|Year : 1968 | Volume
| Issue : 1 | Page : 32-36
Clinical picture of trachoma
New Civil Hospital, Ahmedabad, India
|Date of Web Publication||22-Dec-2007|
R P Dhanda
New Civil Hospital, Ahmedabad
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Dhanda R P. Clinical picture of trachoma. Indian J Ophthalmol 1968;16:32-6
Trachoma is a disease of established etiology and follows a proven pathology. It however is a disease, the elinical picture of which differs widely from country to country and area to area. That precisely is the reason that clinical staging of Trachoma has been passing through a changing phase ever since McCallum suggested a very elaborate classification. Later W.H.O. with its wide experience of surverys in different parts of the world have classified Trachoma more briefly and more precisely. Useful modifications have been suggested on the basis of individual experiences. It is apparent that regional factors like personal hygiene, social customs, environmental sanitation and climatic variations are all as important if not more, in determing the clinical picture of Trachoma in a particular area. Staging may be an important consideration during national surveys for standardizing the method of recording and statistical assessment. A clinician is however very conscious of the difficulty to demarcate any boundaries of the stages of Trachoma. There is so much of overlapping that the disease appears a continuous pathology. It is an every day observation that cornea may be actively involved even though the lid appears to have entered the healing stage. Similarly active pannus in the cornea is so often seen with degenerative regressive pathology in the lids that the term corneal trachoma is so often mentioned.
What is however important from the patients' and therapeutic point of view, is whether Trachoma is in an active and progressive stage or in a healing or regressive stage. In the progressive stage, local therapy is better supported by a systemic administration while in the regressive stage when healing has already overtaken the disease, local treatment alone may be adequate. In the complicated and degenerative stages, surgery is of course the treatment of choice. I will therefore deal with the subject from this practical point of view and discuss the pathological basis of clinical features.
I start with a presumption that Trachomatous follicles, fleshy congested islands in the palpabral conjunctiva and pannus in the cornea are indicative of activity of the disease while cicatrization is suggestive of the healing process. I may however at this very stage exclude with a brief description the so called Trachorea-I which has been described as the subclinical stage of infection and inflammation difficult to diagnose specifically. Trachomatous manifestations have not become apparent at this stage. The condition is obscured by acute conjunctivitis. It has been suggested that examination of upper limbus with slit lamp for the vascular loops encroaching into the cornea for more than 1 mm. and histological and cultural studies may help in more definitive diagnosis at this stage, a rather impracticable proposition in routine ophthalmology. From the clinical point of view I would however make a simple statement. Any conjunctivitis in a child in an endemic area which does not respond to usual treatment within one week or tends to recur again and again should be treated as Trachoma unless proved otherwise.
Small pin head size flat yellow follicles discretely spread over the congested palebral conjunctiva when seen are a very dependable diagnostic feature. They may be numerous and readily apparent or they may be few and may have to be looked for. Unfortunately the follicular stage of treachoma is soon obscured by secondary infection and conjunctival hyperplasia. The follicular stage may also be obscured by lymphoid tissue reaction or when trachoma is associated with spring catarrh, the oedematous conjunctiva completely overshadowing the trachomatous picture. It is in relatively small number of cases that follicles may be visible along the upper limbus or in the upper corea. They have usually to be looked for. Therefore trachomatous folliculosis though a true trachomatous manifestation is a clinical feature not as frequently seen as its significance suggests. In fact I wonder if more than 10% diagnosis of trachoma is based on trachomatous follicles.
A word about the so called papillae. These conglomerate dilated capillary networks in a trachomatous palpebral conjunctiva have been mentioned more often than seen, and are only a part of generalised vascular response of the conjunctiva. A papillary trachoma has been described but the reference is probably to the conjunctival hyperplasia when the term papilla denotes lymphoid vegetations.
Corneal vascularisation is a clinical feature which can be a dependable guide for diagnosis of active and progressive Trachoma. Invasion of the avascular cornea by neocapillaries from across the upper limbus is a definitive and diagnostic feature of Trachoma when associated with involvement of upper palpebral and fornix conjunctiva.
I suggest that pannus is always an indication of active Trachoma whether the concurrent pathology in the lid is follicular, cicatricial or degenerative. The so called regressive panmis is only indicative of less activity of the disease. Trachomatous pannus in the early stages is usually sub-epithelial but in severe cases, aggravated by secondary infection, it may damage the Bowman's membrane and involve the superficial lamellar layers. Clinically a deep trachomatous pannus is best seen either with a high convex lens in the ophthalmoscope or against retroillumination from a slit-lamp.
Pannus may take on a prolifereative appearance in more highly endemic areas for which terms like pannus crasus, fleshy pannus or malignant pannus have been mentioned.
It is not difficult to exclude pannus from other causes of corneal vascularisation like extensive phlyctenular ophthalmia. Pannus of a chemical burn or of specific conditions like mustard gas keratitis, Rosacea keratitis are again not easy to confuse with Trachoma for more than one reasons. Fine vascularisation due to ariboflavinosis and the deep vascularisation of interestitial keratitis are entities in themselves.
Fleshy Palpebral Conjunctiva:
Fleshy and hypertrophied islands in the palpebral conjunctiva are seen for varying periods depending on the response to natural defence and active treatment.
A fleshy palpebral conjunctiva is another guide to the activity of the disease. It is this evidence in relation to the amount of cicatrization that suggests the division of stage 1I1 in IIIa and IIIb because IIIa is more on the active side and stage IIIb more on the regressive side. These fleshy areas again become grossly masked when trachoma is associated with palpebral spring catarrh, a situation not quite infrequent and often difficult to isolate one from the other. A term called "trachoma like" has been used by clinicians in areas with low incidence of trachoma. A congested and fleshy appearance in either angles of upper palpeble conjunctiva has been termed `trachoma like'. There is however no pathological basis for such a criterion and these cases are mostly the result of a chronic inflammation or irritation of a non-specific nature.
Like any other chronic diseases, trachoma heals by cicatrisation though not necessarily always so. Even a moderate degree of active trachoma usually leaves behind permanent evidence of its past existence. Cicatrization involves not only the palpebral conjunctiva but also the fornix and bulbar conjunctiva. The degree of cicatrization is directly proportional to the severity of associated secondary bacterial infection. Cicatrization of the palpebral conjunctiva may be really fine and visible only tinder bright illumination and magnification. However subclinical, it permanently changes the normal pattern of the vascular tree in the palpebral conjunctiva. Disturbance of this pattern can be enough guide for confirming the presence of subclinical cicatrisation. I suggest that any upper palpebral conjunctiva through which Meibomian ducts are not visible and where normal pattern of vertically dividing vessels is altered has definitely undergone chronic inflammation and some amount of cicatrization. Cicatrization may however be more extensive involving the lid margin along the muco-cutaneous junction which not only leads to the frequently mentioned typical sinuous appearance of lid margin but also explains the incidence of trichiasis in trachoma. Cicatrization of the bulbar conjunctiva although present in large percentage of cases is not clinically manifest. It becomes however very apparent when a surgeon makes a flap along the tipper limbus or attempts a peritomy. Cicatrization of the bulbar conjunctiva may explain the possible higher incidence of glaucoma in trachoinatous eyes, and may be responsible for many failures of iridencleisis and trephining operations. Cicatrization at limbus and in cornea is however the most significant evidence of past trachoma. Herbert's pits along the upper limbus are a feature caused by no other ocular disease. They have been observed even in cases where palpebral conjunctiva have been declared free from present or past trachoma. It is this observation which has further supported the suggestion of existence of corneal trachoma.
Cicatrization of the upper cornea of any degree is usually present only in cases of severe trachoma. It leads to gross corneal astigmatism and marked diminution of vision though the pupillary area of cornea is clear. This cicatrization is a hazard in getting into a proper plane of dissection in lamellar keratoplasty. I should also explain why trachoma involves mostly the upper conjunctiva. Upper fornix is a potentially closed space less efficiently cleaned by nature and not easily accessible for medication. The pathology extends along the upper fornix and upper bulbar conjunctiva and therefore more frequently involves the upper cornea. Lower cornea and lower fornix are also involved but only in very severe cases. Obliteration of lower fornix and presence of symblepharon along the lower limbus are enough evidences. Lower cornea is mechanically demaged by entropion and trichiasis of a ptotic upper lid and due to exposure keratitis caused by ectropion of lower lid.
The normal process of healing by cicatrization may be vitiated by degenerative changes particularly in the tarsus. This is probaboy due to the persistence of deeply situated islands of active disease in the tarsal plate. The common clinical features are cystic degeneration, calcareous degeneration and pigment degeneration. Degenerative changes in the bulbar conjunctiva and corneal epithelium are histologically manifest by keratinisation of corneal and conjunctival epithelium, and droplet type degeneration in the lamellar layers resembling an amyloid type degeneration. A hazy cornea without any vascular reaction, without manifestation of an active disease in the lid is a common observation in old cases surrounded by unhealthy bulbar conjunctiva.
One factor, whether a particular case of Trachoma will go on to complicated trachoma or not is the degree of secondary infection. As. I have often said, though rather exaggerated, "we might turn in a tube of Trachoma virus culture into the conjunctical sac and if we only kept the eye clean, Trachoma will pass through its clinical phases and die out without leaving any gross defects." The grade of secondary infection decides the depth and extent of cicatrization which in turn is responsible for complications of trachoma.
Entropion, trichiasis, ectropion, conjunctival symblepharon, obliteration of fornices, extensive secondary xerosis can all be explained as being directly due to cicatrization. Extension into and involvement of lacrimal sac and lacrimal ducts has been known to be responsible for trachomatous dacryocystitis and dacryoadenitis respectively. The surprising thing is that the severity of the complications is indefinitely related to the severity and activity of the disease.
We have particular experience of trachmatous involvement of cornea, clinical, surgical and histopathological, during the last 5 years at the regional eye bank and the Corneal surgery unit at Indore where we Lave handled 888 donor corneas and have performed 322 corneal grats todate. Over 37% of recipients had a definite evidence of trachoma in the lids or in the cornea. Cornea may be involved as an extension of pathology from the upper limbus into its upper one fourth which is densely fibrosed and hard to dissect. This fortunately is non-progressive once the active disease is controlled and apart from being responsible for high corneal astigmatism and apparent cosmetic defect does not lead to further complications.
Corneal involvement may be a diffuse haze in the superficial layers with or without vascularisation but without any deep scarring. This is a condition we have described as "trachomatous cornea" because the corneal change has been caused by pure trachomatous pathology without any secondary infective ulcer of the cornea. Trachomatous cornea is usually associated with extensive changes in the surrounding bulbar conjunctiva. Histopathologically this cornea shows marked hyperplasia, hyperkeratosis and parakeratosis of the corneal epithelium, the changes extending into the basal cells and even into the superficial lamellar layers.
The third corneal change, damaging but luckily less frequent, is trachomatous keratectasia when part or whole of the cornea spontaneously becomes thin and ectatic leading to marked diminution of vision. This ectatic cornea looks very clear although there is extensive involvement of surrounding tissue.
I have of course excluded gross corneal scars due to corneal ulcers either due to trachoma or associated with trachoma. These gross scars are more due to secondary infection than trachoma itself.
To make a long story short, I have tried to emphasize a clinical approach to trachoma from a therapeutic and pathological point of view. I once again emphasize that what is important for a clinician is to decide whether trachoma is in an active and progressive stage or is healed and in regressive stage. The labels of Tr-O, Tr-I Tr-II, Tr, III-a and Tr-III-b can all be absorbed within these two categories. .1 have emphasized that systemic adminstration in addition to local therapy is important during the progressive stage. Activity of the disease is best determined by looking for pannus in cornea, fleshy active areas in palpebral conjunctiva and of course follicles, if visible. It is the balance between these and the amount of cicatrization that will determine whether the patient has entered the healing stage when local therapy alone will be adequate.
I may suggest that just as a loose diagnosis of immature cataract without ophthalmoscopy has often resulted in incurable blindness due to undiagnosed glaucoma, an overenthusiastic diagnosis of trachoma when there is none has often given mental worry to the patient. A simpler approach to the understanding of clinical trachoma is therefore important if routine clinical ophthalmology is to contribute to amelioration of blindness of trachomatous origin.
| Summary|| |
From the clinical point, it is more important to determine whether trachoma is progressive or healing rather than put it under an exact specified category.
Pannus, fleshy palpebral conjunctiva and follicles are signs denoting activity. Corneal trachoma has been precisely defined.
The pathological basis of clinical features of the follicles, papillae, pannus, cicatrization and complications in trachoma are discussed to determine the activity of the disease and the consequent therapy.
In the progressive stage, systemic therapy is indicated along with local applications, whereas in complicated cases surgery may be needed. In healing trachoma local therapy alone may be adequate.