Oral opiates as discharge medications

Date implemented – 04/2015

Date for review – 04/2018

Author – Dr Roger Swift



Pain is a leading presenting complaint to the ED.  Failure to adequately relieve pain may be viewed as a failure of treatment.  Pain can neither be verified nor disproved.  Err on the side of the patient.  Acute pain that is unrelieved by non-pharmaceutical measures and unrelieved by paracetamol or NSAIDs may require use of opiates after discharge from ED.

The patients most likely to have a serious adverse event from oral opiates are older patients on high-dose, long-acting opiates and benzodiazepines. The most serious adverse event is excessive sedation and respiratory depression.

Prescribing long courses of oral opiates for non-cancer pain risks the patient becoming physically dependent on opiates without any long term relief of their pain. Prolonged courses of opiates may lead to habituation, requiring ever higher doses, with diminishing effectiveness and physical dependence.

Although there are some patients that game the system to obtain opiates for non-medical use, identifying them in the Emergency Department can be difficult. Some will be obvious from frequent presentations, grossly abnormal illness behaviour, history of drug misuse, or those seeking prescription for lost or stolen S8 drugs. Other more skilled individuals may easily go undetected. Be familiar with drug seeking behaviours (listed below). Check registries for opiate users or suspected doctor shoppers;

  • Drug Dependency Register WA DoH phone 9388 4945 during office hours – only available for Medical Practitioners with a prescriber number.
  • Prescription Shopping Information Service phone 1800 631 181
  • For Next Step clients dosing at the Next Step Clinic, telephone 9219 1919 and ask for the dispensary.



  1. Only use short-acting opiates for the treatment of acute pain when opiates are indicated.
  2. Use non-opiate alternatives including; paracetamol, NSAID, carbamazepine, amitriptyline, gabapentin, pregabalin, diazepam, clonidine, dexamethasone, etc.
  3. Start with the lowest possible effective dose of opiate.
  4. Discuss with ED Consultant or most senior ED doctor before prescribing discharge opiates.
  5. Prescribe no more than three days or 20 tablets of short acting opiate if indicated.
  6. Make clear to anyone given a prescription for opiates that no repeat prescriptions will be provided by ED.
  7. Do not prescribe opiates to patients on opiate dependence program (e.g. methadone) before contacting dispensing source, confirming dose and advising that dose has been given ED (i.e. patients requiring admission or prolonged stay in ED).
  8. Counsel patients on the risk of adverse reactions, especially sedation and respiratory depression, and not to drive or operate heavy machinery.
  9. Patients already taking benzodiazepines and/or other opiates have a higher risk of adverse event.
  10. Do not initiate treatment with long-acting or extended-release opiates in the Emergency Department.
  11. Opiates are not generally useful for the management of chronic pain. Address exacerbations of chronic or recurrent pain conditions with non-opioid analgesics and non-pharmacological therapies. Liaise with Chronic Pain clinician when possible.
  12. Do not use parentral opiates for exacerbation of chronic pain.
  13. Do not prescribe opiates if a patient claims a lost, stolen, or destroyed prescription unless exceptional circumstances and then only provide a one to two-day supply.
  14. Contact the usual practitioner if prescribing opiates (e.g. phone or Communik8 letter)
  15. Consider prescribing opiate agonist/antagonist if risk of drug seeking behaviour.


Drug Seeking Behaviour

From The Journal of Emergency Medicine, Vol. 42, No. 1, page 18, 2012. Note, these behaviours are suggestive but not diagnostic.

Behaviours associated with patients who had a pre-existing management plan including referral to a drug dependency program or to reduce use of opiates or muscle relaxants (compared to a control group with no management plan).


Table 3. Odds Ratios for Studied Behaviours

Odds Ratio 95% CI
Requesting parenteral analgesia N/A N/A
>10/10 pain N/A N/A
Three visits in 7 days 30.8 10.84–87.30
Over 3 pain complaints 29.3 12.18–70.33
States out of medication 26.9 12.28–58.72
Drug requested by name 26.3 11.54–59.86
Presents for prescription refill 19.2 7.42–49.52
Lost or stolen medication 14.1 1.82–109.37
10 out of 10 pain 13.9 7.98–24.19
Back pain 13.6 7.17–25.60
Headache 10.9 5.48–21.85
Dental pain 6.3 1.79–21.81
Non-narcotic allergy 3.4 1.55–7.57


Also examine for evidence of current or previous IVDU. Search electronic records for history of IVDU or drug dependence, frequent presentations to different hospitals with pain related problems, and use of aliases.


Non-Opiate Pharmaceuticals

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e  Chapter 38. Acute Pain Management in Adults

Drug Use Initial Dosage Titrate Typical Effective Dosage (maximum daily dose)
Amitriptyline Chronic pain 0.1 milligram/kg PO once in the evening Increase over 2–3 weeks 0.5–2.0 milligrams/kg/day

(150 milligrams per day)

Carbamazepine Trigeminal neuralgia 100 milligrams PO twice a day Increase 100–200 milligrams per day 200–400 milligrams PO twice a day (1200 milligrams per day)
Gabapentin Neuropathic pain, post-herpetic neuralgia 300 milligrams PO per day Increase up to 300 milligrams per day 300–1200 milligrams PO three times a day

(3600 milligrams per day)

Pregabalin Neuropathic pain, post-herpetic neuralgia 50 milligrams PO three times a day Increase over 1 week 300 milligrams per day divided twice a day or three times a day (600 milligrams per day)




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Does this patient have a seizure or syncope?

There are many components to this topic, and the knowledge is variable from junior to senior physicians. So, I put together this Q&A style post to consolidate all the web resources, my collection, and hopefully educate someone. Enjoy :)


 A universally challenging problem facing emergency physicians; this Lancet article sums up the topic very well, in fair detail. (See this reference).

It really boils down to a good history - here is where the eyewitnesses and paramedics are really helpful (sometimes). And no... urinary incontinence doesn't quite help (See this reference). This questionnaire may be useful:

Syncope scoring

Or this flowchart combining history, physical and eye-witness account:

Syncope clinical features

Convulsions are often seen in syncope as well (convulsive syncope), and are more common than you think (70-90%), but the duration is usually brief.

Seizure is more likely if:
  • Tonic-clonic movements are usually prolonged and their onset coincides with loss of consciousness
  • Hemilateral clonic movement
  • Clear automatisms such as chewing or lip smacking or frothing at the mouth (partial seizure)
  • Tongue biting (especially laterally)
  • Blue face
  • Prior to the event: aura (such as unusual smell)
  • Post-ictal confusion
Syncope is more likely if:
  • Tonic-clonic movements are always of short duration (<15 sec) and they start after the loss of consciousness
  • Prior to the event: Nausea, vomiting, feeling of cold, sweating (neurally-mediated)
  • short duration


Nope, serum prolactin is almost completely hopeless. (See this reference - report form the American Academy of Neurology)

 What the article recommends:
  • Serum prolactin assay does NOT distinguish epileptic seizures from syncope (in both conditions, serum prolactin are elevated). Level of Evidence B
  • Elevated serum prolactin assay, when measured in the appropriate clinical setting at 10 to 20 minutes after a suspected event, is a useful adjunct for the differentiation of generalized tonic-clonic or complex partial seizure from psychogenic nonepileptic seizure among adults and older children. Level of Evidence B


 A misconception is that transient LOC are commonly due to a TIA. The fact is, to have LOC in TIA/stroke, there must be either bilateral carotid artery disease or posterior circulation disease, in which there must be other accompanying neurological signs and symptoms! (e.g. cerebellar signs)

(See this reference - TIA definition) - What it says:

Syncope: A transient self-limited loss of consciousness, usually leading to falling. The onset is relatively rapid, and the subsequent recovery is spontaneous, complete and relatively prompt. The underlying mechanism is a transient global cerebral hypoperfusion.

Transient ischemic attacks are different in that they represent focal cerebral or retinal hypoperfusion. In general, syncope is brief loss of consciousness without focal neurologic signs or symptoms, whereas transient ischemic attacks are brief focal neurologic signs and symptoms without loss of consciousness.

 European Society for Cardiology syncope guidelines say this:

TIA related to a carotid artery does not cause T-LOC. When almost all cerebral arteries are occluded, transient obstruction of the remaining vessel subtending a large portion of the brain may extremely rarely affect consciousness only in the standing position. Moreover, focal neurological signs are much more prevalent.

TIA of the vertebrobasilar system can cause LOC, but there are always focal signs, usually limb weakness, gait and limb ataxia, ocu-lomotor palsies, and oropharyngeal dysfunction. For all practical purposes a TIA concerns a focal deficit without LOC, and syncope the opposite.


This is a common mis-understanding. Somehow, many doctors think that patients with syncope mandates a CT brain. In fact, European Society for Cardiology guidelines and ACEP guidelines DO NOT recommend routine CT / MRI for syncope. Image only if a seizure is suspected to be the more likely cause.

ALIEM goes on to advise when a CT brain is advised:

Clinicians might consider obtaining a Head CT as part of the syncope evaluation for the following findings:
  • Trauma above the clavicle 
  • Persistent neurologic deficit or complaint 
  • Age >65 
  • Sudden onset headache 
  • Patients on warfarin (coumadin)


 The most well known tools are the San Francisco Syncope Rule and the Boston Syncope Rule.

  Syncope risk stratification

 This is from ALIEM post on Management of Syncope, it is a good read. What do they say?

Bottomline: "Educated clinician judgment based on EBM guidelines (European Society for Cardiology and ACEP) seems to be the best strategy for management. Syncope prediction rules can certainly aid this process, but they do not yet fit for use alone for risk stratification in any population."

I generally agree with that, and don't use any form of risk stratification tool for syncope. If you do use the SFSR for example, use it as an adjunct to clinical judgement. So what then? See below...  


In my opinion, I like what Dr Smith's ECG blog has laid out, and more recently on emDocs as well. What they say also follow fairly closely what ACEP guidelines recommend. In fact, all you really need is HISTORY, PHYSICAL and a good read of the ECG! (Dr Smith's post is longer than mine, and contain very valuable info, references to this topic). After that, it is about a GOOD CLINICAL ASSESSMENT and investigating for what you think the likely causes are.

Only last month in Aug 2015, ESC published a consensus syncope risk stratification in the emergency department. (See this reference). A very simple conceptual flow chart:

  ED syncope model

 A short 6 page article well worth your time and to think about.  

Web References