Category: Useful Evidence


Medical Myths: Fever = blood cultures now!

Filed Under: Emergency, Internal Medicine, Useful Evidence by Casey Parker — 6 Comments
May 1, 2012

When I was an intern in a big old hospital one of the tasks we did was taking blood cultures off of patients who spiked fevers on the wards.  In fact thinking back on it, I think I was taking cultures to appease the senior ward nurses and not really stopping to think about the why?  Probably stabbed any number of patients with early sepsis and happily continued onto the next job without even worrying about the BP, lactate, line sepsis etc etc…  It was an annoying task as it was “time critical” – you had to get the cultures ASAP as the fever spiked – or else the boss would be grumpy, we might “miss the sepsis”.

Were we right to worry about getting the cultures done in a timely fashion?  Did it have to be “during the rigors?”

My colleague pointed out this paper by Riedel et al, Journ Clinical MIcro (April 2008).  This case-review looked at 1436 patients and their fever – culture timing profile and found that it really didn’t matter when you took the cultures in realtion to the spike of a fever – the majority of positive came from cultures taken hours after a fever.  This study cannot comment on the numbers of “missed” bacteremias as a result of wrong / delayed timing.

So what does it all mean for you, next time the nurse calls to tell you Mr Jones has spiked a temp….

  1. Walk, don’t run – it really doesn’t matter if you do it now or in an hour.
  2. Go there, look at the patient and think “what is going on here?”  Does he have a reason to be febrile already documented, on appropriate therapy?  Or, is he someone who needs to be reassessed for sepsis – does he have a line infection?  Does he have a wound infection?  Is he in SIRS or worse?  Do you need other sites cultured – urine, chest etc?
  3. Take cultures as clean as possible – aseptic approach – try and avoid those frustrating false positive BCs
  4. Contemplate changing the plan – look at the AB cover – is is sensible? Do you need to yank a line or call a surgeon to drain some pus?

Thanks Ben for the article.  Interns – relax, but do a more thorough job!    Casey

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Case 044: the answer

Filed Under: Clinical Cases, Useful Evidence by Casey Parker — 8 Comments
March 19, 2012

Ok, 24 hours in and we have a winner.  The most comprehensive and correct / first in (20 minutes) answer was from Egerton Yorrick Davis IV (I wonder what happened to the first 3 EYDs?)  His answer went right to the red heart of the problem and picked up the diagnostic pitfalls en route.  Here it is:

“Most 40y old women will have gallstones – it is easy to get entrapped by this diagnosis as a cause of epigastric pain.
Dyspepsia + anemia = upper GI bleed until proven otherwise – but penicious anemia or gastritis with parietal cell depletion and intrinsic factor deficiency leading to VitB12 is in the DDX.
Depression is also common – but can be a feature of anemia, or even B12 deficiency.
When she has her op she may have got nitrous oxide as part of her anesthetic – which could exacerbate B12 deficiency – and was probably fasted +/- eating a low B12 diet (meat, eggs, milk)
Neurological symptoms (including paraestheiae) are the other component of the triad for B12 deficiency.
EYD IV”

If you want to see more on Subacute Combined cord degeneration – check out this link(Neurology, Neurosurgery and Psychiarty 1998) which was sent in by Minh Le Cong as part of his answer (too slow sorry Minh).

Great answers though, thanks for the input.  Casey

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C-spine Trauma: in a town with no CT

Filed Under: Critical care / ICU, Emergency, Pearls and Pitfalls, Useful Evidence by Casey Parker — 3 Comments
March 12, 2012

I worked for 4 years in a town with no CT (but plenty of beer) – and it is fair to say that the protocols for managing C-spine trauma were often makeshift.  Logistics rather than clinical acumen often determined who got a CT rather than ‘just’ clinical exam and a set of plain films.  But…. why should my patient get less than gold-standard care – just because of geography?   I realize this is a bit idealistic, but when it comes to life-long disability – do we really want to take that risk?

Now in recent months there has been a lot of posting and banter about C-spine trauma on the popular medical blogs / podcasts.  So I thought I would trawl through the literature and come up with a pragmatic protocol for those of us who work in CT-isolation, or where it is not available 24/7.  Amusingly here is a hot debate about whether you need to MRI patients with pain and a normal CT – Yep, true!  We are not even close to that debate in regional Australia!

The logistics of distance mean that I break (‘scuse the pun) C-spine trauma into 3 main groups:

  1. The minor trauma – these are the patients whom you can clear with clinical history, exam and NO imaging is required.
  2. The fuzzy middle group: they cannot be cleared on clinical grounds for whatever reason, or they have failed the clinical clearance. Yet, they remain asymptomatic, have no high risk features –  your “gestalt” is that they are probably OK.
  3. The major trauma: these patients are high risk – based on the mechanism of injury, associated injuries or the presence of neurology suggestive of a cord injury

I will try and explain how I think each of these should be managed based on my reading of the recent evidence, the reality of rural practice and a measure of common-sense.  If you want to get some great background and refresher in anatomy I have a few suggestions for your valuable time:

OK, without further waffling – lets analyse these 3 groups and try to cook up a rough protocol for each.
In some ways this should be the easiest group – but is also the one that causes the most frequent consternation!
Clearing a C-spine is one of those moments in medicine when you just have to trust your call. This is especially true in the bush – if you decide not to clear them – you are probably committing them to a long transfer strapped to a spinal board: uncomfortable and expensive!
So how do you clear a C-spine clinically? Here is how I do it – I use MDCalc’s Canadian C-spine tool – but be warned – you have to use it properly. These rules are derived and validated by following the protocol to the letter – if you do not follow the protocol as described you cannot achieve the same sensitivity. The Canadian C-spine seems to be better than the NEXUS rule (NEJM, 2003) – but you must have an alert, sober, orientated and cooperative patient – so a lot of our customers are self-excluded! Scot Weingart describes an interesting combination of the 2 rules.
As the receiving doctor in a CT+ town – I really want to know that the patient has had a proper attempt at C-spine rule clearance – otherwise we are squandering valuable flight resources and irradiating unnecessarily.
This group includes the people whom you cannot clear clinically as they are too drunk, disorientated, in pain, etc to qualify for a clear Canadian C-spine rule PLUS those who have failed the rule – ie. they have tenderness, pain on rotation, are too old etc.
So according to the rules they get “imaging”.  Easy: off for a set of plain films, right?  well maybe not such a great idea.
A good number will have sub-adequate views, and then you need to ask – what is the sensitivity OR the negative predictive value of plain films for C-spine injuries…?  Well they are not so great – in fact the term ‘suck’ has been used to describe them!
This series from the Journ. Trauma 2009 showed a sensitivity of plain films c/w CT for serious injury of less than 50% – that is worse than a coin toss!
However, some protocols continue to advocate plain films as a ‘screen’ for fracture in the lower-risk groups.  I guess this means the patient who so nearly passed the clinical clearance test (eg. were just 65 years old only, had transient pain…) But it is a small group – so the role of plain films is vanishing rapidly.
So in summary – there are not many patients we can reliably clear with plain films if you follow the evidence and guidelines as written.
Therefore if you are in a CT-less town, and have one of these patients – you probably should transfer for a CT.  If you think they are low-end risk, and have a good set of films then it is a judgement call on your part.  Traditionally we have cleared patients on this basis – but is it still the standard of care?
This is really the easiest group to decide upon. Sure, the toughest to manage, but the easiest to make a call on C-spine imaging.
If you have a patient with a high-energy mechanism, bony tenderness, neurological signs or major injury (esp head) then you need not bother with plain films. These patients need transfer – not imaging. This is the scenario where you want to get them to a trauma centre ASAP – probably for more than their neck injury. Taking them through the Xray Dept, moving them 3 or 4 times – for a series of images will add little to your management! Assume they have an unstable injury and manage them appropriately. If you are wrong – great, if you are right – then you have done the right thing!
Finally a quick note on C-Spine collars
  • Rigid C-Spine collars are omnipresent in ED trauma patients, they are almost like religious artifacts – there is a lot of belief in their powers, but is there the evidence to back them up??
    • The Journ Emerg Med 2012 published an article by Holla which looked at healthy people and the effect of collars – basically they did not actually immobilize any more than the padded boards / straps and decreased mouth opening.
    • There is no hard evidence to say they actually decrease neurological injury / improve outcomes.
    • We all know they are a pain, ill-fitting and your worst enemy when trying to intubate!
    • So here is my take – immobilisation is good, collars are window dressing.  If you really want to keep the neck still – provide good analgesia and anti-emesis, supervise the patient closely (esp. if they are drunk, head-injured etc), they will need a nurse / doc by the bedside constantly to do this right!
    • If you use a collar  and it is causing problems: pressure, pain, airway obstruction or really making the patient hostile – then take it off and keep a close eye on them.  Prima non nocere.
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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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Paracentesis: are you stabbing in the dark?

Filed Under: Emergency, General Practice, Internal Medicine, Pearls and Pitfalls, Useful Evidence by Casey Parker — 8 Comments
March 3, 2012

Had a few problematic ascitic taps recently in our place – so I thought I would have a look at the evidence around paracentesis, what is new and what works.  There are a few medical “rules” out there for this procedure, but are they supported by the data?

Click to see my review of each of these questions:

Ultrasound has many advantages in this procedure – reduces the rate of failed taps, the number of “unecessary” taps for dry belly and I find it really helps to map out the best place, the depth and location of your needle. I would never do another one blind after doing a lot under US-guidance.  This retrospective case review series from the Journ of Med Economics 2012 showed benefits alround to using US guidance.  There was decrease in adverse events, infection and a drop in the budget costs associated with these outcomes.

Oh, and using an US is cool – you get great pics, practice you FAST technique with real collections to find.

here is how I do it – no evidence, just experience….

  1. Do a scout scan to identify the deepest pocket of fluid and where the organs are that you want to miss- liver, spleen, bowel…
  2. Pick a spot – I don’t mind if it is left or right, as long as it is clear on the US
  3. Roll the patient with a pillow under one buttock (procedure side-down) and leave them for 15 minutes
  4. Rescan to confirm you have a clear space, measure the depth to the peritoneum and the depth of fluid beyond that.
  5. Prep / aseptic technique.  Inject some local with adren. into your spot and infiltrate to the peritoneum
  6. I use a suprapubic catheter kit, but a central line or dedicated kit is fine
  7. Put the probe anteriorly, insert the needle lateral to the probe in plane so you can watch the tip.  In you go
  8. Drain as much as you think / need. Send your samples.  Leave the drain in if you want to remove big volumes
  9. Monitor the patient for circulatory failure, and use albumin – especially for the sicker patient / big volume taps.

I remember being an intern on the Gastro unit, and being growled at by the boss because the INR wasn’t done on a patient due to have a belly tap. OK, I might have been an imperfect intern – but was my boss justified in worrying about an increased INR when doing a tap?

Well – there is not much evidence – certainly I could find no positive evidence – studies which demonstrated an increased rate of bleeding with coagulopathy for this paracentesis.  There are a few studies and reviews which came to the conclusion that there was no significantly increased bleeding risk.  For example this retrospective case review series of 600 chest and abdo taps from Transfusion 2003;  and this literature review in Transfusion 2005.

This series from Pache & Bilodeau Alimentary Pharmacology and Therapeutics 2005 looked at nearly 5000 taps and found the rate of bleeding was 0.2%, and death was rare - 0.016%.  They note that these outcomes occurred in the patients with the most severe liver disease.  So maybe the patient’s predisposition is the problem rather than the procedure?

Now I am sure if you accidentally stab the patient in the liver, IVC or inferior hypogastric artery they will bleed – but being coagulopathic is probably not the issue here!  Sure it makes the resuscitation a bit trickier, but it is not the cause!  I think this is one of those medical myths where we all see or hear about a bad outcome, somebody retrospectively looks at the INR and blames it for the bleed – retrospectoscopic bias!

Probably my boss should have used an US to guide him, rather than blame the intern if he hit something bleedy!

Traditionally patients undergoing big paracentesis volumes were given IV albumin infusion to prevent post-tap circulatory collapse, hyponatremia etc.  Over the last few years a few other strategies have been suggetsed and used -  in 2011 there was a meta-analysis in Hepatology - this showed that IV albumin was generally the best bet for circulatory dysfunction and hyponatremia.  There was also a small mortality benefit – so it seems like a reasonable thing to do.  The previous Cochrane reviews on the topic in 1998 and 2002 showed no benefit, a trend towards increased mortality – so it is interesting that the latest review comes to a new conclusion.

Once again, the complications of circulatory dysfunction and hepatorenal syndrome are associated with the more severe / decompensated end of the spectrum of liver disease. So tread carefully in the patient with advanced disease, renal impairment and poor cardiac function at the outset.

OK, that is paracentesis in a page or so.  Let me know if you have any other pearls

Casey

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Paracetamol: mostly harmless?… the sequel

Filed Under: General Practice, Paediatrics, Pharmacology, Useful Evidence by Casey Parker — 1 Comment
February 28, 2012

Got a comment from my colleague – Dr Y Levy that got me thinking about fever, the big picture and all those little kids getting dosed up by well-meaning parents.  So I have revisited the Panadol debate

Here is what Hoods had to say in his comment:
“Way back in 1927 Julius Wagner-Jauregg won a nobel prize in medicine for showing the beneficial effects of fever in certain infectious diseases.
He delibrately infected his tertiary syphillis (general paresis of the insane) patients with malaria and they partially improved.
He then treated the malaria with quinine.
These days we treat all fevers with ceftriaxone”. [Ed: cynical, but sadly often true!]

Wagner-Jauregg won the Nobel Prize in 1927, joined the Nazi Party a few years later and did some reasonably (by todays standards) radical and semi-ethical experiments on the mentally ill of Austria back in the day.  Anyway, a fascinating citation – we have long ago been shown that fever can have some good effects on infectious disease and immune response.  But what recently?

I found a few interesting papers that support the fever defense hypothesis:

The Lancet, 1997 published this paper which was a small case-control study from Gabon, looking at paediatric malaria Plasmodium clearance – paracetamol vs. no paracetamol.  The outcome was 1) parasite clearance and 2) TNF / IL-6 / free radical production.   The kids getting paracetamol had the same amount of fever (trend towards less fever), but significantly longer parasite clearance times.  So it seemed paracetamol might have blunted the immune response – but it was a small trial and the mechanism is unclear.

 Prymula et al in Lancet 2009 ran a Czech study that looked at kids getting vaccinations – 2 groups: 1 with prophylactic paracetamol, 1 without.  What did they find?  Well the kids who got paracetamol were less likely to have a fever after vaccination, but they had significantly reduced antibody response to common vaccines – unclear if this correlates with in vivo reduction in immunity.

So to continue the soapbox lecture on paracetamol…..

The Big Picture – we work as doctors to treat symtoms, but also to achieve the best outcomes for our patients.  Fever is a symptom, not a disease.  Unfortunately most parents / patients do not make this distinction – from a patient  perspective a fever is a sign of illness, easily measured and remembered. The people that make and sell antipyretics have the easiest job in the world – paracetamol looks great to the patient – you take it and the fever abates – perfect!  Of course, we know it was going to swing down in an hour anyway, and then it returns a few hours later – just in time for the next dose!  This setup is marketing-gold!  Our patients and parents have been well trained by the TV, pharmacist and folklore to want to treat fever ASAP.

Fever is a harmless symptom in the vast majority of patients that we treat.  There is likely immune / host response benefit from fever.  Evolution tends to keep the bits that work, and fever looks like it has a beneficial function to the organism.  So I think I will agree with Dr Levy and other commenters…

Treating fever (in the absence of other symptoms) doesn’t really make sense -

  1. We might be interfering with a perfectly useful host defense mechanism
  2. Paracetamol works a bit, but you still get some fever and it will return in a few hours
  3. The reason you feel terrible when we get a virus etc is not just because of a fever – it is the result of a lot of factors, none of which antipyretics fix!
  4. The commonest Paeds toxicology OD scenario involves parents / health care professionals overdoing the dose / frequency of paracetamol.  So chasing fever with multiple doses of paracetamol might lead to serious mischief in some cases
Now, how do we go about changing one of the biggest behavioral automatisms of modern parents, nurses and medical staff?  Any suggestions?


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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

Twitt
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Ultrasound for pneumonia – sounds crazy?

Filed Under: Emergency, Internal Medicine, Paediatrics, Useful Evidence by Casey Parker — 10 Comments
February 9, 2012

You may have noticed my recent obsession with all things respiratory.  Seeing and personally experiencing a lot of LRTIs recently. 

A few weeks back Cliff Reid @resus.me put up this article for discussion: Lung US for pneumonia in ED, Emerg Med Journ 2012.  Which suggests that US is at least as good as an CXR for the early diagnosis of pneumonia and actually picked a few more when the CTs were compared as a gold standard.  It was a small study of 120 patients – so I thought I would look further into the literature – see what else is out there.  Here is what I found:

Evaluation of lung ultrasound for the diagnosis of pneumonia in the ED. Amer Journ Emerg Med 2009

Ultrasound diagnosis of pneumonia in children.  Radiol Med. 2008

Clinical application of transthoracic ultrasonography in inpatients with pneumonia.  Europ Journ Clinical Investigation 2011.

Diagnosis of radio-occult pulmonary conditions by real-time chest ultrasonography in patients with pleuritic pain.  Ultrasound in Med Biol 2008

It seems the Italian sonographic community have cornered the market in all things chest US in the past few years!

So in summary if you are too busy to read the articles – there are a pile of little observational studies out there that all say the same thing – US is as good as a CXR, maybe a little more sensitive for showing pneumonia / consolidation.  It is very likley to be better than the clinical examination – however that is not how this works. 

If you hear something or are unsure – then use the probe as the next “test” – if you get a positive then likley you have found a pneumonic process.  You can treat this as clinically appropriate, and still get a CXR if necessary later.  However, especially in kids – do you really need to irradiate them?  Or can we use clinical progress, repeat US and still achieve the same ends?

I suspect those of us who grew up on CXR diagnosis will be more comfortable seeing a positive, or a negative – however if you look in the numbers – CXR has a significant false negative rate in pneumonia (especially early in the disease) – so should we be so comfortable?  I think this is one of those common biases in Medicine – we attribute too much weight to a familiar test, even though we know it might be steering us in the wrong direction.  We like yes/no, black/white answers – and believe in CXR as it has been drilled into us from day 1 of Med School!

This is a great example of US being an “extension of the clinical examination” rather than a “test” – after all, with US you are looking at the sound that you might be able to hear with your stethoscope and ears.  I suspect in 10 years this will be something we teach in Medical Schools – the old look, listen, feel, percuss with have “scan” added to the end of the exam.

Love to hear your thoughts

Casey

Twitt
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Who hears a whoop?

Filed Under: Emergency, General Practice, Paediatrics, Useful Evidence by Casey Parker — 1 Comment
February 7, 2012

Whooping cough is a kids disease?  That is the public perception and one docs might believe as well.

We have had an epidemic of B. pertussis in WA this past few months, despite pretty good vaccination rates – so where does this bug come from?

There is a large pool of whooping cough in the adult / older child population, and that is where the babies get it – and get sick.  So how do we go about fixing this problem?

I did a bit of reading and found that the rate of  Pertussis in adults is actually alarmingly high – these trials ( BMJ 2006, school kids,  Clin Vacc Immunol 2010 , Jour Infect Dis 2002 from France. )   show that if you take a patient presenting with a cough of > 2 weeks and swab / test them all between 12 – 37% will test positive.  So by just taking a history – “cough for 2 weeks” you have a pre-test probability of about 25% for a disease that you really want to treat ASAP to decrease the risk of transmission to some innocent neonate / infant.  You might say – “why bother doing the test “- you are going to treat them anyway.  But we do the test to confirm and allow our Public Health colleagues to get a grip on the outbreak.

The pertussis vaccine is possibly the shortest effective duration of all vaccines on the schedule.  Having had a course is not protective into later childhood or adulthood.  In WA the government have been running a campaign to get all new parents, and expectant grandparents vaccinated to try and close the risk of friendly fire from within the new family unit.

I think as healthcare providers we need to be vigilant and consider this diagnosis in patients with a prolonged cough and be prepared to treat and ask the patient to isolate themselves from small infants.

Any comments?

Casey

Twitt
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