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Patient Assessment: Eye Scleritis (Scleral Sclerosis / Scleritis)

Scleritis is the inflammatory condition of the sclera (the white "coat" of the eye) involving oedema and cellular infiltration of the entire scleral thickness. When clinicians refer to "sclerosis of the eye," they typically mean scleritis or scleromalacia - a progressive sclerosing/fibrotic process of the sclera, often linked to autoimmune connective tissue diseases.

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I. BIOGRAPHIC DATA

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II. CHIEF COMPLAINTS

1. Severe, deep, boring pain in the right eye - 3 weeks duration
2. Redness of the right eye - 3 weeks duration
3. Waking from sleep due to eye pain at night - 2 weeks duration
4. Blurring of vision in the right eye - 1 week duration
5. Photophobia (light sensitivity) - 1 week duration
6. Excessive tearing (epiphora) - 1 week duration
7. Pain radiating to the forehead, brow, and temple - 1 week duration

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III. HISTORY OF PRESENT ILLNESS

• Onset: Insidious
• Duration: 3 weeks
• Progression: Gradually worsening
• Aggravating factors: Eye movement, exposure to bright light, touch
• Relieving factors: Darkness, rest (partial)
• Associated features: Pain radiates to the face and temple; disrupts sleep
• Treatment sought so far: Tried OTC lubricating eye drops and paracetamol - no significant relief

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IV. PAST ILLNESS HISTORY

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V. PHYSICAL EXAMINATION

A. General Examination

B. Systemic Examination

• Musculoskeletal: Bilateral symmetrical swelling, warmth, and tenderness of metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints; early morning stiffness reported; no deformity yet; consistent with active Rheumatoid Arthritis
• Cardiovascular: S1 and S2 heart sounds heard; no murmurs
• Respiratory: Air entry bilaterally equal; no added sounds
• Abdomen: Soft, non-tender; no organomegaly; appendectomy scar present
• Neurological: No focal neurological deficit; cranial nerves intact
• Skin: No rash, no subcutaneous nodules over extensor surfaces

C. Ocular Examination - Right Eye (Affected Eye)

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VI. LABORATORY INVESTIGATIONS

Routine Blood Tests

Immunological / Autoimmune Tests

Infectious Disease Screen

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VII. MEDICATIONS PRESCRIBED

1. Step 1 - NSAIDs (First-line for diffuse/nodular scleritis)

2. Gastroprotection (with NSAIDs)

3. Corticosteroids (if NSAIDs fail or disease is severe)

4. Topical Eye Treatment

5. Disease-Modifying Antirheumatic Drug (DMARD) - for underlying RA

6. Immunosuppressives (for refractory or necrotizing disease - if needed)

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VIII. SPECIAL INVESTIGATIONS

Ophthalmic Imaging & Specialized Tests

Systemic Imaging

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IX. NURSING DIAGNOSIS & CARE PLAN (Summary)

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X. FOLLOW-UP & PROGNOSIS

• Review: Every 2 weeks for the first 2 months; then monthly
• Monitor: Visual acuity, IOP, slit lamp findings, inflammatory markers (ESR, CRP), renal/liver function (Methotrexate toxicity)
• Rheumatology referral: Mandatory to optimize RA therapy and coordinate systemic immunosuppression
• Prognosis: For diffuse anterior non-necrotizing scleritis, the long-term visual prognosis is good when treated appropriately. Average disease duration is approximately 6 years, with decreasing recurrences after the first 18 months. The greatest risk to vision is secondary glaucoma from elevated IOP.

"Glaucoma is the commonest cause of visual loss in anterior scleritis, so control of the IOP is critically important."

• Kanski's Clinical Ophthalmology, 10th Edition

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• Kanski's Clinical Ophthalmology: A Systematic Approach, 10th Edition (ISBN 9780443110993), pp. 308-311
• The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease (ISBN 9781975160753), pp. 341-346
• Goldman-Cecil Medicine International Edition, 2-Volume Set (ISBN 9780323930345)
• EyeWiki - Scleritis - Laboratory testing and management
• Medscape - Scleritis Clinical Presentation - Physical examination

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Patient Assessment: Diabetic Retinopathy

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I. BIOGRAPHIC DATA

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II. CHIEF COMPLAINTS

1. Blurring of vision in both eyes - 6 months (gradual, progressive; worse in right eye)
2. Difficulty reading small print - 4 months
3. Floaters (black spots/cobwebs) in front of right eye - 2 months
4. Distortion of straight lines (metamorphopsia) - 6 weeks
5. Decreased color perception - 1 month
6. No pain in either eye

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III. HISTORY OF PRESENT ILLNESS

• Onset: Insidious and gradual
• Duration: 6 months (blurred vision); 2 months (floaters)
• Progression: Slowly progressive
• Aggravating factors: Bright light, reading
• Relieving factors: None significant
• Associated systemic symptoms: Generalized fatigue, polyuria, polydipsia (suggesting poor glycemic control)

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IV. PAST ILLNESS HISTORY

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V. PHYSICAL EXAMINATION

A. General Examination

B. Systemic Examination

• Cardiovascular: S1, S2 audible; no murmurs; mild cardiomegaly clinically; peripheral pulses palpable bilaterally
• Respiratory: Normal vesicular breath sounds; no added sounds
• Abdomen: Soft, non-tender; no hepatosplenomegaly; appendectomy scar noted
• Neurological: Peripheral neuropathy findings - reduced vibration sense in both feet; diminished ankle jerks bilaterally; glove-and-stocking pattern hypoesthesia (consistent with diabetic peripheral neuropathy)
• Feet: No ulcers; dry skin; reduced sensation to monofilament test; nail thickening noted
• Skin: Acanthosis nigricans at the nape; no xanthomas

C. Ocular Examination

External Eye

Fundus Examination (Dilated Ophthalmoscopy - Indirect + 90D Slit Lamp)

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VI. LABORATORY INVESTIGATIONS

Routine Blood Tests

Urine Tests

Cardiac Investigation

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VII. SPECIAL INVESTIGATIONS (Ophthalmic)

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VIII. MEDICATIONS PRESCRIBED

1. Glycemic Control (Systemic - Optimize for DR management)

2. Blood Pressure Control

3. Lipid Management

4. Intravitreal Injections (PRIMARY EYE TREATMENT for CSME)

Anti-VEGF agents are first-line therapy for center-involving DME. - The Wills Eye Manual, p. 813

5. Intravitreal Corticosteroids (Second-line for DME - if poor anti-VEGF response)

6. Laser Treatment (Adjunct / Selected cases)

7. Supplements & Supportive

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IX. NURSING DIAGNOSIS & CARE PLAN

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X. PATIENT EDUCATION

1. Blood glucose monitoring - at least twice daily; maintain a logbook
2. Diet counseling - low-glycemic index diet, reduce simple sugars, high fiber
3. Exercise - 30 minutes of moderate-intensity walking, 5 days/week (after medical clearance)
4. Eye care - Annual dilated retinal examination even without symptoms; urgent visit if sudden vision loss, floaters, or flashes occur
5. Amsler grid use - daily self-monitoring at home for detecting change in macular edema
6. Foot care - daily foot inspection; avoid walking barefoot; regular podiatry review
7. Avoid smoking - smoking accelerates vascular disease and DR progression
8. BP and lipid control - strict adherence to medications; home BP monitoring

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XI. FOLLOW-UP & PROGNOSIS

Prognosis

• Risk of severe visual loss can be reduced to less than 5% with effective screening, glycemic control, and treatment based on ETDRS and anti-VEGF trials. - Kanski's Clinical Ophthalmology, 10th Edition, p. 521
• With current Moderate NPDR + CSME (right eye), the risk of progression to proliferative disease over 5 years is approximately 20-30% if glycemic control remains poor (HbA1c >9%)
• Aggressive HbA1c reduction to <7% significantly reduces the risk of DR progression (validated by the DCCT and UKPDS studies)
• The most common cause of visual impairment in this patient is diabetic macular edema, which is highly treatable with anti-VEGF agents
• Venous beading is noted in 1 quadrant (a significant predictor of progression to PDR) - requires vigilant follow-up

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• Kanski's Clinical Ophthalmology: A Systematic Approach, 10th Edition (ISBN 9780443110993), pp. 506-523
• The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease (ISBN 9781975160753), pp. 811-816
• Goldman-Cecil Medicine International Edition, 2-Volume Set (ISBN 9780323930345)
• Harrison's Principles of Internal Medicine 22E (2025, McGraw Hill Medical)
• Medscape - Diabetic Retinopathy Clinical Presentation
• PMC - Diabetic Retinopathy: Clinical Findings and Management

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Can Scleritis Occur in a Patient with Hypertension (HTN)?

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1. HTN is NOT a Direct Cause of Scleritis

"Up to 50% of patients with scleritis have an associated systemic disease, typically connective tissue or vasculitic in nature."

• The Wills Eye Manual (ISBN 9781975160753)

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2. HTN Co-exists Because Both Share the Same Root Diseases

A. Polyarteritis Nodosa (PAN)

• A systemic necrotizing vasculitis that inflames medium-sized blood vessels
• Causes scleritis (ocular vasculitis) AND hypertension + nephropathy (renal artery inflammation)
• As noted in the EyeWiki Scleritis article: "myalgias, weight loss, fever, purpura, nephropathy, and hypertension may be signs of polyarteritis nodosa" - the same disease that causes scleritis

B. Granulomatosis with Polyangiitis (GPA / Wegener's)

• Causes necrotizing scleritis + renal involvement leading to secondary hypertension (glomerulonephritis → renovascular HTN)
• This is the most vision-threatening form of scleritis

C. Systemic Lupus Erythematosus (SLE)

• Causes scleritis AND lupus nephritis → secondary hypertension
• Both the scleral inflammation and the elevated BP are driven by the same autoimmune process

D. Rheumatoid Arthritis (RA)

• Most common systemic disease associated with scleritis (especially scleromalacia perforans)
• Patients with longstanding RA commonly develop secondary hypertension from long-term NSAID/steroid use, renal involvement, and metabolic effects

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3. HTN Has Its OWN Separate Eye Complications That Add to the Problem

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4. Treatment Interactions - Clinically Important

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Summary

• The Wills Eye Manual (ISBN 9781975160753), pp. 341-346
• Kanski's Clinical Ophthalmology 10th Edition (ISBN 9780443110993), pp. 308-311
• EyeWiki - Scleritis - Systemic associations
• Medscape - Scleritis Overview
• StatPearls - Scleritis (NCBI)

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Rheumatoid Arthritis and Scleritis: The Correlation

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1. Epidemiological Evidence (How Common Is It?)

"RA is the most common systemic disease in patients with scleritis, followed by GPA, Sjögren syndrome, and systemic lupus erythematosus."

• Springer Nature: Management of Scleritis in Older Adults (2024)

"Rheumatoid arthritis accounts for 8% to 15% of all cases of scleritis."

• PMC Review on RA-associated Scleritis

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2. Why Does RA Cause Scleritis? - The Pathological Mechanism

A. Immune Complex-Mediated Vasculitis

• Rheumatoid Factor (RF) - IgM autoantibodies against the Fc region of IgG, present in ~90% of RA patients
• RF forms immune complexes that activate complement and trigger inflammatory cascades
• These same immune complexes deposit in scleral blood vessel walls, causing a vasculitis of scleral tissue

"Biopsy studies have indicated that scleritis is often a vasculitis of scleral tissue."

• Firestein & Kelley's Textbook of Rheumatology, 2-Volume Set

B. VEGF and Inflammatory Cytokines

• Pro-inflammatory cytokines in RA (TNF-α, IL-1, IL-6) damage the microvasculature of the sclera
• VEGF promotes abnormal vessel proliferation and permeability in the sclera
• The same cytokine storm destroying joints simultaneously attacks the scleral tissue

C. Genetic Susceptibility

• HLA-DR4 is strongly associated with seropositive RA and correlates with greater extraarticular disease (including scleritis)
• Patients with HLA-Dw4 are at highest risk

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3. What Type of Scleritis Does RA Typically Cause?

Scleromalacia Perforans - The RA Hallmark

• Seen in elderly women with longstanding, seropositive RA
• Progressive scleral thinning without the typical pain and inflammation
• Necrotic scleral plaques near the limbus without vascular congestion
• Slow progression exposing underlying uvea
• Despite the name, actual perforation is rare as fibrous tissue maintains integrity

"Scleromalacia perforans (5% of scleritis) is a specific type of progressive scleral thinning without inflammation that typically affects elderly women with longstanding rheumatoid arthritis."

• Kanski's Clinical Ophthalmology, 10th Edition

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4. Clinical Profile of RA-Associated Scleritis

"Generally, the rheumatoid arthritis in association with scleritis is long standing and seropositive. Patients often also have nodules, vasculitis, or pleuropericarditis. They have a shortened life expectancy compared with other patients with rheumatoid arthritis."

• Firestein & Kelley's Textbook of Rheumatology

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5. The Critical Warning: Necrotizing Scleritis in RA = Systemic Vasculitis Emergency

"Necrotizing scleritis associated with rheumatoid arthritis is associated with increased mortality due to coronary arteritis or cerebral angiitis and requires urgent, aggressive immunosuppressive therapy."

• The Wills Eye Manual (ISBN 9781975160753)

• The same vasculitis may be attacking the coronary arteries (risk of myocardial infarction)
• Or the cerebral vessels (risk of stroke)
• Immediate referral to rheumatology is mandatory
• Aggressive immunosuppression must be started without delay

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6. Full Spectrum of Ocular Manifestations in RA

"In adults, the ocular manifestations of rheumatoid arthritis mainly affect the anterior part of the eye, cornea, and sclera... Scleromalacia perforans, which is aseptic necrosis of the sclera, is associated with rheumatoid arthritis about 46% of the time."

• Goldman-Cecil Medicine International Edition

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7. Treatment Implication: Treat the RA, Treat the Scleritis

"Scleritis usually responds to treatment of the underlying disease if an associated disease is present. Thus control of rheumatoid arthritis usually results in control of associated scleritis."

• Firestein & Kelley's Textbook of Rheumatology

Note: Periocular steroid injections are contraindicated in necrotizing scleritis - they can cause further scleral thinning and perforation. - The Wills Eye Manual

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Summary

RA → Autoimmune vasculitis (immune complex + TNF-α/IL-6/RF)
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    Deposits in scleral vessels
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    Scleral vasculitis = SCLERITIS
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Spectrum: Diffuse → Nodular → Necrotizing → Scleromalacia perforans
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RA-scleritis = marker of systemic vasculitis + shortened life expectancy

• Kanski's Clinical Ophthalmology 10th Edition (ISBN 9780443110993), pp. 308-316
• The Wills Eye Manual (ISBN 9781975160753), pp. 341-347
• Firestein & Kelley's Textbook of Rheumatology, 2-Volume Set (ISBN 9780323935364), pp. 857-858
• Goldman-Cecil Medicine International Edition (ISBN 9780323930345), p. 807
• PMC - RA-Associated Episcleritis and Scleritis: Treatment Perspectives
• AAO EyeNet - Ocular Involvement in Rheumatoid Arthritis