Day 1: A straightforward SOB case, right?

2pm, 26.07.12. The first patient I saw as a newly qualified doctor was a 26 year old woman with shortness of breath. A glance at her triage notes highlighted a PMH featuring asthma. As I waited for the consultation room to be ready, I wrote down my differentials at the top of the clerking sheet:

  1. Asthma
  2. Pneumonia
  3. PE
  4. Pneumothorax
  5. Panic attack
  6. (DKA)
  7. (Acute heart failure)

I looked at the obs. Temp 37.7 Pulse 122 RR 22 BP 108/80 O2 sats: 98% on air. An early warning score of 2. I felt more nervous as a doctor than I ever felt as a medical student.

“So, what’s brought you in today?”
“Lots of things.”
“What’s bothering you the most?”
“Well, I’ve got this headache.”

This was not what I  expected. Still, this was the patient’s concern, so I had to focus on it.

“Can you tell me more about it?”
“Well, it’s different to my migraines…”
“You suffer from migraines?”

And so I became a statistic. One of the rubbish 77% of doctors who fail to fully let the patient explain their story before a focused question. I was aware of this at the time, and consciously tried to return to her trail of thoughts.

“Yes Doctor.”
“Sorry to interrupt, I just didn’t see it in your notes and wanted to check. You were telling me about your headaches…”

This led to an exploration of no less than 7 presenting complaints:

  1. Headache for 1 month – occipital area, bilateral, worse on coughing, not affected by posture, doesn’t disturb her sleep, 7/10 severity, constant, not throbbing, no aura, no focal neurology, no head injury, never had anything like it before. No rash, neck stiffness or photophobia.
  2. SOB – worsened over the past month, was playing sports with no problem one month ago. Now can’t walk 400 yards. No obvious trigger, not related to work (she works in an office). Actually gets worse during the day, and is worst before sleeping. Constant, but getting worse. Not a particularly sudden onset.
  3. Cough for 1 month. Yellow phlegm, no haemoptysis. No diurnal variation. Quit smoking 2 weeks ago to help; no effect.  No GORD symptoms, no post-nasal drip.
  4. Chest pain for 1 week. non pleuritic. In centre of chest, upper third of sternum. Not affected by pressure. No radiation, sweating, nausea or vomiting. Bilateral. No relationship with food or exertion.
  5. Pins and needles +/- numbness for 1 week. Hands get pins and needles only, whereas the feet can get both. Episodes of minutes then resolves fully.
  6. Constitutional symptoms – 1 week of night sweats and fever. Also loss of appetite (no weight loss) and extreme fatigue. Currently spending >70% of the day in bed. No mood disturbance. Wants to get on with life. Active person before.
  7. Postural dizziness – worse on waking in the morning/sitting up. This patient was actually referred from her GP for the above symptoms and a standing BP of 66/48.

Of note, she had URTI symptoms a month ago which resolved in a week. The GP first treated for asthma 2 weeks ago with a salbutamol inhaler and a 5 day prednisolone course. The patient came back to the GP last week, and was given 500mg amoxicillin as a 7 day course.

She had no previous medical history.

Her mother was diagnosed with hypothyroidism the day before.

She lived with her family and partner. The parents returned from Cuba 6 weeks ago, and the father had a severe productive cough for 2 weeks on return.

On examination, the striking findings were a diffuse, polyphonic end expiratory wheeze and generalised MRC 4/5  in all limb movements.

I could not think of a unifying diagnosis or a plausible combination. I decided to focus on the SOB and cough, as together these offer a fairly compact list:

  1. Asthma exacerbationIn favour: Common things are common. Explains SOB and cough.Against: The diurnal variation was different to that expected in asthma (which is usually worse in the early hours, as the smooth muscle tone of the airways is greatest then in both asthmatics and non-asthmatics). No trigger. The patient had no personal or family history of atopy. It also does not explain the hypotension and would be unusual to cause such severe constitutional upset with asthma.
  2. PneumoniaIn favour: Cough productive of yellow phlegm, SOB and constitutional upset could be explained. Again, common things are common. Could even explain the hypotension if severe. Previous URTI.Against: There was no response to high dose amoxicillin.(This could be explained by patient factors and disease factors. Patient factors include non compliance. Disease factors include bacterial resistance, an atypical pneumonia or an imported infection from the father.)
  3. PEIn favour: A diagnosis that must be considered in any acute breathless patient. Female. Explains cough and possibly chest pain.Against: If present, chest pain would usually be pleuritic. No risk factors. No sudden onset. No calf swelling or tenderness on examination.
  4. PneumothoraxIn favour: If asthmatic, becomes more likely. Explains SOB and possible cough.Against: Does not explain constitutional upset. Does not usually progress over a month.
  5. Addison’s DiseaseIn favour: Possible subclinical Addison’s, which had been unmasked by the recent infection. Infection explains SOB, cough and URTI symptoms earlier on. Addison’s explains constitutional upset, generalised weakness and postural hypotension. Family history of autoimmune disease.Against: Less common (5 cases per million per year incidence in Western countries).



WCC was raised at 12
Neutrophils were raised at 86%
CRP was raised at 14

Everything else was unremarkable.

Chest xray was unremarkable.
ECG showed sinus tachycardia.

My plan was salbutamol 5mg nebulised, ipratropium 500mcg nebulised and a 5 day course of oral prednisolone, I also wanted the amoxicillin switched to doyxycycline or clarithromycin.

I had a lot of internal debate about a d-dimer. On the one hand, if it were positive, we would be obliged to do a CTPA, otherwise it hasn’t really affected management. It would be likely to be positive in any case as the patient is probably infected  and/or has a PE. Given this, then the result is almost definitely positive, which means we should skip the test and go straight to CTPA if clinical suspicion remains.

I presented to the registrar. He felt it was infection and wanted to change to doxycycline. He wanted the patient discharged.

I then presented to the consultant. He was more suspicious of PE, and requested a d dimer and to admit the patient. I was asked to write up therapeutic clexane.

After much paranoid recalculating of the dose based on her weight, my first ever prescription as a doctor was 150mg Clexane SC OD.

Questions I would be grateful for your help on:

  • Why might a pneumonia not respond to amoxicillin?
  • What are the commonest presentations of PE? What are the subtler ones?
  • The U&Es were unremarkable in this patient, and did not even tend toward the lower end for Na or higher end for K. Does this essentially rule out Addison’s? I am aware of the proper investigations for Addison’s; I would really appreciate knowing if well-within-normal U&Es makes Addison’s very unlikely.

Thank you for reading this and I look forward to your comments. I will be sharing my cases here regularly and also turning them into SBAs on


2 thoughts on “Day 1: A straightforward SOB case, right?

  1. The most common cause of pneumonia is strep pneumoniae, which in the UK is pretty much fully sensitive to amoxicillin. However in Spain there is wide spread resistance. Could the patient have perhaps colonised her upper respiratory flora with spanish bacteria. The second point to consider is that mycoplasma is very common as a cause of pneumonia and due to not having a cell wall is intrinsically resistant to penicillins. Treating with simply amoxicillin you will not treat a significant number of pneumonias, hence the reason that empirical treatment of pneumonia is amoxicillin and clarithromycin.

    Commonly PE presents being breathless, low sats, tachycardic. Subtler one being a persistent tachycardia only. I think you are entirely justified in querying it in this case.

    With regards to your U+E question I may be completely wrong but might the short course of prednisolone corrected things and muddied the water on your interpretation of said U+Es

  2. Hey Matt,

    Thanks for reading and posting. The patient hadn’t travelled anywhere recently. Her father had come back from the Dominican Republic 6 weeks before I saw her, and he had had a nasty productive cough for 2 weeks which self resolved. We were thinking along similar lines, namely resistance, atypicals and possibly something imported. Thanks for explaining exactly why mycoplasma will not respond to amoxicillin – it makes sense.

    Regarding PEs, I am appreciating how consultants generally have a very low threshold for PE in breathless/tachycardic patients. I guess this is because they have seen so many real life cases where PE did not present classically and it’s a big one to miss.

    I see what you mean about prednisolone, but my understanding is that prednisolone is chosen as a long term steroid because a) it can be taken orally and b) it has very little mineralcorticoid activity, so would tend not to cause too much Na gain (and hence fluid retention) or K loss. I linked to the BNF in this SBA on this:

    Thanks again Matt, and hope to hear from you again.

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