HYDROMORPHONE HYDROCHLORIDE- hydromorphone hydrochloride injection
West-ward Pharmaceutical Corp.
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Hydromorphone Hydrochloride Injection, USP is a sterile solution intended for subcutaneous, intramuscular or slow intravenous injection. Each mL contains hydromorphone hydrochloride 2 mg, edetate disodium 0.5 mg, methylparaben 1.8 mg and propylparaben 0.2 mg in Water for Injection. The pH range is 3.5-5.5; sodium hydroxide and/or hydrochloric acid added, if needed, for pH adjustment. Hydromorphone is a semisynthetic phenanthrene alkaloid of opium; it is classified pharmacologically as a narcotic analgesic. Hydromorphone hydrochloride may be named chemically as 4,5α-Epoxy-3-hydroxy-17-methylmorphinan-6-one hydrochloride, with the following structural formula:
C17 H19 NO3 • HCl M.W. 321.80
Hydromorphone hydrochloride occurs as a fine, white or practically white, crystalline powder and is freely soluble in water and sparingly soluble in alcohol.
Hydromorphone resembles morphine both structurally and pharmacologically. Like other narcotic analgesics, hydromorphone exerts its principal pharmacological effects on the central nervous system and gastrointestinal tract. Its primary action of therapeutic value is analgesia. The analgesic effects of hydromorphone are due to its central action; however, the precise mechanism of action of hydromorphone and other opiates is not known, although it is believed to relate to the existence of opiate receptors in the central nervous system. Hydromorphone, like other narcotic analgesics, appears to increase the patient’s tolerance for pain and to decrease the perception of suffering, although the presence of the pain itself may still be recognized.
In addition to analgesia, narcotics commonly produce such CNS effects as drowsiness, alterations in mood and mental clouding. Hydromorphone is reported to produce analgesia with less sedation than morphine. This may be an advantage in the postoperative period, since the patient with a less-clouded sensorium is better able to cooperate in early ambulation procedures. Likewise, cancer patients can be relieved of pain yet remain sufficiently alert to function within the scope of their underlying physical disorder. Narcotic analgesics also depress various respiratory centers, depress the cough reflex, constrict the pupils, elevate cerebrospinal fluid pressure, produce transient hyperglycemia and enhance parasympathetic activity.
Narcotic analgesics may cause nausea and vomiting by stimulating the chemoreceptor trigger zone (CTZ); however, they also depress the vomiting center, so that subsequent doses are unlikely to produce vomiting. Nausea and vomiting are significantly more common in ambulatory than in recumbent patients. Narcotic analgesics, including hydromorphone, increase the tone and decrease the propulsive contractions of the smooth muscle of the gastrointestinal tract. The resultant prolongation in gastrointestinal transit time is responsible for hydromorphone’s constipating effect. Because narcotics may increase biliary tract pressure, some patients with biliary colic may experience worsening rather than relief of pain.
While narcotics generally increase the tone of urinary tract smooth muscle, the net effect tends to be variable, in some cases producing urinary urgency, in others, difficulty in urination. Narcotics have also been reported to cause antidiuretic hormone (ADH) to be released, thereby reducing urine output.
In therapeutic dosage, opiates do not usually exert major effects on the cardiovascular system. However, some patients exhibit a propensity to develop orthostatic hypotension and fainting. Rapid intravenous injection is more likely to precipitate a fall in blood pressure than are intramuscular or subcutaneous injections.
Narcotic analgesics cause histamine release, which appears to be responsible for wheals or urticaria sometimes seen at the site of injection. Histamine release may also produce dilation of cutaneous blood vessels, with resultant flushing of the face and neck, pruritus and sweating.
Hydromorphone is well absorbed after parenteral administration.
After intramuscular administration, hydromorphone has a slightly more rapid onset and slightly shorter duration of analgesia than morphine. The major pathway of hydromorphone metabolism is conjugation with glucuronic acid in the liver; hydromorphone glucuronide is excreted primarily in the urine.
Hydromorphone Hydrochloride Injection is indicated for the relief of moderate to severe pain such as that due to: surgery, cancer, trauma (soft tissue and bone), biliary colic, myocardial infarction, burns, renal colic.
Hydromorphone Hydrochloride Injection 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). [See WARNINGS.]
Narcotic analgesics, including hydromorphone, are contraindicated in premature infants or during labor when delivery of a premature infant is anticipated.
Hydromorphone produces dose-related respiratory depression by acting directly on brain stem respiratory centers. Hydromorphone also affects centers that control respiratory rhythm and may produce irregular and periodic breathing.
The respiratory depressant effects of hydromorphone and its capacity to elevate cerebrospinal fluid pressure may be markedly exaggerated in the presence of head injury, other intracranial lesions or a pre-existing increase in intracranial pressure.
Furthermore, hydromorphone produces adverse reactions which may obscure the clinical course of patients with head injuries. In such patients, hydromorphone must be used with extreme caution and only if its use is deemed essential.
The administration of hydromorphone may obscure the diagnosis or clinical course of patients with acute abdominal conditions.
Hydromorphone should be used with extreme caution in patients having an acute asthmatic attack, patients with chronic obstructive pulmonary disease or cor pulmonale, patients having a substantially decreased respiratory reserve and patients with pre-existing respiratory depression, hypoxia or hypercapnia. In such patients, even usual therapeutic doses of narcotics may decrease respiratory drive while simultaneously increasing airway resistance to the point of apnea.
If necessary, hydromorphone may be given intravenously, but the injection should be given very slowly (over a period of at least 3 to 5 minutes). Rapid intravenous injection of narcotic analgesics, including hydromorphone, increases the incidence of adverse reactions; severe respiratory depression, apnea, hypotension, peripheral circulatory collapse, cardiac arrest, as well as anaphylactoid reactions, have occurred. Hydromorphone should not be administered intravenously unless a narcotic antagonist and the facilities for resuscitation and assisted or controlled respiration are immediately available. When hydromorphone is given parenterally, especially intravenously, the patient should be lying down.
The administration of hydromorphone may result in severe hypotension in an individual whose ability to maintain blood pressure has already been compromised by a depleted blood volume or concurrent administration of drugs such as the phenothiazines or certain anesthetics.
Hydromorphone may produce orthostatic hypotension in ambulatory patients.
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