Betamethasone + Neomycin Sulphate (Ophthalmic) interactions

Clostridioides difficile-associated diarrhea (CDAD), formerly pseudomembranous colitis, has been reported with almost all antibacterial drugs and may range from mild diarrhea to fatal colitis. The most common culprits include clindamycin and lincomycin. Antibacterial therapy alters the normal flora of the colon, leading to overgrowth of C difficile, whose toxins A and B contribute to CDAD development. Morbidity and mortality are increased with hypertoxin-producing strains of C difficile; these infections can be resistant to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea after antibacterial use. Since CDAD has been reported to occur more than 2 months after antibacterial use, careful medical history is necessary. Therapy with broad-spectrum antibacterials and other agents with significant antibacterial activity should be administered cautiously in patients with history of gastrointestinal disease, particularly colitis; pseudomembranous colitis (generally characterized by severe, persistent diarrhea and severe abdominal cramps, and sometimes associated with the passage of blood and mucus), if it occurs, may be more severe in these patients and may be associated with flares in underlying disease activity. Antibacterial drugs not directed against C difficile may need to be stopped if CDAD is suspected or confirmed. Appropriate fluid and electrolyte management, protein supplementation, antibacterial treatment of C difficile, and surgical evaluation should be started as clinically indicated.

Adequate hydration is crucial to minimize the risk of oto- and nephrotoxicity associated with the use of aminoglycosides. Dehydration should preferably be corrected prior to initiation of therapy. In patients who may be at risk for dehydration, such as those with severe and/or prolonged diarrhea or vomiting, fluid status should be monitored closely. If signs of renal irritation develop during therapy, hydration should be increased as indicated, accompanied by a reduction in dosage if necessary. Therapy should be withdrawn if urinary output decreases progressively or azotemia increases.

The use of neomycin oral solution is contraindicated in patients with inflammatory or ulcerative gastrointestinal diseases because of the potential for enhanced absorption of neomycin. Like other aminoglycosides, neomycin is potentially oto- and nephrotoxic, and systemic exposure should be avoided if possible.

The immunosuppressant and anti-inflammatory effects of corticosteroids, particularly in higher dosages, may decrease host resistance to infectious agents, decrease the ability to localize infections, and mask the symptoms of infection. Secondary infections may be more likely to develop. In general, corticosteroids should not be used in patients with active infections, especially systemic fungal infections, unless they are medically necessary and effective antimicrobial therapy or other appropriate treatment has been instituted. However, for corticosteroid-dependent patients who develop a severe or life-threatening infection, continuation of corticosteroid therapy with at least physiologic replacement dosages should be considered, since these patients may have secondary adrenocortical insufficiency. Removal of external steroid during periods of stress may be detrimental to these patients.

The use of oral aminoglycosides is contraindicated in patients with intestinal obstruction. Orally administered aminoglycosides are poorly absorbed from the gastrointestinal tract and primarily eliminated unchanged in the feces. Drug retention and enhanced systemic absorption may occur in the presence of intestinal obstruction, increasing the risk of oto- and nephrotoxicity associated with these drugs.

Aminoglycosides are potentially oto- and nephrotoxic. Eighth cranial nerve damage may manifest as vestibular and/or auditory toxicities, including dizziness, nystagmus, vertigo, ataxia, tinnitus, and varying degrees of hearing impairment. Nephrotoxicity is usually evidenced by tubular necrosis; increases in BUN, nonprotein nitrogen, and serum creatinine concentration; decreases in urine specific gravity and creatinine clearance; proteinuria; and cells or casts in the urine. Rarely, renal electrolyte wasting may occur, resulting in hypocalcemia, hypomagnesemia, and hypokalemia that may be associated with paresthesia, tetany, confusion, and positive Chvostek and Trousseau signs. Although aminoglycoside- induced nephrotoxicity is generally reversible following discontinuation of the drug, death from uremia has occurred rarely. Therapy with aminoglycosides should be administered cautiously at reduced dosages in patients with renal impairment, since they may be at increased risk for oto- and nephrotoxicity due to drug accumulation. To minimize the risk of toxicity, patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other neuro- and nephrotoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be periodically determined and dosage adjusted to maintain desired levels. Renal and eighth cranial nerve function should be closely monitored, and the dosage reduced or therapy withdrawn if toxicity develops.

Aminoglycosides can cause dose-related neuromuscular blockade and muscle weakness, particularly in patients with neuromuscular disease or hypocalcemia and in patients receiving general anesthetics, neuromuscular blocking agents, or massive transfusions of citrate-anticoagulated blood. Although aminoglycoside- induced neuromuscular blockade is generally self-limiting, it may rarely result in respiratory paralysis. Neomycin is thought to be the most potent neuromuscular blocking agent in the class. However, the risk is greatest with intraperitoneal or intrapleural instillation of large doses or rapid intravenous administration of parenteral aminoglycosides. Therapy with aminoglycosides should be administered cautiously in patients with neuromuscular disorders (e.g., myasthenia gravis, parkinsonian syndrome, botulism) or hypocalcemia. If signs of respiratory paralysis occur during aminoglycoside therapy, the drug should be discontinued and mechanical respiratory assistance provided if necessary.

Aminoglycosides can cause eighth cranial nerve damage, resulting in vestibular and/or auditory toxicities. Symptoms include dizziness, nystagmus, vertigo, ataxia, tinnitus, and varying degrees of hearing impairment. Permanent hearing loss may occur, including, rarely, total or partial irreversible bilateral deafness after the drug has been discontinued. Therapy with aminoglycosides, particularly if prolonged (> 10 days), should be administered cautiously in patients with preexisting vestibular and/or auditory impairment, since it may delay the recognition or confound the diagnosis of a drug-induced ototoxic effect. To minimize the risk of toxicity, patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other ototoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be periodically determined and dosage adjusted to maintain desired levels. Serial audiograms should be obtained in patients old enough to be tested, since loss of high- frequency perception usually precedes clinical hearing loss. The dosage should be reduced or therapy withdrawn promptly if signs and symptoms of toxicity develop.

Corticosteroids mimic the effects of endogenous cortisol and aldosterone. Use of these agents may aggravate conditions of hyperadrenocorticalism in a dose-dependent manner.

Corticosteroids can raise blood glucose level by antagonizing the action and suppressing the secretion of insulin, which results in inhibition of peripheral glucose uptake and increased gluconeogenesis. Therapy with corticosteroids should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during corticosteroid therapy, and their antidiabetic regimen adjusted accordingly.

Corticosteroids may have enhanced effects on patients with cirrhosis due to decreased metabolism of these agents. Patients with cirrhosis should be monitored more closely for excessive cortisol effects. Dosage adjustments may be required in these patients.

Corticosteroids may elevate serum triglyceride and LDL cholesterol levels if used for longer than brief periods. Patients with preexisting hyperlipidemia may require closer monitoring during prolonged corticosteroid therapy, and adjustments made accordingly in their lipid-lowering regimen.

Corticosteroids may have enhanced effects in hypothyroidism due to decreased metabolism of these agents. Patients with hypothyroidism should be monitored more closely for excessive cortisol effects. Dosage adjustments may be required secondary to changes in their thyroid condition.

Pharmacologic dosages of corticosteroids should be used cautiously in patients with ocular herpes simplex because of the risk of corneal perforation. Corticosteroids are not recommended for patients with active ocular herpes simplex.

In patients with latent tuberculosis or tuberculin reactivity, the use of pharmacologic dosages of corticosteroids may cause a reactivation of the disease. Close monitoring for signs and symptoms of tuberculosis is recommended if corticosteroid therapy is administered to patients with a history of tuberculosis or tuberculin reactivity. During prolonged corticosteroid therapy, tuberculosis chemoprophylaxis may be considered.

Corticosteroids are primarily metabolized by the liver and may have enhanced effects in patients with liver disease. Dosage adjustments may be necessary in these patients.

Toxic myopathy has been observed with the chronic use or the administration of large doses of corticosteroids, often in patients with disorders of neuromuscular transmission such as myasthenia gravis or in patients receiving neuromuscular blocking agents. Fluorinated corticosteroids such as betamethasone, dexamethasone, and triamcinolone appear to cause more severe muscle atrophy and weakness than the nonfluorinated agents. Moreover, multiple-daily doses are more toxic than once-daily or, preferably, alternate-day morning doses. Steroid myopathy is generalized and sometimes accompanied by respiratory weakness and dyspnea. In some cases, it has resulted in quadriparesis. Elevations of creatine kinase (CK) may also occur, albeit infrequently. After withdrawal of corticosteroid therapy, recovery may be slow and incomplete. Therapy with corticosteroids should be administered cautiously in patients with preexisting myopathy or myoneural disorders since these conditions may confound the diagnosis of steroid-induced myopathy. The presence of a normal serum CK level, minimal/no changes of myopathy on electromyography, and type 2 muscle fiber atrophy on biopsy are helpful in suggesting steroid-induced weakness. If steroid myopathy is suspected, a dosage reduction or discontinuation of the steroid should be considered.

Although corticosteroids are commonly used in the treatment of myasthenia gravis to increase muscle strength, these agents should nevertheless be administered with caution in such setting. Patients should be treated in an intensive care unit and receive respiratory support, since muscle strength may markedly decrease initially, particularly with high dosages. Preferably, therapy should begin with relatively low dosages (15 to 25 mg/day of prednisone or equivalent) and be increased stepwise as tolerated (approximately 5 mg/day of prednisone or equivalent at 2- to 3-day intervals until marked clinical improvement or a dosage of 50 mg/day is reached). Improvement may be delayed and gradual. Thus, it is important not to discontinue therapy prematurely.

The use of corticosteroids may be associated with left ventricular free-wall rupture in patients who have had a recent myocardial infarction. Pharmacologic dosages of corticosteroids should be administered with great caution in such patients.

Corticosteroids reduce osteoblastic function and inhibit the absorption of intestinal calcium, which can result in bone resorption and bone loss during prolonged therapy. In addition, bone matrix may be affected by the protein-catabolic effects of corticosteroids, especially when given in high dosages or for prolonged periods, leading to aseptic necrosis and fractures. Long-term or high-dose corticosteroid therapy should be administered cautiously and only if necessary in patients with or at risk for osteoporosis. Adverse skeletal effects may be minimized by alternate-day or intermittent administration. Any patient receiving prolonged therapy with the equivalent of 7.5 mg prednisone/day or more are at risk for glucocorticoid-induced osteoporosis and should be managed according to The American College of Rheumatology (ACR) guidelines.

Corticosteroids may cause peptic ulcer disease and gastrointestinal (GI) hemorrhage, usually when given in high dosages or for prolonged periods. However, even conventional dosages may aggravate symptoms in patients with a history of peptic ulcers. Delayed healing of ulcers has also been reported. Therapy with corticosteroids should be avoided or administered cautiously in patients with active or latent peptic ulcers or other risk factors for GI bleeding. Some clinicians recommend the use of prophylactic antacids or H2-antagonists between meals when large doses of corticosteroids are necessary.

Corticosteroids may cause gastrointestinal perforation and hemorrhage, usually when given in high dosages or for prolonged periods. They may also mask symptoms of complications such as peritonitis or intraabdominal sepsis. Therapy with corticosteroids should be avoided or administered cautiously in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or recent intestinal anastomoses.

Corticosteroids may aggravate the symptoms of psychosis and emotional instability. Patients with these conditions should be monitored for increased or worsened symptoms during corticosteroid therapy.

In patients with scleroderma, corticosteroids may precipitate renal crisis with malignant hypertension, possibly via steroid-induced increases in renin substrate and angiotensin II levels and decreases in vasodilator prostaglandin production. Renal failure may ensue. Therapy with corticosteroids should be administered cautiously in patients with scleroderma. In addition, they should be limited to short-term use.

Unlike most helminths, Strongyloides stercoralis has the ability to replicate in the human host. In patients with strongyloidiasis, the use of pharmacologic or immunosuppressive dosages of corticosteroids may result in Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia. Therapy with corticosteroids should be administered with extreme caution, if at all, in these patients. For patients on corticosteroids who develop known or suspected Strongyloides infestation, withdrawal of corticosteroids or reduction of the dose of corticosteroids is recommended.

Corticosteroids may increase blood coagulability and have rarely been associated with the development of intravascular thrombosis, thromboembolism, and thrombophlebitis. Therapy with corticosteroids should be administered cautiously in patients who have or may be predisposed to thrombotic or thromboembolic disorders.

Prolonged use of corticosteroids may cause posterior subcapsular cataracts and elevated intraocular pressure, the latter of which may lead to glaucoma and/or damage to the optic nerves. Long-term therapy with corticosteroids should be administered cautiously in patients with a history of cataracts, glaucoma, or increased intraocular pressure.

Corticosteroids can cause hypernatremia, hypokalemia, and fluid retention. These mineralocorticoid effects are most significant with fludrocortisone, followed by hydrocortisone and cortisone, then by prednisone and prednisolone. The remaining corticosteroids, betamethasone, dexamethasone, methylprednisolone, and triamcinolone, have little mineralocorticoid activities. However, large doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. All corticosteroids also increase excretion of calcium and can cause hypocalcemia. Therapy with corticosteroids should be administered cautiously in patients with preexisting electrolyte disturbances. Caution is also advised when treating patients with seizure disorders, since electrolyte disturbances may trigger seizure activity.

Corticosteroids may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. These mineralocorticoid effects are most significant with fludrocortisone, followed by hydrocortisone and cortisone, then by prednisone and prednisolone. The remaining corticosteroids, betamethasone, dexamethasone, methylprednisolone, and triamcinolone, have little mineralocorticoid activities. However, large doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. Therapy with corticosteroids should be administered cautiously in patients with preexisting fluid retention, hypertension, congestive heart failure, and/or renal dysfunction. Dietary sodium restriction and potassium supplementation may be advisable.

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