Urticaria with opioids

Contraindications fc>r nonsalicylate NSAID therapy are the same as those for aspirin (see Box 7-I).The formation of a gastric ulcer or erosion that may bleed profusely is a serious potential problem with NSAIDs. Consequently, the nonsalicylate NSAIDs should be avoided or used with great caution in patients with active peptic ulcer disease. NSAIDs may increase the risk of GI complications even when used in conjunction with low-dose aspirin for cardioprotection. In addition, because of potential crosssensitivity to other NSAIDs, the nonsalicylate NSAIDs should not be given to patients in whom aspirin or other NSAIDs have caused symptoms of asthma, rhinitis, urticaria, angioedema, hypotension, bronchospasm, or of symptoms of hypersensitivity reactions. Opioids, tramadol, or acetaminophen may be suitable alternatives for patients with known or suspected susceptibility. 

Urticaria at the site of injection is due to histamine release. It is seen with pethidine and morphine, but not with oxymorphone, methadone, fentanyl, or sufentanil. Wheal and flare responses to various opioids differ (41). 

Cetirizine competitively antagonizes histamine at the Hi-receptor site and is indicated in the symptomatic relief of symptoms (e.g., nasal, nonnasal) associated with seasonal and perennial allergic rhinitis treatment of uncomplicated skin manifestations of chronic idiopathic urticaria. Histamine is a potent vasodilator, bronchial smooth-muscle constrictor, and stimnlant of nociceptive itch nerves. In addition to histamine, mnltiple chemical itch mediators can act as pruritogens on C-fibers, including neuropeptides, prostaglandins, serotonin, acetylcholine, and bradykinin. Furthermore, new receptor systems such as vanilloid, opioid, and canna-binoid receptors on cutaneous sensory nerve fibers that may modulate itch offer novel targets for antipruritic therapy. 

Therapeutic doses of morphine cause dilation of cutaneous blood vessels. The skin of the face, neck, and upper thorax frequently becomes flushed. These changes may be due in part to the release of histamine and may be responsible for the sweating and pruritus that occasionally follow the systemic administration of morphine. Histamine release probably accounts for the urticaria commonly seen at the site of injection, which is not mediated by opioid receptors and is not blocked by naloxone. It is seen with morphine and meperidine but not with oxymorphone, methadone, fentanyl, or sufentanil. 

The adverse effects of extended-release hydromorphone are similar to other opioid medications with constipation, nausea, vomiting, pruritus, and urticaria being common. Other possible side effects include confusion, somnolence, euphoria, and respiratory depression. Respiratory depression is the most dangerous side effect of hydromorphone as it may result in hypoxia, coma, and death. Hydromophone should be used with caution in patients taking other CNS depressant medications. High doses of hydromorphone can result in the accumulation of neuroexcita-tory metabolites which may cause seizures and myoclonus. One advantage over morphine is that hepatic metabolites of hydromorphone have minimal analgesic or respiratory depressant activity. 

---