Morphine sulfate is an opioid agonist indicated for the management of pain not responsive to non-narcotic analgesics
Morphine is a phenanthrene derivative which acts mainly on the CNS and smooth muscles. It binds to opiate receptors in the CNS altering pain perception and response. Analgesia, euphoria and dependence are thought to be due to its action at the mu-1 receptors while resp depression and inhibition of intestinal movements are due to action at the mu-2 receptors. Spinal analgesia is mediated by morphine agonist action at the K receptor.
Direct Intravenous Injection: The usual starting dose in adults is 0.1 mg to 0.2 mg per kg every 4 hours as needed for pain management. The dose should be adjusted according to the severity of pain, the occurrence of adverse events, as well as the patient?s underlying disease, age, and size.Morphine Sulfate Tablets: 15 to 30 mg every 4 hours as needed.
Morphine should be used with caution in patients who are concurrently receiving other central nervous system depressants including sedatives or hypnotics, general anaesthetics, phenothiazines, other tranquilisers, muscle relaxants, antihypertensives and alcohol. Interactive effects resulting in respiratory depression, hypotension, profound sedation, or coma may result if these drugs are taken in combination with the usual doses of morphine. Mixed agonist/antagonist opioid analgesics (e.g. buprenorphine, nalbuphine, pentazocine) should not be administered to a patient who has received a course of therapy with a pure opioid agonist analgesic. Medicinal products that block the action of acetylcholine, for example antihistamines, anti-parkinsons and anti-emetics, may interact with morphine to potentiate the anticholinergic adverse effects. Cimetidine inhibits the metabolism of morphine. Monoamine oxidase inhibitors are known to interact with narcotic analgesics producing CNS excitation or depression with hyper- or hypotensive crisis. Morphine should not be co-administered with monoamine oxidase inhibitors or within two weeks of such therapy. Plasma concentrations of morphine may be reduced by rifampicin. Although there are no pharmacokinetic data available for concomitant use of ritonavir with morphine, ritonavir induces the hepatic enzymes responsible for the glucuronidation of morphine, and may possibly decrease plasma concentrations of morphine.
Known hypersensitivity or allergy to morphine ? Bronchial asthma or upper airway obstruction ? Respiratory depression in the absence of resuscitative equipment ? Paralytic ilieu
Apnea, circulatory depression, respiratory arrest, shock, and cardiac arrest. Other common frequently observed adverse reactions include: sedation, lightheadedness, dizziness, nausea, vomiting, and constipation.
Pregnancy: Based on animal data, may cause fetal harm.
Signs of morphine toxicity and overdose are pin-point pupils, skeletal muscle flaccidity, bradycardia, respiratory depression, hypotension, somnolence and central nervous system depression which can progress to stupor or coma. Circulatory failure and deepening coma may occur in more severe cases. Overdose can result in death. Rhabdomyolysis progressing to renal failure has been reported in opioid overdose. Primary attention should be given to the establishment of a patent airway and institution of assisted or controlled ventilation. Oral activated charcoal (50g for adults, 1g/kg for children) may be considered if a substantial amount has been ingested within one hour, provided the airway can be protected. The pure opioid antagonists are specific antidotes against the effects of opioid overdose. Other supportive measures should be employed as needed. In the case of massive overdose, administer naloxone 0.8 mg intravenously. Repeat at 2-3 minute intervals as necessary, or by an infusion of 2 mg in 500 ml of normal saline or 5% dextrose (0.004 mg/ml). The infusion should be run at a rate related to the previous bolus doses administered and should be in accordance with the patient’s response. However, because the duration of action of naloxone is relatively short, the patient must be carefully monitored until spontaneous respiration is reliably re-established. For less severe overdose, administer naloxone 0.2 mg intravenously followed by increments of 0.1 mg every 2 minutes if required. Naloxone should not be administered in the absence of clinically significant respiratory or circulatory depression secondary to morphine overdose. Naloxone should be administered cautiously to persons who are known, or suspected, to be physically dependent on morphine. In such cases, an abrupt or complete reversal of opioid effects may precipitate an acute withdrawal syndrome.
Store in a cool and dry place, protected from light.
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