Clinical Case 110: Sepsis, Scans and Surgeons

Here is a case that may keep you guessing.  One for the US nerds.  Here we go:

25 year old tourist – visiting the town, she has been backpacking for 6 months and the history is a little vague… but basically she thinks she may have had a miscarriage about 5 months ago.

She had a positive pregnancy test and two weeks later developed pain and PV bleeding.  Didn’t see a doctor as she had no travel insurance…  the pain settled and she thinks she may have passed some large clots  – anyway the symptoms settled and she carried on her travels.  No imaging was done.

Fast forward to now – 5 months later.

The history is of 24 hours of lower ado pain. The pain started in the left iliac fossa.  Was well localised but has since become more generalised – on examination she is guarding and has clear peritonism across the lower belly.  Certainly she is more tender on the left.  She is febrile (39.8 C = 103.6 F), tachycardia 110 and has a BP of 90/60.  She denies any recent PV loss, discharge or urinary symptoms.  Her bowels were OK until yesterday – no motion since the pain started.  A VBG shows a mild, compensated metabolic acidosis, normal lactate.

He UA shows some pyuria but no nitrites.  And the B-hCG is…..   [drum roll] .. negative.

So in summary – a 25 yo lady who may have had a spontaneous miscarriage 5 months ago now presents with a sepsis picture, left iliac fossa pain and peritonism.  We need a scan!  So I will show you a series of 6 TV US images now and let you interpret them…  here we go.   [I have added captions to orient you if you are not familiar with TV scan which can look a bit weird to the uninitiated ]

I think I will let this case linger here for a few days.  Would really love to hear your thoughts on these images, the possible diagnoses and where to next!

Of course I will tell you what the final outcome and diagnosis was – but first lets see what you think of these images in this scenario.

Comments please.  Are you a super sleuth with a scanner?


Right ovary on TV

Right ovary on TV

Longitudinal pelvis view

Longitudinal pelvis view

Left pelvis adnexa

Left pelvis / adnexa

Left ovary

Left ovary

Left pelvis mass long.

Another look at the left pelvic mass

And so what happened in this case? What was the diagnosis?

After some fluid resuscitation and empirical antibiotics we headed off to the OT. Gynae started with a laparoscope – which showed: – a lot of purulent fluid – a long inflamed appendix which was adherent to theft anterior pelvic peritoneum, wrapped in omentum. – the appendix had a terminal abscess which contained a sac of frank pus in a strange casing! – Presumably a partially walled off appendix abscess in an odd location. Moral of the story: an unusual appearance of a common disease is commoner than the usual appearance of a rare disease ! The pregnancy was “noise” unhelpful clinical data

Clinical Case 109: Eyes, Air and Ultrasound

A quick case that shows how we can use ultrasound in clinical assessment of eyes and why US makes me look like a better doctor.

30 year old woman – was punched in the face 3 days ago at a disco.  She sustained a small laceration over the inferior orbital rim – but went on dancing.

The next day she awoke with a really swollen face, unable to open her eye at all.  The laceration had sealed itself  – so she decided to wait a few days to “see it it would get better”.  That is the type of people we see a lot of in Broome!

By day 3 the swelling was no better and she was beginning to get a bit annoyed by the pain and inability to open her eye…  so off to ED.

The left eye was severely swollen – despite analgesia and a firm hand – the best I could do was glimpse the sclera and a bit of cornea.  She had a small subconjunctival haemorrhage, no hyphema and a clear looking cornea [in the half second that she tolerated my prying her lids apart.]  Far from an ideal assessment.  So how do you assess an eye that is occluded by swelling in the middle of the night?  Ultrasound of course!

Here is a rough guide to looking into eye trauma using the US machine.

  1. Linear probe set to 4 – 5 cm depth.  “Small parts” preset works OK.
  2. Get heaps of gel onto he probe / upper lid (use cooled gel if you want to make a gel heap as a stand-off pad.)
  3. Easiest to have the patient supine with pillow to stop the head moving.
  4. Set the gain to make the vitreous black, however it can be useful to turn it up if you are looking for subtle intra-vitreal bleed etc
  5. Scan over the upper lid fanning from superior to inferior, then in sagittal plane from side to side.

There are some cool things you can do with ocular US when the eye is unexaminable:

– Assess range of extra ocular movement.  This is really important for assessing for rectus entrapment.

– Assess pupil response (check out the video here)

So I went through my routine and scanned the closed eye.  In trauma I look for the following injuries on my scan:

  • lens dislocation,
  • retinal tear,
  • intra-vitreal bleed / detachment,
  • globe rupture and
  • retrobulbar haematoma [tip is a “guitar pick-shaped” posterior globe]
  • Check the optic nerve sheath diameter (ONSD)

As I was scanning the orbit I kept getting this weird artefact – thought it was maybe due to some cellulitis or loss of contact – but it “just didn’t look right”.

So when I do a scan and it is “not quite right” I tend to imagine the worst case scenario.  I was seeing a normal eye with good pupil response, extra ocular movement etc. No pathology – just this odd artefact that obscured my views.  So I decided to investigate further.

Here is the CT of her orbit: Clearly an inferior orbital fracture with a nice teardrop of fat extruding into the antrum.

And you can see quite a bit of air that has escaped into the orbit – which was the sourcephoto-2 copy of my mystery artefacts.

So I thought I had just discovered a new sonographic sign – but of course I was wrong.

There was a paper published on this phenomenon way back in AJEM, 2004 from Michael Blaivas et al (here)

So I managed to fluke finding air in the orbit – though I wash’t really sure what I was seeing!

Lessons learned here:

  1. If you are not sure what you are seeing – don’t ignore it! It might be the key to the diagnosis
  2.  Air in the orbit equals blowout fracture and looks like a dirty gas shadow (kinda like bowel in the orbit)
  3.  Correlate your bedside scan with formal images and you will learn a lot faster.

Happy scanning


Clinical Case 108: Planes, Drains and Pneumothoraces

Another case inspired by a Twitter debate today.

A Tweet Case was put forward by @FlyingDrBen  (Ben Darwent) who is based in Perth WA – home of LITFL. My friends Minh le Cong, Karim Brohi and Tim Leeuwenburg started a discussion around the case.  Fair to say it got way too big for twitter!  So I am posting this case to get you all thinking and source expertise on the topic.  Here we go…

Rodknee is a 27 yo. man who has presented to a remote hospital following an “incident” in which his girlfriend stabbed him in the right lateral chest with a small kitchen knife ( ~ 12 cm blade).  She apparently found out he had been sleeping with his wife despite his assurances to the contrary.  The oldest story in the book!

Rodknee is a stoic individual and managed to sober up and have a sleep before presenting to the ED about 3 hours after the injury.  There was not much blood loss at the scene and he managed to patch things up with his +1 in the meantime.

On arrival his Obs are all normal ( P = 70, BP = 125/80, RR 14, SpO2 = 99% RA, he is well perfused and alert.  He does complain of some pleuritic pain on inspiration over the site of the wound.  On inspection he has a very neat stab wound ~ 2cm long at the anterior axillary line – 6th intercostal space.  There wis no active bleeding or bubbling.

The attending Doctor is a semi-retired GP from an affluent Sydney suburb who is doing a few locums “for fun” to round out his career.  He has asked for your advice – fortunately you have a High-def VC link up to their ED which is about 250 km away.   So you have a virtual look at the patient.  He is as advertised.

Being an ultrasound enthusiast – you talk the locum through a FAST scan and look for a pneumothorax / haemothorax.  The very rough and ready images reveal a tiny right pleural fluid collection (less than a centimetre) and no clear pneumothorax – although it is hard to exclude in a mobile vertical patient who is 250 km away!  So we think he has a small haemothorax and either no pneumothorax – or a very small pneumo we have not been able to find on US.  He remains haemodynamically stable.

The locum is super keen to get Rodknee transferred out to your bigger ED ASAP – he is the solo cover and has been up all night already.  Fair call – lets get the aeromedical team in to swoop and run.  But……   what about the potential pneumothorax?  Does it need a drain before we put this chap on a small plane?  The textbook says it will expand and might cause tension effect if it does.

Just out of interest – you ask the locum if he is comfortable with placing an ICC if required…  he tells you that he last did one in 1979.  Then he starts waving a metal trocar around like the Swedish chef from the Muppets!  Hmmm, maybe not so soon!

So here is the question – is it better to perform a prophylactic intercostal catheter in a well lit ED under sterile conditions, OR should we fly him without an ICC.  What is the risk of his developing a tension pneumothorax or becoming hypoxic is his possible pneumo expands?

Is a drain mandatory for a 30 minute flight in a small aircraft that will be going to altitude?

Controversial!  Lets hear your thoughts.


Here is a nice physiology experiment from the Journ of Trauma & Acute Surgery Nov 2014 – small pneumothoraces did expand – but not with any clinical implications at cabin pressure up there.


Clinical Case 107: Subarach Sans Scan

This case is inspired by a Twitter conversation started by Dr Brent May ( @DocBrent ) – he is an Anaesthetist and motorsport doc in Australia.

Brent asked the simple question: “SAH Q – no CT available. What is the “usefulness” of RBC count on LP? Lab “unable to do xanthochromia”.  This is a real problem in many hospitals – especially the smaller places with no CT or specific lab crew.  So lets look at a case and try to get to the bottom of this one!

You are working in a remote clinic with a small Emergency area.  It is a slow day.  You are 400 km from the closest hospital which has a CT and laboratory services.


Jan is a 45 year old local woman.  She presents with a bad headache – this is not usual for her, she is not usually a “headachy” person. No PMHx of migraine or other headache syndrome.  It woke her from sleep this AM – about 4 hours ago. Maximal intensity from the onset.  She says it has not responded to simple analgesia and resting at home.  She has had no syncope or neurological symptoms.  The headache has remained relatively constant.  She is complaining of neck stiffness – though has normal ROM in her neck.  She has no fever, vomiting or photophobia.

On examination she has no neurological signs.  Her obs are all normal, BP = 140/85, afebrile.  You cannot reproduce any objective neck stiffness.

So – first question.  Based on that clinical info – what would you estimate Jan’s “probability” of having a subarachnoid haemorrhage ?  Have a Gestalt guess… 2%, 5%, 10%, 50 %???

How low would you want your “probability” to be to avoid a transfer and subsequent work-up?  i.e.. what is your lower test threshold for SAH? 1:100,  1: 1000, less?

Here is a copy of Perry & Steill’s landmark paper in the BMJ 2011 – check out tables 1 & 2.  Jan is pretty much a “average Jan” for the cohort of 3000 pts in their paper.

About 7.7  % ended up having a subarachnoid bleed – and another 2 – 3 % had another non-benign cause for their headache.  So 10% is a reasonable “pretest probability” for badness in Jan’s case.

Now a 10% risk of serious intracranial pathology.  That would mandate a work up in most places.  Unfortunately your hospital only has rudimentary lab gear – you can do an LP and get red cell counts, but not xanthochromia.   A CT would be helpful if you can do it in less than 6 hours – but even if you called for transfer now – it would be well past 6 hours by the time Jan made it into the doughnut 400 km away.

So here we are.  You can do an LP and get red cell counts on the CSF.  Xanthochromia is probably not helpful as it is early (less than 12 hours) and simple visual inspection for yellow change is inaccurate. [Best read by non-colour blind female lab techs apparently!  Can you ask for that on the forms?]  Most Australian labs use automated spectroscopy to analyse for xanthochromia – and this is usually only available in larger, tertiary labs.

The accepted gold standard diagnostic features of SAH are variable – but the Canadian group who do a heap of research use the following:

“Subarachnoid haemorrhage was defined by:-

– subarachnoid blood on unenhanced computed tomography of the head,  OR

– xanthochromia in the cerebrospinal fluid,  OR

– red blood cells (>5×106/l) in the final sample of cerebrospinal fluid,

PLUS  an aneurysm or arteriovenous malformation evident on cerebral angiography.”

So now the big question.  Is there any way that you can effectively “rule out” SAH in Jan without transferring her 400 km to the next hospital?

Does a low CSF red cell count allow us to “exclude” SAH?  Can we use any other tests to decrease the risk for Jan?

Tough yet common problem in many rural areas in Australia.  I would love to hear your thought and comments below.  Does it depend on the timing?  Can we watch and wait if the initial LP is clear?  Or do we need to get imaging and a review for xanthochromia on all the Jan’s we see in ED?

If you are interested in the diagnostic dilemma that is the “SAH work up” then I highly recommend listening to David Newman’s SMART EM episode on the topic from way back in 2010. (WARNING: it is nearly 2 hours of podcast!)

Let me know what you think


Clinical Case 106: The mysterious Pink Lady

Time for another quick clinical case

Your next patient is Joan – a semi-regular attender to your family practice.

Joan is a 67 yo woman who is usually reasonably well.  She works as a book keeper in a small business.

She has been troubled by some gastro-oesophaeal reflux symptoms over the last few years and has been taking some omeprazole “most days” for symptom relief.

Today she presents with a sheaf of discharge letters from the local ED.  7 in total!  She has been seen in the ED 7 times in the last 6 weeks with “chest pain – non-specific”.

She tells you that she has been experiencing dull, spasms of pain in her substernal area that sometimes radiate to her back.   They are not really like her usual ‘heartburn’ symptoms.  She doesn’t feel sick or sweaty.  Just worried.

These are quite unpleasant and stop her from working at her computer.  The last couple of episodes have occurred at night and woken her from sleep – her husband has called the ambulance service twice in the last fortnight!  On each attendance to the ED she has been “fast tracked” into the chest pain protocolised management.  And spent a few uncomfortable nights on a stretcher in the corridor of the ED…..  awaiting a second  troponin.

Amidst the paperwork there are formatted letters from ED interns, Registrars and even one from a consultant ED Physician.

There are a batch of plumb normal ECGs and photocopies of many negative troponin results.  She even stayed in for an exercise stress test one day – which was non-suggestive of ischemia.

She has been diagnosed consistently with:  “Chest pain – non-specific.”  or “Chest pain, not cardiac.” on each occasion.  On the latest visit the senior Doc has ventured a positive diagnosis – “Probable Oesophageal spasm.”

Interestingly there have been a number of therapeutic trials of “Pink Lady” i.e.. the Mylanta & Xylocain viscous cocktail so loved by triage nurses the world over!  Joan says that the pain is usually short-lived – coming in spasms. It seems to go away after a few minutes then return.  She says a lot of the doctors ordered the Pink stuff and when her pain got better…  told her it was from her oesophagus. [ see this post from Dr Seth Trueger on this topic. ]  Maybe best left until after the troponin has settled the question!!

She has received advice to take her omeprazole twice a day and to follow up with her GP.  OK, here she is….

So, it seems clear that she is in the low-risk group for cardiac disease as a cause of her chest pain.  Let us assume that the ED Docs have excluded ACS as a cause.

SO, if you are the GP how do you go about making an actual diagnosis in this scenario?

Is a therapeutic trial of PPIs a reasonable strategy?

Depends…. are you trying to give relief to the patient or make a diagnosis? After searching through the databases I found this decent sized trial from Flook et al, in Amer Journal of Gastroenterology (January 2013)

It looked at 600 patients with reflux symptoms giving chest pain.  A placebo, RCT (esomeprazole 40 mg BD for 4 weeks) They found a significant improvement in symptoms at the end – but this was really only for patients with less frequent reflux sx at the outset.  Not so effective for the pts with more than 2 days a week of symptoms.

There is also a meta-analysis [Wang et al, JAMA, June 2005 ] looking at 6 papers ( only 220 pt in total) which tried to answer the question about the diagnostic characteristics of a “trial of PPI” for reflux-related chest pain in patients with “non-cardiac chest pain” .  The conclusion of the authors was that is was an acceptable “test” with a sensitivity of 80% and specificity of 74% roughly.  So – it might help – but to my mind those are not stellar numbers.  I would want a reasonable high or low pretest probability of “GORD” before hanging my patient’s hat upon those figures.

Should she have endoscopy to look for serious upper GI problems?

Well that is a tricky one.  Not a lot of data.  Just opinion.  The surgeons that I work with would suggest everyone with severe enough , persistent symptoms should probably have a scope to exclude malignancy or other correctable lesions in the oesophagus.  In the good old days we would send them for a Barium swallow.  But nowadays it seems easy to get a scope, and then you have the option of a CLO, biopsy or whatever else they need on the day.

So I think it is reasonable to get a scope if you have persisting symptoms or severe symptoms so that you know what you are dealing with.  It would be disastrous and unfortunate to treat a malignant process for months and months with symptomatic care.

What is the role of manometry or pH monitoring to try and correlate her symptoms with  events in her oesophagus?

This is not something that I really see much of – but I work a long way from any Gastroenterolgists!  Certainly I have seen this done in patients with bad GORD – i.e.. those whom are contemplating a fundoplication procedure.

Found this paper in the BMJ – Barham et al from Gut, 1997. [Diffuse oesophageal spasm: diagnosis ] It is old – but suggests that for intermittent symptoms like our patient is suffering – you really need to get continuous outpatient / 24 hour ambulatory monitoring of pH and pressure in order to make this diagnosis.  Diffuse oesophageal spasm is also known as “nutcracker oesophagus” or “corkscrew oesophagus” as it has characteristic appearances on imaging.  However – you would be lucky to see this phenomenon as it is fleeting!  IN order to correlate symptoms with measured anomalous peristalsis or pH spikes – you would need ambulatory monitoring.  I guess it is like the Holter of the gut?

Image courtesy of Figure 1


The task of the ED team is to exclude life threatening diseases and give relief from symptoms.

When it comes to chest pain – once the serious diagnoses have been “excluded” to a reasonable degree of certainty [aortic dissection, ACS, pneumothorax, large PE….] then we are left with a cluster of other possibilities.

These are rarely “diagnosed” in the ED.  The evidence would suggest that the oesophagus is a major source of chest pain in this group – with GORD and motility disorders being the most likely disease processes.

So – if you want to have a go at symptom relief after excluding the bad diagnoses then it seems reasonable to tackle the oesophagus as your first  step.

Given to complex and costly nature of the investigations involved – this is not really within the scope of the ED provider to actually ‘make’ these diagnoses.  They can wait until review by the primary care doc or Gastro team if warranted.

But…  it would seem that a trial of a decent dose of PPI is not a bad option.  There seems to be little on the downside and a good number of patients will get symptomatic relief.  In my opinion – if you are going to do this then give a good dose for a reasonable period [as in above study] e.g.. a month of b.i.d. PPI-de jour seems like a good start. ** This is my opinion – not evidence*

This may even prevent them needing to come back to the ED with subsequent chest pain and go through the whole rigmorole again!  Not that this should be a primary objective of therapy – but it does seem to be a win-win for patient and the ED.