Paracetamol + Dextropropoxyphene

Generic Medicine Info
Indications and Dosage
Chronic pain
Adult: Each tablet/capsule containing dextropropoxyphene 32.5 mg and paracetamol 325 mg: 2 capsules 3-4 times daily. Max: 8 capsules/day.
Elderly: Dose reduction is required.
Renal Impairment
Dose reduction is required.
Hepatic Impairment
Dose reduction is required.
May be taken with or without food.
Concurrent admin with alcohol or paracetamol-containing products.
Special Precautions
Hepatic or renal impairment, pregnancy, lactation, children, elderly. Dextropropoxyphene may impair mental alertness and co-ordination. Not recommended for use in patients who are suicidal or prone to drug dependence.
Adverse Reactions
Dizziness, sedation, nausea, vomiting, weakness, constipation, abdominal pain, rash, euphoria, dysphoria, visual disturbances, liver dysfunction, abuse potential.
Potentially Fatal: Hepatic necrosis (especially in chronic alcoholics).
Overdosage with dextropropoxyphene may cause the patient to be stuperose or comatose and convulsing. Respiratory depression , decreased ventilatory rate and/or tidal volume leading to cyanosis and hypoxia may occur. Subsequently, BP may fall and cardiac performance worsens resulting in pulmonary oedema and circulatory collapse. Paracetamol overdose may result in anorexia, nausea, vomiting, diaphoresis, general malaise and abdominal pain. Evidence of hepatic toxicity may become obvious up to 72 hr after ingestion. Treatment includes establishing a patent airway and restoring ventilation. Naloxone may be used to reduce the degree of respiratory depression; 0.4-2 mg can be administered promptly, preferably via IV route. May repeat naloxone dose at 2-3 min intervals if needed. If no response is observed after 10 mg of naloxone has been administered, the diagnosis of dextropropoxyphene toxicity should be questioned. Obtain a serum paracetamol assay as early as possible, but no earlier than 4 hr after ingestion. N-acetylcysteine, should be administered as early as possible, and within 16 hr of the overdose ingestion for maximal results.
Drug Interactions
Dextropropoxyphene may inhibit the hepatic metabolism of antidepressants, anticonvulsants and warfarin-like drugs; paracetamol may enhance anticoagulant activity. Concurrent admin may increase serum levels of carbamazepine and result in neurotoxicity. Ritonavir may increase serum levels of dextropropoxyphene when used together.
Potentially Fatal: CNS depressant effect of dextropropoxyphene is additive with other CNS depressants, including alcohol. Concurrent admin with alcohol or paracetamol-containing products.
Mechanism of Action: Dextropropoxyphene is a centrally-acting opioid analgesic. It binds to opioid receptors at several sites within the CNS. Paracetamol is a non-opioid analgesic and antipyretic. In combination, they exert greater analgesic effect than that produced by either drug administered alone.
Absorption: Dextropropoxyphene: Readily absorbed from the GI tract; undergoes considerable first pass effect. Paracetmol: Readily and completely absorbed after oral admin.
Distribution: Paracetamol: Evenly distributed throughout most body fluids with an apparent volume of distribution of 1-1.2 L/kg.
Metabolism: Dextropropoxyphene: Metabolised hepatically. Paracetamol: About 90-95% of a dose is metabolised by the hepatic microsomal system.
Excretion: Dextropropoxyphene: Half-life: About 6-12 hr. Paracetamol: Excreted mainly in the urine as the glucuronide and sulfate conjugates. Elimination half-life: 1-4 hr.
MIMS Class
Analgesics (Non-Opioid) & Antipyretics / Analgesics (Opioid)
Disclaimer: This information is independently developed by MIMS based on Paracetamol + Dextropropoxyphene from various references and is provided for your reference only. Therapeutic uses, prescribing information and product availability may vary between countries. Please refer to MIMS Product Monographs for specific and locally approved prescribing information. Although great effort has been made to ensure content accuracy, MIMS shall not be held responsible or liable for any claims or damages arising from the use or misuse of the information contained herein, its contents or omissions, or otherwise. Copyright © 2023 MIMS. All rights reserved. Powered by
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