Interactions between Buprenorphine and Hydrostat IR

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Adrenal Insufficiency.

Buprenorphine should be used with caution in patients with adrenal insufficiency (e.g., Addison's disease). Cases of adrenal insufficiency have been reported with opioid use, more often with use beyond 1 month. If adrenal insufficiency has occurred with a particular opioid, other opioids may be tried as some cases reported use of a different opioid without recurrence of adrenal insufficiency. Available information does not identify which opioids are more likely to be associated with adrenal insufficiency.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a major potential interaction with Alcoholism.

Buprenorphine exposes users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing buprenorphine analgesics, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed buprenorphine analgesics but use in such patients requires intensive counseling about the risks and proper use of buprenorphine, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered. All patients using buprenorphine for opioid dependence should be monitored for progression of opioid use disorder and addictive behaviors.

Buprenorphine is sought for nonmedical use (including by individuals with opioid use disorder) and is subject to criminal diversion. These risks should be considered when prescribing or dispensing buprenorphine. Strategies to reduce such risks should be used (e.g., prescribe smallest appropriate quantity, careful storage during use, proper disposal of unused drug).

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a major potential interaction with Altered Consciousness.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Arrhythmia.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

The HYDROmorphone in Hydrostat IR has a moderate potential interaction with Arrhythmia.

Opiate agonists have cholinergic activity. Large doses and/or rapid intravenous administration may produce bradycardia and arrhythmias via stimulation of medullary vagal nuclei. Therapy with opiate agonists should be administered cautiously in patients with a history of arrhythmias. Clinical monitoring of cardiovascular status is recommended during therapy.

Buprenorphine has a major potential interaction with Asphyxia.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Benign Prostatic Hyperplasia.

Buprenorphine should be used with caution in patients with prostatic hypertrophy or urethral stricture. Urinary retention has been reported with buprenorphine.

Buprenorphine 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 HYDROmorphone in Hydrostat IR 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.

Buprenorphine 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.

Buprenorphine has a major potential interaction with Brain Tumor.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

The HYDROmorphone in Hydrostat IR 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 HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a major potential interaction with Cachexia.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine 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.

Buprenorphine has a major potential interaction with Cerebral Vascular Disorder.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

The HYDROmorphone in Hydrostat IR 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 HYDROmorphone in Hydrostat IR 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.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a major potential interaction with Cor Pulmonale.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Dehydration.

Buprenorphine may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating buprenorphine. In patients with circulatory shock, buprenorphine may cause vasodilation that can further reduce cardiac output and blood pressure; buprenorphine analgesics should be avoided in patients with circulatory shock.

Buprenorphine has a major potential interaction with Depression.

Buprenorphine exposes users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing buprenorphine analgesics, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed buprenorphine analgesics but use in such patients requires intensive counseling about the risks and proper use of buprenorphine, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered. All patients using buprenorphine for opioid dependence should be monitored for progression of opioid use disorder and addictive behaviors.

Buprenorphine is sought for nonmedical use (including by individuals with opioid use disorder) and is subject to criminal diversion. These risks should be considered when prescribing or dispensing buprenorphine. Strategies to reduce such risks should be used (e.g., prescribe smallest appropriate quantity, careful storage during use, proper disposal of unused drug).

Buprenorphine has a major potential interaction with Drug Dependence.

Buprenorphine exposes users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing buprenorphine analgesics, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed buprenorphine analgesics but use in such patients requires intensive counseling about the risks and proper use of buprenorphine, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered. All patients using buprenorphine for opioid dependence should be monitored for progression of opioid use disorder and addictive behaviors.

Buprenorphine is sought for nonmedical use (including by individuals with opioid use disorder) and is subject to criminal diversion. These risks should be considered when prescribing or dispensing buprenorphine. Strategies to reduce such risks should be used (e.g., prescribe smallest appropriate quantity, careful storage during use, proper disposal of unused drug).

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine 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.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a major potential interaction with Gastrointestinal Obstruction.

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

The HYDROmorphone in Hydrostat IR has a major potential interaction with Gastrointestinal Obstruction.

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

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine 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.

Buprenorphine has a major potential interaction with Head Injury.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

The HYDROmorphone in Hydrostat IR 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 HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Heart Failure.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

Buprenorphine has a moderate potential interaction with Hypokalemia.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Hypotension.

Buprenorphine may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating buprenorphine. In patients with circulatory shock, buprenorphine may cause vasodilation that can further reduce cardiac output and blood pressure; buprenorphine analgesics should be avoided in patients with circulatory shock.

The HYDROmorphone in Hydrostat IR 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.

The HYDROmorphone in Hydrostat IR 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.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Liver Disease.

Buprenorphine is metabolized in the liver, and its activity may be increased and/or extended in patients with impaired liver function.
-Buccal film or sublingual tablets: A dose adjustment is recommended for patients with severe liver dysfunction; patients with moderate or severe liver dysfunction should be periodically assessed for signs/symptoms of toxicity or overdose caused by increased buprenorphine levels.
-IM/IV injection: This product should be administered with caution in patients with severe liver dysfunction.
-Subcutaneous injection or subdermal implant: The effect of liver dysfunction on the pharmacokinetics of this product has not been studied. Due to the long-acting nature of the subcutaneous injection, dosage adjustments are not rapidly reflected in plasma buprenorphine levels. Because buprenorphine levels cannot be rapidly adjusted when using the subcutaneous injection, and because the subdermal implant cannot be titrated, patients with preexisting moderate to severe liver dysfunction are not candidates for treatment with these products.
-Transdermal system: This product has not been evaluated in patients with severe liver dysfunction; because this product is only intended for 7-day application, use of an alternate analgesic that may permit more flexibility with dosing in these patients should be considered.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Long QT Syndrome.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

Buprenorphine has a moderate potential interaction with Magnesium Imbalance.

Thorough QT studies with buprenorphine have shown QT prolongation 15 msec or less; this QTc prolongation effect does not appear to be mediated by hERG channels. Based on these 2 findings, buprenorphine is unlikely to be proarrhythmic when used alone in patients without risk factors. However, these observations should be considered in clinical decisions when prescribing buprenorphine to patients with risk factors (e.g., hypokalemia, bradycardia, recent conversion from atrial fibrillation, congestive heart failure, baseline QT prolongation, subclinical long-QT syndrome, severe hypomagnesemia).

Buprenorphine 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 HYDROmorphone in Hydrostat IR 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 HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a major potential interaction with Psychiatric Disorders.

Buprenorphine exposes users to the risks of addiction, abuse, and misuse. Each patient's risk should be assessed before prescribing buprenorphine analgesics, and all patients should be monitored regularly for development of such behaviors and conditions. Risks are increased in patients with personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression); the potential for such risks should not prevent proper pain management in any given patient. Patients at increased risk may be prescribed buprenorphine analgesics but use in such patients requires intensive counseling about the risks and proper use of buprenorphine, as well as intensive monitoring for signs of addiction, abuse, and misuse; prescribing naloxone for the emergency treatment of opioid overdose should be considered. All patients using buprenorphine for opioid dependence should be monitored for progression of opioid use disorder and addictive behaviors.

Buprenorphine is sought for nonmedical use (including by individuals with opioid use disorder) and is subject to criminal diversion. These risks should be considered when prescribing or dispensing buprenorphine. Strategies to reduce such risks should be used (e.g., prescribe smallest appropriate quantity, careful storage during use, proper disposal of unused drug).

Buprenorphine has a major potential interaction with Pulmonary Impairment.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Renal Dysfunction.

Buprenorphine is substantially excreted by the kidney; the risk of adverse reactions to this drug may be greater in patients with impaired renal function. Buprenorphine has not been studied in patients with renal dysfunction; caution is recommended when used in patients with severe renal dysfunction.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a major potential interaction with Respiratory Arrest.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a major potential interaction with Scoliosis.

Buprenorphine analgesics are contraindicated in patients with significant respiratory depression. Serious, life-threatening, or fatal respiratory depression may occur with buprenorphine. Patients should be monitored closely for respiratory depression, especially during initiation of therapy or after a dosage increase. Prescribing naloxone for the emergency treatment of opioid overdose should be considered; however, naloxone may not be effective in reversing respiratory depression produced by buprenorphine due to its slow rate of dissociation from mu receptors.

The use of buprenorphine analgesics in patients with acute or severe bronchial asthma in an unmonitored setting or without resuscitative equipment is contraindicated. Buprenorphine-treated patients with significant chronic obstructive pulmonary disease or cor pulmonale, and those with substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression are at increased risk of decreased respiratory drive (including apnea), even at recommended dosages of buprenorphine analgesics; buprenorphine for opioid dependence should be used with caution in such patients with compromised respiratory function. In patients who may be susceptible to the intracranial effects of carbon dioxide (CO2) retention (e.g., those with evidence of increased intracranial pressure or brain tumors), buprenorphine analgesics may reduce respiratory drive, and the resulting CO2 retention can further increase intracranial pressure; these patients should be monitored for signs of sedation and respiratory depression, especially when starting therapy. Buprenorphine for opioid dependence should be used with caution in patients with head injury, intracranial lesions, and other circumstances where cerebrospinal pressure may be increased. Opioids may obscure the clinical course in a patient with a head injury; use of buprenorphine analgesics should be avoided in patients with impaired consciousness or coma.

Life-threatening respiratory depression is more likely to occur in older adult, cachectic, or debilitated patients as they may have altered pharmacokinetics (or altered clearance) compared to younger, healthier patients. These patients should be monitored closely, especially when starting and titrating buprenorphine analgesics and when coadministering with other drugs that depress respiration; alternatively, the use of nonopioid analgesics should be considered. Buprenorphine should be used with caution in patients with kyphoscoliosis.

Buprenorphine 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).

The HYDROmorphone in Hydrostat IR 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).

The HYDROmorphone in Hydrostat IR 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.

Buprenorphine has a moderate potential interaction with Shock.

Buprenorphine may cause severe hypotension (including orthostatic hypotension, syncope) in ambulatory patients. Risk is increased in patients whose ability to maintain blood pressure has already been compromised by reduced blood volume or coadministration of certain CNS depressant drugs; these patients should be monitored for signs of hypotension after starting or titrating buprenorphine. In patients with circulatory shock, buprenorphine may cause vasodilation that can further reduce cardiac output and blood pressure; buprenorphine analgesics should be avoided in patients with circulatory shock.

Buprenorphine has a moderate potential interaction with Urinary Retention.

Buprenorphine should be used with caution in patients with prostatic hypertrophy or urethral stricture. Urinary retention has been reported with buprenorphine.

The HYDROmorphone in Hydrostat IR 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.