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

Why is hypoxia not part of the Wells Criteria?

Whether you have done medical or surgical runs you will have spent plenty of time trying to figure out whether a patient has a pulmonary embolism. Many clinicians will hang their hat on the presence or absence of hypoxia. You may then wonder why hypoxia is not actually part of the esteemed Wells criteria.

Well, it turns out the presence of hypoxia in PE is quite variable. In fact, not uncommonly patients with massive PE may have normal oxygen saturations, a phenomenon confirmed both by the literature (1) and my own observations. To understand why, we have to understand why hypoxia might occur in the first place.

It has actually taken a while for people to figure out why hypoxia occurs in PE, although it is still not 100% transparent. Many people assume that the problem is V (ventilation)/Q (perfusion) mismatching, where Q is decreased due to the obstruction. This is not quite correct. V > Q results in hypercarbia, but not hypoxia. The problem is that Q is redistributed to other lung units, without a matching rise in V. This results in regions of lung with low V/Q, away from the embolism (2,3). This seems to be the most likely cause of hypoxia.

This explains why massive pulmonary embolism may not cause hypoxia. Remember that massive pulmonary embolism is defined by the presence of RV strain and cardiogenic shock. If most of the pulmonary arterial tree is obstructed there is nowhere for the blood to be redistributed, minimizing the ability for areas of low V/Q to form. Additionally, if the patient has cardiogenic shock, low cardiac output reduces Q, reducing the inequality. Therefore, paradoxically, improving oxygen saturations may be a sign of worsening shock (4).

Hypoxia is therefore not correlated with the severity of pulmonary embolism. Patients with severe PE may not be hypoxic. If your patient appears shocked, or just looks terrible, you cannot use the absence of hypoxia to rule out PE.

On the other hand, small PEs may also not cause hypoxia, if they are too small for significant redistribution of pulmonary blood flow to occur.

All of this leads onto the next point, which is the utility of ABGs when you suspect PE. No doubt at some point you will have been asked to obtain an ABG in a patient where PE is suspected. The origins of this were some small, flawed studies suggesting that a normal A-a gradient on an ABG could rule out PE in combination with other features. This has been proven false in a more rigorous study (5) – a normal A-a gradient is equally likely in patients with or without PE initially suspected of having PE. This study concluded that ABGs had limited diagnostic value in the investigation of PE. Hopefully now you understand why.

Additionally most of these ABGs are requested on patients in whom it is clearly obvious from the end of the bed that there is an elevated A-a gradient. If you are on 5L of oxygen to maintain normal saturations and there is no clinical reason for hypoventilation, then you will have an elevated A-a gradient.

Till next time…

 

  1. Intensive Care Medicine. June 1977, Volume 3, Issue 2, pp 77–80| Cite as Massive pulmonary embolism without arterial hypoxaemia Pathophysiology in two cases. F. Jardin, J. Bardet, A. Sanchez, F. Blanchet, J. P. Bourdarias, A. Margairaz.
  2. Pulmonary Circulation. Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet? John Y. C. Tsang, James C. Hogg First Published June 1, 2014 Review Article.
  3. Journal of Applied Physiology. Pulmonary embolization causes hypoxemia by redistributing regional blood flow without changing ventilation. William A. Altemeier, H. Thomas Robertson, Steve McKinney, and Robb W. Glenny. 01 DEC 1998https://doi.org/10.1152/jappl.1998.85.6.2337
  4. Hemodynamic Factors Influencing Arterial Hypoxemia in Massive Pulmonary Embolism with Circulatory Failure FRAN(OIS JARDIN, M.D., FRANCIS GURDJIAN, M.D., PIERRE DESFONDS, M.D., JEAN-LUC FOUILLADIEU, M.D., AND ANDRI MARGAIRAZ, M.D. Circulation 59, No. 5, 1979.
  5. Diagnostic Value of Arterial Blood Gas Measurement in Suspected Pulmonary Embolism. MARC A. RODGER , MARC CARRIER , GWYNNE N. JONES , PASTEUR RASULI , FRANÇOIS RAYMOND , HELENE DJUNAEDI , and PHILIP S. WELLS. https://doi.org/10.1164/ajrccm.162.6.2004204   PubMed: 1111212 Received: April 24, 2000