Category Archives: Lab


I had a patient gifted to me from the nigh/day handover.  Don’t we just love ‘em?  

“Wait for the bloods and then talk to the surgeons”

I just had to wait for the bloods on a pleasant chap in his mid 50’s who had woken at 5am with severe central abdominal pain.  The pain had been adequately treated by the paramedics with 5mg of IV morphine, he had no fever, no Ds or Vs.  He might, if pushed, concede to some mild nausea.  Examination as reported to me was – slightly tender in the RIF, not peritonitic.

Bloods came back, totally in the black.  Except his troponin – 168ng/ml, [our house negative level is less than 32].   WTF – why had we done a troponin??

I went to re-examine the patient, and re-visit the history.  I took a slightly more cardiovascular bent.  No chest, back, neck, or tooth pain.  This gentleman could have been anaesthetist he cycled so much; 30km daily (no unhealthy obsession with apple products though).  I asked about changes in exercise tolerance, nada.

My examination echoed that of the overnight doctor who saw him at 5:30; tender RIF.

I did a bit of bedside USS, aorta looked normal calibre, heart was contracting slowly,  but well.   His resting HR was around 34,  Sinus bradycardia with ?high take off in the anterioseptal leads, I wondered about an inferior MI .  Posterior leads didn’t help.   CXR looked normal.  We repeated the TNI and did a VBG (VBG was normal).

Risk Factors?  Well after Prof Carley’s talk I’m less interested in these, but he had none.

I explained the result of the blood test, in the context of him not having chest pain (which he confirmed patiently to me for the nth time), was confusing.

Back to the history.  Sudden onset abdominal pain, started in the middle of his stomach, now beginning to hurt in the RIF.  No fever, mild nausea.  No constipation, no diarrhoea.  WCC and CRP normal.  I googled the list of non ACS causes of troponin rise:

System Causes of Troponin Elevation
Cardiovascular Acute aortic dissection
Medical ICU patients
Heart failure
Apical ballooning syndrome
Cardiac inflammation
• Endocarditis, myocarditis, pericarditis
Infiltrative disease
• Amyloidosis, sarcoidosis, hemochromatosis, scleroderm
Left ventricular hypertrophy
Myocardial Injury Blunt chest trauma
Cardiac surgeries
Cardiac procedures
• Ablation, cardioversion, percutaneous intervention
Hypersensitivity drug reactions
Respiratory Acute PE
Infectious/Immune Sepsis/SIRS
Viral illness
Thrombotic thrombocytopenic purpura
Gastrointestinal Severe GI bleeding
Nervous system Acute stroke
• Ischemic stroke
• Hemorrhagic stroke
Head trauma
Renal Chronic kidney disease
Endocrine Diabetes
Musculoskeletal Rhabdomyolysis
Integumentary Extensive skin burns
Inherited Neurofibromatosis
Duchenne muscular dystrophy
Klippel-feil syndrome
Others Endurance exercise
Environmental exposure
• Carbon monoxide, hydrogen sulfide


Now appendicitis wasn’t on that list.  SIRS was.  I went back to something I heard over and over again at medical school.  The history gives you the answer 90% of the time.  This man was complaining of abdominal pain which started in his umbilicus and was migrating to the RIF.  If I ignored his bloods or didn’t have his bloods what would I do?

A kind cardiologist came to review him for me, and agreed that ACS was not the cause of this gentleman’s elevated TNI.

I asked the surgeons to take a look, which they dutifully did.  I told them about the trop rise (which was falling again now 128ng/ml at 2 hours).  They took him for observation, with the diagnosis “?biliary”.

He had an USS the next day which demonstrated a thickened appendix, and had a laparoscopic appendectomy that evening.

Why had we done a troponin?  Someone who was just coming off their night shift had ticked the box by accident.

I’m wondering whether this was a true false positive because this chap was fit enough to have the generally elevated TNI that some endurance athletes have been shown to have1, or if his small pocket of intra-abdominal sepsis was enough to cause some mild myocyte damage.  Hell could it be mix of the 2?

Should I have just disregarded the first result and ignored?  This chap was adamant he had no chest pain, and had no risk factors for silent-MI.  On reflection the elevated TNI meant I felt that there was ‘something’ to find, and I went digging.  If I had had no blood tests at all, I’d have probably sent him to the surgeons, just like the tired overnight doctor who handed him over to me was going to.

  1. Shave, Rob, et al. “Exercise-Induced Cardiac Troponin ElevationEvidence, Mechanisms, and Implications.” Journal of the American College of Cardiology56.3 (2010): 169-176.


So a couple of weeks ago we got a lovely gentleman through our doors who had a medical problem.  He was mid 60s and had a pneumonia, but was tolerating it pretty well.  He had HTN, and CLL.

 What irked our collective team noodle was his K+ of 8.9, his ECG was normal, and he wasn’t in renal failure.

No tenting, sineing, PR prolongation, or P wave abnormality, or weird block.

“No, the sample isn’t haemolysed” the lab told us.

The repeat came back 8.7. – not haemolysed (this time written in block capitals).

The VBG we did, and ran to ICU to analyse gave us a value of 8.2.

So we turned to google, pubmed, and litfl, and all learnt about pseudohyperkalaemia:

The commonest cause is sloppy venepuncture, but it can also occur in patients with thrombocytosis, or leucocytosis.  Effectively it is a measurement error that occurs if you have tonne of cells in the sample all gently, slowly lysing.

Our gentleman’s WCC was 200

Pseudohypokalaemia has also been reported with leucocytosis as well.  As always I suppose we should always interpret lab results in light of what the patient looks like in front of us.