Year : 1966 | Volume
: 14 | Issue : 5 | Page : 191--196
The lacrimal secretory system and its treatment
Lester T Jones
Portland, Oregon, USA
Lester T Jones
|How to cite this article:|
Jones LT. The lacrimal secretory system and its treatment.Indian J Ophthalmol 1966;14:191-196
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Jones LT. The lacrimal secretory system and its treatment. Indian J Ophthalmol [serial online] 1966 [cited 2021 Sep 18 ];14:191-196
Available from: https://www.ijo.in/text.asp?1966/14/5/191/38653
It has been estimated that in as high as one out of every three patients who consult an ophthalmologist, the lacrimal system is in some way involved. It is also evident that treatment of the secretory part of this system is not well understood, nor its abnormalities accurately diagnosed.
The Secretory System should first be divided into two parts, I the basic secretors and II the reflex secretors.
I. Basic Secretors
A. Mucin secretion.
1. The conjunctival mucin-secreting goblet cells.
2. The crypts of Henle found along the full length of the upper 1/3 of the conjunctiva) surface of the upper tarsus and similarly along the lower 1/3 of the lower tarsus.
3. The glands of Manz, found in a circumcorneal ring of limbus conjunctiva.
These not only contrbute most to the lubrication of the lids but form the inner or "fixed" polysaccharide layer of the precorneal film.
B. Lacrimal secretion.
1. The accessory lacrimal glands of Kraus, about 40 of which are in or about the upper conjunctival fornix and about 6 in the lower.
2. The accessory glands of Wolfring, like Kraus' glands, but bigger,- about 3 adjacent to the upper margin of the upper tarsus and one below the lower tarsus.
3. Occasionally one in the plica, one in the caruncle, and an "infraorbital gland" may be found.
All of these are exocrine glands lying in the subconjunctival tissue and form the intermediate layer of the precorneal film.
C. Oil Secretion.
1. The tarsal (Meibomian) glands, about 25 in the upper tarsus and 20 in the lower.
2. The glands of Zeis at the palpebral margin of each eyelid.
3. The glands of Moll, found at the roots of the eyelashes.
The oil secretors form the outer layer of the precorneal film, most important of which are the tarsal glands. The oily secretion prevents the escape of lacrimal fluid over the lid margins. Mishma (1965) states that absence of the oily layer allows the precorneal film to decrease in thickness and rapidly "run off of the cornea", and that evaporation is from 10 to 20 times as fast as normal.
Basic secretion is the fundamental, indispensable part of the secretary system. Every vertebrate that spends part, or all of its life on land possesses this type of secretion, including the whale which is completely aquatic. In a high percent of newborn humans, it is the only source of lacrimal supply for a few days or weeks. Many individuals go through life in fair comfort with nothing but a basic secretion. In the Shirmer -1 test, it accounts for the first 8 to l5 mm. of wetting of the filter paper. Margaard (1932) estimates the normal excretion in 24 hours to be 6.4 grains, which we can assume is entirely from the basic secretors. There is no proven efferent nerve supply to the basic secretors, although it is generally agreed that during sleep it is at a low ebb and that mucin secretion increases during inflammation. Basic secretion decreases in amount with age, is always involved in hyposecretion and never involved in true hypersecretion.
II. Reflex Secretors
These consist of the main lacrimal gland (O.T. orbital "lobe") and the accessory palpebral gland (O.T. palpebral "lobe"). They are also exocrine glands, but differ from the glands of Kraus and Wolfring in that they have an efferent, parasympathetic nerve supply. This efferent nerve supply is often incomplete at birth.
Because of the many afferent sources from which these glands may be stimulated, reflex secretion is subdivided into peripheral sensory and central sensory or psvcogenic types.
1. Peripheral Sensory.
This occurs whenever the sensory nerve endings of the conjunctiva, cornea, uvea, nasal mucosa and surrounding skin are abnormally stimulated by trauma, inflammations, foreign bodies, chemicals, gases, heat, wind, etc. Conjunctival sensory stimulation activates the reflex system whenever the basic secretors become inadequate. Also, a sensory stimulus in one eye usually activates the reflex system in both eyes.
Of all the vertebrates, including the primates, man alone possesses this type of reflex secretion. It may be started by any disturbing emotional reaction to an individual's environment, including joy and laughter and it too is normally, always bilateral. Cases with disease of the central nervous system may also give evidence of increase or absence of this type of tearing but we can assume it would have no bearing on hyposecretion.
In secretory problems, diagnostic tests are necessary to differentiate the following conditions:
1. Hypersecretion from epiphora due to lacrimal passage obstruction.
The primary dye test is used. One drop of 0.5% fluorescein solution is instilled in the conjunctival sac. After waiting for I to 5 minutes, a small wire nasal applicator with a small moistened piece of cotton at the tip, is placed under the anterior end of the inferior nasal turbinate, 35 to 40 mm. from the anterior nares. If it comes out coloured with the dye, a hypersecretion is diagnosed. If negative, the epiphora is due to lacrimal duct obstruction.
2. Hyposecretion and pseudoepiphora from normal secretion.
The Shirmer -1 test is used. A piece of Whatman No. 41 filter paper, 5 mm. wide and 35 mm. long is partially folded 5 mm. from one end. The folded short end is placed on the lateral 1/3 of the lower tarsal conjunctiva and the patient is asked to fix his eye on any object slightly above the direct line of gaze for 5 minutes. If the amount of wetting is less than 10 mm., it denotes a hyposecretion of both basic and reflex secretors. If the wetting is between 10 and 30 mm., it may denote a "pseudoepiphora". If above 30 mm., it has no differential value, as the patient may have pseudoephiphora, hypersecretion, or a normal secretion.
3. Basic secretion from reflex secretion.
The basic secretion test is used. Two or more drops of a local ophthalmic anesthetic are instilled in the conjunctival sac of both eyes. After waiting 1 or more minutes for complete topical anesthesia and for any hyperemic reaction from a previous test to subside, the lower cul-de-sac is gently dried with a cotton applicator and filter paper is used as in the Shirmer -1 test. If less than 10 mm. of wetting occurs, a hyposecretion due to failure of the basic secretors alone is present. When this test follows the -1 test described above, where a hyposecretion has already been diagnosed, the difference between the two readings denotes the amount of fluid contributed by the reflex secretors. When the Shirmer -1 has shown more than 10 mm of wetting and the basic secretion test less than 10 mm. of wetting, it denotes a basic secretion failure with a reflex secretion effort to compensate, sometimes referred to as "pseudoepiphora".
4. Reflex secretion failure versus peripheral sensory "fatigue-block".
When the Shirmer -1 or basic secretion tests show no reflex secretion is present, the Shirmer -2 test is used. The conjunctiva of one eye only is anesthetized. Filter paper is installed and then the unanesthetized nasal mucosa in the region of the middle turbinate is irritated by rubbing it with a fairly large, dry cotton tipped applicator. If no increase in rate of wetting occurs, it usually denotes total failure of the reflex secretors. If the rate increases, the reflex secretors are assumed to be normal but do not react because of a "fatigue block" at the efferent center to Conjunctival sensory nerve impulses only.
There is no objective test for psycogenie reflex tearing, but patients with a proven reflex secretion decrease or absence due to a "fatigue-block" of the peripheral sensory impulses, will give a history of having copious tearing during emotional stress. Reflex tearing is often the result of a combination of peripheral sensory and psycogenie stimulation.
This is primarily found in older adults together with fibrocystic changes in the two reflex lacrimal glands. The symptoms are a burning, smarting, stinging sensation. The patient may even complain that the eyes are wet. Sharp pains are often felt on awakening when the lids first open. Photophobia and asthenopia may be severe. Fibrous strands of mucoid material may irritate the eye. As the condition progresses, pain, inflammation and impaired vision accompanied by keratoconjunctivitis sicca, corneal abrasions and uveitis may occur.
Hyposecretion may accompany chronic disease, endocrine disorders, anemia, vitamin deficiencies and Sjogren's Syndrome. It is found in acute exfoliative dermatitis, Stevens Johnson Syndrome, filamentous keratitis, ocular pamphigus, and Mikulicz's disease. Infiltration and replacement of lacrimal gland cells by lymphoid tissue are present.
Trauma and surgery of the lids may damage major portions of the basic secretors or the ducts of the reflex secretors. Paralysis of the latter may accompany central nervous system lesions, especially in the hypothalamus.
Exposure to heat, dry air, sun and wind accentuate the hyposecretion. Drugs such as atropine and scopolamine may decrease an already barely adequate secretion. Recent reports indicate that contraceptive pills also may cause decreased secretion.
Pseudoepiphora should be classed with hyposecretion for, when the basic secretors begin to fail, the peripheral sensory nerves call upon the reflex system to make up the shortage. I n response, the reflex secretors may oversecrete. In spite of such adequate or over-compensation, the symptoms of hyposecretion often persist.
When hyposecretion accompanies a general disease, it usually improves as the general condition improves. This is especially true in endocrine hypofunction, anemia and vitamin deficiency diseases. It is not always true of the more acute diseases that destroy the basic secretors such as acute exfoliative dermatitis, etc.
For local treatment, prescriptions with a viscid vehicle such as methylcellulose of 0.5, 1.0, or 1.5% or polyvinyl alcohol are used. Their advantage is not only as a lubricant to replace the loss of mucin and fluid but also to prevent escape of the medicament through the canaliculi. Cauterization of the puncta or destruction of the canaliculi should never be done as a primary procedure as some hyposecretion cases have remission or respond to conservative treatment. It is also a handicap should parotid duct transplantation be done later.
Once the diagnosis is made, the treatment is often self evident. In ovarian deficiency the patient is usually started on 0.625 mg of premarin, from one tablet twice a week to one a day. Stilbesterol in women and testosterone in men have also been used. Thyroid tablets are indicated where a deficiency exists.
When the palpebral fissure is wide because of atonic lids or ectropion, repair of the condition should be done even to the extent of medial and lateral canthoplasties to narrow the fissure.
Moist chambers, goggles with side protectors, scleral contact lenses are often beneficial. Increasing the humidity of the air and eliminating irritating dusts and gasses may bring some relief.
In the most severe and resistant cases, parotid duct transplantation has often made the difference between vision and blindness.
This condition has the same symptoms as nearly any other type of epiphora but without blenorrhoea and can best be differentiated by a positive primary dye test. Seldom will a thorough investigation fail to disclose the cause.
Among the most frequent causes are trichiasis, ectropion, ectropion, and facial paralysis. Inflammations of the conjunctiva, uvea, cornea, orbit, lids, sinuses, teeth and ears must be ruled out. In much of the world, trachoma is the most frequent offender. Allergic reactions are a common source of trouble. Ammetropia, photophobia, the various tropias and phorias, glaucoma, eye strain and fatigue may be responsible. Chemical and drug irritations, such as eye medication, gases and dust may be responsible. It may accompany endocrine disorders such as Grave's disease.
During certain stages of central nervous system disease, especially of some cortical areas, the thalamus, hypothalamus, and cervical sympathetic ganglia, the lacrimal nucleus may be stimulated and at other stages depressed. Following a Bell's palsy of the facial nerve, parasympathetic fibres to the otic ganglion may become "sidetracked" and grow back into the great superficial petrosal nerve causing "alligator tears". Psycogenic causes must also be considered in hypersecretion.
For most of these conditions, the diagnosis alone will indicate the treatment such as antibiotics, antihistaminics, cortisone, refractions, muscle and lid surgery, etc.
When paroxysmal tearing (Alligator tears) follows Bell's palsy, GoldingWood (1961) states that surgical destruction of the tympanic plexus will cure the condition.
In the exceptional cases where the cause cannot be found, two methods of approach have been tried: 1. Destruction of one or both of the reflex glands or their ducts. 2. Destruction of the sphenopalatine ganglion.
It would seem that the ideal treatment would be to destroy the main lacrimal gland without damaging the accessory palpebral gland. This, however, is practically impossible to do. As we have seen, the parasympathetic nerve supply of the latter comes through the main gland. And to destroy the accessory palpebral gland would destroy the ducts of the main gland.
The sphenopalatine ganglion can be paralyzed temporarily by a local anaesthetic consisting of cocaine applied in the region of the posterior end of the middle turbinate or by novocaine injected into the fossa. An alcohol injection would give longer relief but would almost certainly involve the sensory maxillary nerve and the sympathetics. Surgery of the ganglion would involve a transantral approach to the pterygopalatine fossa with destruction of the Vidian nerve and all its nonlacrimal branches.
Whitwell (1958) has devised an operation by which he separates the lateral side of the main gland from the periosteum and cuts the anastomotic branch as it crosses to the gland. Rycroft (p.c.) states that this is unsuccessful in a fairly high percent. Golding-Wood (1961) has used the transantral approach in which, after he has exposed the pterygopalatine fossa, he ligates the sphenopalatine artery and severs the Vidian nerve as it enters the fossa.
My opinion is that the surgical procedure should be used that is least traumatic, that does not damage nonrelated structures and functions, and that only partially paralyzses the reflex sectors. This can be done by everting the upper lid and prolapsing the palpebral gland into view. The overlying conjunctiva and posterior lamella of the levator are cut horizontally enough to expose the gland. The medial half of the gland, which encompasses one or two of the main ducts, is then excised. The conjunctiva may be closed with one or two 6-0 catgut sutures if desired.
If the hypersecretion is not sufficiently controlled, it is relatively easy to repeat the procedure, taking a little more of the gland. The Jameson (1939) method of simply cutting through the ducts from 5 to 10 mm. above the upper edge of the tarsus is less easy to control.
Xray therapy consisting of 500 R in divided doses over the gland has also been used with varying results.
The lacrimal secretory system can be divided into (1) basic type and (2) reflex type.
The basic secretions are of three types-mucinous, watery and oily, produced by three types of glands.
Reflex secretion is engineered by psychogenic and peripheral sensory stimuli.
With the help of primary dye test and Shirmer -1 and -2 tests the etiological basis of hypo- and hypersecretions can be differentiated in most cases.
The causes and treatment of hypoand hyper-secretion on basis of this study are dealt with.
|1||Mishima S. (1965), Arch. Ophth. 73: 233-241.|
|2||Magaard as quoted in by Whitnall S. E.. (1932), Anatomy of the Human Orbit, Oxford Univ. Press, p. 216.|
|3||Golding-Wood, (1963, Br. Med. Jr., June 8, p. 1518,|
|4||Whitwell. J. (1958), Br. J. Ophth. 42: 518.|
|5||Rycroft B., Personal Communication.|
|6||Golding-Wood P. H. (1961), Jr. Laryng. 75: 232.|
|7||Jameson P. C., (1939). Archives Ophth.,17: 207.|