Clinical Case 118: Thinking outside the box

OK team – a Paeds case for you today.  It’s one where I am going to give you just a few clues and you have to think up the diagnosis.

Here we go…..

Jemimanisha is an 8  yo. girl who lives in an Aboriginal community about an hour away.

She has been brought to ED by her mother after being up all night complaining of a headache.  She has never had headaches before.  Her Mum is concerned that she ate too much junk food at her friend’s home the night before.

On further questioning – the headache is really quite global – she points at both parietal areas and rubs her head on both sides to show where it hurts.  She has had no recent URTI sxs, no fevers, cough or injury.  She isn’t bothered by lights or the ED noise.  Up until bedtime she was fine.  She woke around 11 PM with the headache &  slept in with her mother after that – her mum says she was restless and crying out all night long [Mum looks tired!].  This morning she vomited after eating toast.  Her belly feels OK and she reports no diarrhoea.

PMHx:

  • Obese with a BMI of 32 [currently seeing dietician]
  • Recurrent ear disease with grommets as a child, multiple presentations with acute OM in last 5 years. None recently.
  • Had a laceration to her ankle last month that required repair under sedation in ED – that went well and she was discharged.  Wound healing OK.

On examination

  • Afebrile, HR 90 SR, well perfused,  SpO2 = 99% RA,  RR = 15/min
  • Neuro exam is NAD – PEARL, no meningism, walking well, coordinated and fundi look ok – no papilloedema.
  • ENT – old scarred TMs bilaterally, no coryza, throat NAD
  • Chest and abdo unremarkable, soft, no signs of lung disease
  • No LN or rash, mucosa looks moist.
  • Leg wound has healed but there is a 3mm dehiscence of the edge of the scar – there is clear, serous fluid oozing out.  It is non-tender, no pus or cellulitis.

OK, that is all I am going to give you at this stage…

Here are the questions:

Q1:  What further information do you want [it is a weekend in Broome – so no labs or X-rays !]

Q2:  What is the diagnosis?

Q3:  What do you need to confirm the diagnosis?

I am sure you super sleuths can work this out!  Who is fastest?

OK – after that whirlwind diagnostic Tweetoff – I have uploaded a BroomeDocs podcast looking at the diagnosis and the our recent experiences with this disease here in the Kimberley – there’s a few pearls in there if you care to listen – 10 minutes!

The summary – its a disease that you will not diagnose if you do not think about it!  Ok Here is the podcast:

DIRECT DOWNLOAD

 

Clinical Case 117: Cancer Fishin’

OK – this case is for all the GPs and Internal Medicine types out there.  This is a relatively common scenario…  how do you play it?

Here’s the case.

Bruce is a 53 y.o. accountant.  He is a little overweight at 89 kg (BMI 31).  He is otherwise relatively well, he cycles to the cafe each morning in lycra and drinks a cappuccino in his helmet… why do they do that?

He has hypertension which is controlled by ramipril 5 mg daily.  No other meds or relevant medical history.  He is interested in his health and even has annual “Mens’ Health checks”.  He was in last month for one – which was unremarkable other than a borderline BP and his prostate screen (post full consent and shared decision-making) revealed a normal DRE and PSA level.

Today he has come to see you with a discharge letter from the local hospital.  He was admitted for work-up of “unilateral leg swelling” which occurred spontaneously last Friday.

The letter reads:

Dear Dr Leeuwenburg,

Thanks for following up Bruce who had an unprovoked DVT diagnosed on Doppler.  US showed a 5 cm proximal DVT at the Femoral-saphenous junction (L) leg.

He also had a series of tests: FBP, UECr, LFTs, Ca, Mg, PO4, CRP, TFTs, a prothrombotic screen was unhelpful and serum rhubarb – these were all normal.  WE did a CXR to be sure and this was also reported as normal.  

Bruce was commenced on enoxaparin until his warfarin was therapeutic.  He’s on 8 mg nocte with an INR of 2.3 today .  Please chase his subsequent INRs

Oh – and – please screen for occult malignancy as we have not found anything yet.

Yours truly….

So Bruce is sitting in front of you looking a bit worried.  He says that he feels fine, and the leg swelling is improving.  He was a bit spooked when the “young-looking” hospital doctor told him that DVTs “like this” are usually due to some underlying problem “like cancer”.  He really wants to know what to do next.  Does he have cancer?

OK – so here are my questions to you:

Q1:  What is the chances that Bruce has an occult malignancy?

Q2:  what screening tests, inquiries, imaging etc would you recommend / order for Bruce?

Specifically will you get a CT of the torso?

Q3:  Does it really matter if he has an asymptomatic cancer? Will it reveal itself in time anyway?

Let me know your thoughts…

But in case you were wondering.  Here is the link to the recently published SOME trial out of Canadia in the NEJM in June 2015

They looked at a limited vs. “limited + CT ado-pelvis” strategy and found not much difference.  Both groups had about a 1% cancer rate at work up and had a similar “diagnosis rate” of cancer in the following year.  So the CT didn’t help reduce the time lag to diagnosis much.

However, there is of course a risk of finding incidentalomas and the harms associated with those and their further IX or Rx…

So for me it si back to simple thorough Hx, Exam, do the things you would normally do for a 50 yo bloke and watch him.  Really a great case for Shared decision-making here now that we have some rough numbers that we can present to the patient as risk ?

Thoughts
Casey

Clinical Case 115: Pneumothorax puzzle

This case was interesting for a number of reasons.  It starts with a 50 year old lady whom has been assaulted.  She says she was kicked in the head and chest.  In ED she is looking sore but stable – and it was felt that she had enough mechanism to warrant a CT of her head and neck.  On the neck CT it was noted that she had some surgical emphysema on the lower slices – so she stayed in the tube for a chest scan too!  Here it is:

Pneumothorax = Tense CT!

 

Now – I know what you are all thinking…  that is a CT image that should never had been captured!  We have all heard the addage that you should always pick a tension clinically and never need to image it… but…  the honest truth is that we just are not that good at picking pneumothorax clinically.  As you know I am an ultraosund tragic – and I believe we can certainly pick em with a quick chest probe.  However, relying on clinical exam is just not, well, reliable.

In recent years one error that I have seen creeping into my practice is the tendency to “fast-track” trauma patients to imaging where appropriate without completing a fully thorough secondary survey.  There are a lot of reasons (? excuses) for this:

– trying to get the imaging done in office hours,

– trying to get patients out of collars ASAP,

– relying on second-hand info via handover which may be innaccurate….

– search satificing. Stopping at one major injury!

So my “lesson learned” here is to be systematic and make sure that you are imaging everything that needs imaging and that you have excluded the big “killers” before settling for a CT.

OK – back to the case.

A chest tube was placed and the pneumothorax decompressed.  Post ICC films showed a well expanded lung.  Our patient was admitted to the ward.  Lets jump to the next day…..

Our patient starts to deteriorate.  She is becoming more hypoxic with tachypnoea.  What is going on?

Well there is a few possibilities.  The chief concern was that the tube was occluded / dislodged resulting in reaccumulation of the Ptx.  So another CXR was performed…

Take a few minutes to look at this CXR.  It was reported by the Radiologist as “recurrence of pneumothorax on the right, with overlying subcutaneous emphysema mimicking lung markings.”

There is no recurrence of the pneumothorax. Clinically: the ICC is “swinging” but not “bubbling” – so the tube is patent and CXR shows it is still intrapleural. There is of course considerable mediastinal shift – which is due to the loss of volume on the left side which is collapsed.

Of course – Ultrasound will be useful. The left side is going to be tricky as there is a heap of SubQ emphysema – so the pleura will be hard to visualise. However, if you can find a gap you can see sliding, great. Really the utility of US is to define the collapse on the left side – consolidation, is there an effusion?

So here is where it gets easy – back to basics. The problem here on ultrasound was consolidation with likely atelectasis. The nurses noted the patient was too sore from rib fractures and had been positioning herself right-side up with some haemoptysis. It was very likely that she had plugged some largish bronchi with blood and debris. So we engaged a trusty expert chest Physio to bang out some mucus and blood. Provided good analgesia and got her up and walking. The next day – here lung was re-expanded and her hypoxia was resolved

OK –  let’s hear your comments.  I you were at #SMACCUS last week then you will have a distinct advantage over the other readers as this case was put up in a session there and discussed.

There are so many potential errors that we can make in even the simplest of cases.  Trauma is a complex scenario with information overload, serious sequelae and time critical decisions to be made. So over the next few months I am hoping got run with a theme of “common errors and their mitigation”.  Hoping to have a few special guests on to help show how we can avoid the pitfalls and do better on the floor.

Casey

Clinical Case 114: Skull and Crackedbones

This case is inspired by a recent Twitter discussion with fellow Pads ED enthusiasts – Tessa Davis [ @TessaRDavis ] , Andrew Tagg [ @andrewjtagg ] , Rachael Rowlands [ @rachrwlnds ] and whoever else was reading.

As a background – you probably should read my previous ramblings about Paediatric head injury assessments here: Kids Coconuts and CTs

I think that the PECARN decision tool [MdCalc clickable version HERE ] is probably the most useful and robust data out there for making the call on children with minor head injuries in the ED.  In the past we have often taught or been taught to observe kids for hours and hours, or CT them.  The PECARN data set certainly has changed my practice in the last 5 years.

I now use it to identify children whom are at extremely low risk and feel confident to discharge them with follow-up instructions of course , one needs to be assured that the parents / carers are comfortable with this and able to access appropriate follow-up if required.  The PECARN study also gives us a basis for discussing the risks of observation, imaging and non-investigation in kids who are not in the low-risk group.

Now take a look at this part of the PECARN Algorithm – this is the section for kids aged under 2 years of age.

Screen Shot 2015-03-21 at 10.16.20 pm

The majority of kids that I see in this group are little ones who have walked / run / fallen head first into something solid.  They usually have a frontal “egg” or laceration over the forehead.

So lets walk through the algorithm.  If this kid has a large frontal haematoma then it is going to be tough to say that they do not have a skull fracture, or at least you may think you can feel something.  Let’s face it – pushing on a fresh, boggy swelling over a kids head is just plain cruel!

If you think that you can palpate a fracture – then they immediatley jump into the ‘high risk’ group i.e. the group that is recommended to CT early.  This was about 1 in 8 of the kids in this age group.

However, if there is no fracture palpable then you are very likely heading down the pathway to simple observation, or possibly into the super low-risk group.

Hence the question of the presence or absence of a skull fracture seems to be a big hinge-point when it comes to making this decision.  And here is what I suspect:  we are terrible at picking these!  OK, I understand that the PECARN trial is a pragmatic set-up.  It was a simple clinical call – was the clinician able to palpate a fracture.  However, in reality this does seem very subjective and prone to bias.

Enter our friend – the Ultrasound.  Is there nothing we cannot do with the probe?

Ultrasound is useful in picking fractures elsewhere in the body – particularly in superficial bones.  So can we detect skull fractures with any accuracy?

Well there are a few smallish trials looking gat this question in the literature:

One form New York, Jim Tsung and co. in Paediatrics, June 2013 – “Accuracy of Point-of-Care Ultrasound for Diagnosis of Skull Fractures in Children”

Another from Riera et al in Paediatric Emergency Care, May 2012 – “Ultrasound Evaluation of Skull Fractures in Children: A Feasibility Study”  This one had more small kids in it – i.e.. mean age 2 years

These are small trials – 115 patients combined.  19 had a fracture on CT – so the incidence was ~ 16%.  Like many POCUS papers they show the usual characteristics of bedside ultrasound techniques – very specific and reasonably sensitive – so if you see a fracture – there almost certainly is a fracture, but you will miss 15 – 20 % potentially based on the numbers here.  In the Tsung paper – only one fracture was missed – that was a fracture that was adjacent to the hematoma – rather than directly beneath it.  So you could improve this with a more thorough scan field.  In terms of likelihood ratios: bedside US give a +LR of 27 (excellent!) and a -LR of 0.13 (pretty good!).  As always – we need more data to validate this and make it more generally applicable.

So how would a bedside skull US fit into the PECARN pie?

Hard to say what our “Sensitivity and specificity” is for clinical palpation of skull fractures – I would guess we are 50% sensitive and 75% specific.

So using that as a comparison – we should be able rule in a few more kids who should probably get an early CT.

So will this mean we do more CTs?  I think not – as there are a lot of kids who have a nasty looking egg on the head – and we are often biased by the external picture into believing that we can feel a ‘step’ as we are worried and want to rule out badness.  So if we scan the kids with the ugly looking hematoma and find no fracture on US – then this would probably be a group where it is safe to push them into the “observe, wait ‘n see” strategy.  Although US is not super sensitive – it surely must be better than a subjective prod over a boggy lump.

[Note: if you use a stand-off pad or lots of gel – you can do this US without inflicting much pain at all.  No pressure needs to be applied.  So I think this is a more humane approach to the kids with a large, boggy swelling of the noggin.]

So overall I think that US would allow us to separate the goats from the sheep – allow us to create a bit of diagnostic daylight between these 2 groups:

(1) Those who definitely have a fracture and may need early imaging of the brain

(2) Those at lower risk of fracture who can be safely observed.

Bedside US probably doesn’t add too much to the kids whom can be classified as very low risk by the PECARN algorithm.

My practice is to promptly discharge kids who meet the “extremely low risk” criteria.  I give the parents reassurance and information for what to look out for.  But… this is my new pet peeve…  forcing a kid / family to sit in the ED for 4 – 6 hours to have “Neuro obs” completed seems like a really antisocial and low-yielding exercise in this group.  So if I am satisfied that the parents understand the risk and what to do if… happens, and there is no NAI question – I will send them home from triage.

Love to hear how you manage this common problem in your ED.

 

Casey

Clinical Case 113: Feeding Me Softly

Today’s case comes from Dr Trent Little – chronic Broome JMO and now my right-hand man in the Education Department (  i.e.. we share a desk ;-]  ).  This is a great Kimberely case – all the usual mix of third and first world medicine that just doesn’t happen much in the city.  Lets jump right in:

Solomon is a 44 y.o. man, he presents to the ED with a painful finger.

On examination he has a gangrenous looking right index finger. He is febrile, but not particularly looking that unwell. He also incidentally complains of having an increasing productive cough over the last week.

He is however well known to our department here and has a long medical history.
Previous TB
Chronic pancreatitis
Malnourished and ETOH abuse
Chronic normocytic anaemia
CKD stage 2
Smoker

He reluctantly agrees to admission and is brought into hospital with presumed osteomyelitis and commenced on IV piperacillin / tazobactam tds to cover his chest and finger.

Some clever doctor thought we best do a full blood work up given his history which showed:
Hb =98
Na = 124 (134-146)
K = 2.4 (3.4-5.0)
Cl = 86 (98-108)

Urea = 8.4 (3.0  – 8.0)

Creat = 183 (about double upper range of normal for US readers.)

Phosp = 0.92 (0.8-1.50)
Mag = 0.38 (0.7-1.10)
Cal = 2.20 (2.15-2.60)
Alb = 37 (35-50)
CRP = 220  [Ed: we do not encourage the use of CRP around here, but if you must….]
Lipase = 220 (ever so slightly elevated)

His electrolyte abnormalities were thought to be largely due to malnutrition and chronic disease.

In addition to his anti-microbial cover he his given initially IV K + Mag and then high oral doses. 2g oral Mag tds and 1200mg BD slow K.
His K rises slowly as planned, but despite the high doses oral Mag his serum Mag concentration does not reach >0.4.

On the third day of his admission he absconds from the ward for a few hours to have a couple of cigarettes. On return he his tachycardic with a rate of 110. He is completely asymptomatic and he gets and ECG.

ECG shows:

ECG 1 113

new ST elevation in V3 V4 and perhaps V5. What do you think may be going on here? Would you treat for STEMI/ACS?

Advice from the remote cardiologist is sought.  Solomon is given

-aspirin,

– enoxaparin  1mg/kg bid

– bisoprolol (bisoprolol was thought to be a better B-blocker option given his respiratory history).

The next morning his ECG had returned to normal and his high sensitivity Troponins were all negative at 6 & 12 hours

Now we are confused. What other investigations?

His bloods were revisited that morning.
Na = 126
K  = 4.2
Cl = 90
Cr  = 186
Urea= 8.4
Cal = 2.12
Phosp = 0.44
Mag = 0.38
Lipase 979
CRP is now 10  [Ed: wooohooo! Cured, discharge – hurrah for us…  sorry I just really don’t like CRP as a test. CP]

So, what was all that about then?  Whats the diagnosis ??

He was diagnosed with refeeding syndrome. Our ICU friends thought that the ECG changes were presumed myocardial dysfunction secondary to refeeding syndrome.

How do we manage refeeding sydnrome?  We would be interested to hear anyones opinion who has experience in this area.

What patients are at risk of Refeeding syndrome?

The best way of preventing re-feeding syndrome is identifying those who are at high risk. This BMJ article gives a nice summary.

Anyone not feeding for more than >5 days is at theoretical risk of refeeding syndrome. Our common high risk groups patients groups include:

Anorexia nervosa
Chronic Alcoholism
Postoperative (particularly GI surgery)
Oncology patients
Patients with uncontrolled diabetes
Malabsorptive syndromes such IBD, CF and chronic pancreatitis
Some patients who we would be less likely to consider, but who are also at risk include long term antacid users (Mag and aluminium salt binding phosphate) and long term diuretic users (loss of electrolytes).

It is largely a clinical diagnosis with a few characteristic biochemical abnormalities. Here is a nifty flow diagram from the BMJ review of the NICE guidelines for managing referring syndrome

refeed mx

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