CODEINE SULFATE Drug Interactions
Also known as: Codeine sulfate
CODEINE SULFATE (brand name: Codeine sulfate) is a Opioid Analgesics. 1 INDICATIONS AND USAGE Codeine Sulfate Tablets are indicated for the management of mild to moderate pain, where treatment with an opioid is appropriate and for which alternative treatments are inadequate. Limitations of Use: • Because of the risks of addiction, abuse, misuse, overdose, and death,…CODEINE SULFATE has 17 documented drug interactions in our database, including 5 contraindicated, 12 major, 0 moderate, and 0 minor interactions.
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Contraindicated
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Major
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Moderate
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Minor
The combination significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, bradycardia, and hypotension. These effects can be life-threatening and require immediate medical intervention.
Mechanism
Both codeine (an opioid analgesic) and clonazepam (a benzodiazepine) are central nervous system (CNS) depressants. Their co-administration leads to additive CNS depression, primarily by enhancing GABAergic activity (benzodiazepines) and inhibiting neuronal activity through opioid receptor agonism (codeine), resulting in synergistic effects on respiratory drive and sedation.
Clinical Management
Concomitant use of codeine and clonazepam is generally contraindicated due to the high risk of severe adverse outcomes. If no alternative treatments are adequate, and the benefits outweigh the risks, prescribe the lowest effective doses for the shortest duration possible, and monitor patients closely for respiratory depression and sedation. Educate patients and caregivers about the risks and symptoms of CNS depression.
This combination significantly increases the risk of severe respiratory depression, profound sedation, hypotension, psychomotor impairment, coma, and death. Patients may experience decreased respiratory rate, shallow breathing, extreme drowsiness, confusion, and unresponsiveness.
Mechanism
Codeine, an opioid analgesic, and oxazepam, a benzodiazepine, both exert central nervous system (CNS) depressant effects. When co-administered, their synergistic depressant actions on GABA-A receptors (benzodiazepines) and opioid receptors (opioids) lead to profound and additive CNS depression, particularly affecting the respiratory drive.
Clinical Management
Concomitant use of opioids and benzodiazepines should be avoided due to the high risk of severe adverse outcomes, including respiratory depression and death. If no alternatives are available and co-administration is absolutely necessary, the lowest effective doses should be used for the shortest possible duration, with close monitoring for respiratory depression and sedation. Patients and caregivers must be educated on the risks and signs of CNS depression.
The combination significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may exhibit slowed or shallow breathing, extreme drowsiness, unresponsiveness, and hypoxemia. This interaction can rapidly progress to life-threatening respiratory arrest.
Mechanism
Both codeine (an opioid analgesic) and temazepam (a benzodiazepine) are central nervous system (CNS) depressants. Their co-administration leads to an additive depressant effect on the CNS, particularly affecting the respiratory drive and level of consciousness. This synergistic depression is mediated through different but converging pathways that enhance GABAergic inhibition and opioid receptor agonism.
Clinical Management
Concomitant use of opioids and benzodiazepines should be avoided due to the high risk of severe adverse outcomes, including death. If no alternatives are available, and the benefit outweighs the risks, use the lowest effective doses and shortest possible duration, and closely monitor for respiratory depression and sedation. Educate patients and caregivers on the risks and symptoms of respiratory depression.
The combination significantly increases the risk of profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, bradycardia, and hypotension. This interaction can be life-threatening due to the synergistic depressant effects on the respiratory drive.
Mechanism
Codeine sulfate is an opioid analgesic that acts as an agonist at mu-opioid receptors in the central nervous system (CNS), leading to CNS depression, including respiratory depression and sedation. Triazolam is a benzodiazepine that enhances the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at GABA-A receptors, also resulting in CNS depression. The concomitant use of these two drug classes produces additive CNS depressant effects.
Clinical Management
Concomitant use of codeine sulfate and triazolam is contraindicated due to the severe risks. If no suitable alternatives exist, and the benefits outweigh the risks, the lowest effective doses should be used for the shortest duration possible, with close monitoring for respiratory depression and sedation. Patients and caregivers must be educated on the signs and symptoms of respiratory depression and sedation.
The concurrent use of codeine and chlordiazepoxide can lead to profound sedation, respiratory depression, coma, and death. Patients may experience dizziness, confusion, psychomotor impairment, and hypotension. The risk is heightened in patients with pre-existing respiratory conditions, the elderly, and those receiving higher doses of either medication.
Mechanism
Codeine sulfate is an opioid analgesic that acts on mu-opioid receptors in the central nervous system (CNS), leading to CNS depression, including respiratory depression and sedation. Chlordiazepoxide hydrochloride is a benzodiazepine that enhances the effect of gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the CNS, resulting in further CNS depression. The additive CNS depressant effects of these two drug classes significantly increase the risk of severe adverse outcomes.
Clinical Management
The co-prescription of codeine and chlordiazepoxide is generally contraindicated due to the severe risks. If co-administration is unavoidable and no safer alternative exists, it should be done with extreme caution, using the lowest effective doses for the shortest possible duration, and with close monitoring for signs of respiratory depression and sedation. Patients and caregivers must be educated on these risks and advised to seek immediate medical attention if symptoms occur. Consider naloxone availability.
Patients may experience profound sedation, dizziness, confusion, and impaired psychomotor function. The most serious clinical effect is an increased risk of respiratory depression, which can be life-threatening. Hypotension and syncope may also occur.
Mechanism
Codeine sulfate is an opioid analgesic that exerts its effects primarily through mu-opioid receptor agonism, leading to central nervous system (CNS) depression, including respiratory depression and sedation. Cyclobenzaprine hydrochloride is a centrally acting skeletal muscle relaxant structurally related to tricyclic antidepressants, which also causes significant CNS depression through its actions on the brainstem and spinal cord. The concomitant use of these two agents results in an additive depressant effect on the CNS.
Clinical Management
Concomitant use should generally be avoided due to the significant risk of additive CNS depression. If co-administration is unavoidable, initiate both medications at the lowest possible effective doses and monitor patients closely for signs of respiratory depression, excessive sedation, and altered mental status. Educate patients and caregivers about the risks and instruct them to seek immediate medical attention for symptoms such as difficulty breathing or extreme drowsiness.
Patients may experience profound sedation, dizziness, confusion, and psychomotor impairment. The most serious clinical effect is an increased risk of respiratory depression, which can be life-threatening. Impaired motor function and coordination can also increase the risk of falls and accidents.
Mechanism
Both codeine sulfate, an opioid analgesic, and methocarbamol, a centrally acting muscle relaxant, exert their primary effects through central nervous system (CNS) depression. The co-administration of these agents leads to an additive depressant effect on the CNS, potentiating their individual sedative and respiratory depressant properties.
Clinical Management
Concomitant use should be avoided if possible. If co-administration is necessary, initiate therapy with the lowest effective doses of both drugs and titrate carefully, monitoring closely for signs of CNS and respiratory depression. Educate patients about the risks, including avoiding driving or operating heavy machinery, and provide naloxone for at-risk patients.
Patients may experience profound sedation, dizziness, confusion, psychomotor impairment, and respiratory depression, which can be life-threatening. The risk of falls, accidents, and overdose is significantly increased due to the synergistic CNS depression.
Mechanism
Both codeine, an opioid analgesic, and carisoprodol, a centrally acting muscle relaxant, exert their primary effects through central nervous system (CNS) depression. Carisoprodol is metabolized to meprobamate, which also possesses significant CNS depressant and anxiolytic properties. This combination results in an additive depressant effect on the CNS.
Clinical Management
Concomitant use should generally be avoided. If co-administration is unavoidable, reduce the dosage of one or both drugs, initiate at the lowest effective dose, and monitor closely for signs of respiratory depression and sedation. Educate patients about the risks and advise against driving or operating heavy machinery.
Patients may experience severe CNS depression, including profound sedation, somnolence, and confusion. There is an increased risk of life-threatening respiratory depression, characterized by decreased respiratory rate and depth, potentially leading to hypoxia and hypercapnia. Additionally, impaired psychomotor function, dizziness, and ataxia are common, increasing the risk of falls and accidents.
Mechanism
Codeine sulfate, an opioid analgesic, and baclofen, a central nervous system (CNS) depressant and muscle relaxant, both act on the CNS to produce sedative effects. Their co-administration results in an additive depressant effect on the CNS, leading to enhanced inhibition of neuronal activity. This synergistic action can significantly impair respiratory drive and neurological function.
Clinical Management
Concomitant use should be avoided if possible. If co-administration is unavoidable, initiate both medications at the lowest effective doses and titrate slowly while closely monitoring for signs of CNS and respiratory depression. Educate patients and caregivers about the risks and symptoms of CNS depression and respiratory compromise, advising them to seek immediate medical attention if these occur. Consider alternative therapies if the risks outweigh the benefits.
Patients may experience increased sedation, dizziness, confusion, and psychomotor impairment. The most serious clinical effect is an enhanced risk of respiratory depression, which can be life-threatening. Other effects include profound drowsiness, hypotension, and impaired coordination.
Mechanism
Codeine sulfate is an opioid analgesic that exerts its effects by agonizing mu-opioid receptors in the central nervous system, leading to CNS depression, analgesia, and respiratory depression. Tizanidine is an alpha-2 adrenergic agonist that reduces spasticity primarily by increasing presynaptic inhibition of motor neurons at the spinal cord level, also causing significant CNS depression. The co-administration of these agents results in an additive depressant effect on the central nervous system.
Clinical Management
Avoid concomitant use of codeine and tizanidine if possible. If co-administration is necessary, initiate both medications at the lowest effective dose and titrate slowly while closely monitoring for signs of CNS and respiratory depression. Educate patients about the risks and advise them to avoid driving or operating heavy machinery. Consider alternative non-opioid analgesics or non-pharmacological treatments for pain.
Patients may experience increased sedation, dizziness, confusion, and psychomotor impairment. The most serious clinical effect is an enhanced risk of respiratory depression, which can be life-threatening. Other effects include hypotension and profound drowsiness.
Mechanism
Codeine sulfate, an opioid analgesic, primarily acts as a mu-opioid receptor agonist, leading to central nervous system (CNS) depression. Metaxalone, a centrally acting muscle relaxant, also produces CNS depression through an unknown mechanism, possibly by general CNS depression. 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 medications 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 heavy machinery or driving. Consider alternative non-opioid analgesics or non-pharmacological therapies if appropriate.
Patients may experience increased sedation, dizziness, confusion, and psychomotor impairment. The most serious clinical effect is an increased risk of respiratory depression, which can be life-threatening. Other effects include profound drowsiness, decreased cognitive function, and impaired coordination.
Mechanism
Codeine sulfate, an opioid analgesic, exerts its effects primarily through agonism of mu-opioid receptors in the central nervous system (CNS), leading to CNS depression. Chlorzoxazone, a centrally acting skeletal muscle relaxant, also produces CNS depression by inhibiting multisynaptic reflex arcs in the spinal cord and subcortical areas. The co-administration of these agents results in additive CNS depressant effects.
Clinical Management
Avoid concomitant use of codeine sulfate and chlorzoxazone if possible. If co-administration is necessary, initiate therapy with the lowest effective doses of both drugs and titrate carefully while closely monitoring for signs of CNS and respiratory depression. Educate patients about the risks of additive sedation and advise against operating heavy machinery or driving.
Patients may experience profound sedation, dizziness, confusion, and impaired psychomotor function. The most serious clinical effect is an increased risk of respiratory depression, which can be life-threatening. Hypotension and severe constipation may also occur.
Mechanism
Codeine sulfate, an opioid analgesic, produces central nervous system (CNS) depression through its agonistic effects on mu-opioid receptors. Orphenadrine citrate, an anticholinergic and skeletal muscle relaxant, also causes CNS depression through its central anticholinergic and sedative properties. The concurrent use of these agents results in an additive depressant effect on the CNS.
Clinical Management
Concomitant use should generally be avoided due to the significant risk of additive CNS depression and respiratory compromise. If co-administration is unavoidable, initiate therapy with the lowest effective doses of both drugs and monitor patients closely for signs of sedation and respiratory depression. Educate patients about the risks and advise them to avoid activities requiring mental alertness, such as driving.
The co-administration of codeine and lorazepam can lead to profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, apnea, and hypotension. These effects can be life-threatening and require immediate medical intervention.
Mechanism
Codeine is an opioid analgesic that primarily acts as a mu-opioid receptor agonist, leading to central nervous system (CNS) depression, including respiratory depression. Lorazepam is a benzodiazepine that enhances the effect of gamma-aminobutyric acid (GABA) at the GABA-A receptor, resulting in further CNS depression. The combined CNS depressant effects are synergistic, significantly increasing the risk of adverse outcomes.
Clinical Management
Avoid concomitant use of codeine and lorazepam whenever possible. If co-prescription is unavoidable, use the lowest effective doses and for the shortest duration necessary, carefully titrating and monitoring for signs of respiratory depression and sedation. Educate patients and caregivers about the risks and symptoms of CNS depression and respiratory depression, advising them to seek immediate medical attention if these occur.
Concomitant use can lead to profound sedation, respiratory depression, coma, and death. Patients may experience extreme drowsiness, confusion, slowed or difficult breathing, and unresponsiveness. The risk is heightened in patients with pre-existing respiratory compromise or those who are opioid-naive.
Mechanism
Codeine sulfate, an opioid analgesic, primarily acts as a mu-opioid receptor agonist, leading to central nervous system (CNS) depression, including respiratory depression. Diazepam, a benzodiazepine, enhances the effect of gamma-aminobutyric acid (GABA) at GABA-A receptors, also resulting in CNS depression. The synergistic CNS depressant effects of both drugs significantly increase the risk of adverse outcomes.
Clinical Management
Avoid concomitant use of codeine and diazepam whenever possible. If co-prescription 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 about the risks and symptoms, and consider prescribing naloxone if appropriate.
The concomitant use of codeine and alprazolam significantly increases the risk of severe CNS depression, including profound sedation, respiratory depression, coma, and death. Patients may experience slowed or difficult breathing, excessive drowsiness, dizziness, and unresponsiveness.
Mechanism
Codeine is an opioid analgesic that acts as an agonist at mu-opioid receptors, leading to central nervous system (CNS) depression, including respiratory depression and sedation. Alprazolam is a benzodiazepine that enhances the effect of gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the CNS, resulting in an additive depressant effect on the CNS and respiratory drive.
Clinical Management
Concomitant use of opioids and benzodiazepines should generally be avoided due to the FDA Black Box Warning. If co-prescription is absolutely necessary, use the lowest effective doses for the shortest possible duration, monitor patients closely for signs of respiratory depression and sedation, and educate patients and caregivers on these risks. Consider alternative therapies that do not involve co-prescribing these drug classes.
The primary clinical effects include profound sedation, respiratory depression, coma, and death. Patients may exhibit reduced level of consciousness, decreased respiratory rate, hypoxemia, and hypotension.
Mechanism
Codeine is an opioid analgesic, and midazolam is a benzodiazepine. Both drug classes are central nervous system (CNS) depressants. Co-administration leads to additive pharmacodynamic effects, particularly on GABA-A receptors (benzodiazepines) and opioid receptors (codeine), resulting in enhanced CNS depression.
Clinical Management
Avoid concomitant use of codeine and midazolam unless the benefits outweigh the risks, and alternative treatment options are inadequate. 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. Have naloxone readily available.
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