Opioid · Analgesic
Hydromorphone (Dilaudid)
Also called Dilaudid
Indications
- Acute severe pain, IV, IM, SC or by PCA
- Analgesia in ventilated ICU patients, by bolus or infusion
- Alternative to morphine when histamine release or, with dose reduction, kidney impairment is a concern
- Opioid-tolerant patients who need large doses (high-potency 10 mg/mL product)
Dosing
Hydromorphone drip card and mL/h converterStart: 0.5–1 mg/h (PADIS range 0.5–3 mg/h)
| Where | Dose |
|---|---|
| Other common pushes | Hydromorphone: 0.2–0.5 mg IV every 5–15 min (about 7 times morphine) |
| Opioid equianalgesic doses | Hydromorphone: 1.5 mg IV = 7.5 mg PO |
| Other ICU drugs | Hydromorphone: Use lower doses; metabolite causes neuroexcitation |
On the quick cards
- Other common pushesPush and Emergency Meds: Analgesia, antiemetics, steroids, diuretics, TXA
- Opioid equianalgesic dosesEquivalents and Conversions: Equal to morphine 10 mg IV
Mechanism of action
Hydromorphone is a full μ-opioid agonist with little κ or δ activity, acting through the same Gi/o signaling as morphine: less cAMP, open GIRK potassium channels and closed presynaptic calcium channels in pain pathways. It binds the μ receptor more tightly than morphine (Ki under 1 nM, Volpe 2011), which helps explain its 5–7-fold potency by weight. Its main metabolite, H3G, has no analgesic action but excites neurons when it accumulates.
Pharmacology
- CNS: analgesia and sedation like morphine with a faster peak; myoclonus, agitation, allodynia or seizures when H3G accumulates
- Respiratory: dose-related depression, the main danger in potency mix-ups
- Cardiovascular: less histamine release and hypotension than morphine, though both occur
- GI and Other: constipation, nausea, itching, urinary retention
Pharmacokinetics
| Onset | Within 5 min IV (Coda 1997) |
|---|---|
| Peak | 10–20 min IV (Coda 1997) |
| Duration | About 2–4 h IV |
| Half-life | About 2.3 h IV (label) |
| Distribution | Vd about 300 L (about 4 L/kg, label) |
| Protein binding | 8–19% (label) |
| Metabolism | Liver glucuronidation (UGT2B7) of over 95% of a dose to H3G; minor 6-hydroxy reduction products; no 6-glucuronide (label) |
| Elimination | Urine, mainly as H3G; about 7% unchanged |
| Organ failure | Exposure doubles in moderate and quadruples in severe kidney impairment and rises 4-fold in moderate liver impairment; start at one-quarter to one-half the usual dose (label) |
| Bioavailability | Oral low and variable (about 25–50%), so IV:PO is about 1:5 |
Chemistry
- Semisynthetic phenanthrene from morphine: the 6-hydroxyl becomes a ketone and the 7,8 double bond is saturated (4,5α-epoxy-3-hydroxy-17-methylmorphinan-6-one)
- Keeps morphine's natural (−) stereochemistry; pKa about 8.2, so mostly ionized at pH 7.4, and only modestly more lipid soluble than morphine
- Hydrochloride 0.2–4 mg/mL in citrate buffer, pH 3.5–5.5, plus a high-potency 10 mg/mL for opioid-tolerant patients only; protect from light (label)
Adverse effects and cautions
In the one-pagers
- Sedation, Pain and Delirium ScalesPharmacology and ICU pitfalls: Hydromorphone: 0.5–3 mg/h: Potency errors; metabolite myoclonus
- End of Life, Brain Death and Organ DonationSymptom control and the ethics of comfort: Opioids are the mainstay for pain and dyspnea. Truog 2008 names morphine the agent of choice, with fentanyl (by infusion, since a bolus wears off quickly) or hydromorphone as alternatives. Benzodiazepines add anxiolysis, sedation and amnesia but no analgesia; midazolam peaks in 5–10 minutes, lorazepam in 20–25. When distress recurs, bolus and raise the in
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Sources
- FDA label: Dilaudid Injection (2026)
- FDA label: Hydromorphone HCl Injection, Fresenius Kabi (2026)
- PubChem: hydromorphone
- Coda 1997 (IV onset and potency)
For education and exam preparation only. Follow your institution’s protocols. Typical adult values for study. Follow the order, the label and your institution's protocols.