Dry Eye Syndrome Clinical Presentation

Ocular irritation of dry sensation, burning, itching, pain, foreign body sensation, photophobia, and blurred vision are common in patients with dry eye. These symptoms are often exacerbated in smoky or dry environments, by indoor heating, or by excessive reading or computer use. These symptoms are quantified objectively in the Ocular Surface Disease Index (OSDI) questionnaire, which lists 12 symptoms and grades each on a scale of 1-4.

In KCS, symptoms tend to be worse toward the end of the day, with prolonged use of the eyes, or with exposure to extreme environmental conditions. Patients with meibomian gland dysfunction may complain of redness of the eyelids and conjunctiva, but, in these patients, the symptoms are worse on awakening in the morning.

Paradoxically, some patients with dry eye syndrome complain of too much tearing. When evidence of dry eye syndrome exists, this symptom often is explained by excessive reflex tearing due to severe corneal surface disease from the dryness.

Certain systemic medications also decrease tear production, such as antihistamines, beta-blockers, and oral contraceptives.

Past medical history may be significant for coexisting connective tissue disease, rheumatoid arthritis, or thyroid abnormalities. A thorough review of systems should be obtained, asking specifically about dry mouth.

Within the veteran population, a study found an increased incidence of dry eye syndrome in both men and women that was also strongly connected to cases of posttraumatic stress disorder and depression.^[4]

Signs of a dry eye include the following:

• Bulbar conjunctival vascular dilation
• Decreased tear meniscus
• Irregular corneal surface
• Decreased tear break-up time
• Punctate epithelial keratopathy
• Corneal filaments
• Increased debris in the tear film
• Conjunctival pleating
• Superficial punctuate keratitis, with positive fluorescein staining
• Mucous discharge
• Corneal ulcers in severe cases

Symptoms often do not correlate with signs.

In severe cases, there may be an epithelial defect or a sterile corneal infiltrate or ulcer. Secondary infectious keratitis also can develop. Both sterile and infectious corneal perforations can occur.

The International Dry Eye WorkShop (DEWS) recently developed a 3-part classification of dry eye, based on etiology, mechanisms, and disease stage.^[1]

The classification system, which is updated as an etiopathogenic classification by the DEWS Subcommittees, formulated by the National Eye Institute (NEI)/Industry Dry Eye Workshop Report in 1995, distinguishes 2 main categories (or causes) of dry eye states, as follows: an aqueous deficiency state and an evaporative state.

• Deficient aqueous production

  • Sjogren syndrome dry eye
    • Primary
    • Secondary
  • Non-Sjogren syndrome dry eye
    • Lacrimal gland deficiency
    • Lacrimal gland duct obstruction
    • Reflex hyposecretion
    • Systemic drugs
• Evaporative

  • Intrinsic causes
    • Meibomian gland dysfunction
    • Disorders of lid aperture
    • Low blink rate
    • Drug action (eg, Accutane)
  • Extrinsic causes
    • Vitamin A deficiency
    • Topical drugs and preservatives
    • Contact lens wear
    • Ocular surface disease (eg, allergy)

Deficient aqueous production can be further classified as follows:

• Non-Sjögren syndrome

  • Primary lacrimal gland deficiencies
    • Idiopathic
    • Age-related dry eye
    • Congenital alacrima (eg, Riley-Day syndrome)
    • Familial dysautonomia
  • Secondary lacrimal gland deficiencies
    • Lacrimal gland infiltration
    • Sarcoidosis
    • Lymphoma
    • AIDS
    • Graft vs host disease
    • Amyloidosis
    • Hemochromatosis
    • Lacrimal gland infectious diseases
    • HIV diffuse infiltrative lymphadenopathy syndrome
    • Trachoma
    • Systemic vitamin A deficiency (xerophthalmia) – Malnutrition, fat-free diets, intestinal malabsorption from inflammatory bowel disease, bowel resection, or chronic alcoholism
    • Lacrimal gland ablation
    • Lacrimal gland denervation
  • Lacrimal obstructive disease
    • Trachoma
    • Ocular cicatricial pemphigoid
    • Erythema multiforme and Stevens-Johnson syndrome
    • Chemical and thermal burns
    • Endocrine imbalance
    • Postradiation fibrosis
  • Medications – Antihistamines, beta-blockers, phenothiazines, atropine, oral contraceptives, anxiolytics, antiparkinsonian agents, diuretics, anticholinergics, antiarrhythmics, topical preservatives in eye drops, topical anesthetics, and isotretinoin
  • Reflex hyposecretion – Reflex sensory block and reflex motor block
    • Neurotrophic keratitis - Fifth nerve/ganglion section/injection/compression
    • Corneal surgery - Limbal incision (eg, extracapsular cataract extraction), keratoplasty, refractive surgery (eg, PRK, LASIK, RK)
    • Infective - Herpes simplex keratitis, herpes zoster ophthalmicus
    • Topical agents - Topical anesthesia
    • Systemic medications – Beta blockers, atropine-like drugs
    • Chronic contact lens wear
    • Diabetes
    • Aging
    • Trichloroethylene toxicity
    • Cranial nerve VII (CN VII) damage
    • Multiple neuromatosis
• Sjögren syndrome

  • Primary (no associated connective tissue disease [CTD])
  • Secondary (associated CTD)
    • Rheumatoid arthritis
    • Systemic lupus erythematosus
    • Progressive systemic sclerosis (scleredema)
    • Primary biliary cirrhosis
    • Interstitial nephritis
    • Polymyositis and dermatomyositis
    • Polyarteritis nodosa
    • Hashimoto thyroiditis
    • Lymphocytic interstitial pneumonitis
    • Idiopathic thrombocytopenic purpura
    • Hypergammaglobulinemia
    • Waldenstrom macroglobulinemia
    • Wegener granulomatosis

Evaporative loss can be further classified as follows:

• Intrinsic causes

  • Meibomian gland disease
    • Reduced number - Congenital deficiency, acquired meibomian gland dysfunction
    • Replacement - Distichiasis, distichiasis lymphedema syndrome, metaplasia
    • Meibomian gland dysfunction
      • Hypersecretory - Meibomian seborrhea
      • Hyposecretory - Retinoid therapy
      • Obstructive – Simple, primary or secondary to local disease (eg, anterior blepharitis), systemic disease (eg, acne rosacea, seborrheic dermatitis, atopy, ichthyosis, psoriasis), syndromes (eg, anhidrotic ectodermal dysplasia, ectrodactyly syndrome, Turner syndrome), and systemic toxicity (eg, 13-cis retinoic acid, polychlorinated biphenyls); or cicatricial, primary or secondary to local disease (eg, chemical burns, trachoma, pemphigoid, erythema multiforme, acne rosacea, VKC, AKC)
  • Low blink rate
    • Physiological phenomenon, such as during performance of tasks that require concentration (eg, working at a computer or a microscope)
    • Extrapyramidal disorder, such as Parkinson disease (decreasing dopaminergic neuron pool)
  • Disorders of eyelid aperture and eyelid/globe congruity
    • Exposure (eg, craniostenosis, proptosis, exophthalmos, high myopia)
    • Lid palsy
    • Ectropion
    • Lid coloboma
  • Drug action (eg, Accutane)
• Extrinsic causes

  • Vitamin A deficiency
    • Development disorder of goblet cells
    • Lacrimal acinar damage
  • Topical drugs and preservatives (surface epithelial cell damage)
  • Contact lens wear
  • Ocular surface disease (eg, allergy)

A classification of dry eye on the basis of mechanisms includes tear hyperosmolarity and tear film instability.

For a classification of dry eye on the basis of severity, the Delphi Panel Report was adopted and modified as a third component of the DEWS.^[1] See Table.

Table 1. Dry Eye Severity levels^{[1, 5]} (Open Table in a new window)