HYDROMORPHONE HYDROCHLORIDE Drug Interactions
Also known as: Hydromorphone Hydrochloride
HYDROMORPHONE HYDROCHLORIDE (brand name: Hydromorphone Hydrochloride) is a Opioid Analgesics. INDICATIONS AND USAGE Hydromorphone Hydrochloride Injection is indicated for the relief of moderate to severe pain such as that due to: surgery, cancer, trauma (soft tissue and bone), biliary colic, myocardial infarction, burns, renal colic.HYDROMORPHONE HYDROCHLORIDE has 17 documented drug interactions in our database, including 4 contraindicated, 13 major, 0 moderate, and 0 minor interactions.
4
Contraindicated
13
Major
0
Moderate
0
Minor
Patients may experience profound sedation, respiratory depression, coma, and death. Other symptoms can include severe psychomotor impairment, hypotension, and decreased level of consciousness. The onset of these effects can be rapid and life-threatening.
Mechanism
Both hydromorphone, an opioid agonist, and diazepam, a benzodiazepine, are central nervous system (CNS) depressants. Their co-administration leads to an additive depressant effect on the CNS, particularly on the respiratory drive, leading to profound sedation and respiratory depression. This synergistic action occurs through distinct but converging pathways that reduce neuronal excitability.
Clinical Management
Concomitant use of opioids and benzodiazepines should be avoided whenever possible due to the high risk of severe adverse outcomes, including death. If co-administration is absolutely necessary, use the lowest effective doses for the shortest possible duration, monitor patients closely for respiratory depression and sedation, and ensure naloxone is readily available. Consider alternative treatments that do not involve co-prescribing these classes.
Concomitant use can lead to severe and potentially fatal adverse effects, including profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, bradycardia, hypotension, and diminished protective reflexes. The risk of overdose is significantly increased.
Mechanism
Both hydromorphone (an opioid agonist) and oxazepam (a benzodiazepine) are central nervous system (CNS) depressants. Their co-administration leads to an additive pharmacological effect on GABAergic neurotransmission and opioid receptors, resulting in profound CNS depression. This synergistic depression significantly impairs respiratory drive, leading to hypoventilation and respiratory arrest.
Clinical Management
Concomitant use of hydromorphone and oxazepam is generally contraindicated due to the high risk of respiratory depression and death, as highlighted by an FDA Black Box Warning. If co-administration is unavoidable, patients must be closely monitored for signs of respiratory depression and sedation, with reduced dosages of one or both agents. Naloxone and flumazenil should be readily available, and alternative therapies should be considered.
The combination significantly increases the risk of severe adverse events including profound sedation, respiratory depression, coma, and death. Patients may experience extreme drowsiness, confusion, dizziness, slowed or stopped breathing, and unresponsiveness.
Mechanism
Both hydromorphone (an opioid agonist) and triazolam (a benzodiazepine) are central nervous system (CNS) depressants. Their co-administration leads to additive pharmacodynamic effects, primarily by enhancing GABAergic neurotransmission (benzodiazepine) and agonizing mu-opioid receptors (opioid), resulting in profound CNS and respiratory depression.
Clinical Management
Concomitant use is contraindicated. If co-administration is unavoidable, the lowest effective doses should be used for the shortest possible duration, with close monitoring for respiratory depression and sedation. Naloxone should be readily available for opioid overdose reversal, and flumazenil for benzodiazepine reversal, though the latter is generally not recommended for benzodiazepine overdose due to seizure risk.
The primary clinical effects include profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, hypoxia, and hypotension. These effects can be rapid in onset and life-threatening.
Mechanism
Hydromorphone, an opioid agonist, binds to mu-opioid receptors in the central nervous system (CNS), leading to CNS depression, including respiratory depression and sedation. Chlordiazepoxide, a benzodiazepine, enhances the effect of the inhibitory neurotransmitter GABA at GABA-A receptors, also resulting in CNS depression. The co-administration of these two CNS depressants produces additive and synergistic effects on GABAergic and opioid pathways, significantly increasing the risk of severe CNS and respiratory depression.
Clinical Management
Concomitant use of hydromorphone and chlordiazepoxide is generally contraindicated due to the high risk of severe adverse outcomes, as highlighted by an FDA Black Box Warning. If co-administration is absolutely unavoidable, use the lowest effective doses for the shortest possible duration, and closely monitor patients for signs of respiratory depression and sedation. Consider alternative therapies that do not involve co-prescribing opioids and benzodiazepines.
Patients may experience profound sedation, respiratory depression, coma, and even death. Other potential effects include dizziness, confusion, impaired psychomotor function, and hypotension. The risk is particularly elevated in elderly patients or those with pre-existing respiratory compromise.
Mechanism
Both hydromorphone, an opioid analgesic, and cyclobenzaprine, a centrally acting skeletal muscle relaxant, cause central nervous system (CNS) depression. When co-administered, their individual CNS depressant effects are additive, leading to an increased risk of severe adverse reactions. This additive effect primarily involves GABAergic potentiation and inhibition of neuronal excitability.
Clinical Management
Avoid concomitant use of hydromorphone and cyclobenzaprine if possible. If co-administration is necessary, use the lowest effective doses for the shortest duration possible, and closely monitor patients for signs of respiratory depression and sedation. Advise patients against operating heavy machinery or driving and educate them on the risks of CNS depression.
Patients may experience profound sedation, respiratory depression, hypotension, and psychomotor impairment. Symptoms can include excessive drowsiness, dizziness, confusion, difficulty breathing, and slowed or shallow respiration. The risk of falls and accidental injury is also significantly increased.
Mechanism
Both hydromorphone, an opioid agonist, and methocarbamol, a centrally acting muscle relaxant, exert depressant effects on the central nervous system (CNS). The concomitant use of these agents leads to an additive pharmacological effect, increasing the overall CNS depression. This synergy primarily affects neuronal activity in the brain and spinal cord.
Clinical Management
Avoid concomitant use of hydromorphone and methocarbamol if possible. If co-administration is unavoidable, initiate both medications at the lowest effective doses and titrate cautiously while closely monitoring for signs of CNS and respiratory depression. Educate patients and caregivers about the risks and instruct them to seek immediate medical attention if symptoms of severe sedation or respiratory compromise occur.
Patients are at significantly increased risk for profound sedation, respiratory depression, coma, and even death. Other clinical effects include dizziness, impaired psychomotor function, and hypotension. The risk is heightened by carisoprodol's active metabolite, meprobamate, which also contributes to CNS depression.
Mechanism
Hydromorphone, an opioid agonist, primarily exerts its effects through mu-opioid receptors, leading to central nervous system (CNS) depression. Carisoprodol, a centrally acting muscle relaxant, is metabolized to meprobamate, which has anxiolytic and sedative properties through GABA-A receptor potentiation. The co-administration results in additive CNS depressant effects.
Clinical Management
Concomitant use should generally be avoided due to the high risk of severe adverse effects. If co-administration is unavoidable, initiate with the lowest effective doses of both medications and monitor patients closely for signs of respiratory depression and sedation. Consider alternative non-opioid analgesics or non-benzodiazepine muscle relaxants.
The concurrent use of hydromorphone and baclofen significantly increases the risk of severe CNS depression, including profound sedation, respiratory depression, coma, and even death. Patients may experience impaired psychomotor function, dizziness, confusion, and hypotension.
Mechanism
Hydromorphone, an opioid agonist, produces central nervous system (CNS) depression by binding to mu-opioid receptors. Baclofen, a GABA-B receptor agonist, also causes CNS depression by inhibiting neuronal activity in the spinal cord and brain. The co-administration of these agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of hydromorphone and baclofen if possible. If co-administration is unavoidable, initiate treatment with the lowest effective doses of both drugs and titrate slowly while closely monitoring for signs of respiratory depression and sedation. Educate patients and caregivers on the symptoms of CNS depression and respiratory compromise.
Patients may experience profound sedation, respiratory depression (ranging from mild to life-threatening), hypotension, and psychomotor impairment. This can lead to decreased level of consciousness, dizziness, extreme drowsiness, and impaired coordination, increasing the risk of falls and accidents.
Mechanism
Both hydromorphone, an opioid agonist, and tizanidine, an alpha-2 adrenergic agonist, exert significant central nervous system (CNS) depressant effects. When co-administered, their individual depressant actions on the brain are additive, leading to an enhanced overall CNS depression.
Clinical Management
Avoid concomitant use if possible. If co-administration is necessary, initiate both drugs at the lowest effective doses and titrate slowly while closely monitoring for signs of CNS and respiratory depression. Educate patients about the risks and advise against driving or operating heavy machinery.
Patients may experience profound sedation, increased risk of respiratory depression, hypotension, and psychomotor impairment. This can lead to decreased level of consciousness, dizziness, confusion, and impaired coordination, significantly increasing the risk of falls and accidental injury.
Mechanism
Hydromorphone, an opioid analgesic, primarily acts on mu-opioid receptors in the central nervous system (CNS) to produce analgesia, sedation, and respiratory depression. Metaxalone, a centrally acting skeletal muscle relaxant, also exerts its effects through general CNS depression. The concurrent administration of these two agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concurrent use of hydromorphone and metaxalone if possible. If co-administration is unavoidable, initiate both medications at the lowest effective doses and titrate cautiously. Closely monitor patients for signs of CNS and respiratory depression, including sedation, respiratory rate, and oxygen saturation. Educate patients about the risks and advise against operating heavy machinery or driving.
Patients may experience profound sedation, dizziness, impaired psychomotor function, and increased risk of falls. The most serious clinical effect is respiratory depression, which can be life-threatening. Other effects include hypotension and coma.
Mechanism
Hydromorphone, an opioid analgesic, acts on mu-opioid receptors in the central nervous system (CNS) to produce analgesia, sedation, and respiratory depression. Chlorzoxazone, a centrally acting muscle relaxant, also exerts its effects within the CNS, primarily by inhibiting polysynaptic reflex arcs. The co-administration of these agents results in an additive depressant effect on the CNS.
Clinical Management
Concomitant use should be avoided if possible. If co-administration is necessary, initiate both drugs at the lowest effective doses and titrate carefully, monitoring closely for signs of CNS and respiratory depression. Educate patients about the risks and advise against operating machinery or driving.
Patients may experience profound sedation, respiratory depression, hypotension, coma, and even death. Impaired psychomotor function, dizziness, and confusion are also common. The risk of these adverse effects is significantly increased when both drugs are used concurrently.
Mechanism
Hydromorphone is an opioid analgesic that primarily acts on mu-opioid receptors in the central nervous system (CNS), leading to dose-dependent CNS depression, including respiratory depression and sedation. Orphenadrine is an anticholinergic agent with muscle relaxant properties that also exerts significant CNS depressant effects. The co-administration of these agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of hydromorphone and orphenadrine due to the high risk of additive CNS depression. If co-administration is unavoidable, reduce the starting dose of one or both medications, monitor patients closely for signs of respiratory depression and sedation, and limit the duration of therapy. Educate patients about the risks and advise them to avoid driving or operating heavy machinery.
The concurrent use of hydromorphone and lorazepam significantly increases the risk of severe respiratory depression, profound sedation, hypotension, psychomotor impairment, coma, and death. Patients may exhibit decreased level of consciousness, bradycardia, pinpoint pupils, and hypoventilation. The FDA has issued a Black Box Warning highlighting these life-threatening risks.
Mechanism
Hydromorphone, an opioid agonist, primarily acts on mu-opioid receptors in the central nervous system (CNS) to produce analgesia, sedation, and respiratory depression. Lorazepam, a benzodiazepine, enhances the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at GABA-A receptors, leading to CNS depression. The co-administration of these two CNS depressants results in an additive and synergistic depressant effect on the brainstem respiratory centers and overall CNS activity.
Clinical Management
Avoid concomitant use of hydromorphone and lorazepam whenever possible. If co-administration is unavoidable, prescribe the lowest effective doses for the shortest duration possible, and closely monitor patients for signs of respiratory depression and sedation. Educate patients and caregivers on the risks and symptoms of CNS depression, and consider prescribing naloxone for at-risk patients.
Concomitant use can lead to profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, bradycardia, hypotension, and hypoxemia. The risk is heightened in opioid-naive patients or those with underlying respiratory conditions.
Mechanism
Hydromorphone, an opioid agonist, binds to mu-opioid receptors in the central nervous system (CNS), leading to CNS depression, including respiratory depression and sedation. Clonazepam, a benzodiazepine, enhances the effect of gamma-aminobutyric acid (GABA) at GABA-A receptors, resulting in further CNS depression. The synergistic CNS depressant effects of both drugs significantly increase the risk of severe adverse outcomes.
Clinical Management
Avoid concomitant use of hydromorphone and clonazepam whenever possible. If co-administration is unavoidable, prescribe the lowest effective doses for the shortest duration possible, and closely monitor patients for signs of respiratory depression and sedation. Educate patients and caregivers on the risks and symptoms, and consider prescribing naloxone for at-risk patients.
The combination can lead to severe adverse effects including profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, bradycardia, hypotension, and psychomotor impairment.
Mechanism
Both hydromorphone (an opioid agonist) and alprazolam (a benzodiazepine) are central nervous system depressants. They act synergistically to enhance GABAergic neurotransmission, leading to profound CNS depression. This combined effect significantly depresses the respiratory drive and reduces consciousness.
Clinical Management
Concomitant use should be avoided whenever possible. If co-prescription is unavoidable, use the lowest effective doses and shortest possible duration. Closely monitor patients for signs of respiratory depression and sedation, and provide naloxone for opioid overdose reversal. Educate patients and caregivers about the risks.
The combination significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, pinpoint pupils, and hypotension.
Mechanism
Both hydromorphone (an opioid agonist) and temazepam (a benzodiazepine) are central nervous system (CNS) depressants. Their co-administration leads to an additive depressant effect on the CNS, primarily by enhancing GABAergic neurotransmission (benzodiazepines) and inhibiting neuronal activity (opioids), resulting in profound respiratory depression and sedation.
Clinical Management
Avoid concomitant use of opioids and benzodiazepines whenever possible due to the high risk. If co-prescription is absolutely necessary, use the lowest effective doses for the shortest possible duration, closely monitor patients for signs of respiratory depression and sedation, and educate patients and caregivers on these risks. Consider alternative non-opioid or non-benzodiazepine therapies.
The combination significantly increases the risk of profound sedation, respiratory depression, coma, and death. Patients may exhibit somnolence, decreased level of consciousness, hypoventilation, hypoxia, and hypotension. This interaction can lead to life-threatening respiratory arrest.
Mechanism
Hydromorphone, an opioid agonist, binds to mu-opioid receptors in the central nervous system (CNS), leading to CNS depression and respiratory depression. Midazolam, a benzodiazepine, enhances the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at GABA-A receptors, also causing CNS and respiratory depression. The concomitant use of these agents results in an additive and synergistic depressant effect on the CNS and respiratory drive.
Clinical Management
Avoid concomitant use of hydromorphone and midazolam whenever possible. If co-administration is absolutely necessary, use the lowest effective doses for the shortest duration possible, and closely monitor patients for signs of respiratory depression and sedation. Have naloxone readily available and educate patients and caregivers on the risks and symptoms of overdose.
For complete prescribing information:
View full HYDROMORPHONE HYDROCHLORIDE monograph →Medical Disclaimer
The information on RxGuide is intended for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician, pharmacist, or other qualified health provider with any questions you may have regarding a medical condition or medication. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.