returns to 20/20; decreases in color vision, contrast sensitivity, and visual field sensitivity may remain.

Figure 3: Optic neuritis

The treatment for patients with optic neuritis is described by the Optic Neuritis Treatment Trial (ONTT). The ONTT demonstrated that MRI is a powerful predictor of the early risk of multiple sclerosis after optic neuritis, and can be used to determine treatment. If the optic neuritis symptoms are of 8 days or less and MRI of the brain demonstrates 2 or more white matter signal abnormalities then IV methylprednisolone (250mg q6h for 3 days) followed by oral prednisone (1mg/kg/day for 11 days) should be instituted. If the patient is found to have less than 2 white matter signal abnormalities, no treatment is indicated. The ONTT therapy provided a short term reduction in the rate of developing clinically definite MS. Unfortunately, after 3 years follow-up, the treatment effect had subsided. The ONTT therapy showed no long-term benefit for vision. Even without treatment visual recovery begins within two weeks in most optic neuritis patients and may show continued improvement for up to one year. If there is a need for more rapid visual recovery the above treatment regimen may be instituted to hasten short-term visual recovery but it will have no long-term effects. It is important to know that the ONTT showed that oral prednisone should not be instituted alone, as such a regimen increased the rate of new optic neuritis attacks by 50% within two years.(7,8). The currently unpublished and ongoing long-term follow up phase of the ONTT is called the Longitudinal Optic Neuritis Study (LONS). Another related National Eye Institute sponsored study called the Intravenous Immunoglobin Therapy in Optic Neuritis is currently underway. The purpose of the study is to determine whether high-dose intravenous immunoglobulin (IVIg) is more effective than placebo in restoring visual acuity in optic neuritis. The results of these studies have not been published to date.

Elevated CSF Pressure - Papilledema

The common causes of increased cerebrospinal fluid (CSF) pressure are intracranial mass, trauma, meningitis/encephalitis, syndromes of elevated venous pressure, and pseudotumor cerebri. Optic disc swelling that results from increased intracranial pressure is called papilledema. Papilledema can be classified into early, fully developed, chronic, and atrophic types. Early papilledema consists of disc changes that occur before the development of obvious disc swelling. These changes include hyperemia, blurring of the disc margin, flame shaped hemorrhages, and loss of spontaneous venous pulsation (SPV). Loss of SPV is believed to occur when intracranial pressure exceeds 200mm of water. Disc swelling becomes more obvious in fully developed papilledema. The retinal veins become engorged and numerous splinter hemorrhages appear on the surface of a grossly elevated disc. There may also be cotton wool spots and tortuous vessels on or surrounding the disc. Chronic papilledema is characterized by several months of persistent swelling. There is resolution of hemorrhages and exudates, the disc takes on a rounded appearance and nerve fiber layer atrophy becomes apparent. Optic atrophy is the end result of uncontrolled papilledema. The nerves become pale, the vessels become narrow and sheathed, and there is a complete loss of nerve fiber layer. Visual symptoms of increased intracranial pressure include transient visual obscurations, and diplopia from compressive sixth nerve palsy. Visual field defects occur most commonly as enlarged blindspots. The non-visual symptoms of increased intracranial pressure include headache, nausea, and vomiting. In severe cases a loss of consciousness, motor rigidity, and pupillary dilation can occur(9).

Intracranial masses elevate the CSF pressure and cause papilledema by occupying space, blocking the cerebral aqueduct, and producing CSF. They may also cause focal or diffuse cerebral edema. Papilledema develops in about 60% of patients with cerebral tumors. Tumors located below the tentorum are most likely to elevate CSF pressure by obstructing the cerebral aqueduct.

Trauma can increase CSF pressure with or without skull fracture. A skull fracture may rupture middle meningeal arteries, and may result in an epidural hematoma within minutes to hours. Epidural hematomas are surgical emergencies which require immediate drainage. Trauma without skull fracture can lead to subdural hematoma. Subdural hematoma results from rupture of some of the bridging veins of the brain where they penetrate the dura mater. They tend to develop slowly with a delayed onset of symptoms. Surgical drainage is required and rebleeding sometimes occurs. In both cases the pooling of blood can elevate the CSF pressure by occupying space and causing diffuse or localized cerebral edema(10).

Meningitis or encephalitis can increase CSF pressure by obstructing CSF flow and causing diffuse cerebral edema. Papilledema occurs in about 2.5% of patients with meningitis and in about 25% of tuberculosis meningitis cases. Papilledema occurs in 19% of patients with viral encephalitis. In almost all CNS infections and inflammations, swelling of the optic nerve can result without increased CSF pressure. (11)

Syndromes of elevated venous pressure can cause elevated CSF pressure by obstructing cerebral venous drainage. When cerebral venous drainage is obstructed, the flow of CSF across the arachnoid villae is reduced. Such obstructions are most commonly caused by compression of the superior sagital or lateral sinuses. Specific entities include venous thrombosis, hematologic disorders, cancer, and inflammatory or infectious disease. (ibid)

Pseudotumor cerebri (PTC) is a syndrome characterized by increased intracranial pressure, normal or small ventricles on neuro-imaging, no evidence of intracranial mass or lesion, and normal CSF composition. The cause of pseudotumor cerebri remains unknown in 90% of cases. The underlying resistance to flow by the arachnoid villae may occur as a result of obstruction to venous drainage, endocrine disorders, or nutritional disorders. Many exogenous substances are associated with PTC including antibiotics, corticosteroids, oral contraceptives, phenytoin, and vitamin A. The most common group of patients to experience PTC are women 20-44 years of age that are 20% overweight. They have an incidence of 15 per 100,000. Obesity is found in 50% of PTC patients. The most common symptom of PTC is headache, occurring in about 90% of patients. Transient visual obscurations occur in 72% and decreased acuity in 68% of cases. Diplopia occurs in 36% of cases secondary to a compressive sixth nerve palsy. Other common symptoms include nausea, vomiting, dizziness, and tinnitis. About 5% of cases are asymptomatic(12).

Pseudotumor cerebri is a diagnosis of exclusion. The keys to diagnosis are the occurrence of papilledema with a typically patient profile, a negative CT or MRI, and intracranial pressure above 200mm H20 with normal CSF contents. Papilledema occurs in almost 100% of cases of PTC.

The treatment for PTC and related papilledema is to institute weight reduction. Asymptomatic cases with no vision loss should be followed every three months. If vision loss or symptoms are present then Acetazolamide (Diamox) 500mg bid should be instituted. Carbonic anhydrase inhibitors have been shown to play a large role in PTC and are recommended as the initial means to control increased intracranial pressure. If CSF pressure fails to respond to oral therapy, then a lumbar peritoneal shunt may be surgically placed. Indications for surgery include recent or progressive visual field loss and debilitating headache. Serial lumbar puncture and oral corticosteroids have been a common treatment in the past but have gone out of favor in recent years. Optic nerve sheath decompression is the second form of surgery used in the management of patients with severe vision loss from papilledema(ibid).

Figure 4: Pseudotumor cerebri

Hemodynamic abnormalities

Cardiovascular disease including hypertension and hyperlipidemia, diabetes mellitis, and blood dyscrasias are the most common hemodynamic risk factors for swollen optic discs are. The classification of systemic hypertension for those 18 and over begins at stage one 140-159 mmHg systolic and 90-99 mmHg diastolic and goes up to stage 3 at greater than or equal to 180/110 mm Hg. Hyperlipidemia is considered present when total cholesterol levels become greater than or equal to 240 mg/dL. Additionally a ratio of total to HDL ratio greater than 4.5 imparts risk(13). The increasing appreciation of the significance of hyperglycemia has lead to a revision of diagnostic criteria for diabetes by the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. The threshold for diagnosis based on the fasting glucose level has been revised downward from 140mg/dL to 126mg/dL(14). Blood dyscrasias such as anemias, myeloproliferative disorders, hemorrhagic disorders, leukemias, lymphomas, and plasma cell dyscrasias may also be risk factors for swollen discs.

Figure 5: Non-arteritic anterior ischemic optic neuropathy

Non-arteritic anterior ischemic optic neuropathy (NAION) is caused by a vascular insufficiency of the optic nerve head leading to ischemia. Anatomic factors such as small scleral openings with crowded nerve fibers appear to increase the risk for NAION. Hypertension is present in about 40% of cases and diabetes in 20%. NAION produces a sudden painless loss of vision that may be unilateral or bilateral. The disc is usually segmentally swollen and may have associated flame hemorrhages. The disc edema typically has an altitudinal configuration with the inferior half of the disc most commonly involved. Patients are typically younger than those with arteritic AION and in the range of 40-60 years of age. The incidence of NAION has been estimated at 2.3 per 100,000 over the age of 50(15).

No proven treatment currently exists to reverse or arrest the vision loss from NAION. The recommended management for NAION is to first rule out giant cell arteritis. Westergren ESR will be in the age appropriate normal range. C-reactive protein values will be less than 5.0 mg/L. Case history should be reviewed for the associated cardiovascular, diabetic, and hematological risk factors. Blood pressure should be taken to rule out uncontrolled hypertension. Immediate correspondence to the patient’s primary care provider should be made and steps taken to identify and control identified risk factors. The Ischemic Optic Neuropathy Decompression Trial (IONDT) was a randomized clinical trial designed to assess the safety and efficacy of the widely used optic nerve sheath decompression surgery for NAION. The study sought to compare the improvements in visual acuity at six months in patients assigned to receive surgery with those assigned to careful follow up. Unfortunately the results of the IONDT showed that optic nerve sheath decompression surgery is not effective, may be harmful, and should be abandoned. The IONDT Follow-up study is underway to follow all patients originally enrolled in the IONDT. The goal of the follow-up study is to determine the incidence of NAION in the second eye, changes in visual acuity over time in both the study and second eye, and other aspects of the natural history of NAION. No results from the follow-up study have been reported to date(16).

Diabetic papillopathy is more common in young type I diabetics. It is characterized by transient and frequently bilateral disc edema. With glucose control it carries a good prognosis with a low incidence of optic atrophy. Despite evidence of optic nerve hypoperfusion, diabetic papillopathy carries a much better visual prognosis than other optic neuropathies because spontaneous regression is likely.

The treatment for diabetic papillopathy is continued glucose control and monitoring. Case history should be reviewed for associated cardiovascular and other hematological risk factors(17).

Central retinal venous occlusion (CRVO) will often produce a swollen optic disc. Accompanying signs include involvement of four quadrants with intraretinal hemorrhages, retinal edema, cotton wool spots, and wide spread capillary non-perfusion. CRVO can manifest in two forms, typically described as being ischemic or non-ischemic. In the more severe ischemic variety, vision is typically reduced to 20/400 or worse and a relative afferent pupillary defect is present.

The immediate treatment for CRVO is to review the case history for associated cardiovascular, diabetic, and hematological risk factors. Blood pressure should be taken to rule out uncontrolled hypertension. Timely correspondence to the patient’s primary care provider should be made and steps taken to identify and control identified risk factors. Unfortunately, no therapy is known to be effective against non-ischemic CRVO. The Central Retinal Vein Occlusion Study Group endeavored to answer the question of whether prophylactic panretinal photocoagulation (PRP) in ischemic CRVO prevents the development of iris neovascularization or any neovascularization (INV/ANV) or whether it is more appropriate to apply PRP only when INV/ANV occurs. They also evaluated the efficacy of macular grid photocoagulation in preserving or improving central visual acuity in eyes with best corrected visual acuity of 20/50 or poorer due to macular edema from CRVO. The Study Group conclusion was that prophylactic PRP does not totally prevent INV/ANV, and prompt regression of INV/ANV in response to PRP is more likely to occur in eyes that have not been treated previously. The authors recommend careful observation with frequent follow-up examinations including undilated slitlamp examination and gonioscopy in the early months. Prompt PRP is recommended in eyes which develop INV/ANV. The Study Group also identified that grid pattern photocoagulation for macular edema in CRVO does not produce improved visual acuity. Patients with non-ischemic CRVO should be followed for signs of ischemic CRVO every 4 weeks for the first 6 months. Likewise, patients with ischemic CRVO without neovascularization should be followed every 4 weeks for the first 6 months to monitor for NVI/ANV. If PRP is performed because of NVI/ANV, follow-up is recommended every 3-4 weeks to monitor for progression of neovascularization(18,19).

Figure 7: Central retinal venous occlusion

Malignant hypertension is also known as malignant nepharoangiosclerosis. It is uncommon, but can lead to swollen discs. This condition arises secondary to renal arteriolar necrosis and is associated with rapidly progressive renal failure. In most cases it appears as accelerated cardiovascular disease in the course of idiopathic hypertension. Renal insufficiency leads to dramatic fluid retention and severe hypertension. Patients present with varying degrees of symptoms depending on the involvement of the brain, heart, and kidney. The heart may be enlarged with left ventricular hypertrophy. Renal insufficiency produces urinary findings of proteinuria and microscopic hematuria. Hematologic abnormalities are common including coagulopathies and hemolysis. Headache, blurry vision, and mental changes are common symptoms. Diagnosis is based on a persistent diastolic blood pressure above 120mm Hg, presence of neuroretinopathy, and the other features of cardiac and renal involvement. This entity typically occurs in the 5th to 6th decade of life(20).

Figure 8: Malignant hypertension

Malignant hypertension is a medical emergency. Blood pressure must be measured and transportation to a hospital emergency room made without delay. Calling an ambulance is appropriate. Untreated patients die in a relatively short period of time. Untreated survival rate is about 50% in 6 months and most of the rest die within one year. Death usually results from uremia (40%), cerebral atherothrombotic infarction (40%), or myocardial infarction (15%). Fortunately with therapy fewer patients die. Aggressive lowering of BP and management of renal failure greatly reduce the mortality and morbitiy rate. Patients will lesser degrees of renal failure improve the most. If hypertension can be reduced most patients will survive beyond 3-5 years. (ibid)

Conclusion

Common causes of optic disc swelling include vasculitis, demylination, elevated cerebrospinal fluid pressure, and abnormal hemodynamics. The underlying systemic causes of swollen optic discs are quite varied and so too are the appropriate treatment regimens. It is vitally important that optometric physicians understand these common pathologic entities so that an accurate diagnosis is made and appropriate treatment is instituted when optic disc swelling presents.

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Questions or concerns about courses should be directed to the individual authors and/or the Continuing Education Department at the College of Optometry at kundart@pacificu.edu.