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DRY EYE SYNDROME
(Keratoconjunctivitis Sicca)
Stj.Dr. Feyza Pelin HAKSEVER
 Inadequate lubrication of eyes.
 Multifactorial disease of the tears and the ocular surface.
 Results in discomfort, visual disturbance, and tear film
instability with potential damage to the ocular surface.
 Common form of ocular surface disease (OSD) and may
overlap with other causes of OSD, such as ocular allergy and
meibomian gland dysfunction (MGD).
ANATOMY
The ocular surface is an integrated anatomical unit consisting of 7
key interactive and interdependent components:
 the tear film,
 the lacrimal and accessory lacrimal apparatus,
 the nasolacrimal drainage system,
 the eyelids,
 the bulbar and tarsal conjunctiva,
 cranial nerve V, and cranial nerve VII.
Abnormalities or deficiencies in any of the 7 ocular
surface components may worsen dry eye syndrome
The tear film covers the normal ocular surface. It has 3 layers as
following:
 A superficial thin lipid layer (0.11 µm) – This layer is produced by
the meibomian glands, and its principal function is to retard tear
evaporation and to assist in uniform tear spreading.
 A middle thick aqueous layer (7 µm) – This layer is produced by
the main lacrimal glands (reflex tearing), as well as by the
accessory lacrimal glands of Krause and Wolfring (basic tearing)
 An innermost hydrophilic mucin layer (0.02-0.05 µm) – This layer
is produced by both the conjunctiva goblet cells and the ocular
surface epithelium. It is the hydrophilic quality of the mucin that
allows the aqueous layer to spread over the corneal epithelium.
CLASSIFICATION
Dry eye syndrome may be subdivided into 2 main types as
follows:
 Dry eye syndrome associated with Sjögren syndrome (SS)
 Dry eye syndrome unassociated with SS (non-SS KCS)
Dry eye syndrome can also be subdivided into 2 main types as
follows:
 Pure aqueous deficiency dry eye
 Evaporative dry eye
Eighty-six percent of patients with dry eye syndrome also
have signs of meibomian gland dysfunction.
PATHOPHYSIOLOGY & ETIOLOGY
 A genetic predisposition in SS-associated dry eye syndrome
(high prevalence of human leukocyte antigen B8 (HLA-B8)
haplotype)
 Decrease in circulating sex hormones (both androgen and
estrogen receptors are located in the lacrimal and meibomian
glands; the deficiency possibly affecs the functional and
secretory aspect of the lacrimal gland)
 In meibomian gland dysfunction, androgen deficiency results in
loss of the lipid layer—specifically, loss of triglycerides,
cholesterol, monounsaturated essential fatty acids such as oleic
acid, and polar lipids, including phosphatidylethanolamine and
sphingomyelin. Loss of polar lipids, which are present at the
aqueous-tear interface, exacerbates evaporative tear loss, and loss
of unsaturated fatty acids raises the melting point of meibomian
gland secretions, or meibum, leading to thicker, more viscous
secretions that obstruct ductules and cause stagnation of
secretions.
 Patients on antiandrogenic therapy for prostate disease also have
increased viscosity of meibum, decreased tear breakup time
(TBUT), and increased tear film debris, all of which indicate a
deficient or abnormal tear film.
 Defect in mucin-synthesizing genes (MUC1-MUC17; have
roles in hydration and stabilization of the tear film.
Particularly significant is MUC5AC, which is expressed by
stratified squamous cells of the conjunctiva and whose
product is the predominant component of the mucous layer
of tears)
 Decreased production of tear proteins (lysozyme, lactoferrin,
lipocalin, phospholipase A2)
 Lipocalin deficiency (Previously known as tear-specific
prealbumin, is inducible lipid-binding proteins produced by
the lacrimal glands and present in the mucous layer. They
lower the surface tension of normal tears, which provides
stability to the tear film and also explains the increase in
surface tension seen in dry eye syndrome characterized by
lacrimal gland deficiency. Lipocalin deficiency can lead to
precipitation in the tear film, forming the characteristic
mucous strands seen in patients with dry eye symptoms)
Deficient Aqueous Production
(Non-Sjögren syndrome & Sjögren syndrome)
Non-Sjögren syndrome
 Primary lacrimal gland deficiencies (Idiopathic, Age-related,
Congenital alacrima, Familial Dysautonomia)
 Secondary lacrimal gland deficiencies (Lacrimal gland
infiltration/ablation/denervation/infectious diseases, Sarcoidosis, Lymphoma,
AIDS, Amyloidosis, Hemochromatosis, Trachoma, Systemic vitamin A
deficiency (xerophthalmia), Malnutrition)
 Lacrimal obstructive diseases (Trachoma, Ocular cicatricial
pemphigoid , Erythema multiforme, Stevens-Johnson syndrome , Chemical and
thermal burns, Endocrine imbalance , Postirradiation fibrosis )
 Medications (Antihistamines , Beta blockers, Phenothiazines, Atropine,
Oral contraceptives, Anxiolytics, Antiparkinsonian agents, Diuretics,
Anticholinergics, Antiarrhythmics, Isotretinoin)
 Reflex hyposecretion (Neurotrophic keratitis, Chronic contact lens
wear, Diabetes, Aging, Trichloroethylene toxicity, CN VII damage,
Corneal surgery - Limbal incision, keratoplasty, and refractive surgery,
Infective - Herpes simplex keratitis and herpes zoster ophthalmicus,
Topical agents - Topical anesthesia,
Systemic medications – Beta blockers and atropinelike drugs )
Sjögren syndrome
 Primary SS has no associated CTD.
 Secondary SS may be associated with some CTDs (RA, SLE,
Scleroderma, Primary biliary cirrhosis, Interstitial nephritis, Polymyositis and
Dermatomyositis, PAN, Hashimoto thyroiditis, Lymphocytic interstitial
Pneumonitis, ITP, Hypergammaglobulinemia,Waldenstrom macroglobulinemia,
Wegener granulomatosis)
Evaporative Loss
(Intrinsic causes & Extrinsic causes)
Intrinsic causes
 Meibomian gland disease
Hypersecretory (Meibomian seborrhea)
Hyposecretory (Retinoid therapy)
Obstructive
 Low blink rate
Physiologic phenomenon (may occur during performance of tasks that require
concentration)
Extrapyramidal disorder (such as Parkinson disease)
 Disorders of eyelid aperture and eyelid-globe congruity
(Lid palsy, Ectropion, Lid coloboma, Exposure; craniostenosis, proptosis/
exophthalmos, and high myopia)
Extrinsic causes
 Vitamin A deficiency (Development disorder of goblet cells, Lacrimal
acinar damage)
 Topical drugs (surface epithelial cell damage)
 Contact lens wear
 Ocular surface disease (allergy)
SYMPTOMS
 Foreign-body sensation
 Grittiness
 Hyperemia
 Mucoid discharge
 Ocular irritation
 Ocular dryness
 Excessive tearing (secondary to reflex secretion)
 Photophobia
 Itching
 Fluctuating or blurry vision
DIFFERENTIAL DIAGNOSIS
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Adult Blepharitis
Allergic Conjunctivitis
Atopic and vernal keratoconjunctivitis
Bell Palsy
Contact Lens Complications
Floppy Eyelid Syndrome
Neurotrophic Keratopathy
Ocular Manifestations of HIV Infection
Ocular Rosacea
Superior Limbic Keratoconjunctivitis
Thyroid Ophthalmopathy
Topical preservative sensitivity
Toxic keratopathy
THANK YOU!