The diagnosis of episcleritis is based upon the history and physical examination. The history should be explored for the presence of the diseases associated with episcleritis, and the symptoms they cause, such as rash, arthritis, venereal disease, and recent viral infection. Episcleritis may be differentiated from scleritis by using phenylephrine or neosynephrine eye drops, which causes blanching of the blood vessels in episcleritis, but not in scleritis. A blue color to the sclera suggests scleritis, rather than episcleritis.

After anesthetizing the eye with medication, the conjunctiva may be moved with a cotton swab to observe the location of the enlarged blood vessels.

Scleritis is best detected by examining the sclera in daylight; retracting the lids helps determine the extent of involvement. Other aspects of the eye exam (i.e. visual acuity testing, slit lamp examination, etc.) may be normal. Scleritis may be differentiated from episcleritis by using phenylephrine or neosynephrine eye drops, which causes blanching of the blood vessels in episcleritis, but not in scleritis.

Ancillary tests CT scans, MRIs, and ultrasonographies can be helpful, but do not replace the physical examination.

Scleritis can be classified as anterior scleritis and posterior scleritis. Anterior scleritis is the most common variety, accounting for about 98% of the cases. It is of two types : Non-necrotising and necrotising. Non-necrotising scleritis is the most common, and is further classified into diffuse and nodular type based on morphology. Necrotising scleritis accounts for 13% of the cases. It can occur with or without inflammation.

Episcleritis is a benign, self-limiting condition, meaning patients recover without any treatment. Most cases of episcleritis resolve within 7–10 days. The nodular type is more aggressive and takes longer to resolve. Although rare, some cases may progress to scleritis. However, in general, episcleritis does not cause complications in the eye. Smoking tobacco delays the response to treatment in patients with episcleritis.

Intraocular pressure should be measured as part of the routine eye examination.

It is usually only elevated by iridocyclitis or acute-closure glaucoma, but not by relatively benign conditions.

In iritis and traumatic perforating ocular injuries, the intraocular pressure is usually low.

In an eye with iridocyclitis, (inflammation of both the iris and ciliary body), the involved pupil will be smaller than the uninvolved, due to reflex muscle spasm of the sphincter muscle of the iris.

Generally, conjunctivitis does not affect the pupils.

With acute angle-closure glaucoma, the pupil is generally fixed in mid-position, oval, and responds sluggishly to light, if at all.

Shallow anterior chamber depth may indicate a predisposition to one form of glaucoma (narrow angle) but requires slit-lamp examination or other special techniques to determine it.

In the presence of a "red eye", a shallow anterior chamber may indicate acute glaucoma, which requires immediate attention.

A limbal nodule is any nodular lesion at the limbus (junction of the cornea and sclera) of the eye.

The differential diagnosis for a limbal nodule can include:

- Pinguecula

- Early Pterygium

- Foreign body / foreign body granuloma

- Phlycten, an inflamed nodule of lymphoid tissue

- Episcleritis

- Scleritis

- Granuloma

- Limbal dermoid, a kind of choristoma (NB: in other organs "dermoid" can refer to a teratoma)

- malignant melanoma

Late congenital syphilitic oculopathy is a disease of the eye, a manifestation of late congenital syphilis. It can appear as:

- Interstitial keratitis – this commonly appears between ages 6 and 12. Symptoms include lacrimation and photophobia. Pathological vascularization of the cornea cause it to turn pink or salmon colored. 90% of cases affect both eyes.

- Episcleritis or scleritis – nodules appear in or overlying the sclera (white of eye)

- Iritis or iris papules – vascular infiltration of the iris causes rosy color change and yellow/red nodules.

- Chorioretinitis, papillitis, retinal vasculitis – retinal changes can resemble retinitis pigmentosa.

- Exudative retinal detachment

Congenital syphilis is categorized by the age of the child. Early congenital syphilis occurs in children under 2 years old, and late congenital syphilis in children at or greater than 2 years old. Manifestations of late congenital syphilis are similar to those of secondary syphilis and tertiary syphilis in adults.

Inflammatory myofibroblastic tumours are diagnosed based on their appearance under the microscope, by pathologists. Medical imaging findings are non-specific.

Photophobia may also affect patients' socioeconomic status by limiting their career choices, since many workplaces require bright lights for safety or to accommodate the work being done. Sufferers may be shut out of a wide range of both skilled and unskilled jobs, such as in warehouses, offices, workshops, classrooms, supermarkets and storage spaces. Some photophobes are only able to work night shifts, which reduces their prospects for finding work.

Erythema nodosum is diagnosed clinically. A biopsy can be taken and examined microscopically to confirm an uncertain diagnosis. Microscopic examination usually reveals a neutrophilic infiltrate surrounding capillaries that results in septal thickening, with fibrotic changes in the fat around blood vessels. A characteristic microscopic finding is radial granulomas, well-defined nodular aggregates of histiocytes surrounding a stellate cleft.

Additional evaluation should be performed to determine the underlying cause of erythema nodosum. This may include a full blood count, erythrocyte sedimentation rate (ESR), antistreptolysin-O (ASO) titer and throat culture, urinalysis, intradermal tuberculin test, and a chest x-ray. The ESR is typically high, the C-reactive protein elevated, and the blood showing an increase in white blood cells.

The ESR is initially very high, and falls as the nodules of erythema nodosum. The ASO titer is high in cases associated with a streptococcal throat infection. A chest X-ray should be performed to rule out pulmonary diseases, in particular sarcoidosis and Löfgren syndrome.

The best treatment for light sensitivity is to address the underlying cause. Once the triggering factor is treated, photophobia disappears in many but not all cases.

People with photophobia will avert their eyes from direct light, such as sunlight and room lights. They may seek the shelter of a dark room. They may wear sunglasses designed to filter peripheral light and wide-brimmed sun hats.

Wearing sunglasses indoors can make symptoms worse over time as it will dark-adapt the retina which aggravates sensitivity to light. Indoor photophobia symptoms may be relieved with the use of precision tinted lenses which block the green-to-blue end of the light spectrum without blurring or impeding vision.

A paper by Stringham and Hammond, published in the "Journal of Food Science", reviews studies of effects of consuming Lutein and Zeaxanthin on visual performance, and notes a decrease in sensitivity to glare.

PTGC is treated by excisional biopsy and follow-up. It may occasionally recur and in a small proportion of patients has been reported to subsequently develop Hodgkin lymphoma (usually nodular lymphocyte predominant Hodgkin lymphoma).

Any potential ocular involvement should be assessed by an ophthalmologist as complications such as episcleritis and uveitis may occur.

Anterior uveitis develops in 40–50% of cases with HZO within 2 weeks of onset of the skin rashes. Typical HZO keratitis at least mild iritis, especially if Hutchinson's sign is positive for the presence of vescicles upon the tip of the nose.

Features:

This non-granulomatous iridocyclitis is associated with:

- Small keratic precipitates

- Mild aqueous flare

- Occasionally haemorrhagic hypopion.

HZO uveitis is associated with complications such as iris atrophy and secondary glaucoma are not uncommon. Complicated cataract may develop in the late stages of the disease.

PTGCs is characterized by:

- follicular hyperplasia (many follicles),

- focally large germinal centres, with poorly demarcated germinal centre (GC)/mantle zone interfaces (as GCs infiltrated by mantle zone lymphocytes), and

- an expanded mantle zone.

Colloid nodules are usually small enough to be undetectable without an ultrasound or other imaging techniques. They usually produce no symptoms, so patients are unlikely to notice them until their size makes them easier to detect. Like other thyroid nodules, they are usually first noticed in a routine physical examination.

"Xanthelasmata" can be removed with a trichloroacetic acid peel, surgery, lasers or cryotherapy. Removal may cause scarring and pigment changes, but it is an uncommon side-effect of treatment.

Inflammatory myofibroblastic tumours are characterized by a mix of inflammatory cells, e.g. plasma cells, lymphocytes and eosinophils, and bland spindle cells without nuclear atypia. These tumours may have necrosis, hemorrhage, focal calcification and mitotic activity.

The histologic differential diagnosis includes:

- calcifying fibrous pseudotumour

- inflammatory fibroid tumour

- nodular fasciitis.

Approximately half of IMTs have a rearrangement of the ALK gene.

Xanthelasma is a sharply demarcated yellowish deposit of fat underneath the skin, usually on or around the eyelids. While they are neither harmful nor painful, these minor growths may be disfiguring and can be removed.

A "xanthelasma" may instead be referred to as a "xanthoma" when becoming larger and nodular, assuming tumorous proportions. Still, "xanthelasma" is often classified simply as a subtype of "xanthoma".

Colloid nodules may be initially identified as an unspecified kind of thyroid nodule. Follow-up examinations typically include an ultrasound if it's unclear whether or not there really is a nodule present. Once the presence of a nodule has been confirmed, the determination of the kind of thyroid nodule is done by fine needle aspiration biopsy.

Colloid nodules are distinguished by an apparently gelatinous mass of colloid both surrounding and contained within follicular cells. Colloid nodules are not surrounded by a fibrous capsule of compressed tissue. However, they are surrounded by flattened epithelial cells. Both the number of cells and the type of colloid may vary considerably.

Erythema nodosum is self-limiting and usually resolves itself within 3–6 weeks. A recurring form does exist, and in children it is attributed to repeated infections with streptococcus. Treatment should focus on the underlying cause. Symptoms can be treated with bedrest, leg elevation, compressive bandages, wet dressings, and nonsteroidal anti-inflammatory agents (NSAIDs). NSAIDs are usually more effective at the onset of EN versus with chronic disease.

Potassium iodide can be used for persistent lesions whose cause remains unknown. Corticosteroids and colchicine can be used in severe refractory cases. Thalidomide has been used successfully in the treatment of Erythema nodosum leprosum, and it was approved by the U.S. FDA for this use in July 1998.

Weber–Christian disease, also known as relapsing febrile nodular nonsuppurative panniculitis, is a cutaneous condition characterized by recurrent subcutaneous nodules that heal with depression of the overlying skin.

It is type of panniculitis.

It is a rare disease seen in females 30–60 years of age. It is a recurring inflammation of fatty layers of tissue present beneath the skin. Clinical course is characterised by exacerbations and remissions. Lesions are bilaterally symmetrical and are usually seen in the lower legs.

Diagnosis is based on visual examination and the presence of itching. A skin biopsy is often performed to exclude other diseases. Lesion biopsies will typically show a high level of eosinophils in PN. A culture of at least one lesion will rule out staphylococcus infection, which has been significantly linked to atopic dermatitis.

Some specific reactive lymphadenopathies with a predominantly follicular pattern:

- Rheumatoid arthritis

- Sjogren syndrome

- IgG4-related disease (IgG4-related lymphadenopathy)

- Kimura disease

- Toxoplasmosis

- Syphilis

- Castleman disease

- HIV-associated lymphadenopathy

- Progressive transformation of germinal centers (PTGC)