Clinical Case 130: Painful Palate Puzzle

OK crew.

Today I have a super quick clinical case for you.

42 year old man presents to the ED with a week history of pain in the palate.  He says he thought it was referred pain from a “sinus infection”.  He has had a series of these “sinus infections” recently and his GP has treated them with oral Amoxicillin / Clav…  not getting any better. We can debate if this is a good use of antibiotics, but just agree it is ‘clinical equipoise’ for now! (Check out the NNT take on this from 2013 here,  Cochrane agreed in 2012.. but they are looking at it again right now).

The antibiotics didn’t really help after 5 days.  He went to another GP who prescribed another antibiotic…  But today, on day 7,  he has a new symptom.  He has noticed a painful lump on his hard palate.  He cannot recall feeling it before.  It just “appeared” over the week as he was struggling through the pain of his “sinus infection”.

A cursory ENT exam shows all to be normal.  He does have some fullness and percussion tenderness over the left maxillary sinus.  But there is a definite lump on the palate:

The lump is firm, tender but not particularly hot.  It is bang in the midline:

palate lumpOK

Q1: spot diagnosis – what is it?

Q2: what imaging will you request if any?

Q3: what is the treatment ?

Casey

 

Pneumonia Ultrasound Diagnostic Strategy

In June I will be travelling to the Emerald Isle to attend and learn at the SMACC Conference in Dublin.  One of my jobs whilst I am there is to help out on the SMACC Mini workshop – I will be talking about using lung US to diagnose paediatric pneumonia.  Clearly, I am a self-confessed sonophile. I think that we can get a lot of information in quick time by using the bedside scanner to interrogate the lungs.  BUT, there is always a BUT…  what we do with this information is most important.  Lung ultrasound is really very simple, technically easy and there are not many subtle anatomical findings to keep you guessing.  However, when we interpret our scans we need to know a few things:

  1. What is the clinical question?  Are we “Diagnosing” or “excluding pneumonia”, “Septic screening?” or “differentiating pneumonia from bronchiolitis?”
  2. Do the findings represent “hard” or “soft” signs of pneumonia – could the signs be false positives?
  3. What is the plan – are we going to act on our findings? Hit then with antibiotics? OR get more tests?

Dr Rory Spiegel posted a great critique of the recent evidence around lung US for pneumonia at EMNerd this week. “A Case of Shadows II”   His post has prompted me to respond by explaining how I think we should use this tool in the light of our current evidence.

If you read the abstracts you will come away with a somewhat “black n white” view of the world.  However, there are a few shades of grey.  You will read impressive numbers – a positive likelihood ratio of 15, a negative LR of 0.06…  this is a great test! It discriminates in both directions.  BUT… here’s the next BUT… you need to know what these investigators were calling “pneumonia” and what was not.  If you have done any lung scanning you will  know that there exists a spectrum of findings -ranging from hard to soft.  So where on this spectrum can we “call it”?

  • Hepatisation with dynamic air bronchograms
  • Hepatisation with static air bronchograms
  • Large subpleural consolidations
  • Sub centimetre sub pleural consolidations
  • Unilateral B-lines
  • Unilateral effusion

 

Classic hepatized lung with “shred sign” of adjacent B-lines

Basal pleural effusion

The diagnostic characteristics of these signs are not all equivalent – as you go down the spectrum they become less specific [and more sensitive].  This does not make them useless – just less potent as far as diagnosis goes.

There is also a real risk of over-diagnosis  if we start overcalling pneumonia based on the softer signs.  So how do we integrate this “new test” into our practice?  I reckon we need Bayes.  We need to be smart about how we use the information that US provides.

Lets start with a case.  Here is the pretest- probability guesstimation:-  we are not great at picking pneumonia clinically – however if we have a child with fever, cough, tachypnoea and unilateral auscultation changes then I would guess that we are at about 50% at least.  So lets whip out the nomogram!  If we start at 50% and have a hard sign (e.g. dynamic air bronchograms) – +LR around 15 then we are up to about a 94% post-test probability – this is a slam dunk, I think we would all start treating this kid.  If we were to see only a softer sign such as focal B-lines and a tiny unilateral effusion then our +LR is weaker ( wild guess would be about 5??) That still gets us to a post-test probability of 83% – and I would start antibiotics at that level. [Editorial note: these numbers are completely fictional.  Based on my own experience and reading.  We need to have studies that exam these signs].

If you decided that the chest wasn’t convincing on auscultation – then your pretest risk might be lower – let us call it 20%.  In that case a soft +LR of 5 would only get you to 55% post test… maybe not good enough to call it over the “treatment threshold”.  We need more data.

So lets consider another scenario.  2 year old girl with fever, poor perfusion and tachycardia.  No localising signs on examination.  We are definitely going to start empirical antibiotics based on her risk of sepsis.  But we want to run a “septic screen” to find the source.  In this case our pretest probability is lower.  Maybe 10 or 15% chance of pneumonia.  So a CXR probably has a sensitivity of 70%, is that good enough?  Our lung US can have a whole range of sensitivities.  If we draw the line at “completely normal” – i.e.. none of the hard, soft or indeterminate signs listed above then the data suggests a sensitivity of high 90s.  So our strong -LR in this setting allows us to get our post-test probability down, well below 1%.  We need to look elsewhere for the source, maybe she needs an LP?

Now – a tougher case.  A 12 month old boy who has been admitted with bronchiolitis fro 48 hours.  He was initially improving with supportive care, but today has developed increased fever, tachypnoea and oxygen requirements.  He isn’t following the usual branch curve.  Has he developed a superinfection / pneumonia?  Lets scan his lungs…. We expect to see bilateral, small (sub centimetre ) sub-pleural consolidations.  Maybe symmetrical, small basal effusions.   So here we need to be choosy.  I would ignore any of the softer signs listed above.  There is a low signal:noise ratio here.  For our scan to be useful we would need to see a hard (very specific) sign of pneumonia – such as a larger  area of hepatisation with air bronchograms to allow us to make a call.  In terms of post-test probability, out treatment threshold need to be considered.  Given the clinical situation is the best option to start antibiotics.

Lung ultrasound is a test.  Like all tests it has imperfections.  It is not a binary phenomenon – there are a range of “cut off points” that you can use to enhance its ability to rule in or exclude pneumonia.  Unlike a numerical test like troponin or D-dimer it is not as simple as shifting the magical “normal range”.  We need to understand the relative potency of all of the possible findings and use these to our advantage depending on our goal.

So go on!  Use lung US in your practice. Use it wisely.

  1. Think about the context of your patient, estimate the pretest probability.
  2. Decide if you want a sensitive or specific test – what are you trying to do?  Rule in or out?
  3. Scan and interpret you findings – is it negative? Or maybe soft? Hopefully you find some hard signs.
  4. Understand how to apply these findings to the patient
  5. Premeditate your treatment threshold – at what level will you be starting treatment?

The best thing about lung US is that you can play around with it and only waste a few dollops of gel and your own time.  There is no real inherent risk in the test itself – no radiation or the need to bother the nice radiographers!

I hope this all makes sense.  Let me know if not!

Cheers

Casey

 

 

2000px-Fagan_nomogram

 

Clinical Case 129: A SMACC in the Head (ache)

HI ALL

I need a little help with writing my talk for SMACC in Dublin this June – it is all about diagnosis in the ED.

So I want to present a simple case to you here…  and I want you to answer it honestly, without referring to any papers – I am after your “gut instinct” you “Gestalt” for lack of a better English word!  So please have a read of the scenario below and tell me the answer to the simple question by completing the poll

 Karen is a 45 year old accounts manager. She is usually well aside from occasional asthma and long-standing, mild depression.  Takes salbutamol and citalopram.

She presented to her GP this morning with a history of a bi-frontal headache which came on over a period of 15 minutes whilst at work at her computer.  The headache increased rapidly in intensity to “9/10” pain.  It is the “worst headache she has ever had”.  She felt nauseous after it peaked and nearly vomited.  She has had no syncope or light headedness.  She described some neck stiffness to her GP, but here are no objective findings of meningism on examination.

Her Neuro exam is normal with no changes on fundoscopy.

Her BP is 143/82 and she is in sinus rhythm at 80/min.  ECG Normal.

Her GP was worried about a possible subarachnoid haemorrhage (SAH) and sent her into your ED by ambulance.

By the time you have seen her the headache has been present for 3 hours. It has improved a little with paracetamol and a dose of ketorolac en route…

So that is all the data you will get.. now onto he poll:

[Please try and be as instinctual as possible, answer as if you were in your ED and had to guesstimate the answers to these questions]

 

I promise that I will get back to you with some poll results and data once I have mined your minds!  See you in Dublin!

Casey

Any Place for Race on the Coalface?

Last month (Feb 25th 2016) the New England Journal of Medicine published this editorial “Perspective” titled: “Dealing with Racist Patients.

In the article the authors – Drs Kimani,  Alexander K. Smith, Bernard Lo  and Alicia Fernández present this case vignette:

A 77-year-old white man with heart failure arrives in the emergency department of an urban hospital at 3 a.m. with shortness of breath and a fever. When a black physician enters, the man immediately announces, “I don’t want to be cared for by a %$#!{& doctor!” Taken aback, the physician retreats from the room. She’s offended by the man’s rejection and demeaning language — but knows that he may have a serious medical condition and that she cannot treat him against his will. How should the physician proceed?

This is followed by a discussion around the ethics and legalese aspects faced by physicians when dealing with overtly racist patients in the ED.

There is even a flowchart to assist the decision-making around this scenario.  Probably a good idea to have a “checklist” when dealing with a potentially emotional and heated discussion.

Please have a read of the article and come back here for my thoughts.

Last week I had the chance to discuss this paper and the issues raised with a few of my colleagues – and there were some interesting opinions.  To give you some context our ED is very much an Aboriginal ED – about two-thirds of our patients are Indigenous Australian people.  Our staff include a mixture of local, Anglo/European Aussies, overseas-trained doctors and our fantastic local Aboriginal health workers.  Being racist is not really an option if you work in the Kimberley – or at least it would be a very unpleasant existence. We do see a bit of “reverse racism” particularly directed at our overseas-trained doctors.  So it was interesting to read this article and see how it works in the U.S of A.

The authors of the paper broke down the ethical considerations based upon the patient’s reasons for refusing a particular doctor

  • Incompetent patient: – clearly these folk need to be treated under a duty of care. Don’t see much to gain by fuelling a conflict in this scenario.  If a patient does not have capacity to make decisions then it comes down to the family.  I would tend towards uber-pragmatism here and offer whichever physician will cause the patient the least distress.  But… Racism on the part of the family should not be included in this compromise.
  • Patient preference based on “clinically or ethically appropriate reasons” – this is a little bit tricky.  Examples are given:
    • Female patients requesting a female doctor.  (This is often the case in Aboriginal Health in Australia – it is generally culturally inappropriate for male clinicians to perform intimate examination of female patients [and vice versa].  There are of course degrees of ‘intimacy’ and traditional beliefs.  We also have varying capacity to accomodate this scenario – I work solo nights, so cannot offer this at all times.)
    • Patients who request clinicians with same language.
    • Patient with negative experiences with a particular racial group – e.g. veterans of war conflict rejecting clinicians from their former enemy country.
  • I would add another group of patients that I have come across; patients that request a different clinician based upon “undisclosed” reasons… for example a homophobic patient may refuse to see a doctor that they suspect to be a homosexual.
  • Finally there is the overtly racist or bigoted patient.  These are somewhat easier to classify, however the conflict is usually front-and-centre.

The authors also raise the potential for conflict between the patient’s wishes and the employer’s [hospital] duty to provide a safe and non-discriminatory workplace.

Of course, being the USA there is alway the potential for physicians to take civil legal action against these patients.  This hasn’t happened yet.  I cannot imagine it happening in Australia  – but it does raise another set of ethical questions.  Should a physician take legal action against a patient in this setting?  Certainly we pursue criminal charges in the case of staff being assaulted.  How is this different ethically?  Is a verbal “assault” based on race, gender, religion or sexuality different if a punch is never thrown?

So after a bit of debate and thought I have boiled this down to two basic options in my head.  If I was in this situation there are 2 practical options:

  1. Acquiesce to the patient’s request and provide another clinician
  2. Decline the request, run the risk of conflict, but remain “ethically intact”.  That is, place the principle before the patient.

So how to decide which way to play any given scenario…..

For me the central, critical question is around the underlying patient motivation.  You might ask yourself the following questions:

Is the patient refusing a particular doctor in a genuine attempt to enhance their own care?

OR

Are they placing their care behind their irrational, false belief that the treating doctor is in some way inferior.

So put yourself in this situation:- you are the duty consultant and a patient is kicking up a bit of fuss after being allocated a doctor who was trained in Pakistan.  The patient has no other information about the junior doctor other than his name – Dr Mohommed Hafeez Bilal and that he has a strong Pakistani accent.  The patient doesn’t appear to have a life-threatening condition but it is looking like he will need admission for ongoing investigation.

Q1. How will you deal with this patient?

Q2. What will you tell Dr Bilal?

Q3.  Do you have another, smarter way of breaking this down?

 

Clinical Case 128: Northern Knee Nasty

OK, team.  This is a bit of a teaser for my SMACC Dublin talk “On How I Do Diagnostics”.  I won’t be giving too much away, but wanted to share a bit of local flavour when it comes to diagnosing a relatively common problem.  Acute monoarthritis of the knee….

Lets do a case.

Jimmy is a 30 year old man who is usually “fit and well”.  Despite this he has a BMI of 37, a starting BSL of 16 [288 for the States].  He denies any chronic symptoms of knee or other joint pain.

He had a few footy injuries when he played Aussie Rules in his 20s. But that was 8 years ago and 60 kg lighter.  He specifically denies a childhood history of rheumatic fever [sadly this is a high yielding question in Broome..]

On specific questioning he has had a recent STI (gonorrhea is 1000 times more prevalent in my ED than in urban EDs)… though this is not really surprising. He was treated with a ZAP PACK ( single doses of azithromycin, probenecid and Amoxicillin 3G) 2 weeks ago.

Jimmy has never heard of gout. He cannot recall any injury to the knee – though he had “a big weekend” – so it’s all a bit blurry…..

On examination:

  • there is a crusted, sloughy superficial skin sore ( impetigo) over the patella – looks quiescent
  • he cannot weight bear due to pain
  • his ROM is about 20 – 30 degrees flexion
  • the knee has a moderate sized effusion
  • it is warm ( not hot) to touch
  • no specific sites of bony or ligament tenderness

So there we are.  This is a classic tropical Aussie case.  Our differentials are a bit different up here.  To start investigating we need 2 things:

  1. an estimation of pretest probability
  2. an idea of the test characteristics for our next Ix

This is my real- world differential diagnosis in this chap – and they are all weighted pretty evenly!!

  1. septic (Staph / MRSA/ streptococcal) arthritis – biggest DANGER Dx here
  2. gonococcal arthritis – tends to present as subacute arthritis
  3. gout – he’s syndrome X and recently binged on EthOH
  4. Recurrence of acute rheumatic arthralgia – common even if no primary Dx
  5. Reactive arthritis ( eg. Reiter’s ) – we know he had an STI, so can happen
  6. occult trauma – needs excluding or I’ll look like a goose
  7. Ross river virus ( local flavivirus) – presents with lower limb swelling, rash

From a diagnostic perspective this differential is a bit of a disaster. Six or 7 potential causes, roughly evenly weighted.  So our pretest probability for any of these is 20% at best! In order to get over the “test threshold” and “diagnose” any of the above we will need to choose our investigations wisely.  What we need is a test that will sort the goats from the sheep, one with a low signal-to-noise ratio.

The ideal test here would have a potent positive likelihood ratio (+LR) for the less dangerous diagnoses AND a strong negative likelihood ratio (-LR) for the serious, destructive diseases – esp.  acute septic arthritis…  so what will work?

I would argue that there is no known blood test that will hel us in this scenario. Please let me know if you think this is wrong. WCC, CRP, ESR, uric acid, ASOT, serology

X-ray is really only going to help us exclude an occult fracture eg. tibial plateau – it is cheap, safe, available – so let’s do it. RESULT: Drum roll….. Normal, some periarticular fluid in the tissues.

So let’s just stick a needle in and suck out the fluid, send it off – GOLD STANDARD. Yes, this is the best option. My test of choice up front……but…. the knee is covered in crusty looking sores. Do we really want to poke a needle into this and onto the joint? I’d worry I am causing septic joint whilst trying to exclude it!

Whilst pondering this dilemma I do what I usually do – ultrasound!

Really I am just having a gander to check where I could place a needle into a pocket of synovial fluid safely.  This is an image I caught…. It contains a sign which is supposedly very specific for one of the above diagnoses. Maybe we can spare the needle?

Can you tell me what the sonographic sign is? And which differential does it suggest?

Is it enough to ‘settle’ this diagnostic dilemma?

Let me know if you have any clinical pearls that might help here!

more soon, Casey

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