Migraine Prophylaxis: preventing you a headache

Migraine headaches are common.  They can be really disabling for patients and if they occur with any frequency they can make life miserable.  Fortunately there are many options out there for the longer term management and prophylaxis of migraine and other primary headaches.

The only problem for us is that there are so many, seemingly effective remedies – it can be a real headache deciding which to try with your patient.

A dive into the literature reveals a broad range of medications and classes of medications that may be suitable – but the data is difficult to get one’s head around.  There are many ways that headache prevention can be measured and weighed – making it hard to compare apples with apples.  And to make things worse – a lot of newer agents come with a hefty price tag if you are prescribing off-schedule…   so how to choose?

Well I have been diving into the literature and have tried to summarise the data around migraine prophylaxis as cleanly as I possible.  How?  The NNT and the NNH for these meds are a fair place to start – you can weigh the risks and benefit with your patient if you know the rough numbers.  And then it is a matter of individualising care to your patient’s other needs and medical problems.

So here we go a whirlwind tour through Migraine Prophylaxis !

A quick explanation of the statistics is required!  When researchers look into migraine prophylaxis interventions – they tend to use a slightly odd, but useful measure of “effect”.  Clearly if you wanted you could measure the number of headaches per month / year etc and have a scale of effect – but that is a bit messy.  So instead they use the arbitrary bar of “50% reduction in headache frequency”.  So when I tell you that the NNT for drug X is 7 – that means that you would have to treat 7 patients with that drug for whatever time period in order to reduce their headaches from 12 to 6, or 8 to 4 – or whatever you like.  Hope that makes sense.

Now usually when we look at drugs in medicine – they get NNTs of 10 or 20 – which most folk would regard as useful.  [NB: aspirin has an NNT of 42 for mortality in acute STEMI.  Its NN to harm is about 167.]

When we look at migraine prophylaxis we are talking about NNTs in the range of 3 – 10.  Now that may sound like these drugs are really great!  But recall we are using “50% reduction in headache frequency” as the end point.  That is a reasonably low hurdle to jump over.  If we were to ask for “complete prevention, absolute prophylaxis” then the NNT would be much higher- I am guessing in the 100s.

So who needs prophylaxis?

  • Most Neurologists would consider 2 – 3 severe / disabling headaches per month a reasonable threshold for considering prophylaxis
  • This may vary depending on the patient’s choice
  • Some patient’s will feel strongly about preventing any headaches due to the severity; interference with life, work, family etc.
  • This needs to be explored with each migraine sufferer  on a case-by-case basis.  That is what they pay us the big bucks to do!
  • Remember that this is an “optional” intervention – so do not be too precious with particular drugs – it is a fine balance between potential harms and benefits – very much in the realm of “shared-decision making” and being pragmatic.

Most of the agents used for abortive therapy / acute management of migraine run the risk of causing rebound if used more than 10 – 15 times a month.  So another way of looking at it would be to use prophylaxis as a means to limit the amount of “acute abortive care” required and therefore maintain its efficacy.

OK – so that is the boring biostats explained.  Lets look at the candidates available to you and your patient to choose from.  I have lifted this very useful table from the Med Journal of Australia 2008 – link is here – it is a really well written piece.

Migraine prophylaxis (Click for the summary table from the MJA 2008 paper)

The Players:

This is a really old agent dating from the 60s. There is not a lot of quality evidence – but it has been the benchmark and default drug for a lot of doctors for many years. It is the oldest 5HT antagonist – the main side effects are weight gain and drowsiness. It is cheap and we know it. Specifically it is touted to help more with vestibular migraines.

Propranolol is the 2nd oldest agent out there. Usually dosed at 20 mg BD (not great for a long term med). It has been well studied. A NNT of 4, and a NNH of 40. Dirt cheap Some benefit for the anxious, tremulous or hypertensives – but can cause exacerbation of asthma / COPD in some punters.

Old TCA well known to most GPs. Going out of favour in Psych but still widely used.  Has it share of anticholinergic side effects and we all worry about OD! There is consistent evidence that amitriptyline works over a long period.  Of course, if the patient has depression as a comorbid diagnosis – this is a good option. None of the SSRIs etc have been shown to help.  Generally the dose required is at the lower end of the spectrum

This is a tough one – these agents have been looked at and I find mixed signal when I read the papers.   Some say it works, but the Forest plot is inconsistent!  At best I would say that there are better / more efficacious agents out there.  Also there was a pretty strong harm signal – dizziness, somnolence and cognitive dysfunction all being  significantly more common with these drugs!  So I would imagine a reasonably high rate of drop out after a period taking these drugs.  Here’s the Cochrane review from 2013.

This is the drug I would take if I needed migraine prophylaxis.  Unfortunately, it is expensive and the PBS in Australia only covers it if you have failed on the other agents. But it was in the top performers in terms of NNT = 4.  Also it seems to be effective at lowish doses 50 – 100 mg – so less side effects potentially.  The NNH is quoted as 3 – 25, a big range! And it depends on the dose.  But one of the “harms” counted is weight loss.  So this is probably a welcome effect for many patients!  In fact this makes Topiramate the only agent that seems to not be associated with weight gain.  The other common SE was taste disturbance (maybe related??)  Biggest downside is the potential for birth defects – so you need to use with care in fertile women!

Another effective drug – with an NNT of 4. But the NNH a little harsher at 7 – 14. The major problem with Valproate is weight gain and the metabolic syndrome. There are whole websites devoted to this syndrome! Valproate 400 mg has been trialled head-head against topiramate 50 mg…. and Topiramate came out on top

Another epilepsy med that has been looked at. Not a lot of great data – small trials showed a NNT of 2 . Was effective – but had a NNH of just 2!  Nausea, vomiting, drowsiness, dizziness… not easy to sell as a long term solution to migraine I think.

There have been a few ACE inhibitors and ARBs tried – so I have chosen candesartan as it the most widely used in Australia for hypertension. In head to head against propranolol – it was equally efficacious and well tolerated. Clearly this is a viable option for a large group of patients who might get benefit from BP control or renal / diabetic disease.

Yes Botox! I am including this in my review as it is out there and used. Your patients will find it when they Google their options. In summary: there is not a lot of quality evidence. Some Neurologists believe it helps with some subtypes (“imploding”) of migraine. And it is sometimes used in patients where other options have failed with a modest 10 – 30 % rate of response. So it is certainly not first line! Maybe 3rd or 4th line! Of course, in patients with coexisting wrinkles or narcissism there maybe additional benefits (Jokes ;-))

 

OK – that is it for my quick review of the literature around migraine prophylaxis.  Would love to hear your experience or views on the data.  I stingily recommend reading the great MJA piece that is linked above.

Casey

Clinical Case 105: Headache Take 5

Ok Neuro nerds…  here’s a quick case to test your diagnostic skills.  It is one of those common scenarios we see.

35 year old man presents for the 5th day in a row complaining of the same headache he came in with on the 1st day!

He is usually fit and well, but has been prone to headaches over the years – never really diagnosed.

He describes the headache as being very similar each day, starting at various times during the day.  He get sharp, boring intense pain around his right eye which throbs into his temple.  He describes spasm of pain which last for 10 – 20 minutes and then fade to a dull ache.  He has noticed his right eye waters a lot during the attacks and nothing seems to help.  The pin is disabling in intensity and he needs to stop doing whatever he is doing and go sit / lay down until it passes.  In between attacks he is pain free but is starting to feel apprehensive – as he knows it is coming back!

There is accompanying nausea but no vomiting.  No real photophoia or odynophobia.  He cannot recall any aura or visual symptoms prior to these headaches.

He has been under some stress lately at work and this week his boss has had a go at him for “slacking off” and suspects these headaches are artifactual! There has been tension about money in the business for weeks.

Looking back through the chart of the past 4 visits – he has had a range of treatments – paracetamol, hot compresses, IM ketroloac, aspirin, caffeine, oral tramadol and oxygen therapy.

Nobody has been able to document any focal neurological signs of neck stiffness. He has had no syncope or trauma.

Ah 0 easy you think!  Classical cluster headache – we can fix this with high flow oxygen pronto!

As you make a move to place a Hudson mask over his face he slaps it away….

“Everyone has tried that all week!  It hasn’t helped.  It just annoys me and I feel claustrophobic with that mask on.!!”

Hmmm…. maybe not so typical.

So what is going on?

Q1: What is the probable diagnosis?

Q2:  What is the treatment of choice?

Q3: Will you get any neuro imaging?  This is day 5!  Is this something nasty?

Clinical Case 104: FAST Thinking

This is a trauma case.  I want to use this case to illustrate something about the way we think about trauma when it comes to making calls using ultrasound – specifically the FAST exam.  FAST exams are ubiquitous in modern ED practice – but if executed and interpreted poorly – they are potentially a source of error.

Now you may be aware that I am an US tragic – and when it comes to trauma I have been seriously drinking from the gel fountain.  OK – onto the case.

Typical Broome case:  a lot of unknown unknowns.  30 y.o male who is brought in by the Ambos after being found on the roadside.  Appears to be very drunk.  There wis a vague history from the Ambos that a few “innocent bystanders” saw our patient getting a “proper flogging” [being kicked and punched by a group of fellows].

On initial assessment there is not much to find externally – no bruises or lacerations .  His Obs are really very normal [BP 110/70,  pulse 80, RR = 12, breath alcohol level 0.3%.... normal for Broome].  He has a normal neurological examination [ which is of course the bluntest test in Medicine! ] And equally reassuringly has equal and reactive pupil responses.

Now it is a few hours since the injury and his belly is sore.  Despite his relatively pickled state he is really not wanting you to examine his belly at all.  He seems very tender though there is no distension or bruising.

So being me – it is time to get some gel onto the patient and find the badness.  The scan is basically negative, well almost.  The LUQ, pelvis and subxiphoid views are all normal… but. The RUQ view is just not quite right. Take a look and think – is this a positive, a tiny bit of free fluid? Or is it OK?  This is the sort of call you need to be really sure about when doing these bedside scans.

Because it would be easy to look at this and say – “it is OK” and move on, but if you cannot convince yourself of normality – then you need to act.  So what is it going to be?
RUQ FAST view
So – here is the summary: a Very drunk man with normal obs.  Not a clear mechanism of injury – but we think he has been “flogged”.  Not much to find on examination.  And his FAST exam looks pretty good – but is that RUQ view as it ought to be?  It all hinges on this!

OK I ma going to leave it hanging there and wrap up the case in a few days.

Let me know – what will you do next?

If you are interested in the finer points of the FAST exam then I highly recommend Dr Laleh Gharabaghian’s Sonospot website, or check out her podcast with Scott Weingart on “Don’t Half Ass your FAST”

OK, after a few days to consider the FAST  - here is the conclusion to the case.  But first a rant about “half-arsing the FAST” [Love that line from Dr Laleh]

Obviously it would be a bad idea to make a call on a single still image from a FAST protocol – and yet I see this a lot!  I see a lot of Docs getting a little too focussed on getting a “text book picture” on the screen.  I think we should be exploring the area, as Laleh says: fanning through the whole potential space around Morison’s pouch and into he paracolic gutter if the gas allows.

Lots of folk use a single angle of attack – this often gives a nice image – but to be sure that you are not missing something down at the inferior edge of the liver – you need to look at it from a few sides.  This requires one to have a few tricks in the quiver – not just 4 “standard” points to cover.

Now – point number 2.  FAST (and a lot of bedside US) is not the most sensitive test – it requires a decent volume of haemoperitoneum to be present before you notice it.  So what does that mean in practical terms?  Well I looked at the image above – and thought: “it is nearly normal”.  There just might be a slip of blood there anterior to the kidney.  On a second fan through – I was convinced that there was something “not right”.  It was not clearly NEGATIVE.  Now human nature makes us want to think like this:  ‘if it is close to normal – it can’t be too bad.  Could it?’  But that is wrong – FAST is insensitive, so any subtle abnormality could potentially mean serious pathology.  When you interpret a FAST – you need to be certain of normality.  There is no room for “close enough” here.  And when I rescanned this patient – I was not certain.  So I decided to go onto CT.

A slice from the CT

liver cT

Liver laceration with associated pancreatic contusion. No fresh blush of contrast

So – as you can see.  A small anomaly on the FAST can bely serious injury.

So – our patient remained stable and was managed conservatively.  HE did have a lipase bum and went onto develop some traumatic pancreatitis.  [ we would never blame the alcohol! ]

And for the record he had serial FAST scans which become more obviously positive over time.  One could even see the laceration with the aid of the CT!.  But that is not what FAST is about – you should not be looking for solid organ injury.

And here is the liver lesion on the subsequent UltrasoundLiver laceration

So remember – DON’T HALF_ASS YOUR FAST

Have a low threshold to call it “not normal”.

Scan like you are hunting for blood – not just taking a snapshot!

Repeat the scan if in doubt.  And remember to interpret in the clinical context – i.e.. a NORMAL FAST in a crashing patient means little.  You need to find the badness when the pressure is dropping – either in CT or the operating room!

Happy scanning – Casey

Quantum Quandaries, Diagnostic Decoherence and Probabilisticians

So I imagine you have just read the title of this post and thought – “Casey has finally lost it!” – or something to that effect….

Diagnostic Decoherence – it sounds like the title of an obscure SMACC lecture.

So what am I rambling on about – what is this concept? Where does it come from? And why do you care?

Let me explain.

At SMACC 2013 I had the pleasure of meeting Prof. Simon Carley – a man with a brain the size of a small planet.  One evening over a beer he stumped me with a statistical problem – the Monty Hall paradox

It is a simple problem that demonstrates our often-flawed intuition when it comes to probability and decision-making.  And even smart, experienced clinicians get it wrong a lot of the time.   I recall walking away from that conversation feeling like a small part of the rug had been pulled from under my clinical gestalt.

The next morning Simon gave a great lecture on the real world application of statistics at the bedside – this talk was called “Wrestling with Risk” – you can see it on the 2013  SMACC podcast.  Free, awesomeness.

Simon’s talk was great – a beautiful illustration of  balancing risk of missing vs. over investigation and diagnosis that leads to unnecessary intervention.  It is all about understanding the imperfection of our science and being able to think past the “results” of tests. We need to be thinking about what the results really mean and how they apply to the individual in your care.  IN recent months Simon has teamed up with Dr Ian Beardsell [@docib] to produce the St. Emlyn’s podcast - the first few episodes go right to the heart of probability and testing in ED.

Simon used the PE workup as an example – it is one of those diagnoses where we have good data – well-defined pretest risk assessment tools and calculated likelihood ratios for our “diagnostic tests”.  The problems we see with PE workup come from the common misunderstanding many clinicians have about the use of these tests.  For example, performing a CTPA on a Well’s Score low-risk patient is more  likely to yield a false positive over a true positive if reported as “PE”.

OK, great.  We need to teach our students and trainees all these stats – educate them about test characteristics and application to various populations.  If they knew all the LRs, scores and risks then they could make statistically-sensible decisions.  Less harms, less false diagnoses and probably a swag of money saved.

But…. here’s the problem.  We are still practicing in the Wild west of science. There are not a lot of rules, plenty of unknown unknowns and yet we need to get the job done – for most of what we do there is just not a great evidence base.  Even when we do have evidence – it is often of questionable quality or cannot be applied to our patients’ particular context.  Would lead many of us to EBM-nihlism or drink!

Ever since that talk I have been thinking – contemplating and trying to come up with a counterpoint.  Examining the way I use probability in daily practice and searching for a good analogy in another field of science.  And I think I have found it!  So here it goes…. but first a quick disclaimer.

I, Dr Casey Parker, am a total physics nerd and make no apology for this.  So the following rant makes complete sense to me and maybe a few other people I know!  This next bit is very heavy on non-medical, theoretical ideas which I believe are a nice analogy to the conundrum posed by Prof. Carley.  If this type of thing bores you to tears – stop reading now! OK, still there? Begin…

Einstein is famously quoted as stating that “God does not play dice with the Universe.”  Possibly the most famous quote from the great man – and possibly the most flawed!  Einstein was expressing his incredulity at the emerging quantum physics of the early 20th Century – he felt fundamentally uneasy with the idea that probabilistic mechanisms determined the nature of the universe.  Specifically the Copenhagen interpretation stated that: “A system is completely described by a [probability] wave function , representing the state of the system, which evolves smoothly in time, except when a measurement is made, at which point it instantaneously collapses to an eigenstate of the observable that is measured.”

Here is where the infamous thought experiment of Schrodinger’s cat comes in (or doesn’t… if it is dead ;-).  The cat exists in a state where it is both alive and dead (probabilistically) up until the point that the box is opened and an observation is made.

So when you are working up a lowish-risk PE patient – you might have a Well’s score, a modified Geneva or your trusty clinical gestalt.  You plug it into MDCalc and you get a probability of a PE being present.  The D-dimer is done… DOH!… it is “not negative” and you are unable to say “go home!”   So you decide to make an ‘observation’ ie. a CTPA – which really just changes the probability.  There is no waveform collapse, no eigenstate, no.   Medicine is not like physics – there is no absolute.

But, here is the but…  at some point you have to make a call.  We work in the real world – you cannot go to the patient and tell them that they have a 73.2% PE.  You cannot give them a 73 % dose of heparin? We need to be able to to decide who gets treated and who does not.  This is analogous to the classical-quantum divide:  we know that particles are composed of probability waves, yet when you look around you – you see objects, collisions, hard surfaces all of a predictable nature.  When your patient falls – their radius breaks, when the clot sticks, they get ST elevation.  So how can we reconcile this in our practice.

For the vast majority of diseases or problems that we see in the ED there are no numbers, no starting position – we are sailing in uncharted waters and would be lost.  I say “would”.  Because we do have our own personal onboard navigation systems – we all carry a rich library of experience and “gut instinct” around in our heads.  This is what we call “Gestalt” – that oft spoken German word which is rarely understood.  So how does this work?

Back to the quantum world… For most of the 20th century theoretical physics was stuck with a big headache.  On one hand there was a great theory that explained the big things – Einstein’s relativity.  And then there was the new kid on the block – quantum theory which used probability and wave equations to describe and predict the tiny world of the fundamental particles.  However, there was a demarcation dispute.  At some scale the particles had to start behaving like classical physical objects.  But there was no way to marry these two perfectly functional theories in such a way that made any sense.  This is where Decoherence comes in.

When we take a history and examine a patient – we are building up a set of probabilistic waves.  Each piece of data increases or decreases the amplitude of the wave.  Each wave carries the probability of a diagnosis – and to reach the threshold of action / reality / or the “treatment threshold” the wave must break over the wall.  Stick with me – it gets clearer soon.

Simon has beautifully described how various factors create waves of various amplitude in the work up of chest pain.  Check out his SMACC Gold lecture from 2014 - on risk factors.  When we take the history from a chest pain patient – we know that the typical atherosclerosis risk factors are poor predictors of acute coronary syndromes.  In other words – they produce only small waves, they are subtle ripples in the ACS pond.  In order to get over the threshold – we need a collection of waves which positively interfere with one another in order to make it to an “actionable” probability.  Chest pain is easy – we have good data to measure the waves and the amplitude of the threshold.  Alas, when you are floating on the “non-specific abdo pain pond” the waters are choppy.  Lots of waves interfering with one another – leaving us with murky water.  That is why these patients seem tougher to sort out.  And by the way – no matter what the Surg Reg tells you – the white cell count is merely a ripple on that pond!

Now of course, some of our “tests” create big waves – think about “thunderclap headaches”, “shingles rash” or a “3 mm of ST elevation pattern in II, III and aVF”.  These features create waves that easily carry us over the “action threshold”.  This is the stuff we all learn in Med School.  Sometimes it is wrong – for example – Framingham risk factors and ACS – no real wave in the ACS setting.  However, more often it is just plain messy.

When the quantum physicists look at probability waves – they isolate a couple of particles and do complex probability wave calculations  - very smart.  But if you try and do this with more than 3 particles (waves) at a time – the numbers get crazily complex – it is just too messy.  And yet we all do this intuitively on a daily basis.   One of my mentors believed in “Diagnostic Triads” – the idea that many diseases could be reduced to 3 symptoms – this is an example of three simple probability waves interfering to create an ‘eigendisease’ -e.g.  fever, jaundice plus (R)UQ pain = cholangitis.  Unfortunately during our daily grind in the ED the act of taking a clinical history and exam is an infinitely complex assessment in which we are constantly integrating new data and probability waves into the mix.  At some point the waves may coalesce into a meaningful reality – and this is what a quantum physicist might describe as Decoherence.  The waves become a real thing – something that we can name, refer, incise or thromobolyse.

So in summary – I agree with Simon. [ 'twould be daft not to! ]  We are probabilisticians rather than diagnosticians.  However, the math is far more complex than our textbooks and teachers would have us believe.   Medical students have always struggled with the complexity of clinical diagnosis.  There are just too many variables for even the brightest minds to integrate into a cohesive model of what is going on in most patients.  Of course – spending more time, doing more tests can give us more data points and help us “realise” a diagnosis.  And as we gain experience we learn to recognise “disease scripts” – patterns in the waves that we recognise as “a thing” before they reach the threshold.

Now – one might read all of this and get a sense of nihilism.  It all just seems too complex and hard.  But I think there is a way forward.  Here is what I believe we should do:

1.  We need more research to define the probabilities – clinical medicine is full of dogmatic belief in our clinical skills.  E.g.  “the chest is clear – therefore no pneumonia….”  In reality the negative LR for auscultation in pneumonia is close to 1.0.  Utterly useless!  By knowing and teaching the reality of our skills we can do better, make more reasoned decisions.

2.  We need to teach probability to Medical Students – personally I am a fan of the Bayesian approach and teach likelihood ratios as the most easily applied stats to keep in the back of one’s head.  These are more intuitive than sensitivity or specificity.  They tell you more about the “test” and can be applied directly tot he individual patient in front of you.

3.  We need to change the language that we use when we talk to our patients.  A while back I defined the Zeroth Law of Diagnostics - “there is no such thing as Zero risk”.  And I believe that we ought to fess up to our patients – certainty is a rare beast in Medicine.  We should tell our patients this.  We can have a reasonable belief that they do not have a PE, or that they do have ‘smouldering diverticulitis’ – however, there is a real chance that we are wrong.  If things change, or they get new symptoms [waves - new waves ] then they need a review and rethink.  The catch phrase for this is = “shared decision-making”… or as we in GP-land call it : consultation.  The patient is the one with the disease [or not] and they take the risk.

4.  We need a bit of Dogmalysis – there are a lot of pseudo axioms and long-held truths in our game that need re-examination.  David Newman has produced a nice series of podcasts on this topic – check it out at SMART EM.

5.  We need to develop a healthy insight into the way we think – I believe the buzz word is metacognition.  Understanding the sources of error and recognising the false waves will help us to make better, more accurate decisions – and to do better by our patients.

Ok.  That was quite a ramble.  Back to something more concrete soon!   Or is that concrete really just the summation of a pile of waves of probable concrete particles ?

Let me know what you think.

Andif you want to read more about Decoherence in quantum physics – I recommend reading this quick review paper.  For more reading check out the Decoherence website here.  Or just go outside and get some sun ;-)

C

Clinical Case 103: Midnight MacGyver Medicine

This is an exercise in medical minimalism.  I am going to throw you a case and a set of resources – you need to say how you would manage it.  I am going to release my strategy in a few days.  So here we go – here is the case…

Firstly, a little bit of background you get from the old file:

Monica is a 49 yo woman who has had a long history of renal trouble.

She was diagnosed with type 2 DM at age 21, with early nephropathy.

By age 40 she was on CAPD, and by 43 was dependent on haemodialysis.

She got lucky and was the recipient of a cadaveric transplant at age 45…..  but, that kidney isn’t doing so well. She has had multiple episodes of threatened rejection and ongoing renal impairment.

In the last year her new kidney started to pack it in and she has had yet another AV fistula formed… in anticipation of ongoing HD.

So here we are – most recently her creatinine was 500, with normal K+ and bicarb of 18.  She has advanced renal osteodystrophy, hypertension, anaemia [on darbopoeitin],  also has chronic asthma / COPD.  Oh, and her BMI is 40, with really tough IV access due to previous fistulae surgery…  good luck.

On the bright side – she has no documented ischemic / valvular heart disease.

Meds: prednisolone 5 mg, ramipril 10 mg, amlodipine 5 mg,  tacrolimus 1 mg, salmeterol inhaler, CaCO3, cinacalcet 30mg and aspirin 150 mg.

It is 5 minutes to midnight on your night shift at “Janus General” hospital in a remote location.  You are on your own.

Here is the scenario:

The Ambos roll in the door with Monica on the stretcher – she is looking pretty crook.  She called ’000′  as she was getting increasingly ‘short-winded’ and her puffers were not helping.

The ambulance crew have her on 8 L/min via a nebuliser mask with salbutamol nebs over the last 20 minutes.

Obs are:  Resp rate 36/min, pulse 110/min, SpO2 = 94%, BP is 180/110, she is afebrile and coughing with green sputum.  She is alert and oriented.  Her new fistula is buzzing nicely

A quick auscultation of her chest reveals diffuse, bilateral, coarse crackles.  A few scattered wheezes but reasonable air entry.  She is working pretty hard – tripoding.

In between gasps she indicates some (R) sided chest pain  - it appears to be pleuritic.

Her legs are both really oedematous – with pitting oedema up to her kneess… maybe a little more on the right.

The monitor shows sinus tachycardia and an ECG the same  - with maybe some slight depression of the ST segments laterally.

The differential diagnosis is looking pretty broad at the moment!  Take a moment to contemplate the possibilities….

Here is what you have:

  • A well stocked, small, rural ED
  • Oxylog ventilator – capable of NIV
  • a POC blood gas analyser (basic biochem and gas panel + lactate)
  • a bedside ultrasound machine [ of course ;-)  ]
  • two really great nurses
  • a telephone to phone a friend / specialist  - but none will be able to attend.

Here is what you do not have:

  • Any formal radiology
  • Any laboratory tests other than the POC machine
  • Any immediate, physical backup
  • Any way of transferring Monica anywhere in the next 12 hours. [ though the sun will rise in 6- usually makes things seem better!]

So – here is the challenge:

  1. Get IV access somehow!
  2. Initiate empirical therapy – what would you use up front
  3. make some sort of diagnosis (es)
  4. Make a plan for the next 12 hours (the lab and Xray department will be available then…)

Welcome to Broome.    Go!

Casey