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8/19/2017 Scleritis Clinical Presentation: History, Physical, Causes

Scleritis Clinical Presentation


Updated: May 09, 2017
Author: Manolette R Roque, MD, MBA, FPAO; Chief Editor: Andrew A Dahl, MD, FACS more...

PRESENTATION

History
When interviewing the patient, investigate the following: the major complaint; a history of the
present illness; the past history, including infection, injury, or surgery; and the review of systems.

Symptoms of scleritis can include pain, tearing or photophobia, tenderness, and decreased visual
acuity. The primary sign is redness.

Pain is the most common symptom for which patients seek medical assistance, and it is the best
indicator of active inflammation. Pain results from both direct stimulation and stretching of the
nerve endings by the inflammation.

The following pain descriptions are characteristic of scleritis:

Severe, penetrating pain that radiates to the forehead, brow, jaw, or sinuses
Awakens the patient during the night
Exacerbated by touch; extremely tender
Only temporarily relieved by analgesics

Tearing or photophobia without mucopurulent discharge, which is usually mild or moderate, may
occur in about 25% of patients with scleritis.

Unfortunately, many patients with scleritis first present to the emergency room or urgent care clinic,
where a diagnosis of conjunctivitis is typically treated inappropriately with topical antibiotics. This
practice generally leads to a significant delay in the initiation of anti-inflammatory therapy and a
prolonged clinical course and more guarded prognosis.

Upon palpation, the patient may describe tenderness that is diffuse with possible radiation to other
parts of the head.

Decreased visual acuity may be caused by extension of scleritis to the adjacent structures, leading
to reactive blepharitis, myositis, keratitis, uveitis, glaucoma, cataract, and fundus abnormalities.

Redness gradually increases over several days. It has a bluish red tinge, which is seen best when
the examination is performed in natural light, not through the slit lamp. It may be localized in one
sector or involve the whole sclera; most frequently, it is in the interpalpebral area. This discoloration
does not blanche after topical applications of routine sympathomimetic dilating agents (Neo-
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8/19/2017 Scleritis Clinical Presentation: History, Physical, Causes

Synephrine 2.5%).

Past medical and ocular histories may elucidate systemic diseases, trauma, drugs, or surgical
procedures that might cause scleritis:

Connective-tissue or vasculitic diseases


Infectious diseases
Miscellaneous diseases (eg, atopy, rosacea, gout, chemical injuries)
Blunt or penetrating ocular trauma
Drugs, such as pamidronate (Aredia), alendronate (Fosamax), risedronate (Actonel),
zoledronic acid (Zometa), and ibandronate (Boniva)
Past ocular surgical procedures, especially within a year prior to the onset of scleritis, might
be significant.

Past medical history is also important for discovering certain conditions (eg, gastric ulceration,
diabetes, liver disease, anemia, renal disease, hypertension) that eventually might modify future
therapy.

Past and present therapies and responses to these interventions should be investigated.

Because scleritis can be associated with systemic disorders, make a routine inquiry that covers
various bodily systems, as follows:

Dermatologic (eg, skin, hair, nails)


Respiratory
Cardiac
Genitourinary
Rheumatologic
Gastrointestinal
Neurologic
Hematologic and lymphatic
Pulmonary
Ear, nose, sinus, and throat

Physical
The head and extremities (eg, nose, mouth, external ear, skin, joints) examinations may reveal
significant signs, which might be compatible with a particular underlying disease. An eye
examination might detect and characterize scleral disease. Include scleral and general eye
examinations.

Scleral examination

Daylight

The sclera may appear diffuse, deep bluish red, or violaceous. After several attacks of scleral
inflammation, areas of scleral thinning and translucency may appear, allowing the dark uvea to
show.
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8/19/2017 Scleritis Clinical Presentation: History, Physical, Causes

A black, gray, or brown area that is surrounded by active scleral inflammation indicates a
necrotizing process. If tissue necrosis progresses, the scleral area may become avascular,
producing a white sequestrum in the center that is surrounded by a well-defined black or dark
brown circle. The slough may be removed gradually by granulation tissue, leaving the underlying
uvea bare or covered by a thin layer of Tenon and conjunctiva.

Slit lamp light

In scleritis, maximum congestion is in the deep episcleral network with some congestion in the
superficial episcleral network. The posterior and anterior edges of the slit lamp beam are
displaced forward because of underlying scleral and episcleral edema.

In scleritis, topical application of 2.5% or 10% phenylephrine only blanches the superficial
episcleral network without significant effect on the deep episcleral network.

Red-free light

Red-free light is helpful to the following study areas:

Areas that have maximum vascular congestion


Areas that display new vascular channels
Areas that are totally avascular

General eye examination


Evaluate adjacent structures in scleritis at every follow-up visit, since involvement is an important
reason for vision loss, as follows:

Extraocular muscles
Lids and orbit
Cornea
Uvea
Lens
Intraocular pressure (IOP)
Dilated fundus

Causes
Scleritis may occur isolated (43%) or in association with several types of disorders (57%), as
follows:

Autoimmune (48%)
Connective-tissue diseases and other inflammatory conditions include the following [3] :
Rheumatoid arthritis
Systemic lupus erythematosus
Ankylosing spondylitis
Reactive arthritis
Psoriatic arthritis
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8/19/2017 Scleritis Clinical Presentation: History, Physical, Causes

Gouty arthritis
Inflammatory bowel diseases
Relapsing polychondritis
Polymyositis
Sjgren syndrome
Mixed connective tissue disease
Progressive systemic sclerosis
Vasculitic diseases include the following [4] :
Polyarteritis nodosa
Allergic angiitis of Churg-Strauss syndrome
Granulomatosis with polyangiitis (Wegener granulomatosis)
Behet disease
Giant cell arteritis
Cogan syndrome
Infectious (7%) - Bacterial, fungal, viral, or parasitic
Miscellaneous (2%) - Atopy; rosacea; or secondary to foreign bodies, chemical injuries, or
drugs (eg, pamidronate, alendronate, risedronate, zoledronic acid, ibandronate) [5]

Differential Diagnoses

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