Adverse effects of Opioid
| Opioids: adverse effects |
The adverse effects of opioids are summarised in Table 1.5. Opioid withdrawal syndrome includes body aches, diarrhoea, ‘goose flesh’, loss of appetite, nervousness or restlessness, runny nose, sneezing, tremors or shivering, stomach cramps, nausea, sleeplessness, diaphoresis, yawning, asthenia, tachycardia and unexplained fever.
The majority of opioid adverse effects (except those due to withdrawal) can be reversed with the pure opioid antagonist naloxone (see Opioid antagonists). Naloxone is available for parenteral use. Using naloxone to reverse unwanted opioid effects also attenuates analgesia and the dose must be titrated with care to achieve the desired reversal without unmasking pain. Naloxone is rarely indicated when opioids are used for chronic pain.
Adverse effects of opioids (Table 1.5)
| System | Adverse effects |
| cardiovascular | bradycardia due to stimulation of the vagal nucleus in the medulla histamine release by morphine, morphine analogues and pethidine, which may cause vasodilation and hypotension during intravenous administration postural hypotension from peripheral vasodilation and baroreflex inhibition |
| neurological | dose-dependent mental clouding, delirium, sedation, nausea and vomiting, cough suppression, miosis, respiratory depression or apnoea, excitatory phenomena with myoclonus with high doses relative to renal function, reactivation of herpes simplex (spinal and epidural morphine) following intraspinal use of morphine or hydromorphone, central adverse effects may be considerably delayed (6 to 12 hours) (see Epidural administration) |
| dermatological | sweating, flushing urticaria and pruritus due to histamine release |
| gastrointestinal | vomiting, anorexia, decreased gastric motility, increased antral tone, delayed gastric emptying, biliary colic due to spasm of the sphincter of Oddi and raised intrabiliary pressure, slowed digestion, prolonged intestinal transit time, increased anal sphincter tone, constipation; these are caused by mu and delta receptor agonists acting locally and centrally |
| musculoskeletal | chest wall rigidity (with fentanyl and fentanyl analogues), myoclonus |
| neuroendocrine | hypothalamic effects (including inhibition of gonadotrophin-releasing hormone and corticotrophin-releasing factor) leading to decreased gonadotrophins, adrenocorticotrophic hormone, beta endorphin, testosterone and cortisol, and increased prolactin antidiuretic hormone release is variably increased by mu receptor agonists (leading to fluid retention or oedema ), and inhibited by kappa receptor agonists |
| respiratory | dose-related respiratory depression (which is more marked during sleep or with concomitant sedatives, hypnotics, alcohol and general anaesthetics) bronchospasm due to histamine release |
| urinary | urinary retention and difficulty with micturition, increased external sphincter tone, decreased detrusor muscle tone, antidiuretic effect |
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