Immunosuppressive therapy in inflammatory ocular surface disease

Chronic ocular surface complications are known to occur after SJS. These include symblepharon, entropion, trichiasis, dry eyes, persistent conjunctival inflammation, conjunctival injection and corneal opacification.[2,3] A recent article classifies these complications as Stevens-Johnson ocular surface failure (SJS-OSF), Stevens-Johnson recurrent inflammation (SJS-RI), Stevens-Johnson ocular membrane pemphigoid (SJS-MMP) and Stevens-Johnson scleritis (SJS-scleritis).[3]

The exact pathogenesis of these lesions is unknown. Destruction of the limbus during the acute stage can lead to stem cell deficiency. Although the cornea looks normal after the acute stage abates, the peripheral limbal cells slowly fail over a period of time, sometimes leading to complete surface failure in a few years. Further, some patients also develop prolonged limbal inflammation which eventually leads to limbal cell failure. Kawasaki et al studied the conjunctiva of five patients with chronic ocular problems post SJS. They found that the substantia propria of the conjuctivalised cornea was infiltrated with CD4-positive T-cells, CD8-positive T-cells and macrophages. Further, there was predominant interferon gamma production at the tissue level suggesting that the Th1 axis of the immune system was active. In these patients very little conjunctival inflammation was clinically evident. [4] Conjunctival inflammation in these patients may be due to trichiasis or severe dry eye. These have to be treated effectively by local measures. If in spite of this the inflammation persists and local measures fail, then there is a role for systemic medications. Systemic steroids and various other steroid-sparing agents including cyclosporine, azathioprine, cyclophosphamide, methotrexate have been used with varying success. [3] In our patients, the time lag between the SJS and the late ocular complication varied from a few months to many years. All these patients had not responded to local therapy. The response to oral steroids and other immunosuppressive therapy was not predictable. Except for two patients who showed no response, other patients followed with us at least for six months after stopping therapy. The response was maintained even after stopping immunosuppressive therapy. There are limitations in this study. This is a retrospective observational study. Due to this objective improvement criteria were not used.

Immunosuppressive therapy in inflammatory ocular surface disease post Steven Johnson syndrome
Dear Editor, Stevens-Johnson syndrome (SJS) is an acute inflammatory disease which often affects the skin and mucosal membranes including that of eyes. [1] On recovery, up to 50% of the patients with SJS develop chronic ocular surface problems which may need immunosuppressive therapy. [2] We report our experience with seven patients of SJS with ocular complications who were treated with systemic immunosuppressive therapy. These patients were referred to us by the treating ophthalmologist because local therapy had not helped and they felt that there was chronic inflammation which could respond to systemic immunosuppressive therapy. We are reporting these cases due to the rarity of the condition and lack of data in the literature.
The details of the seven patients are summarized in the Table 1. SJS was secondary to a viral illness in three patients, in two patients it was due to an allergic reaction to sulpha drugs and it was secondary to phenytoin and carbamazepine therapy in one each. Persistent dryness and ocular surface inflammation in spite of local therapy was the presenting symptom in all patients. Other ophthalmic findings were not given to us by the treating ophthalmologist. Laboratory parameters (complete hemogram, erythrocyte sedimentation rate (ESR), liver function tests, renal function tests, urine routine) were normal except for unexplained increase in ESR in two patients.
Oral steroids were the cornerstone of treatment. Steroid sparers were added if steroid alone did not control the inflammation. The choice of steroid sparer was empirical as there are no established guidelines. Methotrexate has been established to treat a variety of inflammatory eye diseases hence it was used in most of the patients. Patient 5 was on topical cyclosporine, since there was no response he was switched to oral cyclosporine which was later stopped due to intolerance. Duration of the treatment was according to patient response and tolerance to drugs. At a mean follow-up of 10.42 months (range 6-30 months) there was no treatment-related complication.

Use of smart lacrimal probes
Dear Editor, Nasolacrimal duct probing is the treatment of choice for an unresolved congenital nasolacrimal duct obstruction (CNLDO). [1] We have found routine use of a nasal endoscope (5 mm, 0°) and smart lacrimal probes [ Fig. 1A] as useful adjuncts to probing, especially for older children and repeat probings. [1,2] However, there are two problems: 1. unavailability of endoscope at many eye hospitals and 2. difficulty in visualizing the probe in the nose. I write this communication to bring to the notice of the readers, the utility of smart lacrimal probes that we have found valuable.

The graduated/measured probe [Fig. 1B]
Size of the lacrimal punctum in an infant is 0.3 mm. [3,4] However, even the thinnest probe measures 0.45 mm (Bowman 0000 lacrimal probe). To avoid injury, punctum should be dilated using one end of this instrument which is designed like a Nettleship's punctum dilator.
On the other side, there is a 0.65-mm diameter stainless steel rod with markings at every 10 mm. After inserting the probe through the lacrimal punctum, the probe tip advances into the canaliculus. When the first mark at 10 mm approaches the punctum, the tip of the probe enters the lacrimal sac (canalicular length = 2 mm vertical + 8 mm horizontal). [5] This requires little manipulation to negotiate the probe through the common canaliculus.
After changing the direction of the probe, one continues to insert the probe. When the second marking (20 mm) approaches the lacrimal punctum, the tip of the probe approaches the bony canal. One can feel the resistance of the bony part of the nasolacrimal canal. With little manipulation, the probe tip enters the canal (the functional diameter of the bony canal is around 1 mm). [3,4,6] If the canal is stenotic, a gritty sensation is felt or the probe cannot be negotiated any further.
As the probe is advanced, third mark on the graduated probe (30 mm) approaches the punctum. One can feel slight resistance of the imperforate valve of Hasner and a sudden give away of the resistance as the probe tip enters the inferior meatus. When the probe is inserted beyond 30 mm mark, the tip of the probe can be visualized in the inferior meatus with the endoscope or can be felt as a metallic touch with another probe inserted in the inferior meatus. [2] 2. The cannulated/irrigating probe [ Fig. 1C] This is 0.7 mm in diameter with 0.3 mm cannulation. The end of the probe is knurled and tubular with a side opening for an easy entry and manipulation. The stainless steel cannulated rod is mounted on a holding member and connected to a silicon tube connected to a syringe containing fluorescein dye. Once the inferior meatus is reached, the fluid is injected which wells up in the inferior meatus momentarily and can be easily visualized by an endoscope or retrieved in suction catheter or on nasal gauze.
These probes do not improve the success rate by themselves but there are advantages. Graduated probe makes it easy to guess the location of the tip of the probe in the lacrimal system. When combined with the tactile feedback, good comprehension is achieved to decide what manipulation or maneuver may be required to proceed further and where exactly the stenosis or atresia may be located in the case of resistance or failure to proceed. It also helps to avoid unwarranted use of force when correct manipulation is required and it helps to decide when