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Opioids and palliative care |
The palliative care article "An approach to pain management in palliative care" dealt with the four step approach to pain management in palliative care namely:
1. Diagnose and treat the cause of pain where possible.
2. Raise the pain threshold.
3. Consider adding an opioid.
4. Recognise and treat neuropathic pain appropriately.
This article covers step 3 – “Adding an opioid”, and for the most part will discuss the use of morphine in palliative care as it remains the strong opioid of choice in palliative pain management. It is most effective for visceral and soft tissue pain, and can be less effective with bone, nerve and colicky pains.
Uses
While morphine is predominantly used for analgesia, it is also effective for the symptomatic relief of cough, dyspnoea and diarrhoea (although loperamide is a peripherally acting opioid and 30 times more potent than codeine.)
Morphine is not an effective sedative; its sedative properties are a side effect, not a desired effect. Giving morphine as a sedative especially in the terminal phase will cause myoclonus, confusion and possibly agitation. If sedation is necessary benzodiazepines or phenothiazines are much more effective.
Mechanism
Pain receptors when stimulated by noxious stimuli initiate firing in primary afferent fibres that synapse in the dorsal horn of the spinal cord. The relay neurones in the dorsal horn transmit pain information to the sensory cortex via neurones in the thalamus. The activity of the dorsal horn relay neurones is modulated by several inhibitory inputs. These include local interneurones, which release opioid peptides, and descending noradrenergic and serotonergic fibres, which originate in the brainstem and are themselves activated by opioid peptides. Thus opioid peptide release in both the brainstem and the spinal cord can reduce the activity of the dorsal horn relay neurones and can cause analgesia. The effects of opioid peptides are mediated by specific opioid receptors.
Opioid analgesics are drugs that mimic endogenous opioid peptides by causing prolonged activation of opioid receptors. However opioid receptors are not solely located in the brainstem. Receptors are located elsewhere in the body and the activation of these receptors give rise to the side effects of opioids.
Limbic system – euphoria
Respiratory centre – respiratory depression
Chemoreceptive trigger zone – nausea and vomiting
Gut – constipation, biliary colic, nausea
Other common opioid analgesics include methadone, fentanyl, oxycodone and codeine. Pethidine, although an opioid, is not used in palliative care because it is very short acting and its metabolite nor pethidine accumulates and lowers the epileptic threshold. 1000mg of pethidine/24 hours will cause grand mal seizures.
Morphine myths
1. Morphine is dangerous because it depresses respiration
Respiratory depression does not occur in patients with pain. Pain acts like a physiological antidote to respiratory depression; the mechanism to this is unclear. It is more accurate to say morphine overdose causes respiratory depression, therefore as long as morphine is titrated and the dose reduced if drowsiness occurs, there is no danger of respiratory depression.
2. Morphine is “addictive”
A physical dependence to morphine will develop with continued use, in that a “withdrawal” syndrome is precipitated with sudden termination of administration. However psychological dependence is a very rare phenomenon in the palliative care population.
3. Tolerance develops rapidly
Not true. A steady increase in dose requirement may occur, but is certainly not automatic and is usually due to progressive disease. However, tolerance can develop rapidly with IV use, which is why subcutaneous paranteral administration is preferred. If tolerance does develop, opioid rotation and the use of an NMDA antagonist, eg. Ketamine, may prove effective in reversing tolerance. (More on NMDA antagonists in later articles.)
Contra-indications
True morphine allergy, ie. producing anaphylaxis, is extremely rare and the only absolute contra indication. However many patients claim to be allergic to morphine when actually what they have experienced is side effects, eg. nausea and vomiting, itch, drowsiness, etc., which is usually related to receiving a larger than necessary dose. It is always worth re-using opioids at low doses initially on these patients. Often substituting one preparation for another can really reduce the side effects, eg. change Kapanol to MS Contin or Oxycontin, or MS Contin to fentanyl patches, etc.
Cautious use (ie. necessitating lower doses)
1. Renal failure
The metabolite of morphine M6G is more potent than morphine and renally excreted. Therefore with renal failure, M6G accumulates and toxicity will develop quickly i.e. myoclonus, delirium, sedation, pinpoint pupils.
This is avoided by using lower doses of morphine or administering less frequently, ie. 8 hourly instead of 4 hourly.
2. Severe hepatic failure
3. Significant pulmonary disease
Administration
Morphine exists in two forms
1. Immediate release - Oral (works within 20 minutes and Subcutaneous)analgesic for 4 hours
2. Slow release – MS Contin – given 12 hourly or Kapanol – given 12 or 24 hourly
Titration
The aim is to find the optimal dose of morphine without producing unnecessary side effects, eg. sedation.
Use 4 hourly morphine to find the optimal dose, then transfer to slow release. Eg. A patient takes 5mg oral morphine which helps his pain but only last 2½ hours. An increase to 10mg helps his pain and lasts for 4 hours. As there are six 4 hourly doses in a 24 hour period, he will require: 10mg x 6 = 60mg/24hrs.
This equates to 30mg bd MS Contin.
In general practice, it is often more practical to start patients on a slow release preparation but you do run the risk of accidentally overdosing or underdosing the patient who may then lose confidence in morphine completely.
Golden rules
1. Starting dose
Opioid naïve – 5mg q4hrs
2. Increasing the dose
If the patient is not pain free for the 4 hours and is not drowsy, increase the dose. Increase the dose by 30-50%
Give breakthroughs as per the usual 4th hourly dose. If more than 3 breakthroughs are required in 24 hours, increase the slow release morphine. Eg. A patient on MS Contin 30mg bd requires 4 x 10mg of mist morphine, therefore increase the total MS Contin by 40mg to 60mg bd.
3. Decreasing the dose
Pain free and drowsy, decrease the dose.
After a nerve blocking procedure, titrate down to avoid excessive drowsiness or respiratory depression.
Decrease the dose by 30-50%.
4. Subcutaneous
Give s/c not oral – for nausea and vomiting, dysphagia, bowel obstruction. Divide the dose by half: e.g. 10mg Mist Morphine = 5mg s/c Morphine
5. The hand that writes the morphine must also write the laxative. Ignore this at your peril!
Two useful statistics:
90% of patients only require 5-60mg oral morphine 4 hourly.
15% of patients with pain will need specialist intervention.
Joanne Doran is the area medical director for palliative care based at St Vincent's Hospital, Lismore, NSW, Australia.
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