Category: Clinical Cases


Clinical Case 054: Just a sip

Filed Under: Clinical Cases, Emergency, General Practice, Paediatrics by Casey Parker — 2 Comments
May 27, 2012

Mother of a 15 month old boy (weighs 11 kg) presents to the clinic with a bottle of massage liniment.

 

A quick glance at the label tells you the active ingredients are;

 

Per 50 milliliter:

 

 

Mum says she just popped out to hang the washing and left him playing on the floor.  She was not aware that her teenage son had left the bottle on the couch after going to footy practice.

 

When she came back inside she immediately smelled the menthol and found the little guy on the floor, playing with the bottle, it was dripping down his chin and he was making a disgusted face – like he had a bad taste in his mouth.  She picked him up and could smell the scent on his breath.  But he was fine, happy and she gave hi a bottle of milk to settle him and get the taste out of his mouth.
Ok, now you are seeing him 45 minutes later – he still looks fine, he is playing happily, smells like a gymnasium.  His obs are all normal and Mum says:
“I am sure it is fine – but I just thought I should bring him in for a quick once over…”
After examining him you agree that he is normal, no signs of respiratory distress, no chest or abdo signs.  Now here are the questions:
Q1:  What is likelihood that a toddler would have swallowed more than a few mils?
Q2: Which of the ingredients are potentially toxic? And how much would be required for potential serious badness?
Q3:  What signs, symptoms and timeframe will you want to keep an eye on this little boy?
Q4:  What resources can you use to help make this assessment and formulate a management plan?


Twitt
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Clinical Case 053: thoracic tortuosity

Filed Under: Clinical Cases, Emergency, General Practice, Internal Medicine by Casey Parker — 6 Comments
May 17, 2012

OK.  This is just plain out there.  We see some unusual stuff in the remote areas – things you only read about in the books!  I am going to put this in the category of medical voyeurism.  This is not how we should go about our business, but I had to share these pics!

20 yo with pleuritic chest pain, not much else, but hypertensive BP =  160/90 [not that unusual up here in the tropics]

He managed to get a D-dimer… and then the inevitable CT angiogram  (probably PERC negative)

Here is a slice from the CT -

OK – spot diagnosis, what is going on?

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Clinical Case 052: Belly, bum and balls…

Filed Under: Clinical Cases, Emergency, General Practice, Paediatrics, Surgery by Casey Parker — 7 Comments
May 14, 2012

Today’s case is not in the ED.  This one unfolds on the ward – the morning after the admission.  So imagine yourself there – on the Paeds surgical ward.

6 year old boy was admitted last evening after referral from the local GP to the on-call Surg team.

He has a 24 hour history of increasing central abdominal pain.  The pain wa initially periumbilical, but overnight it has localized to the lower abdomen – maybe a bit more on the right. Urinalysis was normal

The surgical team have been on their super-early orning rounds and seen the child – they have written in the notes:

“ tender lower abdo, no rebound, guarding, otherwise soft, afebrile.  Bloods all normal.  PLAN:  Med team consult please.? epurients”

OK, now that is Surg -speak for – we aren’t operating on this kid – not a likely appendix.  Turf to med, maybe its constipation?

Half way though your ward round the nurse- coordinator calls you to say:  “You had better come see this kid – he has just had a bout of melena”

Hmmmm… not sounding like your average “un-appendix”.  So you pop in and see him.  Mum is looking worried.  His obs are normal, his belly is ‘as described’ by the Surg team.  When you pull down his jocks for a gander at his bottom you notice his scrotum is a bit red, and on examination his left testis is tender and there is a definite hydrocoele.  Hmmmmm…

OK – can you solve this Paediatric puzzle?

What is going on?  Well here is the clincher.

Rash

What are you going to do next?

Congrats to Dr Bek – who as it turns out practices about 500m down the road from me at the local Aboriginal Medical Service.  Bek gave the right and most insightful answer.  Good call from Maj and Patrick also – honorable commendations.  I happen to know Bek was at a recent talk I gave which covered HSP – so technically she did cheat? But I think she already knew before I got to her!

HSP (Henoch-Shonlein purpura) is an IgA-mediated leukocyoclastic vasculitis which produces a syndrome in children as described by the eponymous gents (and Heberden 30 years earlier). They described the quadrad of: purpura, arthralgia, abdominal pain and melena. Of course, they missed the meat – the renal disease. The disease involves a vasculitis of small vessels in the skin, gut, joints, glomeruli etc. It is pretty much the same disease as IgA nephropahy (Berger’s disease) in adults. HSP ends to occur in young children 4 – 10

I love HSP as a diagnosis as it is one of those end-of-the-bed diagnoses which can present in a number of ways – a rash, joint pain, belly aches etc. You have to keep it in you thoughts or you might miss it. The diagnosis is basically clinical – unless it is unclear as to the cause of the rash – so you might check for other causes of purpura. As opposed to ITP etc the platelets will be normal or elevated.

Treatment is mainly symptomatic – analgesia and “surgical” management of complications such as intussusception or torsion. GI bleeding, abdo pain and joint pain are usually treated with oral steroids. Does it work?  Well – maybe.  There are papers in both direction but they are all small and lack the power to say yes or no.  A rough summary is that they might make you belly pain get better sooner,  make the likelihood of an operation or CT scan lower and just might improve joint symptoms.  Now onto the million dollar question… the beans.

The reason HSP is an important problem in the long term is that there is an incidence of chronic renal disease. Usually a nephritic syndrome (though some mixed or nephrotic). And some of these kids will progress to renal failure. Here is the problem – there are studies that show that early steroids, and even cyclophosphamide do not reduce this progression. So we cannot treat the serious complication.

Monitoring includes urinalysis testing, BP monitoring – as there is about a 7% recurrence rate and the risk of renal disease goes up with recurrence and older-age of the kid.

 

Twitt
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Clinical Case 050: Think Better, Do Better

Filed Under: Clinical Cases, Emergency, General Practice, Pearls and Pitfalls by Casey Parker — 5 Comments
April 30, 2012

Last week I received the following comment from a reader in a country nearby.  This was a great story for me to hear as it made all my long hours of reading and writing seem worthwhile.  There are plenty of podcasts and blogs that will teach you how to do life-saving stuff – but this story is about how a reader took something from Broome Docs and ‘saved a life’ in a very different way.  It is not about a single trick or a procedure – but about how to approach the daily practice of medicine in a better, patient-oriented and effective manner.  For me this is the essence of why I do what I do at Broome Docs.  Here is the story from Dr Tom:

Hi Casey,

Straight after I read your first article on Consult Skills, I clipped and saved it using Evernote so that I could access it on my iPhone whenever needed.

Lo and behold, last week I had my first opportunity to use it when a middle–aged lady presented with a two year history of severe low back pain, bilateral hip pain and right leg pain. She had had multiple visits to her GP, several locums and 3 different orthopedic specialists over that time. Even though she was on a benefit, she had paid to see a couple of specialists privately because she was so desperate.

When she arrived in our ED, one of our relatively new Resident Medical Officer’s went to see her. The RMO came back very frustrated and said that both the patient and accompanying relatives were very angry and demanding, and that she wasn’t really able to get anywhere with her.

At that stage I said to the RMO that we had two important functions to fulfill:

1.      To make sure that the patient didn’t have any emergent orthopedic conditions e.g. cauda equina syndrome, spinal abscess etc.

2.      To try to understand the patient’s point of view.

The latter was met with a slightly quizzical expression so I pulled out my iPhone, opened my Evernote application and showed her the section I had clipped a few weeks ago:

1.      They want to know the doctor is listening to them

2.      They want to know that the doctor cares

3.      They want to make sure the doctor understands what is going on

4.      They want the Doc to “get it right” – that is make the right call / decision / do the right test  etc…

5.      They want to know what to do next “what will happen to me now?”

At that stage I went into the patient’s room and said:

‘Hi, my name is Tom – I am the senior ED doctor on duty today. I understand you have been going through a really rough patch lately. The first thing I am going to do is to take your pain way with some morphine. Once you are comfortable, I would like you to tell me everything that has happened to you over the last couple of years; then I will have a good look at you, review your results, talk to the orthopedic specialist on call today and together, we will try and come up with a plan to get things sorted for you.

After 10mg of morphine she said – ‘Doctor, you know this is the 1st time in over two years that I have not been in pain’.

She then proceeded to tell me:

•       Her marriage had broken up and she was looking after 6 children on her own.

•       She was in so much pain that she was unable to dress herself (mainly because she could not bend down or stand on one leg), was unable to walk more than a few steps, had hardly been out of her house in the past few weeks and was largely confined to her bed or a chair.

•       She had a history of multiple severe drug reactions and was not currently taking any analgesics.

•       She suffered from stress incontinence and wet herself at least 2-3 times every day.

•       When she fell over, she was physically unable to get off the floor unaided.

•       Her teenage son had to take time off school to help dress and wash her, clean the house and do the cooking – this was now starting to adversely affect both his education and their relationship.

•       She was not eligible for any government subsidies (e.g. home help).

•       She was often tearful due to a combination of pain and frustration.

After listening to her history, I briefly re-capped to make sure that I had not missed any important points.  I then examined her and reviewed her recent imaging.

Next I rang the on-call Orthopedic Specialist and said –  ‘I’ve got a lady with chronic severe lower back, hip and leg pain; a plain film of her pelvis and hips shows severe bilateral hip OA; she doesn’t appear to have any new emergent orthopedic conditions but I would like to admit her so that we can sort out her analgesia, home help, mobility and definitive treatment’.

I returned to the patient and told her: ‘Great news, the Orthopaedic Surgeon has agreed to bring you into hospital, sort out your pain, get you a bit more mobile and most importantly, try and fast track some surgery on your hips.’

At that point she started crying and said:

‘You know, of all the doctors I have seen over the last few years, you are the only one who has ever sat down and really listened to what has been going on. Thank you so much’.

PROGRESS REPORT

After initially being admitted to hospital for a week, she has gone on to have her 1st hip replacement done and is due for her 2nd operation in 3 months time.

Great work Dr Tom.  I really appreciate your sharing this story with me and knowing that we can do better by changing the way we think and talk to patients.

Twitt
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Clinical Case 049: the Unseen ECG

Filed Under: Clinical Cases, Emergency, Internal Medicine by Casey Parker — 15 Comments
April 15, 2012

I was sitting at the desk writing up some notes when the triage nurse stuck the following ECG strip under my nose.

The story was that this chap was a hypertensive, obese, diabetic vasculopath with impaired renal function who had presented with a fever of 39 deg and nasty looking diabetic feet (see Clinical case 047 for example…).  He was looking unwell so she did an ECG on the off chance he might be having a silent infarction.

So here we are – sick looking, high-risk sounding patient.

No chest pain; No previous IHD documented; Previous ECGs? – he had a normal exercise stress test 2 years ago with a normal baseline ECG in the chart

OK, all you smart ED types.  Can you make the diagnosis?  What is going on here?  There might be a trick or two …..

Ok a few observant comentators noted the machine was running at 50mm/sec – and the V leads were missing. The patient was running at 126 bpm clinically and on the monitor. Unfortunately our new nurse who was not familiar with the machine pushed the wrong buttons and gave me a terrifying minute or two as I made my way to the bedside! The penny eventually dropped and I could breathe a big sigh of relief!. The true ECG showed a tachy @ 126 with a RBBB pattern and no convincing P waves. So channeling Chris Watford (Emcrit) I did a Lewis lead config – and the P-waves popped up like they should! Sweet – we were back to boring old sinus tachy in a septic patient and all was well!

1. Always look at the patient before the ECG, or at least shortly thereafter!

2. If something doesn’t add up, check the basics, repeat the test and ask, ask, ask

3. Septic patients can develop nasty arrythmias – SVT, AF, transient heart blocks (RBBB), VT etc – so beware the sepsis with tachy, find those P-waves – as all the other options are not good for their cardiac output.

4. Lewis leads (S5) actually works, it is cheap, easy and makes you look smarter!

 

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Clinical Case 048: We Ask an Epidural Expert

Filed Under: Anaesthetics, Clinical Cases, Obstetrics, Pearls and Pitfalls, Specialist Tips by Casey Parker — 7 Comments
April 11, 2012

This case is an opportunity for us to learn from an expert.  Epidural analgesia in labour can be rewarding and infuriating.  So I have enlisted the help of Dr Roger Browning – Consultant Anaesthetist at Fremantle and King Edward Memorial Hospitals {tertiary maternity centre in WA}.  I put a few questions to Roger based around a real case to see how the expert goes about troubleshooting common epidural problems. Here we go:

26 yo primigravida, induced for postdatism @ 41 weeks.  She is now ~ 6cm dilated with slowish progress.  You have been called to put in an epidural after she has tried nitrous and a dose of IM morphine.  As you arrive she is clearly very distressed with each contraction.  They are coming every 4 minutes on an Oxytocin infusion.  She is otherwise fit and well, normotensive.
Practitioners should use the technique they have learnt and are most familiar with. I would place a lumbar epidural using a 16G tuohy kit and loss of resistance to saline, and thread the catheter in leaving 4-4.5 cm in the space and secure it to her back using a “lockit”, medium tegarderm and surrrounding fixomull dressing for reinforcement. I would aspirate the catheter to check for blood or CSF and then test the catheter with a 7-8 ml injection of bupivacaine 0.125% + fentanyl 5mcg/ml. If there is no major motor block within 5min (ie indicating subdural or intrathecal catheter) I would then give another 5-8ml of solution ie 15ml in total to get initial analgesia.
At KEMH we use bupivacaine 0.0625% + fentanyl 2.5mcg/ml background infusion of 5ml/hr and PCEA 10ml with 20min lockout, via a CADD pump. In a rural hospital (and other metro hospitals like osborne park) I would prescribe intermittent topups: bupivacaine 0.125% + fentanyl 5mcg/ml 10-15ml hourly PRN, for breakthrough bupivacaine 0.25% 5ml hourly prn, rectal pressure pethidine 50mg/5ml hourly prn, and instrumental delivery / suturing ligonocaine 2% + adrenaline 1:20000 4ml + 4ml one dose only.
3 hours later….
You are called by the midwife for help.  She states that the epidural you put in worked great initially, but… now it is not so good.  She hasn’t made much progress up to 8 cm now.  We are still expecting a few hours of pain at best….
You need to assess whether or not you think the epidural cathetter is still in the epidural space. Check the patient’s back & dressing, if the catheter is now less than 3cm in the space, or there is a lot of fluid under the dressing don’t waste time trying more drugs etc, it has come out, take it out and place another epidural. If everything looks ok then carefully titrate in more bupivacaine 0.125% + fentanyl5mcg/ml solution, larger volumes will often “spread further” and tend to be better than small volumes of more concentrated LA. I will give up to another 20-25ml in increments over 10-20min. If this doesn’t work you should probably take it out and place a new epidural catheter.
Our 26 yo primi has made it to fully, but not really descending well.  The CTG trace has been getting ugly…  some decelerations at first, but now it has become flat / unreactive.  The Obs team call you for a Csection.  It is not Cat 1 urgent, but you want to get her ready ASAP.
Before starting an epidural topup for a CS once again you want to be sure the catheter is in the epidural space and it is working. Look at her back is the catheter < 3cm in the space? is there a lot of fluid under the dressing? has it been working well down in labour ward? If the answer is no to any of these you are probably better off taking it out and doing a spinal.  At KEMH to topup a epidural we use lignocaine 2% + adrenaline 1:200000 (which comes in a 20ml ampoule) and fentanyl 50-75mcg. You should aspirate the catheter to check for csf / blood and then give 5ml as a test dose, check for early profound block (?intrathecal) or tachycardia, perioral tingling (?iv). You should titrate in the lignocaine in 5ml increments every 5min, to max of 7mg/kg (in the average female this is around 25ml) checking the block height regularly, aiming for loss of cold sensation to T4 (nipples) and signs of sacral spread also (difficulty lifting legs off the bed). If after the maximal dose you have an inadequate block you should consider doing a CSE or spinal (using a smaller dose than usual as there is a risk of a high spinal) rather than causing local anaesthetic toxicity with even more lignocaine. I often also give pethidine 50mg (personal practice not dept) as it decreases the severity / incidence of shivering.
You give your top-up, get her ready and the Obs team start cutting.  As soon as they hit the peritonela layer she winces and says she feels sick.  A minute later and she is crying in pain – her husband is looking very scared.
And how do you go about making this decision?]  This description suggests she has an inadequate block and you should stop the surgeons before they proceed to making a uterine incision. The critical issue here is that once the surgeons incise the uterus they are commited to continuing, placental perfusion and foetal oxygenation is impaired and maternal haemorrhage starts, the surgeons cannot / should not be asked to stop for 15min whilst you try to “fiddle with your block”! You need to make a decision prior to this point. Clarify with the patient are they feeling pain or merely touch, believe them if they say it is pain. Check the dermatomes with ice and get the surgeons to “check with forceps etc in the surgical field. If the patient has significant pain at the point of peritoneal incision as in this scenario, and the block appears to be obviously inadequate I would err on the side of converting to a GA before then letting the surgery proceed. If you have already “topped up” with a decent volume of lignocaine 2% + adr (ie 15-25ml) and given this time to work (15-30min) it is unlikely that stopping for another 10min and giving another 5-10ml will make it into a working block. Having said that if they have a difficult airway or look high risk for a GA and you think some more time and more drugs will make a difference then it might be worthwhile to persist, this is an individual risk/benefit decision and you need to talk to the patient /surgeon and explain all of these issues. The most common scenario for pain during a caesarean occurs post delivery, is usually only mild, and related to temporary surgical stimulation whilst swabbing high in the abdomen or fiddling with the ovaries etc. Often you can get a patient through this with iv opioids, inhaled N20, some surgical infiltration of LA (beware max dose if you used alot in the epidural) and distraction with the baby! Sometimes you still need to do a GA to allow the surgery to finish though…
OK – that is epidurals through the eyes of an expert.   Big thanks to Dr Browning for taking the time to answer my questions. This is certainly a part of medicine with plenty of art, less science and a lot of inter-individual variation.  I am keen to hear your tricks and techniques.  Let us know on the comments.
Casey
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Clinical Case 047: Not so sweet feet

Filed Under: Clinical Cases, Emergency, General Practice, Internal Medicine, Surgery, Tropical disease by Casey Parker — 8 Comments
April 1, 2012

This week a classic Australian remote area case.  There is so much to discuss on this case!  But I have isolated a few key points to put under the microscope, and get your input / expertise.

47 yo. Aboriginal woman has returned to the ED complaining of painless purulent lesions on her left foot.  She was seen a week ago by the nice city locum who diagnosed cellulitis and commenced her on a week of oral flucloxacillin.  She has been taking this for 6 days, but it aint working!

Not so good.  She reports increasing ooze, and the occasional maggot escaping from her improvised dressing.

Here is the background info:

PMHx:  Diabetic (type 2 – is there any other kind?)

  • Hypertensive
  • Nephropathy with significant proteinuria, Cr 100 last visit
  • Retinopathy requiring laser last year
  • No documented ischemic heart disease, CVA or PVD

Meds:  metformin 2 g/day SR, Gliclazide 120 mg MR,  Quinapril 20 mg, aspirin 150 mg/d.  No Allergies

She is overweight with a BMI of 39.  Central adiposity.  Malodourous slough coming off the foot.  She has a good dorsalis pedis and posterior tibial pulse to feel

Obs: T = 38.4,  pulse = 98 SR, BP = 166/102,  RR 14, Sats 97% RA.  Her BSL is 29 mmol (~ 520 in USA)

This is bread and butter for the remote area docs, so i am going to ask 3 questions for you to ponder and comment upon…

Q1:  Antibiotics in this scenario – what are you going to use? Any particular pathogens to keep in mind?

Q2:  Imaging – what do you do?  Are plain films worthwhile?

Q3:  Management of her hyperglycemia (assume she is admitted) – what targets and what to use to achieve this?

….. OK, bonus question… #4 :  Maggots…. good, bad or indifferent?

Get your thinking caps on.  Especially you Dr Dorr – I am gonna quiz you on this this week!

Casey

 

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Clinical Case 046 Rash revealed

Filed Under: Clinical Cases, General Practice, Tropical disease by Jonathan — 2 Comments
March 30, 2012

Cutaneous Larva Migrans!

Once seen never forgotten..

The rash is characterised by the erythematous, serpiginous (snake like) and pruritic trail left by the microscopic larva as they burrow through the skin.

Erythematous, serpiginous and pruritic trail

(C) 2012 Image copyrighted to Jonathan Ramachenderan

It is a parasitic skin infection caused by hookworm larvae. Humans are accidental hosts with the larvae lacking the lytic collagenase enzymes needed to cross the epidermal basement membrane thus making this infection self limiting. Cats and dogs are the intended hosts with the larvae being able to cross into the blood and complete its life-cycle.

Infected animals pass the parasite eggs in their faeces into warm, moist sandy soil where the larvae hatch and make contact with human hosts. They penetrate hair follicles, cracked and intact skin to cause their creeping infection and produce a series of disorganised loops of irritated skin.

There are several treatment options and the non-interventional approach acknowledges Cutaneous Larva Migrans’s self limiting nature but requires adequate patient education and treatment of secondary infection.

Anti-helmintics are used to treat early and active cases. Topical thiabendazole can be used for localised and early lesions whereas oral treatment is used for widespread infection or when topical therapy has failed. Oral ivermectin 200mcg/kg can be used as a single dose, with caution in the elderly and young (<5years) and those with renal and hepatic impairment.

Education of the simple measures such as beach footwear and towels to prevent repeated contact with beach sand is important.

Our patient was promptly contacted soon after the diagnosis was made and received 21mg of ivermectin (7 x 3mg tablets) and on review reported that the rash had completely resolved 5days after treatment.

Thanks for playing guess that rash!

References

1) Dermnet NZ: http://dermnetnz.org/arthropods/larva-migrans.html

2) Medical Observer 2008: http://www.medicalobserver.com.au/news/cutaneous-larva-migrans

3) Reavis M, Jorgensen S. Acute Pruritic rash on the foot. Cutaneous larva migrans. American Family Physician 2010. 15;81 (2): 203

4) Sarasombath PA, Young PK. An unsual presentation of cutaneous larva migrans. Archives of Dermatology. 2007 143(7):955

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Clinical Case 046 Rash in the returned traveller

Filed Under: Clinical Cases, General Practice, Tropical disease by Jonathan — 6 Comments
March 29, 2012

Hi guys! GP land has been going really well with me slowly gaining a following of patients and some interesting cases. I wanted to share with you one which I sought help from and excellent service called Tele-Derm. It was set up by ACRRM and the Queensland Divisions of General Practice (QDGP) with Commonwealth funding in 2004 and it is run by one of the most hard working dermatologists dedicated to providing a reliable service for rural Australia, Dr Jim Muir.

If you are a rural doctor with a dermatology dazzler or puzzler, you can electronically submit cases for assessment and usually within 48hours or in my case 27minutes! Jim will give you a diagnosis or point you in the right direction. He also moderates a forum with great educational cases, links and discussions.

So…

45 year old man came to see me with the rash as depicted below.

It started  4 days after coming back from Thailand where he relaxed on the beach, went snorkelling and ate yummy thai food. He came in to see me 10 days after getting home.

The rash started spreading, beginning on his left flank and moving up toward his axilla with one lesion on his upper back and a few over his lower abdomen.

The main issue was itch and is pain at times (not unbearable). He described it as “catching your skin on a bit of metal”. He has put some over the counter creams to relieve the itch but nothing helped.

He didn’t report a fever or being unwell. He also concurrently did not have a productive cough, dysuria, diarrhoea, cachexia or anorexia.

On examination he was afebrile and other observations within normal limits. He did not have any inguinal or axillary lympadenopathy. He didnt have any other rashes or scaly and dry skin.

He assured me he wasnt bitten by any mosquitos nor was he bitten by any marine life.

Im sitting there scratching my head thinking, “its not cellulitis, its not fungal, its not dermatitis..what is it?”.

What do you think?  Its a once seen never forgotten clinical case!

       

(C) 2012 All images copyrighted to Jonathan Ramachenderan
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Clinical Case 045: Syncopal Salesman

Filed Under: Clinical Cases, Emergency, General Practice, Internal Medicine by Casey Parker — 23 Comments
March 26, 2012

37 yo man who works as a travelling sales rep.  He has a hectic lifestyle and is overweight.  Flies around the country a lot visiting hospitals selling medical equipment.  He presents via ambulance after having a syncopal episode in the local McD’s.

The event was witnessed by a client and staff at the restaurant – he was a bit sweaty, got up to go to the bathroom and fell, he narrowly avoided hitting his head on a chair as he collapsed to the ground. No seizure activity, incontinence or neurolgical deficit noted at the scene. He was unconscious for about a minute.  When the ambos arrived 5 minutes later he was GCS – 15, oriented, though seemed a ‘bit vague’.

Whilst in your small country town for a 3 day visit he notices that he has become increasingly “unwell” – he can’t really put a finger on it -he says he “has been hazy in the head”  and “feeling like nothing seems real”  for the last 48 hours.  No specific vertigo symptoms, headaches or pre-syncopal events have been noted.

Overweight BMI = 35

Hypertensive – was on ramipril, but stopped taking it as it interfered with his ‘performance’

Smoker – 10 -15 per day

1 episode of gout effecting MTP jt

Depression – currently on 40 mg paroxetine/day, good response to this and supportive therapy from GP

Dyslipidemia – trialing “diet and exercise”

He is a fat, slightly sweaty man, looks a good few years older than 37!

Obs: pulse = 85 reg, BP 145/90 no postural drop, SpO2 = 99% RA, RR 14/min, no clinical pallor, anaemia etc

Otherwise his heart, chest, neuro, abdo etc are all normal.

What specific negatives do you want to ensure on physical examination??  What can you exclude by looking and listening?

BSL is 6 mmol (~110 in the U.S.A)

ECG – normal, sinus rhythm, maybe borderline for LVH criteria, normal axis.

What specific features / conditions do you want exclude / or see on the resting ECG in a man with syncope?

Urninalysis is = SG 1.015, 1+protein, otherwise normal

Plum normal

pH 7.41, lactate 0.4 mmol He has a Hb of 156 g/l

Electric lights are all normal

Nothing to write home about… What were you hoping not to see ?

OK, that is it for now.  At this stage I will tell you that any further tests that you want to do are either negative or unavailable in our little ED scenario.

The diagnosis is out there…  first prize goes to the reader who asks the right questions to solve the puzzle.

Ready, set, go…. write your thoughts on the comments and I will respond

Twitt
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