Interactions between Mellaril and Nalbuphine

The thioridazine in Mellaril has a major potential interaction with Abnormal Electrocardiogram.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

The thioridazine in Mellaril has a major potential interaction with Acute Alcohol Intoxication.

Phenothiazines are contraindicated in the presence of large amounts of central nervous system depressants such as alcohol. The risk of suicide and the danger of overdose may be increased in patients who use alcohol excessively. Phenothiazines should be used with caution in patients experiencing alcohol withdrawal.

Nalbuphine has a major potential interaction with Acute Alcohol Intoxication.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Nalbuphine 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 thioridazine in Mellaril has a major potential interaction with Alcoholism.

Phenothiazines are contraindicated in the presence of large amounts of central nervous system depressants such as alcohol. The risk of suicide and the danger of overdose may be increased in patients who use alcohol excessively. Phenothiazines should be used with caution in patients experiencing alcohol withdrawal.

Nalbuphine has a major potential interaction with Alcoholism.

Opioid partial agonists have the potential to cause dependence and abuse, particularly in patients with a history of drug abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use, and abrupt cessation or a significant reduction in dosage may precipitate withdrawal symptoms. Because of their opioid antagonistic effect, withdrawal symptoms may also occur if opioid partial agonists are administered to patients with an opioid dependence or in whom substantial amounts of narcotics have recently been administered. Therapy with opioid partial agonists is not recommended in patients who are physically dependent on narcotics. 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 opioid partial 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 opioid therapy should be undertaken gradually using a dosage-tapering schedule.

The thioridazine in Mellaril has a major potential interaction with Altered Consciousness.

The use of phenothiazines is contraindicated in comatose patients and patients with severe central nervous system depression. Phenothiazines may potentiate the CNS and respiratory depression in these patients.

Nalbuphine has a major potential interaction with Altered Consciousness.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

The thioridazine in Mellaril has a major potential interaction with Arrhythmia.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

The thioridazine in Mellaril has a major potential interaction with Arrhythmia.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Nalbuphine has a major potential interaction with Asphyxia.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Nalbuphine has a moderate potential interaction with Biliary Obstruction.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

The thioridazine in Mellaril has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

Phenothiazines may cause hematologic toxicity. In patients with preexisting blood dyscrasias, bone marrow suppression, or a history of drug-induced leukopenia or neutropenia, phenothiazines should not be used or are contraindicated. Complete blood counts should be regularly monitored in patients with risk factors for blood dyscrasias. If white blood cell counts indicate cellular depression, discontinue treatment and institute appropriate therapy.

Nalbuphine has a major potential interaction with Brain Tumor.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Nalbuphine has a major potential interaction with Brain Tumor.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

The thioridazine in Mellaril has a moderate potential interaction with Breast Cancer.

The chronic use of phenothiazines is associated with persistent elevations in prolactin levels. The clinical significance in patients with a history of breast cancer is unknown and should be considered prior to therapy; approximately one-third of human breast cancers are thought to be prolactin-dependent. Chronic administration of neuroleptic drugs has been associated with mammary tumorigenesis in animal studies; however, evidence is inconclusive in humans.

The thioridazine in Mellaril has a major potential interaction with Cardiovascular Conditions and Disorders.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The thioridazine in Mellaril has a moderate potential interaction with Central Nervous System Disorders.

Phenothiazines can lower the seizure threshold. Caution is recommended during administration in patients with a history of convulsive disorders or EEG abnormalities. Anticonvulsant therapy should be maintained or adequately adjusted during phenothiazine treatment.

Nalbuphine has a major potential interaction with Cerebral Vascular Disorder.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Nalbuphine has a major potential interaction with Cerebral Vascular Disorder.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

The thioridazine in Mellaril has a major potential interaction with Cerebrovascular Insufficiency.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Nalbuphine 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.

The thioridazine in Mellaril has a major potential interaction with Dementia.

Antipsychotic drugs are not approved for the treatment of patients with dementia-related psychosis. Older patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death; although the causes were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. A causal relationship with antipsychotic use has not been established. In controlled trials in older patients with dementia-related psychosis, patients randomized to risperidone, aripiprazole, and olanzapine had higher incidence of cerebrovascular adverse events (e.g., stroke, transient ischemic attack), including fatalities, compared to patients treated with placebo.

The thioridazine in Mellaril has a major potential interaction with Diarrhea.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Nalbuphine has a major potential interaction with Drug Dependence.

Opioid partial agonists have the potential to cause dependence and abuse, particularly in patients with a history of drug abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use, and abrupt cessation or a significant reduction in dosage may precipitate withdrawal symptoms. Because of their opioid antagonistic effect, withdrawal symptoms may also occur if opioid partial agonists are administered to patients with an opioid dependence or in whom substantial amounts of narcotics have recently been administered. Therapy with opioid partial agonists is not recommended in patients who are physically dependent on narcotics. 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 opioid partial 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 opioid therapy should be undertaken gradually using a dosage-tapering schedule.

The thioridazine in Mellaril has a major potential interaction with Electrolyte Abnormalities.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Nalbuphine has a moderate potential interaction with Gallbladder Disease.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

Nalbuphine 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.

Nalbuphine has a major potential interaction with Gastrointestinal Obstruction.

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

Nalbuphine has a major potential interaction with Head Injury.

The hypoventilation associated with administration of opioid partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opioid partial agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opioid partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Nalbuphine has a major potential interaction with Head Injury.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

The thioridazine in Mellaril has a major potential interaction with High Blood Pressure.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The thioridazine in Mellaril has a major potential interaction with History - Cerebrovascular Disease.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The thioridazine in Mellaril has a major potential interaction with History - Myocardial Infarction.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The thioridazine in Mellaril has a major potential interaction with Hypokalemia.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

The thioridazine in Mellaril has a major potential interaction with Hypotension.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Nalbuphine has a major potential interaction with Infectious Gastroenteritis.

Narcotic (opioid) analgesic agents may prolong and/or worsen diarrhea associated with organisms that invade the intestinal mucosa, such as toxigenic Escherichia coli, Salmonella, Shigella, and pseudomembranous colitis due to broad-spectrum antibiotics. These agents decrease gastrointestinal motility, which may delay the excretion of infective gastroenteric organisms and/or their toxins. Other symptoms and complications such as fever, shedding of organisms, and extraintestinal illness may also be increased or prolonged. Therapy with opioids should be avoided or administered cautiously in patients with infectious diarrhea, particularly that due to pseudomembranous enterocolitis or enterotoxin-producing bacteria or if accompanied by high fever, pus, or blood in the stool.

Nalbuphine 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.

Nalbuphine 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.

Nalbuphine has a major potential interaction with Ischemic Heart Disease.

Opioid partial agonists may increase systemic and pulmonary arterial pressure and systemic vascular resistance, particularly when given by IV administration. Data are available for pentazocine and butorphanol. Therapy with opioid partial agonists should be administered cautiously and only if the benefit justifies the risk in patients with acute myocardial infarction (especially if accompanied by hypertension or left ventricular failure) or coronary insufficiency.

The thioridazine in Mellaril has a major potential interaction with Liver Disease.

Therapy with phenothiazines should be administered cautiously or are contraindicated in patients with preexisting liver disease or with a history of jaundice due to phenothiazine hypersensitivity. Patients with a history of hepatic encephalopathy due to cirrhosis may have increased sensitivity to the central nervous system effects of some phenothiazines (e.g., chlorpromazine). Treatment should be discontinued if jaundice occurs.

Nalbuphine has a moderate potential interaction with Liver Disease.

Narcotic (opioid) analgesic agents are extensively metabolized by the liver, and several of them (e.g., codeine, hydrocodone, meperidine, methadone, morphine, propoxyphene) have active metabolites that are further converted to inactive substances. The serum concentrations of these agents and their metabolites may be increased and the half-lives prolonged in patients with impaired hepatic function. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with liver disease. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

The thioridazine in Mellaril has a major potential interaction with Magnesium Imbalance.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

The thioridazine in Mellaril has a moderate potential interaction with Neuroleptic Malignant Syndrome.

Therapy with phenothiazines may precipitate or aggravate a potentially fatal symptom complex known as neuroleptic malignant syndrome (NMS). Treatment should not be initiated in patients with active NMS, and should be immediately discontinued if currently administered in such patients. In patients with a history of NMS, introduction or reintroduction of phenothiazines should be carefully considered, since NMS may recur.

Nalbuphine has a moderate potential interaction with Pancreatitis.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

The thioridazine in Mellaril has a major potential interaction with Pheochromocytoma.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Nalbuphine has a major potential interaction with Prematurity/Underweight in Infancy.

The use of narcotic (opioid) analgesic agents is contraindicated in premature infants. These agents may cross the immature blood-brain barrier to a greater extent than in adults, resulting in disproportionate respiratory depression.

Nalbuphine has a major potential interaction with Pulmonary Impairment.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

Nalbuphine has a moderate potential interaction with Renal Dysfunction.

Although narcotic (opioid) analgesic agents are generally metabolized by the liver, renal impairment can alter the elimination of these agents and their metabolites (some of which are pharmacologically active), resulting in drug accumulation and increased risk of toxicity. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with significantly impaired renal function. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

The thioridazine in Mellaril has a major potential interaction with Respiratory Arrest.

The use of phenothiazines is contraindicated in comatose patients and patients with severe central nervous system depression. Phenothiazines may potentiate the CNS and respiratory depression in these patients.

Nalbuphine has a major potential interaction with Respiratory Arrest.

Opioid partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opioid partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; 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 opioid partial 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 routes are used. Naloxone may be administered to reverse clinically significant respiratory depression.

The thioridazine in Mellaril has a moderate potential interaction with Seizures.

Phenothiazines can lower the seizure threshold. Caution is recommended during administration in patients with a history of convulsive disorders or EEG abnormalities. Anticonvulsant therapy should be maintained or adequately adjusted during phenothiazine treatment.

Nalbuphine 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).

Nalbuphine 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.

The thioridazine in Mellaril has a major potential interaction with Valvular Heart Disease.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.