Can you take Dexasone with Oliceridine?

The dexAMETHasone in Dexasone has a moderate potential interaction with Abnormal Glucose Tolerance.

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.

Oliceridine has a major potential interaction with Acute Alcohol Intoxication.

The use of opiate agonists is contraindicated in patients with acute alcohol intoxication exhibiting depressed vital signs. The central nervous system depressant effects of opiate agonists may be additive with those of alcohol. Severe respiratory depression and death may occur. Therapy with opiate agonists should be administered cautiously in patients who might be prone to acute alcohol intake.

Oliceridine has a moderate potential interaction with Adrenal Insufficiency.

Patients with Addison's disease may have increased risk of respiratory depression and prolonged CNS depression associated with the use of narcotic (opioid) analgesic agents. Conversely, these agents may cause or potentiate adrenal insufficiency. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with adrenocortical insufficiency. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

The dexAMETHasone in Dexasone has a moderate potential interaction with Adrenal Tumor.

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

Oliceridine has a major potential interaction with Alcoholism.

Opiate agonists have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use. Abrupt cessation, reduction in dosage, or administration of an opiate antagonist such as naloxone may precipitate withdrawal symptoms. In patients who have developed tolerance to an opiate agonist, overdosage can still produce respiratory depression and death, and cross-tolerance usually will occur with other agents in the class. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opiate agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opiate therapy should be undertaken gradually using a dosage-tapering schedule.

Oliceridine has a major potential interaction with Altered Consciousness.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

Oliceridine has a major potential interaction with Asphyxia.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

Oliceridine has a major potential interaction with Brain Tumor.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

Oliceridine has a major potential interaction with Brain Tumor.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

The dexAMETHasone in Dexasone has a moderate potential interaction with Cataract.

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.

Oliceridine has a major potential interaction with Cerebral Vascular Disorder.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

Oliceridine has a major potential interaction with Cerebral Vascular Disorder.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

The dexAMETHasone in Dexasone has a moderate potential interaction with Cirrhosis.

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.

Oliceridine has a major potential interaction with Constipation.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Oliceridine has a major potential interaction with Dehydration.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

The dexAMETHasone in Dexasone has a moderate potential interaction with Depression.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Diabetes Mellitus.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Diverticulitis.

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.

Oliceridine has a major potential interaction with Drug Dependence.

Opiate agonists have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use. Abrupt cessation, reduction in dosage, or administration of an opiate antagonist such as naloxone may precipitate withdrawal symptoms. In patients who have developed tolerance to an opiate agonist, overdosage can still produce respiratory depression and death, and cross-tolerance usually will occur with other agents in the class. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opiate agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opiate therapy should be undertaken gradually using a dosage-tapering schedule.

The dexAMETHasone in Dexasone has a moderate potential interaction with Electrolyte Abnormalities.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Fluid Retention.

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.

Oliceridine has a major potential interaction with Gastrointestinal Obstruction.

Opioid analgesics are contraindicated in patients with known or suspected gastrointestinal obstruction, including paralytic ileus.

Oliceridine has a major potential interaction with Gastrointestinal Obstruction.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

The dexAMETHasone in Dexasone has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

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.

Oliceridine has a major potential interaction with Head Injury.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

Oliceridine has a major potential interaction with Head Injury.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

The dexAMETHasone in Dexasone has a moderate potential interaction with Heart Attack.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Heart Failure.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Herpetic Keratitis.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with High Blood Pressure.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with High Cholesterol.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with History, Peptic Ulcer.

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 dexAMETHasone in Dexasone has a moderate potential interaction with History, Thrombotic/Thromboembolic Disorder.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with History, Tuberculosis.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Hyperadrenocorticism.

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

The dexAMETHasone in Dexasone has a moderate potential interaction with Hyperaldosteronism.

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

The dexAMETHasone in Dexasone has a moderate potential interaction with Hypernatremia.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Hypocalcemia.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Hypokalemia.

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.

Oliceridine has a major potential interaction with Hypotension.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

The dexAMETHasone in Dexasone has a major potential interaction with Infection.

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.

Oliceridine has a major potential interaction with Inflammatory Bowel Disease.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Oliceridine has a major potential interaction with Intestinal Anastomoses.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

The dexAMETHasone in Dexasone has a moderate potential interaction with Intestinal Anastomoses.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Liver Disease.

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 dexAMETHasone in Dexasone has a moderate potential interaction with Myasthenia Gravis.

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 dexAMETHasone in Dexasone has a moderate potential interaction with Myoneural Disorder.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Myopathy.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Osteoporosis.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Peptic Ulcer.

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 dexAMETHasone in Dexasone has a moderate potential interaction with Post MI Syndrome.

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.

The dexAMETHasone in Dexasone has a major potential interaction with Prematurity/Underweight in Infancy.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Psychosis.

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.

Oliceridine has a major potential interaction with Pulmonary Impairment.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The dexAMETHasone in Dexasone has a moderate potential interaction with Renal Dysfunction.

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.

Oliceridine has a major potential interaction with Respiratory Arrest.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The dexAMETHasone in Dexasone has a moderate potential interaction with Seizures.

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.

Oliceridine has a moderate potential interaction with Seizures.

Narcotic (opioid) analgesic agents may increase the frequency of seizures in patients with seizure disorders, may increase the risk of seizures occurring in other clinical settings associated with seizures, and, at higher dosages, have been reported to induce seizures in patients without history of seizures. Patients with history of seizure disorders should be regularly evaluated for worsened seizure control during therapy. Prolonged meperidine use may increase the risk of toxicity (e.g., seizures) from the accumulation of the active metabolite (normeperidine).

Oliceridine has a major potential interaction with Shock.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

The dexAMETHasone in Dexasone has a moderate potential interaction with Strongyloidiasis.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Systemic Sclerosis.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Thrombotic/Thromboembolic Disorder.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Tuberculosis, Latent.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Ulcerative Colitis.

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.

The dexAMETHasone in Dexasone has a moderate potential interaction with Underactive Thyroid.

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.

Oliceridine has a moderate potential interaction with Urinary Retention.

Narcotic (opioid) analgesic agents may inhibit the urinary voiding reflex and increase the tone of the vesical sphincter in the bladder. Acute urinary retention requiring catheterization may occur, particularly in patients with prostatic hypertrophy or urethral stricture and in older adult patients. These agents may also decrease urine production via direct effects on the kidney and central stimulation of the release of vasopressin. Therapy with opioids should be administered cautiously in patients with or predisposed to urinary retention and/or oliguria. The effects on smooth muscle tone appear to be the most pronounced with morphine.