Can You Take Furosemide with Kenalog-40?

Using triamcinolone together with alcohol or grapefruit may increase the risk of side effects of triamcinolone. You may want to limit your consumption of grapefruit, grapefruit juice, and/or alcohol during treatment with triamcinolone. Talk to your doctor if you have any questions or concerns. You should seek immediate medical attention if you experience any unusual bleeding or bruising, or have other signs and symptoms of bleeding such as dizziness; lightheadedness; red or black, tarry stools; coughing up or vomiting fresh or dried blood that looks like coffee grounds; severe headache; and weakness. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

Furosemide and ethanol (alcohol) may have additive effects in lowering your blood pressure. You may experience headache, dizziness, lightheadedness, fainting, and/or changes in pulse or heart rate. These side effects are most likely to be seen at the beginning of treatment, following a dose increase, or when treatment is restarted after an interruption. Let your doctor know if you develop these symptoms and they do not go away after a few days or they become troublesome. Avoid driving or operating hazardous machinery until you know how the medications affect you, and use caution when getting up from a sitting or lying position. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

The use of loop diuretics is contraindicated in patients with anuria.

Loop diuretic therapy should be initiated in the hospital under strict observation in patients with liver cirrhosis and ascites. Sudden alteration of fluid and electrolyte balance may precipitate hepatic encephalopathy and coma in such patients, who are also at increased risk for the development of hypokalemia. Supplemental potassium and/or concomitant use of an aldosterone antagonist or potassium-sparing agent may help prevent hypokalemia and metabolic alkalosis. Loop diuretics should be withheld in patients with hepatic coma until the condition improves.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

Tinnitus and hearing loss, both reversible and permanent, have been reported with the use of loop diuretics. Ototoxic effects have generally been associated with rapid intravenous or intramuscular injection, severe renal impairment, unusually high dosages (i.e. several times the usual recommended dosages), and/or concomitant use of other ototoxic agents. Therapy with loop diuretics 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. High-dose parenteral therapy should be administered as controlled infusion.

Loop diuretic therapy should be initiated in the hospital under strict observation in patients with liver cirrhosis and ascites. Sudden alteration of fluid and electrolyte balance may precipitate hepatic encephalopathy and coma in such patients, who are also at increased risk for the development of hypokalemia. Supplemental potassium and/or concomitant use of an aldosterone antagonist or potassium-sparing agent may help prevent hypokalemia and metabolic alkalosis. Loop diuretics should be withheld in patients with hepatic coma until the condition improves.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The immunosuppressant and anti-inflammatory effects of corticosteroids, particularly at higher dosages, may reduce resistance to infectious agents, increase the risk of disseminated infections, mask symptoms of infection, and reactivate or exacerbate latent/resolved infections; fatal cases have been reported. Avoid use of corticosteroids in patients with cerebral malaria. Screen patients for active (or history of) infection with tuberculosis, hepatitis, varicella, measles, and amebiasis, especially prior to prolonged treatment. Closely monitor for reactivation of latent infections; chemoprophylaxis may be required. In general, corticosteroids should not be used in patients with active infections, especially systemic fungal infections, unless medically necessary to control drug reactions. 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 loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The use of certain parenteral formulations of dexamethasone, hydrocortisone, methylprednisolone, prednisolone and triamcinolone is considered by the drug manufacturers to be contraindicated in neonates, particularly premature infants and infants of low birth weight. Some formulations of these drugs contain benzyl alcohol which, when used in bacteriostatic saline intravascular flush and endotracheal tube lavage solutions, has been associated with fatalities and severe respiratory and metabolic complications in low-birth-weight premature infants. However, many experts feel that, in the absence of benzyl alcohol-free equivalents, the amount of the preservative present in these formulations should not necessarily preclude their use if they are clearly indicated. The American Academy of Pediatrics considers benzyl alcohol in low doses (such as when used as a preservative in some medications) to be safe for newborns. Continuous infusions of high dosages of medications containing benzyl alcohol may, however, cause toxicity and should be avoided if possible.

Impaired effectiveness and possible delayed excretion of loop diuretics may occur in patients with severe renal dysfunction. These individuals may require high dosages that are associated with an increased risk of electrolyte abnormalities (hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia, hypocalcemia) and ototoxicity (tinnitus, hearing loss). Therapy with loop diuretics should be administered cautiously in patients with significantly impaired renal function. Prolongation of the dosing intervals may be appropriate to prevent drug accumulation. The patient should be monitored closely for the signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Excessive diuresis should be avoided as it may induce dehydration and hypovolemia, which can result in an abrupt reduction in glomerular filtration and renal blood flow. If increasing azotemia and oliguria occur during treatment of severe progressive renal disease, or if renal function becomes progressively worse as indicated by rising BUN or serum creatinine levels, an interruption or discontinuation of therapy should be considered.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

The use of loop diuretics, particularly at high dosages or during chronic therapy, is commonly associated with loss of electrolytes, including potassium, sodium, chloride, magnesium, and calcium. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Excessive diuresis, as indicated by rapid weight loss, may induce dehydration and hypovolemia, which can result in acute hypotension, orthostasis, circulatory collapse, vascular thrombosis and embolism, and abrupt reduction in glomerular filtration and renal blood flow. Severe dehydration is most likely to occur in the elderly and patients under prolonged sodium restriction. Therapy with loop diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected before initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since the development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower diuretic dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Similarly, to prevent excessive dehydration and hyponatremia, sodium intake should be liberalized if clinically feasible.

Loop diuretics may cause hyperglycemia, glycosuria, and alterations in glucose tolerance tests. Rarely, precipitation of diabetes mellitus has been reported. Therapy with loop diuretics 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 therapy, and their antidiabetic regimen adjusted accordingly.

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

The use of loop diuretics can cause urinary retention in patients with bladder emptying disorders, prostate hyperplasia, narrowing of the urethra. Caution and monitoring is recommended when using loop diuretics in these patients, especially when commencing therapy.

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.

The use of loop diuretics can cause urinary retention in patients with bladder emptying disorders, prostate hyperplasia, narrowing of the urethra. Caution and monitoring is recommended when using loop diuretics in these patients, especially when commencing therapy.

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 cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Large doses of any corticosteroid can demonstrate these effects, particularly if given for longer 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.

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.

Loop diuretics may cause hyperglycemia, glycosuria, and alterations in glucose tolerance tests. Rarely, precipitation of diabetes mellitus has been reported. Therapy with loop diuretics 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 therapy, and their antidiabetic regimen adjusted accordingly.

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 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 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. Large doses of any corticosteroid can demonstrate these effects, particularly if given for longer 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.

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.

Loop diuretics may decrease the rate of uric acid excretion. Hyperuricemia can occur but is usually asymptomatic and rarely leads to clinical gout except in patients with a history of gout or chronic renal failure. Therapy with loop diuretics should be administered cautiously in such patients.

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 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.

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

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

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 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. Large doses of any corticosteroid can demonstrate these effects, particularly if given for longer 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.

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 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 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.

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

The use of furosemide has been associated with exacerbation or activation of systemic lupus erythematosus. Therapy with furosemide should be administered cautiously in patients with a history of lupus.

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.

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.

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.

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.

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.

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

Corticosteroids may cause hypernatremia, hypokalemia, fluid retention, and elevation in blood pressure. Large doses of any corticosteroid can demonstrate these effects, particularly if given for longer 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.

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.

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.

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.

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.

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 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.