How to assimilate information accurately and why aortic dissections and PEs get missed- the pretest probability

Medical school and medical training teaches us that we do tests to confirm the presence or absence of disease. This is the wrong way to think about things. A better concept is to realise that we start with a certain pre-test probability of a disease, which is determined by the base rates of that disease in the population and the patient’s clinical history. Tests can only ever modify this pre-test probability into becoming more or less likely. At a certain point the disease may become so unlikely that testing for it causes more harm than good. This greater harm may come from radiation, reactions to things such as contrast dyes, harmful therapy that might be initiated as a result of a false positive result e.g. antibiotics for a blood culture result that is a contaminant, or simply the fact that time is wasted not pursuing the most likely diagnosis. Other times the disease remains so likely that you may have to pursue repeat testing (take for example the high false-negative rate of COVID swabs).

Consider this scenario. You are the on call house officer. You get paged to the ward to review a 35 year old patient who is having abdominal pain. He was admitted 6 hours ago with severe central chest pain that came on over a matter of seconds and lasted 2 hours. His troponins and ECG have been normal. He has now developed abdominal pain of the same severity and also reaching its peak over a matter of seconds. Concerned about the possibility of aortic dissection you look for mediastinal widening on the chest Xray, pulse defecits, or any neurological symptoms as you know these are the things to look for in a dissection. None of these things are present. Satisfied, you order further ECGs and troponins. The next day you find out he died overnight of an aortic dissection. The next day your consultant tells you “it just shows you how useless clinical exam findings are for aortic dissection- you can’t rely on them. Most dissections have a normal Xray!”

Is this correct? Are these clinical exam findings useless? Is the chest Xray normal in most dissections, as commonly quoted? Well, not quite. They are actually reasonably good tests, including the chest Xray (1,2). The problem is not taking into account the pre-test probability of an aortic dissection, which in this case is high based on the clinical history. Continue reading

What does atypical chest pain mean? Part 1

“I just had my dinner, this hospital food is terrible by the way, look at this, what is this?….anyway  a couple minutes later the pain just grabbed me here”, he says rubbing the back of four fat, tobacco stained fingers up and down from his throat to his epigastrium.

“And you were just sitting down in your chair, right?” – “Yeah. I get this all the time though at home though”.

You sit down to wearily write your note; ‘Impression: Atypical chest pain, probably GORD. Plan: Serial troponins to exclude cardiac’.

Of course, the pain only lasted 10 minutes, so your troponins will probably be negative. So is the pain atypical?

Atypical is another in a series of medical terms that we use all the time which don’t really mean anything- or rather mean different things for different people and should probably be abandoned (1). Some clinicians even use it in order to facilitate admitting the patient to hospital (1).

The question of what exactly is ‘typical’ for angina, or how frequent something needs to be in order to be considered typical, is an interesting one, which provides fodder for many future blog posts. Surely though, positional pain or pain related to food can’t be angina? At least this is kind of what I have been given to understand. Not so easy apparently.

We will run through 3 examples of chest pain presentations well described in the literature which are associated with severe CAD, which many people might consider to be atypical. They go to show that few patients read the medical school textbook. Or maybe the medical school textbook is incomplete.

Post-prandial angina

8.6% of patients with ischemic heart disease experience post prandial angina (angina after meals), with higher incidence of three vessel disease and left main disease, and lower ejection fractions on average. Such angina is more likely to occur after the dinner meal (2). The mechanism is unclear but is thought to be related to either redistribution of blood flow to the gut or increases in cardiac output following meals. Increases in heart rate, blood pressure and systemic vascular resistance are all observed at the onset of angina, which usually occurs within 25 minutes of the meal (2,3). Continue reading