eMedicine Specialties > Emergency Medicine > Rheumatology

Scleritis: Treatment & Medication

Author: Theodore J Gaeta, DO, MPH, FACEP, Clinical Associate Professor, Department of Emergency Medicine, Joan and Sanford Weill Medical College at Cornell University; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine
Coauthor(s): Diana Valcich, MD, Staff Physician, Department of Emergency Medicine, New York Methodist Hospital
Contributor Information and Disclosures

Updated: Apr 14, 2008

Treatment

Prehospital Care

  • Primary complaint of atraumatic eye pain rarely necessitates prehospital care, other than expedient transport to the ED.
  • Take care not to overlook serious comorbidity.
  • If global perforation is suspected, shield the eye and avoid palpation.

Emergency Department Care

  • Recognition of the problem and timely ophthalmology referral are cornerstones of ED management.
  • Pain medications may be prescribed in order to provide comfort for the patient.
  • Detection of scleral thinning mandates shielding of the involved eye to decrease risk of perforation.
  • Scleritis treatment will require immunomodulator therapy once the definitive diagnosis is made.
  • The emergency practitioner can discuss using a topical steroid agent with the ophthalmologist. The caveat being that topical steroid therapy typically fails. However, it could be considered as first-line treatment for nonnecrotizing anterior scleritis, especially in cases in which the likelihood of complications from systemic steroid or nonsteroidal anti-inflammatory drug (NSAID) therapy is high.

Consultations

  • Severity of scleritis and depth of involvement determine the urgency of ophthalmology consultation.
  • Serious systemic illness may require consultation with a qualified internist and/or rheumatologist.

Medication

Therapeutic goals for scleritis are familiar to any emergency practitioner: relieve the patient’s pain and initiate therapy that will positively alter the course of the disease.

From the patient's perspective, pain cessation may be the most important action taken by the emergency practitioner. Outcome will depend on the patient's response to immunosuppressive therapy.

Narcotics and systemic NSAIDs may render temporary pain relief and can be started in the ED.

NSAIDs are generally found to be effective in approximately one third of patients with diffuse anterior scleritis and two thirds of patients with nodular anterior scleritis. NSAIDs have also been found to be helpful in patients with idiopathic posterior scleritis.
   
Initiation of immunosuppressive therapy may require coordination with an internist and/or rheumatologist.

Topical steroids have a high failure rate but should be discussed with the practitioner who will provide follow-up care.

Subconjunctival steroid injections for non-necrotizing scleritis remain controversial. Localized steroid injections may lead to increased intraocular pressure, scleral melting, or globe perforation/scleral rupture.

Surgical management is generally not required except in rare cases of necrotizing scleritis.

Nonsteroidal anti-inflammatory drugs

These agents are used to decrease pain and inflammation. NSAIDs are thought to act by inhibiting prostaglandin synthesis, interfering with migration of leukocytes, and inhibiting phosphodiesterase.


Indomethacin (Indocin)

Often considered the DOC. Indomethacin is rapidly absorbed. Metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation.

Adult

25-50 mg/dose IR PO bid/tid
75 mg SR PO bid; not to exceed 200 mg/d

Pediatric

1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; because of potential cross-sensitivity to other NSAIDs, do not give these agents to patients with hypersensitivity to aspirin, iodides, or other NSAIDs; avoid in GI bleeding; renal insufficiency

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur, (discontinue if leukopenia, granulocytopenia, or thrombocytopenia persists); perform ophthalmologic studies in patients who develop eye complaints during therapy, and discontinue therapy if changes (eg, blurred or diminished vision, corneal deposits and retinal disturbances, scotomata, changes in color vision, macula degeneration) noted


Diflunisal (Dolobid)

Nonsteroidal salicylic acid derivative that acts peripherally as an analgesic. Has antipyretic and anti-inflammatory effects; however, differs chemically from aspirin and is not metabolized to salicylic acid. It is a prostaglandin-synthetase inhibitor.

Adult

Initial: 500-1000 mg PO
Maintenance: 250-500 mg PO divided bid; not to exceed 1.5 g/d

Pediatric

Not established

Antacids may decrease effects; acetaminophen plasma levels may increase when taken with diflunisal; acetaminophen does not affect plasma levels of diflunisal; oral coadministration of diflunisal may increase hypoprothrombinemic effects of anticoagulants; diflunisal competitively displaces coumarin from their protein-binding sites; monitor prothrombin time during coadministration with anticoagulants and adjust dose as needed; coadministration with hydrochlorothiazide can significantly increase hydrochlorothiazide plasma levels; administration of diflunisal with indomethacin can decrease indomethacin renal clearance and significantly increase plasma levels (their combined use has also been associated with fatal GI hemorrhages); coadministration of diflunisal with sulindac may result in significantly lower plasma levels of active sulindac sulfide metabolite

Documented hypersensitivity; active GI bleeding

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

At high doses, diflunisal inhibits platelet function and bleeding time; ophthalmologic examinations should be performed in patients who develop eye complaints during treatment; peripheral edema has been reported with diflunisal use; caution when in cardiovascular conditions that predispose patient to fluid retention; because diflunisal is a salicylic acid derivative, may potentially cause Reye syndrome


Naproxen (Naprelan, Anaprox, Aleve, Naprosyn)

Used for relief of mild-to-moderate pain. It inhibits inflammatory reactions and pain by decreasing the activity of the enzyme cyclooxygenase, resulting in a decrease of prostaglandin synthesis.
Naproxen is rapidly absorbed and has a half-life of 12-15 h. It is highly protein bound.

Adult

375-500 mg PO bid

Pediatric

<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug


Ibuprofen (Motrin, Ibuprin, Advil)

Usually the DOC for treatment of mild- to- moderate pain, if no contraindications exist. Inhibits inflammatory reactions and pain, probably by decreasing activity of the enzyme cyclooxygenase, which results in prostaglandin synthesis.
Highly protein-bound drug that is readily absorbed orally. The half-life is short (1.8-2.6 h).

Adult

400-600 mg PO qid

Pediatric

<6 months: Not established
6 months to 12 years: 10-70 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate to maximum of 2.4 g/d
>12 years: Administer as in adults

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; hypersensitivity to other NSAIDs, aspirin, iodides; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy


Sulindac (Clinoril)

Decreases activity of cyclooxygenase and, in turn, inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

Adult

150-200 mg PO bid or 300-400 PO qd; not to exceed 400 mg/d

Pediatric

Not established

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; hypersensitivity to other NSAIDs, aspirin, iodides; GI bleeding; renal insufficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely, and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if leukopenia, granulocytopenia, or thrombocytopenia persists; caution in anticoagulation defects or in those who are receiving anticoagulant therapy


Piroxicam (Feldene)

Chemically different from other NSAIDs. Extensively bound to plasma proteins. Decreases activity of cyclooxygenase and, in turn, inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Adult

10-20 mg/d PO qd

Pediatric

0.2-0.3 mg/kg/d PO qd; not to exceed 15 mg/d

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; active GI bleeding

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur, (discontinue if leukopenia, granulocytopenia, or thrombocytopenia persists)

Immunosuppressive agents

These agents are used in severe (necrotizing scleritis) and resistant forms of the disease. Only an ophthalmologist experienced with the medication should prescribe these drugs.


Methotrexate (Folex, Rheumatex)

Mechanism of action in treatment of inflammatory reactions is unknown. May affect immune function and usually ameliorates symptoms of inflammation (eg, pain, swelling, stiffness).

Adult

7.5-15 mg PO qwk or 15 mg IM qwk

Pediatric

5-15 mg/m2/wk PO/IM as a single dose or as 3 divided doses given 12 h apart

Oral aminoglycosides may decrease absorption and blood levels of concurrent oral methotrexate (MTX); charcoal lowers MTX levels; coadministration with etretinate may increase hepatotoxicity of MTX; folic acid or its derivatives contained in some vitamins may decrease response to MTX; coadministration with NSAIDs may be fatal; indomethacin and phenylbutazone can increase MTX plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, may increase effects and toxicity of MTX; may increase plasma levels of thiopurines

Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia)

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBCs monthly, and liver and renal function q1-3mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); MTX has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant drop in blood counts; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly with MTX (possibility of increased toxicity with NSAIDs including salicylates has not been tested)


Cyclophosphamide (Cytoxan, Neosar)

Chemically related to nitrogen mustards. As it is an alkylating agent, mechanism of action of active metabolites may involve cross-linking of the DNA, which may interfere with growth of normal and neoplastic cells.

Adult

1-2 mg/kg/d PO

Pediatric

Administer as in adults

Allopurinol, may increase risk of bleeding or infection and enhance myelosuppressive effects; may potentiate doxorubicin-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones; chloramphenicol may increase half-life while decreasing metabolite concentrations; may increase effect of anticoagulants; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity

Documented hypersensitivity; severely depressed bone marrow function

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Regularly examine hematologic profile (particularly neutrophils and platelets) to monitor for hematopoietic suppression; regularly examine urine for RBCs, which may precede hemorrhagic cystitis


Azathioprine (Imuran)

Inhibits mitosis and cellular metabolism by antagonizing purine metabolism and inhibiting synthesis of DNA, RNA, and proteins.

Adult

1 mg/kg/d PO/IV for 6-8 wk; increase by 0.5 mg/kg q4wk until response or dose reaches 2.5 mg/kg/d

Pediatric

Initial: 2-5 mg/kg/d PO/IV
Maintenance: 1-2 mg/kg/d PO/IV

Toxicity increases with allopurinol; concurrent use with ACE inhibitors may induce severe leukopenia; may increase levels of methotrexate metabolites and decrease effects of anticoagulants, neuromuscular blockers, and cyclosporine

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Increases risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur


Cyclosporine (Sandimmune, Neoral)

Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions, such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft versus host disease for a variety of organs.
For children and adults, dosing should be based on ideal body weight.

Adult

3-5 mg/kg PO qd

Pediatric

Administer as in adults

Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease cyclosporine concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase cyclosporine toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin

Documented hypersensitivity; uncontrolled hypertension or malignancies; do not administer concomitantly with PUVA or UVB radiation in psoriasis since it may increase risk of cancer

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin, and liver enzymes; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO

Glucocorticoids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli and are useful in the treatment of recurrent scleritis.


Methylprednisolone (Depo-Medrol, Solu-Medrol, Medrol)

Administered IM or IV. Usually used in addition with other immunosuppressive agents.

Adult

1 g IV 3 times/wk

Pediatric

Not established

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics; grapefruit juice increases prednisolone concentrations; methylprednisolone and cyclosporine mutually inhibit one another resulting in increased plasma levels of each drug

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use; Depo-Medrol contains benzyl alcohol, which is potentially toxic when administered locally to neural tissue
Administration of Depo-Medrol by other than indicated routes, including the epidural route, has been associated with reports of serious medical events including arachnoiditis, meningitis, paraparesis/paraplegia, sensory disturbances, bowel/bladder dysfunction, seizures, visual impairment including blindness, ocular, and periocular inflammation, and residue or slough at injection site


Prednisone (Deltasone, Orasone, Sterapred)

Used to treat inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation.

Adult

60-120 mg PO qd; following satisfactory response, taper over 2-3 wk to approximately 20 mg/d with gradual taper (2.5-mg increments) until discontinuation

Pediatric

2 mg/kg PO qd

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; peptic ulcer disease; hepatic dysfunction; connective tissue infections; viral, fungal, or tubercular skin infections

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

More on Scleritis

Overview: Scleritis
Differential Diagnoses & Workup: Scleritis
Treatment & Medication: Scleritis
Follow-up: Scleritis
References
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References

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Further Reading

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Keywords

scleritis, sclera, leucitis, anterior scleritis, posterior scleritis, necrotizing anterior scleritis, scleromalacia perforans, diffuse anterior scleritis, eye redness, eye pain, sclerokeratitis

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Contributor Information and Disclosures

Author

Theodore J Gaeta, DO, MPH, FACEP, Clinical Associate Professor, Department of Emergency Medicine, Joan and Sanford Weill Medical College at Cornell University; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine
Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, New York Academy of Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Diana Valcich, MD, Staff Physician, Department of Emergency Medicine, New York Methodist Hospital
Diana Valcich, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Joseph A Salomone, III, MD, Associate Professor, Department of Emergency Medicine, Truman Medical Center, University of Missouri at Kansas City School of Medicine
Joseph A Salomone, III, MD is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gino A Farina, MD, Program Director, Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine
Gino A Farina, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

 
 
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