Stability data:
|
| Drug |
Stability
Refrigerated |
Stability
Room Temp. |
Reconstituted
Vial/Powder |
Notes |
| Dilaudid - Hydromorphone |
|
Store at 20° to 25°C (68° to 77°F); excursions permitted to 15° to 30°C (59° to 86°F)
Stable for at least 24 hours at 25°C, protected from light in most common large-volume parenteral solutions |
Solution |
Inspect parenteral drug products visually for particulate matter and discoloration prior to administration, whenever solution and container permit. A slight yellowish discoloration may develop. No loss of potency has been demonstrated.
Protect from light.
Keep covered in carton until time of use. |
| WARNINGS
Drug Dependence
Hydromorphone Hydrochloride Injection can produce drug dependence of the morphine type and therefore has the potential for being abused. Psychic dependence, physical dependence and tolerance may develop upon repeated administration of Hydromorphone Hydrochloride Injection and it should be prescribed and administered with the same degree of caution appropriate for the use of morphine. Since Hydromorphone Hydrochloride Injection is indicated for use in patients who are already tolerant to and hence physically dependent on narcotics, abrupt discontinuance in the administration of Hydromorphone Hydrochloride Injection is likely to result in a withdrawal syndrome.
Infants born to mothers physically dependent on Hydromorphone Hydrochloride Injection will also be physically dependent and may exhibit respiratory difficulties and withdrawal symptoms.
Impaired Respiration
Respiratory depression is the chief hazard of Hydromorphone Hydrochloride Injection. Respiratory depression occurs most frequently in the elderly, in the debilitated, and in those suffering from conditions accompanied by hypoxia or hypercapnia when even moderate therapeutic doses may dangerously decrease pulmonary ventilation.
Hydromorphone Hydrochloride Injection should be used with extreme caution in patients with chronic obstructive pulmonary disease or cor pulmonale, patients having a substantially decreased respiratory reserve, hypoxia, hypercapnia, or preexisting respiratory depression. In such patients even usual therapeutic doses of narcotic analgesics may decrease respiratory drive while simultaneously increasing airway resistance to the point of apnea.
Head Injury and Increased Intracranial Pressure
The respiratory depressant effects of Hydromorphone Hydrochloride Injection with carbon dioxide retention and secondary elevation of cerebrospinal fluid pressure may be markedly exaggerated in the presence of head injury, other intracranial lesions, or preexisting increase in intracranial pressure. Narcotic analgesics including Hydromorphone Hydrochloride Injection may produce effects which can obscure the clinical course and neurologic signs of further increase in pressure in patients with head injuries.
Hypotensive Effect
Narcotic analgesics, including Hydromorphone Hydrochloride Injection, may cause severe hypotension in an individual whose ability to maintain his blood pressure has already been compromised by a depleted blood volume, or a concurrent administration of drugs such as phenothiazines or general anesthetics (see also Precautions - Drug Interactions). Hydromorphone Hydrochloride Injection may produce orthostatic hypotension in ambulatory patients.
Hydromorphone Hydrochloride Injection should be administered with caution to patients in circulatory shock, since vasodilation produced by the drug may further reduce cardiac output and blood pressure. |
Pharmacokinetics
In normal human volunteers hydromorphone is metabolized primarily in the liver. It is excreted primarily as the glucuronidated conjugate, with small amounts of parent drug and minor amounts of 6-hydroxy reduction metabolites.
Following intravenous administration of Hydromorphone Hydrochloride Injection to normal volunteers, the mean half-life of elimination was 2.64 ± 0.88 hours. The mean volume of distribution was 91.5 liters, suggesting extensive tissue uptake. Hydromorphone Hydrochloride Injection is rapidly removed from the blood stream and distributed to skeletal muscle, kidneys, liver, intestinal tract, lungs, spleen and brain. Hydromorphone Hydrochloride Injection also crosses the placental membranes.
In terms of area under the analgesic time-effect curve, hydromorphone is approximately 8 times more potent than morphine (i.e., 1.3 mg of hydromorphone produces analgesia equal to that produced by 10 mg of morphine). After intramuscular administration, hydromorphone has a slightly more rapid onset and slightly shorter duration of action than morphine. The duration of Hydromorphone Hydrochloride Injection analgesia in the non-tolerant patient with usual doses may be up to 4 to 5 hours. However, in tolerant subjects, duration will vary substantially depending on tolerance and dose. Dose should be adjusted so that 3 to 4 hours of pain relief may be achieved.
Source: [package insert]
Dosing:
IV: (opiate naive) Start: 0.2 - 0.6 mg q2-3h prn. Pain, acute: 1-2 mg IV (slow - over 2-3 min) q3h prn.
Mechanically-ventilated pts: 0.7 - 2 mg q1-2h prn or start infusion: 0.5 - 1 mg/hr.
PCA: Usual concentration: 0.2 mg/ml. Demand dose (usual): 0.1 - 0.2 mg (range: 0.05 - 0.5mg). Lockout: 5-15 min. 4 hour limit: 4-6 mg.
Epidural: Bolus: 0.4-1.5 mg. Infusion conc: 0.05 - 0.075 mg/ml. Infusion rate: 0.04 - 0.4 mg/hr. Demand dose: 0.15mg. Lockout: 30 minutes. Alternatively (per Lexi-drugs 2012): Bolus: 0.4 -1 mg. Infusion rate: 0.03 - 0.3 mg/hour. Demand dose: 0.02 - 0.05mg. Lockout: 10-15 minutes.
IM/SC: (opiate naive) Start: 0.8 - 1 mg q4-6h prn. Usual range: 1-2 mg q3-6h prn.
Acute pain: 1-2 mg IM/SC q4-6h prn. |
