Editorial
Evaporative Dry EyeSigns and Symptoms Dont Meshand Other Thoughts
Jules L. Baum, MD - Wellesley Hills, Massachusetts
In the report of the 2007 International Dry Eye Workshop,
the participants offered a definition of a dry eye, which
included its 2 major components, aqueous tear-deficient dry
eye (ATDDE) and evaporative dry eye (EDE).1
In ATDDE, lacrimal tear secretion is reduced, either
through disease or destruction. This leads to tear hyperos-
molarity. This hyperosmotic stress, in combination with
reduced hydration, results in an abnormal corneal epithe-
lium and a cascade of inflammatory events. Evaporative dry
eye may occur in the presence of normal tear gland function
and is most frequently due to increased evaporation from
the ocular surface secondary to a deficient lipid layer in the
precorneal tear film. Symptoms common to both ATDDE
and EDE include discomfort, pain, irritation, foreign body
sensation, a sandy feeling, grittiness, dryness, and itching.
Several signs are characteristic of ATDDE, including an
abnormal Schirmers test, an unstable precorneal tear film,
and a reduced height of the inferior lacrimal tear strip.
Lissamine green or fluorescein staining of the cornea and
conjunctiva may also be seen. However, usually few, if any,
signs of dry eye are seen in EDE. The most common causes
of EDE are meibomian gland obstruction or a decrease in
the secretion of meibum. Meibomian gland obstruction may
occur secondary to lid margin disease. Decreased meibum
secretion is seen mainly in elderly patients and may result in
a precorneal lipid layer abnormality.
A continual frustration voiced by many of the experts in
dry eye concerns the discordance between signs and symp-
toms in patients with EDE.2 Because of this, I would like to
offer some possible explanations for the patients ocular
discomfort and for the ophthalmologists frequent difficulty
in diagnosing EDE.
Patients with EDE often state that their eyes burn or
hurt. I explain to them that evaporation itself may be in
large part the cause of their ocular discomfort. I ask if
tearing increases when these symptoms appear. They
often say yes. Then I explain that they may have a
wet dry eyean eye with discomfort stemming from
evaporation. The increase in evaporation, inducing dis-
comfort, leads to stimulation of the afferent trigeminal
pathway. This, in turn, triggers lacrimal secretion via
efferent fibers of the seventh cranial nerve; thus, a wet
dry eye. I ask patients to describe the feeling they expe-
rience when blowing on wet skin. Cold is a frequent
answer. I next explain that the eye interprets cold as
pain or discomfort. I discuss how nature places meibum
on top of the precorneal tear film to decrease evaporation,
and as one ages, meibum may decrease or change qual-
itatively. Such explanations, time-consuming as they may
be, help patients understand their condition. Such infor-
mation could also be printed and offered to patients.
2010 by the American Academy of Ophthalmology
Published by Elsevier Inc.
One reason that one patient with EDE experiences dis-
comfort, while another having the same set of signs does
not, is a varying threshold of pain among individuals. Much
has been published on this subject in the nonophthalmic
literature, but little, if anything, has entered the EDE liter-
ature to help the practitioner understand symptom differ-
ences and the poor correlation between signs and symptoms
among their patients.35
Another reason for the observation that the symptoms of
EDE patients often fail to correlate with their signs is that
some of the patients reported in epidemiologic studies may
not actually have a dry eye. Let me explain. When I used to
see patients with dry eye who were referred to me by a
general ophthalmologist, and I asked them why they came
to see me, the answer, as expected, would be because I
have a dry eye. When asked how they knew they had a dry
eye, many said the referring ophthalmologist told them
such. I then asked what symptoms they had on first being
seen at the office of the referring ophthalmologist. They
frequently mentioned pain and discomfort. A busy
practitioner, seeing few signs of EDE and with many pa-
tients still to see that day, might suggest a diagnosis of dry
eye and offer a trial of artificial tears. The patient thereafter
considers his/her symptoms as being due to dry eyesrightly
or wrongly. When these patients are then sent question-
naires by epidemiologists, the epidemiologists analyze the
responses, sometimes never having seen or examined the
patients to verify a diagnosis of dry eye. Publications ensue,
with readers told that these patients have dry eyes. The
failure of ocular epidemiologists to verify a diagnosis of
EDE is, I believe, due to their failure to see the patients
themselves and insufficient data received from the primary
ophthalmologists. They rely on the diagnosis of dry eye
found in patient records. The diagnosis may be right or
wrong, as explained previously. Thus, the data collected by
the epidemiologists are a mix from patients either having or
not having a dry eye and a mix of ATDDE and EDE. This
failure to verify a EDE diagnosis is, I believe, another
reason for the poor correlation between signs and symptoms
in patients with EDE.35 The cited references represent
examples rather than a complete listing of articles in which
this failure to verify is apparent.
To offer a closing thought relating to the pathogenesis of
EDE, statins are well known to alter lipid metabolism in
various parts of the body. I have long thought that statins
may also affect meibum, qualitatively, or quantitatively.
Could such an effect prove a risk factor in EDE? It could not
be demonstrated in one such study,4 but the study com-
ingled patients with ATDDE and EDE. A study of EDE
patients alone should be considered.
In summary, with more thought given to the cause of
symptoms of EDE, and with additional discussion between
ISSN 0161-6420/10/$see front matter 1285
doi:10.1016/j.ophtha.2010.05.022
 Ophthalmology Volume 117, Number 7, July 2010
doctors and their patients with EDE, the gap between signs
and symptoms should decrease.
References
1. No authors listed. The definition and classification of dry eye
disease: Report of the Definition and Classification Subcom-
mittee of the International Dry Eye Workshop. Ocul Surf
2007;5:7592.
2. Johnson ME. The association between symptoms of dis-
comfort and signs in dry eye. Ocul Surf 2009;7:199 211.
1286
3. McCarty CA, Bansal AK, Livingston PM, et al. The epidemi-
ology of dry eye in Melbourne, Australia. Ophthalmology
1998;105:1114 9.
4. Schaumberg DA, Dana R, Buring JE, Sullivan DA. Preva-
lence of dry eye disease among US men: estimates from the
Physicians Health Studies. Arch Ophthalmol 2009;127:
763 8.
5. Bandeen-Roche K, Munoz B, Tielsch JM, et al. Self-reported
assessment of dry eye in a population-based setting. Invest
Ophthomol Vis Sci 1997;38:2469 75.