Brands, Medical Use, Clinical Data
- Analgesics, Opioid
- Capsule (controlled-delivery)
Brands / Synonyms
Dihydromorfinon; Dihydromorfinon [Czech]; Dihydromorphinone; Dilaudid; Dilaudid Oros; Dilaudid-HP; DiMo; Dimorphone; Hidromorfona [INN-Spanish]; Hydromorfona [Spanish]; Hydromorphon; Hydromorphone; Hydromorphone HCL; Hydromorphonum [INN-Latin]; Hymorphan; Idromorfone; Idromorfone [DCIT]; Laudacon; Laudicon; Morphinone, dihydro-; Novolaudon; Palladone; Paramorphan
For the relief of moderate to severe pain such as that due to surgery, cancer, trauma/injury, burns, myocardial infarction and colic.
Hydromorphone is a hydrogenated ketone derivative of morphine that acts as a narcotic analgesic. It has a shorter duration of action than morphine. Hydromorphone is approximately 8 times more potent on a milligram basis than morphine. In addition, hydromorphone is better absorbed orally than is morphine. In clinical settings, Hydromorphone exerts its principal pharmacological effect on the central nervous system and gastrointestinal tract. Its primary actions of therapeutic value are analgesia and sedation. Hydromorphone appears to increase the patient's tolerance for pain and to decrease discomfort, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Opioids also produce respiratory depression by direct action on brain stem respiratory centers.
Mechanism of Action
Hydromorphone is a narcotic analgesic; its principal therapeutic effect is relief of pain. Hydromorphone interacts predominantly with the opioid mu-receptors. These mu-binding sites are discretely distributed in the human brain, with high densities in the posterior amygdala, hypothalamus, thalamus, nucleus caudatus, putamen, and certain cortical areas. They are also found on the terminal axons of primary afferents within laminae I and II (substantia gelatinosa) of the spinal cord and in the spinal nucleus of the trigeminal nerve. In clinical settings, Hydromorphone exerts its principal pharmacological effect on the central nervous system and gastrointestinal tract. Hydromorphone also binds with kappa-receptors which are thought to mediate spinal analgesia, miosis and sedation.
Better absorbed orally than morphine
Hydromorphone is a schedule II narcotic which can lead to physical dependence or addiction. High doses lead to respiratory depression, nausea, and vomiting. Overdoses lead to extreme somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, and sometimes bradycardia and hypotension. In severe overdosage, apnea, circulatory collapse, cardiac arrest and death may occur.
Biotrnasformation / Drug Metabolism
Primarily hepatic. After absorption hydromorphone is metabolized by the liver to the glucuronide conjugate which is then excreted in the urine. Hydromorphone is metabolized to the major metabolites hydromorphone-3-glucuronide, hydromorphone-3-glucoside and dihydroisomorphine-6-glucuronide.
DILAUDID is contraindicated in patients with a known hypersensitivity to hydromorphone; in the presence of an
intracranial lesion associated with increased intracranial pressure; and whenever ventilatory function is depressed
(chronic obstructive pulmonary disease, cor pulmonale, emphysema, kyphoscoliosis, status asthmaticus).
Patients receiving other narcotic analgesics, general anesthetics, phenothiazines, tranquilizers,
sedative-hypnotics, tricyclic antidepressants or other CNS depressants (including alcohol) concomitantly with
DILAUDID may exhibit an additive CNS depression. When such combined therapy is contemplated, the dose of one or both
agents should be reduced.