Tag Archive: anaesthesia


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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RSI: made stupidly simple

Filed Under: Anaesthetics, Emergency, Pearls and Pitfalls, Useful Evidence by Casey Parker — 6 Comments
March 8, 2012

The Rapid Sequence Intubation is one of those “gotta have” skills for clinicians who work in frontline medicine. Fair to say there are a lot of sequences out there, but they all follow the same basic plan – prepare, inject the juice, and get the airway secured ASAP.  In recent years there have been a few changes to the long-held anaesthetic dogma, based on good evidence.  So I thought I would take a look at a few, see what is new in RSI.

 Pre-oxygenation strategy:

In case you have been living under a rock and missed the Weingart & Levitan paper on Pre-oxygenation and Avoiding Desaturation in Emergency Airway Management here it is.  The practice of throwing on a Hudson mask at 6 litres/min for 5 minutes is no longer the standard of pre-ox we should be aiming for.   Weingart and Levitan have broken down the evidence and created a 3 tier risk-stratification of sick patients with incredibly practical strategies to optimise the pre-ox and decrease the rate of desaturation that inevitably occurs in the sick patients.

  • NIV as pre-oxygenation device – minimise the shunt, maximise the alveolar recruitment
  • Use of a viva-bag with a cheap PEEP vlave as a poor mans CPAP device
  • USe of high flow (15l/min) nasla cannula oxygen to keep the flow of oxygen throughout the procedure and make your apnoeic time much safer for longer.
  • Check out the tables on the last page of the above paper – it is pretty simple and self-explanatory

 

 

The role of cricoid pressure in emergency airway management has come under a lot of scrutiny in recent years.  As is often the case when we look back at the original data – it seemed like a good idea, had some experimental data to support it – but there was no good large-scale evidence that it made a difference to the outcome which we and patients care about!

There was a good review published last month taht asked the hard questions – in Trends in Anaesthesia and Critical Care 2012, Priebe looked at the data in a systematic manner and tried to separate facts from fiction.

In summary: 

  • Cricoid pressure does not have the evidence to make it a mandatory manouvre
  • Clinicians should use individual judgement to guide its use
  • It may be applied, and may help prevent gastric insufflation during BM ventilation
  • If your glottic view is obscured / inadequate – remove it ASAP, then consider BURP instead
  • There is a paucity of good, reliable evidence to support or deny the use of cricoid pressure!

 

There have been a few recent debates on the use of muscle relaxants.

  1. Should they be used at all in critical care settings?  For me this was a surprise, as I was trained by anaesthesia docs who always used them, but there is a tendency to avoid them in some ICUs.  If you want to hear the low-down on the debate in a very enertaining deabte go to Emcrit and listen to the Paralytics debate. Fair to say it has yet to be decided – but I think for the average GP-intubation it remains the standard to use a muscle relaxant.
  2. Which muscle relaxant?  Roc vs. Sux?   well there have been a few posts and opinions out there – check out my post from last year and links to other resources.
    • In summary – Roc seems to prolong the time to desaturation
    • Give it in a big dose ~ 1.2mg/kg and its onset is comparable to Sux
    • The “back out” plan that Sux ‘allows’ usually is not an option in true critical / emergency RSI
    • You don’y have to worry about the patient fighting the vent anytime soon if you use Roc!

 Last point – The PPPPPPP rule [proper planning and preparation prevents piss poor performance]

Having a well thought-out team-orientated approach to emergency airways is the most important thing to do to make your RSIs go well.  This should be done as part of your departments training / drills and education programme.

Dr Tim (KI Docs) has sent me this nifty little aide-memoir to help get your preparation right and to jog one’s thoughts with asimple checklist included.  I will put it in the Resources section at the bottom of the blog, but click here to have a look at the RSI DUMP kit mat.  Print it out in A# or bigger and put it on your resus room trolley.  Thanks Tim

Let me know if this helps – or if you have other new pearls for the old RSI setup.

Casey

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Medical mythology: Antibiotics for C-section – when?

Filed Under: Anaesthetics, Obstetrics, Useful Evidence by Casey Parker — 2 Comments
October 26, 2011

This clinical question comes from Dr Tim (KI Docs).

He got talking to some specialist O&G and Anaesthesia docs about the timing of prophylactic ABs for LUSCS.  Doesn’t ssound too controversial – but it is one of those ‘memes’ of medicine that persist even well after the evidence is in and accounted for with clear benefits demonstrated.

When do you squirt in your IV ABs if you are doing an anaesthetic for LUSCS?

  • The classic teaching is:  after the umbilical cord has been clamped
  • The new way of thinking – ideally give them 30 – 60 mins prior to the skin incision.
So when I was training in Anaesthesia I was taught to give them after clamping.  I don’t even remember asking “why?” – I just did it.  We would give them, then announce over the drapes we had done it – and the Obs doc would say thankyou and we would go back to small talk with the new mum. Everybody happy…. well maybe not
 
In 2007 Sullivan et al from South Carolina did this RCT which was pretty neat, comparing the two regimes for ABs – they found a decrease in the rate of infections, especially endometritis in the early AB group.  The kids all did the same – no change in neonatal outcomes or the need for a sepsis screen.
 
I changed my practice a few years back when I did a refresher block in Anaesthesia in the big tertiary centre for Anaesthetics – basically i just changed because it seemed to be the done thing there – nobody said “hey, we’ve got evidence for this”.  This is how a lot of us ‘head down – bum up’ doctors get out info, no time to look around – just keep doing what we do until someboby tells us different.
 
Have you got any other memes / myths that need busting?  Let me know
Casey
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Clinical Case 031: Big transfusion, Little Hospital = big trouble

Filed Under: Anaesthetics, Clinical Cases, Emergency, Pearls and Pitfalls, Surgery, Useful Evidence by Casey Parker — 3 Comments
October 19, 2011

I have been working on a post dealing with massive transfusion – Broome style – for a while now.  So last week we landed in a tricky situation.  My colleague had taken a chap with a splenic rupture to theatre and used a good volume or red cells – depleting our small blood bank, when we received another incoming trauma case!  So I thought this case was a good one to illustrate the “Stripped back” approach to massive transfusion / trauma resuscitation as I see it in smaller hospitals with limited agents.

Here is the Case:

40 yo man with major crush injury. The chap’s abdomen was trapped for about ten minutes until the load could be moved.  Remained conscious throughout this period.  Ambos bundled him into ED within 10 minutes and he arrived… then had a PEA (likely combo of hypovolemia and severe acidosis) arrest.  CPR and IV adrenaline en route to OT.  Regained consciousness as the ETT went down (doh).  Anaesthetised and prepped for laparotomy.  Initial ABG came back showing a lactate of 15! pH = 6.8.

Laparotomy showed a bunch of sub-segmental mesenteric vein ruptures, a big rectus haematoma with a few litres of red in the peritoneum.  The lab called to say – only 4 bags of FFP left, more PRBCs coming in by plane from elsewhere…

So – how to proceed?  Lets keep this big picture – what strategies do we want to use for:

(1)  Anaesthesia / analgesia

(2)  Fluid resuscitation – what type, how much?  targets?

(3) How do we monitor / measure if we are winning?  What is useful?

(4)  Surgeon – what should they do? When?

(5)  This chap developed quite good going “ACoTS” – what agents / strategy should we use to treat this?

I hope to do a post soon looking at the new guidelines released in 2010 and strip them down to make them usable in the smaller hospitals where blood doesn’t grow on trees and budgets are non-existent.  Watch this space….

So all you experts – what gives us bang for our buck, what can we store for a while and what is just hard / expensive for a small hospital.  Better still – what is cheap and easy, available and going to make a difference to patients like this?

Casey

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Clinical Case 014: “That’s not a knife….”

Filed Under: Anaesthetics, Clinical Cases, Emergency, Surgery, Useful Evidence by Casey Parker — 3 Comments
June 10, 2011

So this is a typical Broome case.  As always – I will not sugar-coat it for you , just a blow by blow description of how it rolled out. Oh, and this one has a happy ending

30 yo. woman presented via ambulance after being stabbed in the left chest (through the axillary tail of her breast).  Seen at 3AM, primary survey all OK, a bit drunk though.  Secondary survey – single stab wound only, explored under local – could not see any penetration through the intercostals, though difficult to say clinically. portable CXR = no pneumothorax, no effusion. No FAST scan done.  Admitted to the ward for observation, IV fluids and surgical RV in AM.  Obs were not normal, but steady overnight.  Hb 134 g/l on gas.

The next AM, complaining of abdo pain, now some shoulder tip pain on the left.  Repeat formal CXR – no PTX, small effusion left costophrenic angle.  I was on for anaesthetics – so called for pre-op review to explore the wound further.  P= 120/min, BP = 110/50, RR = 25/min, feeling sick / vomited.  Hmmm…. not good

I decided to put in a big IV and send bloods for repeat Hb, VBG, cross match etc…the surgeons opted for a CT to look into the cause of the abdo pain – ? occult visceral injury.  So off to the “doughnut of death”

So the VBG comes back: lactate is 4.2 So – something is up, not perfusing her organs as one might hope.  Meanwhile in CT they have found a large amount of blood in the left upper quadrant, a small left chest effusion but no clear source for the bleeding ? spleen.  Clearly she needs some volume resuscitation – the plan is “Haemostatic Resuscitation“, check out the link for an awesome lecture on this topic.  Bottom line – lots of salty water is a bad thing for a bleeding patient, you gotta give some red stuff and products.

So without further ado we whiz her off to OT for a laparotomy, she does pretty well on induction / RSI, art line, central line, IDC and so on.  We now get the formal Hb back – it is 59 g/l (Doh! not good) and we start the packed-cells.  I called for some FFP to give and well – we don’t have platelets.  Of course the lab want us to document ‘coagulaopathy’ before thawing the FFP.  This is one of my pet peeves – in the 60 minutes they take to thaw the FFP, we will likely be in the deep end of ‘coagulopathy’.  Can’t they just trust me, we need some FFP! (See Emcrit podcast on Massive transfusion for details)  My guess was we were dealing with a concurrent blunt trauma to the spleen.

Well, there was a hole in the diaphragm, about an inch lateral to the left ventricle, this wound continued through the following structures: left lobe of liver, lesser omentum (the source of the ongoing bleed), pancreas and just stopped short of the renal vein/artery. The spleen was intact!

At this point I started to get a bit nervous – I had been ventilating the patient for an hour and was starting to think – there must be a lung injury here, is she gonna blow a pneumothorax?  So what to do?  I got out the USS and took some intercostal views to look for a PTX.  None to be seen.

USS has been shown to be more sensitive and specific than supine CXR in trauma – see this review of the literature

So they got control of the bleeding and we got our PRBCs and FFP in and by the time we were closing she had a Hb of 100 and was peeing like a trooper.  We decided to fly her out – the pancreas injury is not one we wanted to “observe” in our little hospital – if she got sick from this we would be in a lot of trouble.  On follow-up all was well – no further surgery required.

The local con’stab’ulary popped in later to say they had found a very long, fishing knife at the scene – my estimate was that it had to be 40cm from the skin wound to the pancreas!

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Roc vs Sux showdown

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pharmacology, Uncategorized by Casey Parker — Leave a comment
May 17, 2011

I have never used Roc for a RSI, but I think that needs to change.

For me this is a “practice changing” stuff – check it out, many thanks to Dr Cliff Reid at Resus.Me for bringing this to my attention.

In ED when the chips are down and “not intubating” is not an option I will be using Roc in place of Sux from now on.

Chris from LITFL has just released his own comparison – check out Roc rocks and Sux sucks here

Follow the links and let me know if you agree…
Casey

PS (19/5/11):  I did it, I broke free from the shackles of Anaesthetic dogma and used Roc to tube a critically ill patient.  Gotta say, she was a known Grade 1 easy-to-tube larynx, so not super-brave of me…I even let the RMO do it.   All went well, the sky did not fall upon my head!

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PROPOFOL – 1st line in Psychosis?

Filed Under: Anaesthetics, Emergency, Pearls and Pitfalls, Pharmacology, Psychiatry by Casey Parker — Leave a comment
May 3, 2011

OK, now that I have got your attention with a controversial headline lets discuss the real topic – safe sedation and management of acutely unwell psychiatric patients.  This is a hugely difficult scenario for many remote hospitals, which are not ‘Authorized’ Mental Health institutions, and are therefore required to transport patients to tertiary Psych hospitals for evaluation and management.  The sedation and transfer of patients admitted under the Mental Health Act is a minefield of disasters and sentinel events / coronial enquiries.

There has been a lot of paper spent in the various agencies on trying to resolve this dilemma, however the incidents keep happening.  Most efforts have been aimed at coming up with Sedation Protocols, however as a frontline worker I find it difficult to apply a single approach to all patients.  So after a lot of pondering and trial-and-error I have come up with my own approach – it is completely without evidence (other than my limited case series) and based on a lot of common-sense pharmacology and local logistical knowledge.

My hospital has one big ward – Geris, babies, surgical patients and usually 1 or 2 mental health inpatients – often 1 on sedation of some form or another.  There are no locked doors, security guards or even many trained Mental Health nurses.  This is far from ideal, but is the reality in most rural towns in Australia.

The basis of my “Safe Sedation Protocol” is a ‘matrix’ which combines both an assessment of the patient’s current risk – to self and others (Q: how dangerous is this patient?)  along with an assessment of their ‘anaesthetic risk’ (Q: How safe is it to sedate this patient?)  - including the airway assessment, medical risk, likelihood to tolerate prolonged sedation or intubation.

What am I trying to achieve with this approach?

  1. Avoid the morbidity associated with prolonged sedation (sometimes 2 – 3 days awaiting transfer).  This morbidity almost exclusively occurs in the patient after admission / sedation whilst awaiting transfer – NOT in transit.
  2. Avoid injury to the staff and the patient – high rate of staff injury makes it tough to retain good nurses
  3. Prevent the deaths which still occur – these are entirely preventable and iatrogenic.
  4. Maybe even save some $/resources???  Just my guess, no data to support this claim…
  5. Put sedation in Psych on an even footing with other sedation.  No longer should we be sedating these people in darkened corners of the hospital, far from appropriate monitoring, with a single “nurse special” in attendance.  Seems obvious but we keep doing it!
  6. Adhere to the “least invasive, least restrictive” principles of the Mental Health Act

Anyway this post is getting too long – so follow the links below if you are interested and let me know what you think:

SAFE Sedation Matrix:  Try and assess the risk and assign a “colour” to your patient – kinda like the NZ cardiovascular risk tool, eh bro! Print this out so you can follow the colour guide below (or tab back and forth if you know what I mean)

Sedate-by-colour  guide: I realise there is a lot of grey between the colours, but this is a “guide” only – designed to make you think twice before jumping into a possible disaster!  Patients are often in a state of flux – so be prepared to up or – down- grade them a colour if the situation changes.  In fact some of the sedation you use will hopefully move them into a cooler, more happy colour group (ie. you are more happy, not necessarily them!)

Sedative Agents - what I use and why.  It is a poor man’s pharmacy, but I like to keep it simple!  Currently being formulated…

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Preoxygenation Pearls

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pearls and Pitfalls by Casey Parker — 10 Comments
April 10, 2011

This post might become a regular under the banner “What I learned from Scott Weingart this week!”  Scott runs the EMCrit blog and if you haven’t seen it – do yourself a favour and download his podcasts from Itunes – he is a great teacher, and pitches his education in a practical / pragmatic fashion that is well suited to rural GP Anaesthetic / ED types.

I got in contact with Scott a few weeks back to give my 5 cents on “pre-oxygenation”, basically I (and a lot of Anaesthetists) was taught to think of it as “denitrogenation” of the lungs – aiming to get the ET O2 up to 80 – 90% prior to RSI.  This is true, however as Scott has pointed out in his video response – this is missing a few crucial steps.  You cannot directly translate what we do in OT back to the crashing ED patient.

Check out Scott’s video and demonstration of pre-oxygenation on himself.
Then check out Scott’s “DSI: delayed sequence intubation” concept – this is basically how to preoxygenate a sick patient, and hopefully avoid them crashing on induction. The link then links to another video demonstrating the technique.

This is me learning a better way, it does break a few of the “Anaesthetic Commandments”.
Would love to hear your comments
Casey

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