Hydromorphone conversion and pharmacology
A potent semi-synthetic opioid (hydrogenated ketone of morphine), often used for severe pain.
Equianalgesic estimate
1.5mg Parenteral ≈ 7.5mg Oral ≈ 10mg Parenteral Morphine
Published equianalgesic ratios vary between references and with clinical context. Read how to interpret conversion results before applying an estimate.
Mechanism of action
Potent full agonist, primarily acting on mu-opioid receptors. More lipid-soluble than morphine.
Brand names: Dilaudid, Exalgo
Pharmacokinetics
- Protein binding
- 8-19%
- Volume of distribution
- ~4 L/kg
- Half-life
- 2-3 hours (IR), 8-15 hours (ER)
| Route | Form | Bioavailability | Onset | Peak | Duration |
|---|---|---|---|---|---|
| Oral | IR | ~24% | 15-30 min | 30-60 min | 3-4 hours |
| Parenteral | IV | — | 5 min | 10-20 min | 3-4 hours |
Metabolism
- Glucuronidation (Phase II)
Metabolites
- Hydromorphone-3-glucuronide (H3G) No analgesic activity; can accumulate and cause neuroexcitatory effects (myoclonus, delirium, seizures).
Extensive first-pass metabolism. Not significantly metabolized by CYP450 enzymes, leading to fewer CYP-related drug-drug interactions.
Renal and hepatic impairment
Renal
Use with caution. H3G accumulates and can cause neurotoxicity. Often preferred over morphine in renal dysfunction, but still requires monitoring. Metabolites are dialyzable.
Hepatic
Clearance is decreased; dose reduction required (e.g., reduce starting dose by 50-75% depending on severity).
Clinical cautions
- High potency increases the risk of dosing errors; ensure clear differentiation from morphine.
- Less histamine release than morphine.
For qualified healthcare professionals. This page is an educational reference, not prescribing advice. Check medicine information and conversion factors against a current clinical source and local guidance.
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Last updated 30 August 2026. Read how to interpret conversion results and the Terms of Service.