Issue: April 2008
The Definition & Classification of Dry
Guidelines from the 2007 International Dry Eye
BY MICHAEL A. LEMP, M. D. AND GARY N. FOULK S, M. D.,
The diagnosis of dry eye and its treatment has long been approached somewhat
subjectively. Even more so, it's an ocular ailment that hasn't always been treated with
enough gravity given the impact this disease can have on the people who live with it.
We believe this will start to change with the publication of the DEWS Report. The
2007 International Dry Eye Workshop, sponsored by the Tear Film and Ocular
Surface Society [TFOS] was created to provide an evidence-based critical review and
summary of the classification, epidemiology, diagnosis, techniques of basic and
clinical research, and management of dry eye disease.
This report, recently published in The Ocular Surface,1 provides an encyclopaedic,
evidence-based review of dry eye disease. The report was a product of a team of
international experts who spent three years appraising the present state of knowledge
for dry eye disease and the methods used to evaluate, diagnose and manage the
This article summarizes the section of the report addressing the definition and
classification of dry eye disease. Members of the DEWS Definition and Classification
Subcommittee developed a contemporary definition of dry eye disease and a three-
part classification system based on etiology, causative mechanisms and disease
severity. The guidelines described are not intended to override the clinical assessment
and judgement of an expert clinician in individual cases, but they should prove helpful
in the conduct of clinical practice and research.
Definition of Dry Eye Disease
The committee began by reviewing the following definition of dry eye disease that
was adopted by the 1995 National Eye Institute (NEI)/Industry Dry Eye Workshop:
Dry eye is a disorder of the tear film due to tear deficiency or excessive evaporation,
which causes damage to the interpalpebral ocular surface and is associated with
symptoms of ocular discomfort.
The group decided to update this definition to take account of new knowledge about
the roles of tear hyperosmolarity and ocular surface inflammation in dry eye, and the
effects of dry eye on visual function. The following updated definition was produced:
Dry eye is a multifactorial disease of the tears and ocular surface that results in
symptoms of discomfort, visual disturbance, and tear film instability with potential
damage to the ocular surface. It is accompanied by increased osmolarity of the tear
film and inflammation of the ocular surface.
Although the 1995 NEI/Industry Dry Eye Workshop classification has served as a
useful and durable scheme for over a decade, it does not reflect newer knowledge on
pathophysiological mechanisms, effects on vision, and the clinical value of an
assessment of disease severity. To address this, DEWS based the revised
classification scheme on the updated Triple Classification published in 2005 and the
report of the Delphi Panel published in 2006. A three-part classification system was
developed. The first part is etiopathogenic and illustrates the multiple causes of dry
eye. The second is mechanistic and shows how each cause of dry eye may act through
a common pathway, and that any form of dry eye can interact with and exacerbate
other forms of dry eye as part of a vicious circle. The third is a scheme based on the
severity of dry eye disease, which is expected to provide a rational basis for therapy.
Figure 1. Major etiological causes of dry eye disease1
Etiopathogenic Classification of Dry Eye Disease
The etiopathogenic classification developed is shown in Figure 1. As in the 1995
NEI/Industry Dry Eye Workshop report, DEWS regarded the term "dry eye" as
synonymous with the term "keratoconjunctivitis sicca" (KCS). The left hand box in
Figure 1 shows the influence of environmental factors on an individual's risk of
developing dry eye. The term ‘environment’ is used broadly to include physiological
conditions particular to an individual (the milieu interieur), as well as the external
conditions that they encounter (the milieu exterieur).
The recommended scheme retains the two major classes of dry eye used in the 1995
NEI/Industry Dry Eye Workshop classification — aqueous tear-deficient dry eye
(ADDE) and evaporative dry eye (EDE).
ADDE, as its name implies, is primarily due to a failure of lacrimal tear secretion,
although a failure of water secretion by the conjunctiva can also be a contributing
cause. ADDE has two major subclasses, Sjögren Syndrome Dry Eye (SSDE) and non-
SSDE. SSDE is an exocrinopathy in which the lacrimal and salivary glands, as well as
other organs, are targeted by an autoimmune disease. Primary Sjögren Syndrome
consists of this systemic autoimmune disease in the absence of another discrete
autoimmune disease. Secondary Sjögren Syndrome consists of primary Sjögren
Syndrome features together with an overt autoimmune connective disease, most
commonly rheumatoid arthritis. Non-SSDE is a form of ADDE due to lacrimal
dysfunction, where systemic autoimmune features of SSDE have been excluded. It
most commonly presents as age-related dry eye (ARDE), a form that is caused by
lacrimal deficiency and to which the term KCS has sometimes been applied in the
past. Non-SSDE may also result from obstruction of the lacrimal glands due to
cicatrizing conjunctivitis, reflex hyposecretion due to sensory or motor block, and the
use of systemic drugs including antihistamines, beta-blockers, antispasmodics and
EDE is due to excessive water loss from the exposed ocular surface in the presence of
normal lacrimal secretory function. Its causes have been described as intrinsic and
extrinsic, although the boundary between these two categories is inevitably blurred.
Intrinsic EDE is where the regulation of evaporative loss from the tear film is directly
affected, for example, by meibomian lipid deficiency, poor lid congruity and lid
dynamics, low blink rate, and the effects of drugs such as systemic retinoids. Extrinsic
EDE includes those etiologies that increase evaporation by their pathological effects
on the ocular surface. Causes include Vitamin A deficiency, the action of toxic topical
agents such as preservatives, contact lens wear and a range of ocular surface diseases,
including allergic eye disease.
Figure 2. Mechanisms of dry eye1
The Causative Mechanisms of Dry Eye
In general terms, dry eye is caused by a disturbance of the lacrimal function unit
(LFU), an integrated system comprising the lacrimal glands, ocular surface and lids,
and the sensory and motor nerves that connect them. This functional unit controls the
major components of the tear film in a regulated fashion and responds to
environmental, endocrinological and cortical influences. Its overall function is to
preserve the integrity of the tear film, the transparency of the cornea, and the quality
of the image projected onto the retina. While disease or damage to any component of
the LFU can result in dry eye, the core mechanisms of dry eye are driven by tear
hyperosmolarity and tear film instability. In this section the report shows how the
several etiopathogenic subclasses of dry eye activate these core mechanisms, and that
disease initiated in one major subgroup may coexist with or even lead to events that
cause dry eye by another major mechanism. Based upon a schema proposed by
Christophe Baudoin, M.D. and reformatted by Anthony Bron, FRCP, this depiction of
core mechanisms operative in dry eye disease facilitates understanding the complexity
of the disease.
Tear hyperosmolarity is regarded as a central mechanism causing ocular surface
inflammation, damage, and symptoms, as well as the initiation of compensatory
events in dry eye. Tear hyperosmolarity arises as a result of water evaporation from
the exposed ocular surface, in situations of a low aqueous tear flow and/or as a result
of excessive evaporation (Figure 2). Hyperosmolarity causes damage to the surface
epithelium by activating a cascade of inflammatory events and the release of
inflammatory mediators into the tears. Epithelial damage involves cell death by
apoptosis, a loss of goblet cells, and a reduction in mucus secretion, and leads to tear
film instability. This instability exacerbates ocular surface hyperosmolarity, thereby
creating a vicious circle. Tear film instability can also be initiated without the prior
occurrence of tear hyperosmolarity by several etiologies, including xerophthalmia,
ocular allergy, topical preservative use and contact lens wear.
The epithelial injury caused by dry eye stimulates corneal nerve endings, leading to
symptoms of discomfort, increased blinking and, potentially, compensatory reflex
lacrimal tear secretion.
Alteration of normal tear and ocular surface mucins by elevated tear osmolarity
contributes to symptoms by increasing frictional resistance between the lids and the
In the initial stages of dry eye, it is considered that ocular irritation results in reflex
stimulation of the lacrimal gland. However, with time, inflammation accompanying
chronic secretory dysfunction and a decrease in corneal sensation eventually
compromises the reflex response and results in even greater tear film instability.
Classification of Dry Eye Basis of Severity
Regardless of which individual risk factor or group of factors initiates the disease
process, the final common expression involves tear hyperosmolarity and tear
instability leading to ocular surface damage. Since both aqueous tear deficiency and
increased evaporative tear loss occur in most cases of dry eye disease and are linked
by common pathogenetic mechanisms, expert clinicians are increasingly basing
treatment decisions on an assessment of severity rather than discrete deficiencies.
The group believed that a classification of disease based on severity would be of
considerable value in clinical practice, particularly in terms of guiding therapeutic
decisions. This third component of our classification system was based on the severity
grading scheme included in the Delphi Panel report (Table 1).
By establishing these definitions and classification of dry eye disease, we believe
clinicians will be better able to determine the level of DED, as well as the best
treatment course for their patients. OM
1. 2007 Report of the International Dry Eye Workshop (DEWS). The Ocular
Surface. 2007;5:65-204. For a full copy of the DEWS report, please visit the
TFOS website: www.tfos.org.
2. Behrens, A, Doyle, J, Stern, L, et al. Dysfunctional Tear Syndrome: A Delphi
Approach to Treatment Recommendations. Cornea. 25:900-907, Sept. 2006.
Michael A. Lemp, M.D. is clinical professor of ophthalmology at
Georgetown and George Washington Universities and chief medical
officer of OcuSense, Inc. He can be reached at (202) 338-6424 or email
him at email@example.com.
Gary N. Foulks, M.D. is professor of ophthalmology at the Kentucky
Lions Eye Center, University of Louisville. He may be reached at 502-
852-6150 or emailed at firstname.lastname@example.org.
Neither author has any financial arrangement with any of the products or
techniques mentioned in this article.