Clinical findings

What are the typical clinical findings of dry eye disease ?

Typical dry eye clinical findings are

• decreased tears ,

• low stability of the tear film , and thus insufficient wetting of the tissue

• Damage to the tissue surface leads!

Tear film instability / tear film breakup time (BUT) (normal: <10 seconds)

Insufficient tear fluid and unstable tear FILM on the eye, is a typical clinical clinical findings in dry eye:

• the stability of the tear film is determined by the Tear Film Break-Up Time (BUT)

  • is typically examined by staining the otherwise largely invisible tear film with a blue-green vital dye (fluorescein)

  • the normal value should be at least 10 seconds are to the tear film break up and thereby initiating a new blink , which then propagates a new intact tear film.

  • At the onset of dry eye disease, there may also be occasional episodes of increased lacrimation with watery eyes , which alternate with dry eyes

• => Further information can be found HERE

Defects in the cell surface / vital staining (normal: no staining)

An unstable tear film triggers dry spots in the epithelium of the surface of the eye due to the frequent, early opening.

There, the surface epithelium is disturbed by two major damage mechanisms ( secondary pathogenetic factors ): increased mechanical friction and increased osmolarity.

The injured, dried cells can be stained on the cornea with the vital dye fluorescein . On the conjunctiva, lissamin green usually stains better. The defects appear as small spots of staining (as keratitis superficialis punctata , KSP) in biomicroscopy with a slit lamp. You can find more detailed information on vital staining => HERE .

• => This vital staining is another important test for the dry eye, since it shows the severity of the dryness of the tissue damage and thus the dry eye.

Aqueous Tear Production Disorder ( Normal:> 10mm )

With moderate to advanced dry eye, the aqueous tear production is often disturbed - either in the sense of a reduced aqueous production or, occasionally, as excessive secretion.

Mostly (in 4 out of 5 cases) in dry eye oil deficiency in meibomian gland dysfunction with subsequent hyperevaporation is the primary cause of dry eye. But damage to the tissue, including the nerve fibers, can lead to disturbances in neural autoregulation of tear secretion.

It is therefore useful to have an orientation impression of the production performance of the lacrimal gland for the watery tears.

The appropriate test for the maximum production capacity of the lacrimal gland is the Schirmer 1 test (without prior local anesthesia). It is therefore advisable to carry out a preliminary determination of the tear film stability and a subsequent vital staining with fluorescein without the addition of a local anesthetic.

REDUCED TEAR VOLUME

• on the surface of the eye

  • (mostly) by increased evaporation of the tear water - as ' evaporative dry eye' called ... or

  • (much less often) due to a reduced amount of (aqueous) tear secretion from the tear gland

    • referred to as ´ primary watery tears ´

• diagnostic

  • wird ein effektiver Tränenmangel an der Augenoberfläche am einfachsten festgestellt durch eine Beobachtung oder Vermessung des Tränenmeniskus.

  • weiterführend sind: Tränenfilm-Tests und Drüsen Tests

• ÖL MANGEL

  • (nach Menge oder Qualität oder beidem) mit Störung der Lipidschicht auf dem Tränenfilm und nachfolgender verstärkter Verdunstung

    • dies ist eine typische Folge der Meibomdrüsen- Dysfunktion´, (MDD) - sieist der Hauptgrund für ein Trockenes Auge.

    • Diagnostisch:

      • lässt sich die Funktion der Meibomdrüsen am einfachsten prüfen durch eine ´Diagnostische Expression´

      • Genauere Diagnosen und Quantifizierungen werden möglich durch Interferometrie und Meibographie.

• Verschwinden von Meibomdrüsen Gewebe

  • (im Engl. bezeichnet als ´Gland Drop-Out´) bei der optischen Betrachtung (Meibographie) der sonst nicht sichtbaren Meibomdrüsen, die versteckt im Augenlid liegen.

Veränderungen am Lidrand wie:

• Schaum und Ablagerungen auf dem Lidrand durch veränderte Fette der Meibomdrüsen

• verstärkte Rötung und verstärkte Füllung der Blutgefässe

• Demodex Milben an den Wimpern

• blocked meibomian gland openings with protrusion or leaked hardened fats of the meibomian glands

• Rounding and irregularities of the back edge of the eyelid

Epithelial damage => KSP

• Increased friction and increased tear film osmolarity in tear film disorders lead to damage with defects in the surface of the eye. You can find more detailed information on vital staining => HERE .

• This affects the surface epithelium first and can be demonstrated by staining with vital dyes . Defects occur:

  • on the cornea / cornea and conjunctiva / conjunctiva as superficial punctate keratitis (KSP)

  • but also on the back edge of the lid edge - as a lid wiper epitheliopathy (LWE)

Increased amounts of inflammatory mediators

• Inflammation mediators are typically formed by dry eye tissue destruction and occur in tears and tissues. These are various factors, e.g.

  • inflammatory cytokine and chemokine signaling substances

  • subsequent activation of tissue-degrading enzymes (matrix metalloproteinases, MMP ).

  • The most common protease (MMP9) on the surface of the eye can be diagnosed with a rapid test .

Damage to the connective tissue => LIPCOF

• If the surface damage progresses and inflammatory reactions occur, the connective tissue underneath the epithelium is also damaged. Here typically occur Li dkanten- P arallele Co njunctivale F old ( LIPCOF on).

  • LIPCOF are the sign of advanced tissue destruction through the activation of tissue-destroying enzymes , mostly matrix metalloproteinase (especially MMP9).

  • Due to the tissue destruction, the conjunctiva becomes increasingly looser and ´folds wrinkles´. They already occur due to the low forces of the normal blinking of the eye over the surface of the eyeball. The rear edge of the eyelid then pushes the loosened conjunctiva in front of you like a snow plow when gliding over the globe.

  • Diagnostically are LIPCOF wrinkles in the slit lamp easily evaluated - better after staining of the tear film with fluorescein.

• You can find more detailed information about LIPCOF => HERE

Nervous system regulation

The surface of the eye is regulated by the nervous system from the peripheral nerves and the central nervous system.

Important functions such as tear secretion and sufficient blinking are automatically regulated by reflex. At least when blinking, there is an arbitrary influence. For example, arbitrarily performed blinking and particularly powerful blinking are possible, which can help to improve the moisturization of the eye.

Stimulus and neural regulation of lacrimation and blinking

The sensory irritation of the surface of the eye in the dry eye, for example through drying, rubbing, hyperosmolarity or injury, reaches the central nervous system (CNS) via the eye nerves (cranial nerve V, trigeminal nerve).

The signals are processed there and the function of the eye is automatically regulated in the brain stem as required.

For example, the flow of tears and blinking are regulated via nerves that run back from the brain stem and brain to the eye (cranial nerve VII, facial nerve).

• This also explains why chronic irritation in dry eye occasionally on overshooting irritant secretion and 'Wet eye' can lead

• Excessive tear formation is a protective reflex of the eye , in which, in itself, a useful experiment simply ´wash away´ a ´excitement´, like a foreign body on the surface. With chronic irritation in the tissue itself, however, this cannot work.

• At the same time, signals also reach the cerebral cortex, so that this can be perceived consciously and can also be reacted to when necessary.

Eyelid regulation - normal, rare or incomplete blinks

The processing of the signals from the surface of the eye is complex and is influenced by various centers in the CNS.

In principle, the blinking is controlled by the blinking reflex. When the tear film on the surface of the eye breaks open, the tissue begins to dry out, irritating the nerve endings there.

This triggers a blink of an eye, which spreads a new, even tear film and thus makes the nerve stimulus disappear again.

The reflex blink of the eye happens largely unconsciously, although a blink of the eye can of course be perceived consciously and also controlled consciously.

Rare eyelid blinks

• With increased attention due to strenuous visual tasks, eyelid blinks can be deliberately delayed or suppressed

• This affects many everyday activities, e.g. reading , especially on computer screens , watching TV or driving a car , especially at night, etc.

• Then the eye is kept open longer so as not to interrupt the 'important' visual impression, even if a dryness stimulus comes from the surface of the eye.

  • In the illustration, the eye turns red due to the irritation before the blink of an eye finally occurs.

• The eyelid blinks can then occur significantly less than the normal value of approx. 5-10 times per minute. Since the tear film is only stable for about 10-20 seconds , the surface of the eye can dry out easily.

• So rare blinking can create or worsen dry eyes.

Incomplete eyelid blinks

• On the other hand, not only the frequency but also the complete sequence of blinking can be influenced.

• With ´nervous blinking´ due to lack of concentration, nervousness, or habitually, eyelid blinks can be done more often than necessary and are often incomplete without being consciously noticed.

• Incomplete blinking means that the upper eyelid does not close completely when the eyelid is closed (please see animated image). Therefore, the tear film cannot be completely renewed. The lower part of the tear film then always remains relatively dry and there is increased damage to the cell surface .

• Incomplete blinking is quite common and is therefore a common co-factor in dry eyes. However, they are not noticed by the patient and are sometimes difficult for the doctor to diagnose without special equipment .

Irritation and processing to feel pain

In principle there is a certain difference between the pure ´perception´ of a stimulus from the surface of the eye that occurs in the cortex and the evaluation of these stimuli in the ´subordinate´ Limbic system.

´Pain´ is not a perception in the actual sense, but a construction of the brain .

This construction results from the emotional evaluation of a perception. The evaluation takes place above all in the so-called limbic system and through other emotional instances. Numerous other things, such as experiences and expectations, etc., flow into the subjective evaluation.

However, for the individual person the two instances of ´perception´ and what appears as ´pain´ are not always to be clearly separated. So in the end it is not always clear which of the various instances in the brain is ' cook or waiter ' .

On the surface of the eye, this means that the strength of a stimulus on the surface of the eye and the feelings of pain that the patient perceives subjectively are not always closely related.

Difference between clinical findings and patient perception

Why do the SYMPTOMS of the dry eye often not match the clinical FINDINGS?

=> ... this has not yet been fully clarified and is the subject of current research!

It is typical of the dry eye that the severity of the patient's subjective symptoms in terms of pain does not always match the clinically detectable findings .

Subjective evaluation

Therefore, the subjective evaluation of a stimulus from the surface of the eye can dominate over the objective perception. This can depend on the ´day form´ of the individual person, but it can also be very different for different people.

This can be expressed in such a way that the subjective symptoms cause the patient to suffer a great deal of suffering while little or sometimes no objective findings are clinically detectable - this may be a pain syndrome .

On the other hand, however, a patient with significantly pronounced clinical findings, for example a surface damage that can be stained, may have little or no subjective symptoms in the sense of irritation or pain. Such a patient will then probably have little inclination to medically indicated therapy.

Pain syndrome

Disorder of pain processing can lead to pain syndrome.

Pain has the biological meaning to indicate damage to the body and thus give a signal for danger. With chronic chronic pain stimuli , disorders in the area of ​​the pain system can occur. Routes of transmission of the nerves in the pain system can then be cleared and increasingly solidified. Then pain may persist, even if the pain stimuli on the body decrease or the tissue damage has already healed.

It has lost its actual meaning as a warning signal and becomes part of the disease. These pains are described as “neuropathic” pains

This means that a subjective impression of pain can continue to exist for the patient, even though successful treatment of the dry eye has already improved the condition of the surface of the eye.

Psychosomatic influences

Psychosomatic influences on a disease process and on the patient's perception have been an established and serious part of medicine for many years. In addition to, for example, non-specific back pain, functional cardiovascular problems or indigestion, this can also play a role in the dry eye , according to many studies .

If dealing with the disease becomes the most important part of life, this could be an occasion to seek psychosomatic help .

HOW does a dry eye develop?

... and how does it become CHRONIC? ? ?

Dry eye is strongly influenced by regulatory systems and risk factors

Various factors influence the function of the surface of the eye

A disruption of positive factors and the appearance of negative factors (risk factors) worsen the normal functioning of the tissue and therefore increase the risk of the appearance of a dry eye and the severity of the disease.

The complex disturbance of the function and structure of the surface of the eye in the dry eye leads to a lack of the basic functional complexes for the constant moisturization of the tissue.

The development of a dry eye is favored by several factors:

Why does the dry eye tend to get worse?

 ... without adequate therapy

=> Tear deficiency with reduced moistening of the eye surface and subsequent tissue damage have a negative impact and reinforce each other!

Self-reinforcing inflammatory mechanisms

The complex pathological changes in the dry eye influence each other and form self-reinforcing control loops, which are often referred to as vicious circles.

This often leads to exacerbation of the disease if insufficient therapy is given.

Inflammation is an important enhancement mechanism

Inflammation is a powerful mechanism for the exacerbation of dry eye disease.

Inflammation is a basic mechanism for cells to defend themselves. against wounding and damage. This also typically occurs in dry eyes due to the instability of the tear film and the subsequent increased mechanical friction and increased osmolarity of the tear film.

Inflammation mechanisms cause tissue destruction to overcome the supposed pest and should then lead to tissue repair.

In diseases like the dry eye, ongoing tissue damage can lead to chronic inflammation.

If the inflammation becomes chronic, then it turns into a negative and destructive process because the initial tissue destruction cannot be replaced by an adequate repair and thus becomes increasingly severe. This creates self-reinforcing control loops (' vicious loops ') of worsening of the disease.

This powerful mechanism can significantly worsen the disease process.

In such cases of moderate to severe dry eye, it often makes sense if the treatment contains temporarily anti-inflammatory therapy approaches in addition to tear substitutes and physical lid margin therapy with lid margin hygiene .

For detailed information about dry eye therapy, we refer to the longer English language version of the OSCB information portal.

When does a "dry" eye become dry eye disease?

If a ´dry´ eye becomes chronic - then an occasional, temporary disorder can develop into a chronic DISEASE!

An occasional “dry” eye is not a disease

 Most of us have probably already had a temporary feeling of 'dry' eyes, for example when we were exposed to unusually strong drying environmental influences. These are, for example, low air humidity, high temperature, wind, or rare blinking when working concentrated in air-conditioned room air.

Such a ´dry´ eye is typically a short-lived condition, which quickly improves and disappears when we become aware of it and increasingly blink or leave the drying environment.

When “dryness” becomes chronic ... this condition can turn into a disease

Only if the feeling of 'dryness' persists and cannot be improved by avoiding drying out environmental factors and by increasing, consciously and intensely blinking ...

… Then the temporary condition becomes chronic and an occasional “dry” eye can progress to the disease of the dry eye.

This is typically associated with an increase in the DURATION and SERIOUSity of symptoms and clinical findings due to increasing disruption and damage to the surface of the eye. Some important risk factors favor the appearance and severity of the dry eye.

Many different and mutually influencing self-reinforcing control loops of the exacerbation of the disease (often referred to as ´Develskreise´, English ´VICIOUS CIRCLES´) occur in the chronic dry eye and can lead to the clinical full picture of a chronically progressive tissue destruction with a loss of function of the eye surface to lead