Points Suggestive of Infectious Aetiology
• History of trauma/injury with vegetative matter
• History of Contact lens use
• Past history of viral keratitis
• Slit lamp evaluation suggestive of poor ocular surface, presence of corneal infiltrates and hypopyon
Fig. 10.1
Treatment algorithm for presumed infectious peripheral ulcerative keratitis
After starting disease specific therapy for ulcer, it is mandatory to re-evaluate an ulcer after a period of 48 h of medication. An improvement is suggestive of a correct line of management and should be followed and tapered as and when required. Failure to show improvement at the end of 48 h is suggestive of microbial resistance or improper treatment protocol. The management in such cases includes assessing the microbial cultures for antibiotic sensitivity, repeating collection of samples for microbial evaluation and systemic evaluation of the individual. A non healing ulcer may require early surgical intervention.
The following has been summarised in Figs. 10.2 and 10.3 for ease of understanding.
Fig. 10.2
Treatment algorithm in cases of infectious peripheral ulcerative keratitis
Fig. 10.3
Treatment algorithm in cases of suspected infectious aetiology (culture negative)
Treatment for Non-infectious Peripheral Ulcerative Keratitis [1–3]
In case an infectious aetiology has been ruled out and an inflammatory peripheral keratitis is confirmed, a systemic evaluation to identify underlying systemic inflammatory conditions and connective tissue disorders is a must. The main aim of our treatment protocols should be to control inflammation, support the healing and reparative process and to prevent complications (Figs. 10.4, 10.5 and 10.6).
Fig. 10.4
The goals of treatment in cases of an ulcerative keratitis to control the underlying inflammatory process, to promote healing of the ulcer and to avoid or prevent progression and complications
Fig. 10.5
Medical management in cases of inflammatory peripheral ulcerative keratitis
Fig. 10.6
Treatment algorithm for non-infectious immune-inflammatory peripheral ulcers
A. Steroid Therapy:
The first line of management for a non-infectious peripheral ulcerative keratitis is corticosteroids. Local steroid therapy in the form of topical preparations is preferred in unilateral cases when no systemic association is detected on evaluation. They are started at an initial frequency of hourly to two hourly administration followed by a slow and gradual tapering. It is important to remember that corneal melting has been noted in cases where systemic immune conditions are responsible for inflammatory peripheral ulcers.
Systemic steroids are the preferred agents in these conditions where ocular disease is a manifestation of underlying systemic inflammatory condition. Steroids as a first line drug help control inflammation in the initial window period when the effect of immune-modulatory agent has not reached its full potential. Steroids may be administered as intravenous pulse therapy initially in acute cases followed by oral steroids (Dose: 1–1.5 mg/kg body wt.). The regimen for intravenous pulse therapy is administration of 1 gm methylprednisolone for three consecutive days. A full dose of oral corticosteroids based on body weight is given for initial 4 weeks and then tapered, preferably over a period of about 8 weeks. In cases where steroid induced serious side effects are seen or an inappropriate response at the end of initial 1 month is noted a shift to immune-modulators is considered. The side effects of long term steroid therapy include hypertension, dyslipidemia, hyperglycemia, osteoporosis, predisposition to fractures, acne-like lesion, easy bruisability, hormonal imbalance, altered fat distribution in the body (cushinoid facies, buffalo hump) and weight gain. Thus it is important to monitor weight, blood pressure, blood glucose and lipid profile at three monthly intervals along with bone scans annually. While the patient is on long term steroid therapy, calcium and vitamin D supplements should be given routinely.
The therapy should always include use of tear supplements, cycloplegics, anti-glaucoma medications, oral and topical collagenase inhibitors. These adjuvant agents help support the healing process
Artificial tear supplements help improve the ocular surface and tackle the keratoconjunctivitis sicca that is usually associated with systemic immune-mediated conditions. Preservative-free formulations are preferred agents. They help in the epithelial healing process and also dilute the local inflammatory factors. Gel formulations when available can be given along with eyedrops for they coat the ocular surface longer and provide protection.
Cycloplegic agents decrease the ciliary spasm and provide symptomatic treatment by controlling pain.
Anti-glaucoma agents control the intraocular pressure which maybe secondary to local inflammatory process.
Collagenase inhibitors help improve the healing process by inhibiting breakdown of collagen and help in the repair process.
Immunomodulators refers to a group of therapeutic agents that alter the normal immune response of the body. They can either suppress or activate the immune system. Here we are referring to the group of drugs that suppress the immune system aka “immunosuppressant”.
The immunosuppressants are broadly classified as
- 1.
Alkylating Agents: Cyclophosphamide, Chlorambucil.
- 2.
Anti-metabolites: Methotreaxate, Azathioprine, Mycophenolate mofetil.
- 3.
T-cell inhibitors: Cyclosporine, Tacrolismus.
- 4.
Biological agents: anti-TNF agents.
The commonly used immunosuppressants in ophthalmology, their mode of action and adverse effects have been listed in Table 10.2.
Table 10.2
Commonly used medications in the treatment of Peripheral ulcerative keratitis
S. No. | Medications | Mechanism of action | Dose | Frequency | Duration | Side effects |
|---|---|---|---|---|---|---|
1 | Prednisolone | Blocks transcription of anti-inflammatory genes | 1 mg/kg/day | Single dose | Taper over 8–12 weeks [16] | Hyperglycemia, Hypertension, osteoporosis, Gastric ulcers |
2 | Methotrexate | Antimetabolite which inhibits formation of THFR* thus decreasing DNA synthesis It induces apoptosis of T-Helper cells | 5–25 mg/week | Once a week | Taper as required | Hepatotoxity,low WBC count, ulcerative stomatitis, nausea, fatigue, renal failure |
3 | Cyclophosphamide | Alkylating agent Decreases replication of T-cells | 2 mg/kg/day | Single dose | Taper as required | Bone marrow suppression, nausea, vomiting, stomach aches, haemorrhagic cystitis, diarrhoea |
4 | Azathioprine | Purine synthesis inhibitor. It inhibits enzyme required for DNA synthesis, thus affecting proliferating cells | 1–2.5 mg/kg/day | Single/two divided doses | Taper as required | Hypersenstivity reaction, skin rashes, predisposition to neoplasias, nausea, vomiting, hepatic and renal damage |
5 | Cyclosporine
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