Tag Archive: analgesia


Ultrasound for Epidurals… I ask an expert: Dr Mitch

Filed Under: Anaesthetics, Obstetrics, Specialist Tips by Casey Parker — 5 Comments
May 10, 2012

I have had a few readers ask questions about the use of ultrasound for the difficult epidural – usually in the labour ward context, but we sometimes run into this in the OT for combined spinal-epidural blocks.  Now I  love all things ultrasound – but looking at the literature it is tough to get a read on the utility of US in the often troublesome area of epidurals.  All those bones – can we see anything useful?  So I have asked an expert, and gotten a few handy, practical pointers.

Dr Chris Mitchell is a Consultant Anaesthestist at King Edward  Memorial Hospital for Women in Perth, Western Australia. But Mitch is more than an Anaesthetist – before he went into specialist training Chris was a rural GP-Anaesthetist in NW WA.  In fact my first job after my training in Anaesthesia I actually replaced Chris!

Now onto the meat of the post – here are Chris’s tips in beautifully illustrated form – click here [US for Epidurals]

I think it should be said – epidurals in the labour ward are an elective procedure.  There is a risk : benefit pay off.  If you are increasing the risk side of the equation as a result of a difficult insertion, then you need to discuss that with the patient – so before calling for he US machine I think it is worth a pause to consider if this is worth a try – I am sure that for the occasional operator this technique wil help, but is no magic bullet!

We usually try and avoid the patients with really tough anatomy – if the BMI is over 35 we usually start to strongly consider referral to a larger institution for a whole raft of safety reasons.

Huge thanks to Dr Mitch for his pearls on epidurals and US.  I would love to hear your experiences and if you have any questions for Chris I will pass them along.  Comments please

Casey

 

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Clinical Case 048: We Ask an Epidural Expert

Filed Under: Anaesthetics, Clinical Cases, Obstetrics, Pearls and Pitfalls, Specialist Tips by Casey Parker — 7 Comments
April 11, 2012

This case is an opportunity for us to learn from an expert.  Epidural analgesia in labour can be rewarding and infuriating.  So I have enlisted the help of Dr Roger Browning – Consultant Anaesthetist at Fremantle and King Edward Memorial Hospitals {tertiary maternity centre in WA}.  I put a few questions to Roger based around a real case to see how the expert goes about troubleshooting common epidural problems. Here we go:

26 yo primigravida, induced for postdatism @ 41 weeks.  She is now ~ 6cm dilated with slowish progress.  You have been called to put in an epidural after she has tried nitrous and a dose of IM morphine.  As you arrive she is clearly very distressed with each contraction.  They are coming every 4 minutes on an Oxytocin infusion.  She is otherwise fit and well, normotensive.
Practitioners should use the technique they have learnt and are most familiar with. I would place a lumbar epidural using a 16G tuohy kit and loss of resistance to saline, and thread the catheter in leaving 4-4.5 cm in the space and secure it to her back using a “lockit”, medium tegarderm and surrrounding fixomull dressing for reinforcement. I would aspirate the catheter to check for blood or CSF and then test the catheter with a 7-8 ml injection of bupivacaine 0.125% + fentanyl 5mcg/ml. If there is no major motor block within 5min (ie indicating subdural or intrathecal catheter) I would then give another 5-8ml of solution ie 15ml in total to get initial analgesia.
At KEMH we use bupivacaine 0.0625% + fentanyl 2.5mcg/ml background infusion of 5ml/hr and PCEA 10ml with 20min lockout, via a CADD pump. In a rural hospital (and other metro hospitals like osborne park) I would prescribe intermittent topups: bupivacaine 0.125% + fentanyl 5mcg/ml 10-15ml hourly PRN, for breakthrough bupivacaine 0.25% 5ml hourly prn, rectal pressure pethidine 50mg/5ml hourly prn, and instrumental delivery / suturing ligonocaine 2% + adrenaline 1:20000 4ml + 4ml one dose only.
3 hours later….
You are called by the midwife for help.  She states that the epidural you put in worked great initially, but… now it is not so good.  She hasn’t made much progress up to 8 cm now.  We are still expecting a few hours of pain at best….
You need to assess whether or not you think the epidural cathetter is still in the epidural space. Check the patient’s back & dressing, if the catheter is now less than 3cm in the space, or there is a lot of fluid under the dressing don’t waste time trying more drugs etc, it has come out, take it out and place another epidural. If everything looks ok then carefully titrate in more bupivacaine 0.125% + fentanyl5mcg/ml solution, larger volumes will often “spread further” and tend to be better than small volumes of more concentrated LA. I will give up to another 20-25ml in increments over 10-20min. If this doesn’t work you should probably take it out and place a new epidural catheter.
Our 26 yo primi has made it to fully, but not really descending well.  The CTG trace has been getting ugly…  some decelerations at first, but now it has become flat / unreactive.  The Obs team call you for a Csection.  It is not Cat 1 urgent, but you want to get her ready ASAP.
Before starting an epidural topup for a CS once again you want to be sure the catheter is in the epidural space and it is working. Look at her back is the catheter < 3cm in the space? is there a lot of fluid under the dressing? has it been working well down in labour ward? If the answer is no to any of these you are probably better off taking it out and doing a spinal.  At KEMH to topup a epidural we use lignocaine 2% + adrenaline 1:200000 (which comes in a 20ml ampoule) and fentanyl 50-75mcg. You should aspirate the catheter to check for csf / blood and then give 5ml as a test dose, check for early profound block (?intrathecal) or tachycardia, perioral tingling (?iv). You should titrate in the lignocaine in 5ml increments every 5min, to max of 7mg/kg (in the average female this is around 25ml) checking the block height regularly, aiming for loss of cold sensation to T4 (nipples) and signs of sacral spread also (difficulty lifting legs off the bed). If after the maximal dose you have an inadequate block you should consider doing a CSE or spinal (using a smaller dose than usual as there is a risk of a high spinal) rather than causing local anaesthetic toxicity with even more lignocaine. I often also give pethidine 50mg (personal practice not dept) as it decreases the severity / incidence of shivering.
You give your top-up, get her ready and the Obs team start cutting.  As soon as they hit the peritonela layer she winces and says she feels sick.  A minute later and she is crying in pain – her husband is looking very scared.
And how do you go about making this decision?]  This description suggests she has an inadequate block and you should stop the surgeons before they proceed to making a uterine incision. The critical issue here is that once the surgeons incise the uterus they are commited to continuing, placental perfusion and foetal oxygenation is impaired and maternal haemorrhage starts, the surgeons cannot / should not be asked to stop for 15min whilst you try to “fiddle with your block”! You need to make a decision prior to this point. Clarify with the patient are they feeling pain or merely touch, believe them if they say it is pain. Check the dermatomes with ice and get the surgeons to “check with forceps etc in the surgical field. If the patient has significant pain at the point of peritoneal incision as in this scenario, and the block appears to be obviously inadequate I would err on the side of converting to a GA before then letting the surgery proceed. If you have already “topped up” with a decent volume of lignocaine 2% + adr (ie 15-25ml) and given this time to work (15-30min) it is unlikely that stopping for another 10min and giving another 5-10ml will make it into a working block. Having said that if they have a difficult airway or look high risk for a GA and you think some more time and more drugs will make a difference then it might be worthwhile to persist, this is an individual risk/benefit decision and you need to talk to the patient /surgeon and explain all of these issues. The most common scenario for pain during a caesarean occurs post delivery, is usually only mild, and related to temporary surgical stimulation whilst swabbing high in the abdomen or fiddling with the ovaries etc. Often you can get a patient through this with iv opioids, inhaled N20, some surgical infiltration of LA (beware max dose if you used alot in the epidural) and distraction with the baby! Sometimes you still need to do a GA to allow the surgery to finish though…
OK – that is epidurals through the eyes of an expert.   Big thanks to Dr Browning for taking the time to answer my questions. This is certainly a part of medicine with plenty of art, less science and a lot of inter-individual variation.  I am keen to hear your tricks and techniques.  Let us know on the comments.
Casey
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Post op pain puzzler discussion

Filed Under: Anaesthetics, Clinical Cases, Critical care / ICU, Surgery, Useful Evidence by Jonathan — 2 Comments
March 9, 2012

Hope you guys enjoyed the case. Here is the discussion and hopefully some useful take home concepts.

This case illustrated a number of key acute and chronic pain concepts that all GP anaesthetists should consider when anaesthetising an opioid tolerant chronic pain patient, namely opioid induced hyperalgesia (OIH), central sensitization (wind up) and pre-emptive analgesia.

In this case, our patient did not receive adequate perioperative analgesia or pre-emptive analgesia based on his chronic pain and opioid dependent background. He was left in distress for a period of time in which his pain became unmanageable (wind up) and remained so for 16 hours. It seemingly became non-responsive (OIH) to opioids but rotation to a new opioid, a background infusion of a NMDA antagonist and the use of a regional technique helped immensely.

Opioid induced Hyperalgesia

Opioid induced hyperalgesia is a paradoxical response to opioids in which patient receiving opioids have an enhanced response to painful stimuli resulting in hyperalgesia. This results from the upregulation of pronociceptive pathways in the central and peripheral nervous system.

Acute OIH occurs in various settings, most commonly post operatively in the opioid dependent patient but also in low dose and maintenance dose regimes. OIH is distinct from tolerance in that tolerance is reduced effectiveness of an opioid at a receptor over time.

NMDA receptor activation is important in the development of OIH. Antagonism of this receptor has been shown to reduce progression and improve post operative pain especially in opioid dependent patients (Wu + Macintyre + Huxtable et al).

Using an opioid PCA in opioid tolerant patients allows consumption and background requirements to be monitored. A basal infusion equivalent to the patient’s usual daily opioid use should be considered or given orally as tolerated.

Ketamine has been shown to reduce OIH in the post-operative setting (Vadivelu + Huxtable + Macintyre et al). There is evidence that subanaesthetic doses (0.1-0.2mg/kg) of ketamine provides excellent analgesia in opioid dependent patients and prevents opioid induced hyperalgesia in patients consuming high doses of opioid for postoperative relief. (Macintyre et al + Vadivelu et al).

Opioid rotation is the practice switching from one opioid to another to improve analgesia and reduce side effects (OIH in this case). This concept is based on the premise that individual opioids act differently on different opioid receptors and that tolerance between them is likely to be incomplete.

Practically this is preformed by using opioid equivalence charts and commencing with 50% of the equivalent dose and titrating up. (Huxtable)

Methadone together with its mu-receptor agonism has weak antagonistic properties on the NMDA receptor thereby playing a small role in OIH.

Wind up (central sensitization)

Post-operative pain results from peripheral nociception (primary hyperalgesia) from tissue injury and resultant central nociception (secondary hyperalgesia) in the spinal cord.

Any continuous barrage of activity to the spinal chord leads to central sensitization. Perioperatively this is related to periods of inadequate analgesia, extensive surgery or infection (Shipton).

As this central sensitization continues from the noxious stimuli, this maintains secondary hyperalgesia, amplifies post operative pain and contributes to chronic pain.  Central sensitization will manifest clinically as hyperalgesia (increased pain sensitivity) and allodynia (pain in response to a previously non-painful stimulus) (Macintyre et al).

 

NMDA receptor activation plays a key role in central sensitization. Medications such as Gabapentin, Pregabalin and Ketamine have been found to improve post operative pain and thought to reduce the progression to chronic pain.

Using Ketamine at subanaesthetic doses (0.1-0.2mg/kg) antagonizes the NMDA receptor and produces an antihyperalgesic, antiallodynic and anti-tolerance effect. It is useful in pain associated with central sensitization such as severe acute pain and opioid resistant pain.

Pregabalin is a safe and well tolerated and helps to reduce perioperative opioid consumption. It has been shown to decrease the incidence in the progression to chronic pain. Gabapentin similarly has been shown to prevent chronic post surgical pain syndromes (Shipton).

Pre-emptive & Preventative Analgesia

Pre-emptive analgesia is treatment that is initiated before the surgical procedure in order to reduce peripheral and central sensitization. This in effect helps to reduce post operative pain and prevent chronic pain development (Dahl)

Preventive analgesia is simply the well thought out provision of analgesia within the postoperative period and persistence of treatment beyond the expected duration and aims to minimize central sensitisation (Macintyre et al)

Ketamine modulates central sensitization caused by incision and tissue damage and can be used perioperatively to antagonize this (Vadivelu).

Preoperative pregabalin is opioid sparing and improves post operative pain scores. It is a useful adjuvant and anti-hyperalgesic agent used in a multimodal regime.

Prevention of Withdrawal

Inadequate opioid supplementations in the post operative period can lead to withdrawal characterized by excitatory autonomic symptoms. The onset will depend on the individual opioid’s duration of action (Macintyre et al).

Opioid tolerant patients should firstly be identified preoperatively and continue their preadmission opioid regimes with appropriate route substitutions as clinically directed.

Heavily weighted non-opioid regimes should be used with caution as opioid tolerant patient due their risk of withdrawal (e.g.: pure non opioid regime or tramadol as a sole opioid).

If withdrawal is suspected, Clondine can be used orally and intravenously to aid in the symptomatic management.

 

Key Messages

Preoperatively identify opioid tolerant and chronic pain patients and make a peri/post operative analgesia plan

 Always replace a patient’s preoperative opioid use in the post-surgical period

Consider preventative analgesics such as Ketamine, Pregabalin and Gabapentin to prevent central sensitization and subsequently wind up pain.

Consider an opioid rotation in patients who respond poorly to an opioid regime or with escalating requirements

Reverse analgesic ladder on recovery with background opiate titration

 

Hope this helps. Let me know what you think.

Jonathan

 

Baron R (2006) Mechanisms of Disease: neuropathic pain – a clinical perspective. Nature Clinical Practice Neurology 2: 95-106 http://www.nature.com/nrneurol/journal/v2/n2/full/ncpneuro0113.html

Dahl JB, Moinche S (2004) Pre-emptive analgesia. British Medical Bulletin 71(1) 13-27 http://bmb.oxfordjournals.org/content/71/1/13.long

Huxtable CA et al (2011) Acute pain management in opioid-tolerant patients: a growing challenge. Anaesthesia & Intensive Care 39: 804-823 http://www.aaic.net.au/document/?D=20110262

Macintyre PE et al (2010) Acute Pain Management: Scientific Evidence 3rd Edition. Australian & New Zealand College of Anaesthetists & Faculty of Pain Medicine http://www.anzca.edu.au/resources/college-publications/Acute%20Pain%20Management/books-and-publications/acutepain.pdf

Mitra S et al (2004) Perioperative Management of Acute in the Opioid dependent Patient. Anesthesiology 101: 212-27 http://journals.lww.com/anesthesiology/Fulltext/2004/07000/Perioperative_Management_of_Acute_Pain_in_the.32.aspx

Patanwala A et al (2007) Opioid Conversion in Acute Care. Annals of Pharmacotherapy 41: 255-67 http://www.theannals.com/content/41/2/255

Shipton E.A (2011) The transition from acute to chronic post surgical pain. Anaesthesia & Intensive Care 39: 824-836 http://www.aaic.net.au/document/?D=20110056

Vadivelu N et al (2010) Recent Advances in Postoperative Pain Management. Yale Journal of Biology and Medicine 83: 11-25 http://www.ncbi.nlm.nih.gov/pubmed/20351978

Wu CL et al (2011) Treatment of acute postoperative pain. Lancet 377: 2215-25 http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)60245-6/abstract

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Paracetamol: mostly harmless?

Filed Under: Emergency, General Practice, Internal Medicine, Paediatrics, Pharmacology, Useful Evidence by Casey Parker — 7 Comments
February 13, 2012

This post was inspired by Colin Parker (the original C. Parker) and the team at EMPEM.org who did a discussion on the recent paper released by the ISAAC group (International Study of Asthma and Allergy in Childhood).  This collaborative of researchers (based in NZ, but internationally reaching – kinda like Dr C. Nickson) has been looking into the epidemiology of atopic disease and environmental influences for over 20 years.

The EMPEM podcast looked at the latest dataset out of ISAAC  it is titled ISAAC blows wheezy whistle on APAP.  This is going to be a serious debate over the coming years – does paracetamol have a causative association with asthma and other atopic disease?  Causality is nigh on impossible to prove, but this massive multinational data-set has established a statistical association that we cannot really ignore.  Unfortunately it raises a lot more questions than it answers!

So here is my summary of the papers and how I think I will integrate this stuff into my practice.

Beasley et al published this paper in the Lancet,2008. This is analysis of the 3rd phase of the ISAAC cohort, more than 200,000 kids.

  • Paracetamol use in the 1st year of life was associated with increase rate of asthma at 6-7 years age.  The odds ratio was about 1.5 (with a narrow CI)
  • Current use of paracetamol had a dose-related association with current symptoms of asthma
  • There was also an association with other atopic conditions- rhino-conjunctivitis, eczema..

Eyers and the above-mentioned Beasley published this in Clinical & Experimental Allergy 2011

  • Antenatal exposure to paracetamol also had an association with childhood asthma (OR 1.21 – just significant)
  • So, now do we keep saying paracetamol is safe to expecting mums???

What about using ibuprofen in asthmatics with acute febrile illness?  The teaching has always been that Ibuprofen was bad – it might trigger asthma – but is this true?

  • Lesko et al, in Pediatrics 2002 did this neat study of nearly 2000 kids and largely debunked this theory.
  • The paracetamol group did worse – more asthma symptoms than the ibuprofen group.
  • Unfortunately no control / placebo group to get a feel for the true effect – was paracetamol harmful or ibuprofen protecting the kids?

Peirce & Voss (Annals of Pharmacotherapy 2010) did a meta-analysis comparing paracetamol to ibuprofen in terms of safety and efficacy – fever and pain reduction.  For me this is the clincher:

  • Ibuprofen was more effective than paracetamol for the symptom control – fever and pain
  • There was almost no adverse events, they were equally very safe in the immediate sense.
  • So ibuprofen looks like a winner here.

So how does this all fit together and what does it mean for the patient you are about to see in your practice?

  1. Paracetamol might be a bit less safe than we have all been thinking – I think the data is not yet there to show a causative effect – but Vioxx was blacklisted for less heinous crimes!
  2. The medical dogma that ibuprofen is bad for asthmatics and paracetamol is safe has pretty much been reversed.  I am definitely giving ibuprofen as first-line to the next atopic kid I see with an indication for it!
  3. Not sure what to tell the pregnant mums:  take nothing? might be the only truly “safe” option
  4. Ibuprofen does look better for fever and analgesia for kids.  It might have a protective role in atopic disease.  So I think it should be 1st line.
  5. On the whole, the data is still inconclusive, therefore hard to apply to the individual.  However, I think as an institution / hospital we need to look at our policy / practice – is giving every snotty, febrile kid Panadol at triage a wise move?  I think we need to step back and be more selective with our use of these medicaines – after all they don’t really stop anything truly bad (seizures, brain-injury etc) from happening – so the risk must justify the benefits?

 

Ok, this I expect to cause a few ripples through the waters of common practice.  Please let me know – how will you change if at all?

Casey

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Irukandji syndrome – the swarm hits Broome

Filed Under: Emergency, General Practice, Tropical disease by Casey Parker — 1 Comment
January 21, 2012

We had our first ‘swarm’ of Irukandji syndrome victims for the season last week – with associated media frenzy!

For those of you who are not familiar with Irukandji syndrome – it is a jellyfish envenomation, the villain is the Carukia barnesi, a tiny little jelly fish with just 4 tentacles that packs a mighty punch!  It really is a very unpleasant syndrome:

  • Symptoms onset 20 minutes to hours after a sting [after leaving the beach etc]
  • the sting is often invisible or a small wheal
  • symptoms: well imagine a bloke got pregnant, developed pre-eclampsia and went into labour
    • Severe pain that spreads all over the body, hypertension, vomiting, sweating and “a sense of doom”
  • Severe cases: acute pulmonary oedema, off the chart hypertension => intracerebral bleed (2 cases of death by this cause)

Mike Cadogan (LITFL founder) knows the toxicology of this much better than I do – so if you are interested read the posts at LITFL (below)

So how do I treat this syndrome?

  • Lots of fentanyl.  I find intranasal fentanyl great for kids – the milder cases you can manage with a few doses and no need to further upset the usually inconsolable child with a needle
  • IV fentanyl if required, sometimes even a PCA for the prolonged case with significant pain.
  • If you can get the pain under control, then I have not seen a lot of persistent hypertension in the dangerous range
  • IV GTN infusion can be used to manage the catecholamine driven hypertension
  • Magnesium is something that is done a lot in some centres – it is purported to decrease pain significantly and we know it can help drop the BP.  Personally I have not had to go to the second line of therapy in the last few years – so I have not much experience with it – but I think it makes sense if you are not winning with good doses of opiates
  • Other than that the management is supportive – control the BP and watch for neurology and signs of APO.

Oh, and the name – Irukandji – it is not the name of the jelly fish, it is great for Scrabble.  It is the name of the traditional custodians of the coastal lands north of Cairns, sometimes Yirrganydji is the spelling.

So, remember your swimmer suit and 2 litres of vinegar when you go swimming in the north of Australia

If you want to know more about the things that sting in WA – check out this publication from the WA Museum

-  Casey

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Clinical Case 010: Heartattack and Vine

Filed Under: Clinical Cases, Critical care / ICU, Emergency, General Practice, Internal Medicine, Pharmacology, Useful Evidence by Casey Parker — 7 Comments
May 29, 2011
Thanks to Susanna, Med. Student, for this case and clinical question.
“57 year old male presents, cold and sweaty, with central crushing chest pain radiating to left jaw and shoulder.
Only risk factors were being male, aboriginal and a smoker.
Interestingly enough the data from Han et al says that knowing background risk factors is not that useful for the average chest pain work up. Caveats to this – the younger patient (<40 yo) is more likley to have an ACS if they have more than 4 risk factors. Older patients – not so much.  Of all the big risk factors – smoking is the most predictive of an acute coronary syndrome.  My guess is that Aboriginality would probably be a predictor in the younger age groups, but I haven’t seen the evidence.  The best predictors in the ED: the story, the ECG and previous ischemic disease. 

On admission he was hypotensive and bradycardic and ECG showed ST elevation in leads II, III and AVF with likely new onset complete (3rd degree) heart block.
The usual STEMI protocol was put into place but fentanyl was used instead of morphine as an analgesia.  This worked well and the resus went off without a hitch. I’m new to this all still but when I asked the physician and several experienced doctors all said they had never used fentanyl. A literature search brought up little supportive evidence for fentanyl use in an acute MI. What is the efficacy of fentanyl compared with morphine in analgesia for an acute myocardial infarction when is it indicated in AMI? ”
So in response to Susannah’s erudite questions I have decided to do a bit of an evidence-based dissection of the management of STEMI in the average rural hospital. Then outline my preference for fentanyl in seriously unwell patients.  As usual I have basically plagiarised the work off of much smarter gurus – all the links take you to original references eventually…
We have used this for our whole careers – but it seems it is not shown to be helpful and there is a trend towards harm, This is still a bit controversial – so should it be reserved for the hypoxic / crashing patients? The Cochrane review says – not enough data for safety or benefit.
Aspirin is well proven as a safe and efficacious intervention in acute MI. Large studies showing mortality benefit with no serious harm – some minor bleeding events only. Evidence here
The evidence here is a bit more difficult to interpret. A lot of the trials looked at clopidogrel in patients undergoing primary angioplasty – so not quite applicable to our rural patients. The trials looking at short-term outcomes did not show much difference in mortality or further MI – there was a decrease in ‘need for repeat angioplasty’ – hard to sell to the average patient! In addition there was an increase in total number of  ”bleeding events” – so the jury is left a little edgy.   Looking at the longer term data the COMMIT and CLARITY studies showed some benefit.
Thrombolysis is well proven to benefit true STEMI. However, time is crucial – the benefits rapidly decline after the first few hours. There is also good evidence for pre-hospital thrombolytic therapy where it can be delivered by appropriately trained staff. As rural Docs our job is to recognise the signs, ECG changes and know the contraindications – so that treatment can be given as soon as possible. The number-need-to-treat is 43
Well this is interesting. Heparin is part of the thrombolysis protocols for tenecteplase / reteplase – so we give it. However, if you look at the numbers for all ACS, including STEMI it is actually not such a good idea. See the Cochrane review. My practice – I thrombolyse them, then call the Cardiology team wom will be admitting the patient and ask for their opinion – often it depends on the logistics of retrieval / time to angioplasty etc…
Another casualty of a literature survey – B-blockers have not been shown to be beneficial – they have decreased some common complications, but they have caused some cardiogenic shock – so nett effect: no benefit, maybe harmful. See the NNT review
So now to Susanna’s question – why would I use Fentanyl in place of the traditional morphine to control this man’s pain.
As Susanna found, there is no evidence to support this – as I am sure there is none to support the use of morphine.  However, here is my personal rationale for fentanyl – I apply this in any situation (ACS, sepsis, perioperatively, trauma) where the patient is proper sick, changing quickly and at risk of poor end-organ perfusion at some point in the near future.
  • Fentanyl is quick onset, shorter action – easier to titrate.  Morph takes ~15 mins to peak effect – so you have given the second bolus before the first worked usually, then Bam! it all catches up, and you can’t suck it out!  So I feel you end up using less opiate for the same analgesia / outcome.
  • Fentanyl is fentanyl.  Morphine is not just morphine – you are also ‘injecting’ its ugly step-sisters / metabolites which can accumulate in the ill patient and cause unwanted effects – sedation, hypotension, respiratory depression etc
  • Fentanyl is not so reliant on renal clearance as morphine and its metabolites
  • Fent doesn’t cause as much itch / histamine release.  Though an itchy nose is very common (why? somebody tell me)
  • I just like being able to give a drug that works – you inject it and a minute later the patient feels better / less pain.
  • Fentanyl’s short half-life means it can be reversed with naloxone and there is less risk of the rebound seen after naloxone wears off and Morph is still hanging around

Anyway, that is my wrap up on STEMI and all things fentanyl.  I am ignoring the heart block – a whole other post I am afraid.. Love to hear your comments.  Casey

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Case 0003 – Beyond opiates in Chronic pain

Filed Under: Anaesthetics, Clinical Cases, General Practice, Pearls and Pitfalls by Casey Parker — Leave a comment
March 13, 2011

63 yo man with advanced oesophageal cancer, diagnosed 18 months ago.  Now has extensive liver mets, retroperitoneal tumour and fungating open tumour in lower abdomen.

Presents to ED Saturday morning with intractable visceral-sounding pain – “not responding to his usual pain tablets”.  So what is he taking for this pain :

2 x 80 mg OxyContin tabs every 3 hours, plus 10 or 11 Oxynorm tabs for breakthrough each day – yes, thats right a total of 1500 mg of oxycodone/day.  He is NOT taking any other pain medications – does use some oral Movicol for constipation and prn PR Microlax enemas.

So, how can we get control of this pain?  What other options are available to us?  He is keen to stay at home and is relatively active, not keen on parenteral meds…. he reluctantly agrees to stay in for a day or so in order for us to titrate some new meds for the pain – what are you going to write up??

Here is my cocktail, trying to avoid parenteral drugs for discharge. Any comments:

  1. Maintain baseline opiate load – 240 mg SR Oxycontin tds (roughly 1 g background) – don’t let him withdraw!
  2. Breakthrough opiates : oxycodone 40 – 60 mg prn  - in case the next few additions don’t cut it…
  3. Paracetamol: 1g regularly
  4. Consider a trial of NSAID – if tolerated – celocoxib 200 mg
  5. Nocte pregabalin – start with 150 mg – I have had good results with this, especially for the sleep / nocte pain control
  6. Backup plan – try some prn tramadol , either it helps or it doesn’t
  7. If all else fails – rotate opiates, the dose of morphine is huge, too much for standard patches, consider Hydomorph pump?
  8. What about ketamine – if you are struggling to get over the opiate wind-up – “try to reset the clock” with a 48 hour infusion.
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