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

The test is not the disease

When I was a trainee intern we had a patient on my general medical placement present with 2 days of right arm swelling and tenderness, with dilated superficial veins over her arm and upper chest. Her d-dimer was normal. She had an ultrasound of the upper limbs looking for a DVT. This was negative. With a negative d-dimer and USS we were all ready to discharge the patient home (who was otherwise well), however the consultant, a mentor of mine, insisted on a CT venogram. We all rolled our eyes. Eye rolling turned into eye widening as the scan showed the subclavian vein thrombosis we had all been missing. Continue reading

Avoiding harm: the early postoperative fever

One of the most important principles in medicine is to avoid doing harm to your patients. This is easier said than done because sometimes things that are iatrogenic are confused for natural evolutions of the disease process. That leads to writing the first post in a series entitled ‘avoiding harm’.

One good example is the early postoperative fever. I use this term to mean fever occurring in the initial 24-48 hour post operative period. As a house officer my friends and I spent many hours taking blood cultures on these patients, obtaining chest X-rays and chasing urine samples.

Eventually I realised what would happen is we would treat areas of atelectasis that were confused for pneumonia, colonised (but not infected) bladders and skin contaminants on blood culture. All of this represented unnecessary exposure to antibiotics, which have the potential to seriously harm patients.

Fortunately all of this can be avoided. There are 11 articles in the literature which I have taken the time to find for you. They uniformly tell us that if there is no sign of focal infection on clinical exam, the ‘septic screen’ can be safely forgone.

Blood cultures were the most useless. In four studies the pick up rate on blood cultures (excluding contaminant results) was zero. Two of these studies were designed specifically to look into the utility of blood cultures. All studies had large numbers of patients. One study found that of 38 blood cultures only 1 was positive and this was on post-operative day 16. Two further studies reported a 6-7% rate of positive blood cultures. The pick up rate of chest Xrays and urine cultures was about 10%.

Four studies reported that in those patients who were diagnosed with an infection, the majority of the time the source was identifiable based on physical exam and clinical picture, or that the clinical picture guided the need for further investigations.

Three studies actually attempted to quantify the cost. One calculated a cost of $8000 per change in clinical management, one worked out $2000 per infection diagnosed and one concluded that “rote” ordering of tests resulted in a total of $20000 (or $278 per patient) excess expenditure. All eleven studies concluded that “routine” ordering of investigations for early post-operative fever was unnecessary and costly.

  1. Sivakumar B, Vijaysegaran P, Ottley M, Crawford R, Coulter C. Blood cultures for evaluation of early postoperative fever after femoral neck fracture surgery.  J Orthop Surg (Hong Kong). 2012 Dec;20(3):336-40.
  2. Bindelglass DF, Pellegrino J. The role of blood cultures in the acute evaluation of postoperative fever in arthroplasty patients. J Arthroplasty. 2007 Aug;22(5):701-2.
  3. Lesperance R, Lehman R, Lesperance K, Cronk D, Martin M. Early postoperative fever and the “routine” fever work-up: results of a prospective study. J Surg Res. 2011 Nov;171(1):245-50. doi: 10.1016/j.jss.2010.03.009. Epub 2010 May 11.
  4. Fanning J, Neuhoff RA, Brewer JE, Castaneda T, Marcotte MP, Jacobson RL. Yield of postoperative fever evaluation. Prim Care Update Ob Gyns. 1998 Jul 1;5(4):146.
  5. Petretta R, McConkey M, Slobogean GP, Handel J, Broekhuyse HM. Incidence, risk factors, and diagnostic evaluation of postoperative fever in an orthopaedic trauma population. J Orthop Trauma. 2013 Oct;27(10):558-62.
  6. Ward DT, Hansen EN, Takemoto SK, Bozic KJ. Cost and effectiveness of postoperative fever diagnostic evaluation in total joint arthroplasty patients. J Arthroplasty. 2010 Sep;25(6 Suppl):43-8. doi: 10.1016/j.arth.2010.03.016. Epub 2010 May 10.
  7. de la Torre SH, Mandel L, Goff BA. Evaluation of postoperative fever: usefulness and cost-effectiveness of routine workup. Am J Obstet Gynecol. 2003 Jun;188(6):1642-7.
  8. Athanassious C, Samad A, Avery A, Cohen J, Chalnick D. Evaluation of fever in the immediate postoperative period in patients who underwent total joint arthroplasty. J Arthroplasty. 2011 Dec;26(8):1404-8. doi: 10.1016/j.arth.2011.02.019. Epub 2011 Apr 7
  9. Czaplicki AP, Borger JE, Politi JR, Chambers BT, Taylor BC. Evaluation of postoperative fever and leukocytosis in patients after total hip and knee arthroplasty. J Arthroplasty. 2011 Dec;26(8):1387-9. doi: 10.1016/j.arth.2010.12.024. Epub 2011 Feb 25.
  10. Verkkala K, Valtonen V, Järvinen A, Tolppanen EM. Fever, leucocytosis and C-reactive protein after open-heart surgery and their value in the diagnosis of postoperative infections. Thorac Cardiovasc Surg. 1987 Apr;35(2):78-82.
  11. Freischlag J, Busuttil RW. The value of postoperative fever evaluation. Surgery. 1983 Aug;94(2):358-63.

You’re taking the piss

Urinary tract infections are the scapegoat of the medical world. They make us lose our common sense, because once you find something that is easy to treat, you stop looking for anything else. This is termed satisfaction of search.

Let us look at two examples where a positive urine sample may lead the ward house officer astray, related to the domain of surgery.

Firstly, you have a patient who is POD4 after an anterior resection. You are called because they have become febrile. There is no obvious source on examination. You take cultures, and the mid stream urine comes back with a high number of white cells. You start the patient on cefuroxime for a presumed UTI. This is a frequent occurrence.

Unfortunately this decision neglects the basic rule of general surgery. This rule states that the main differentials in a febrile patient after abdominal surgery are as follows; anastomotic leak, anastomotic leak,  anastomotic leak and also anastomotic leak.

“But the urine is positive!”

Unfortunately pyuria is common in intraabdominal sepsis, presumably due to the infection rubbing up against the wall of the bladder and causing inflammation. The rate of sterile pyuria in appendicitis and diverticulitis for example can be anywhere from 25% to 70-80%, depending what literature you read (1,2).

This phenomenon is not even confined to intra-abdominal infection. 30% of patients presenting with pneumonia, sepsis, intra-abdominal infection, or enteritis have pyuria (3). Of these urine samples, only 30% were culture positive. Note that culture positivity does not imply a UTI- there will be a significant proportion of asymptomatic bacteriuria.

The second situation will be when you are not on general surgery, but convincing the surgical registrar to review your patient who has abdominal pain and a clinical presentation concerning for something surgical.

“But the urine is positive, why don’t you just treat the UTI?”

Take home message? Pyuria is common in patients with other serious sources of infection and you should remind yourself and others of this.

Till next time….

  1. Ther Adv Urol. 2015 Oct; 7(5): 295–298. Sterile pyuria: a forgotten entity. Sanchia Goonewardene and Raj Persad
  2. 09 Sterile Pyuria an Indication of Acute Appendicitis in Children. S. Lewis1, C. St. Laurent1, A. Ruiz-Elizalde1 1University Of Oklahoma College Of Medicine,Oklahoma City, OK, USA
  3. Sterile Pyuria in Patients Admitted to the Hospital With Infections Outside of the Urinary Tract. Jared B. Hooker, MS2, James W. Mold, MD, MPH, and Satish Kumar. JABFM March 2013:97-103

 

How to properly interpret the creatinine (Cr)

The house officer wades through a swamp of daily creatinines. Unfortunately there is poor example setting on what to do with these. The classic example is the 90 year old with a “normal” creatinine of 90.

Nobody likes formulae, but it is important to refer to a couple here in order to understand what is to come.

Cr Clearance = (Urine volume x urine concentration of Cr) / Plasma Cr

The exact formula is irrelevant for your purposes but it is important to take home the concept that from this formula we can say that Cr clearance is inversely proportional to serum Cr.

Of course we don’t calculate Cr clearance by taking samples of everybody’s piss. That would be far too unwieldy. Instead we estimate Cr clearance using formulae, such as Cockgrauft- Gault, which takes sex, age and weight and spits out a result.

Of course it would be foolish to think we can accurately determine someone’s muscle mass and rate of Cr production even with fancy maths, so these formulae are estimates only, especially at the extremes of age and weight.

What this really boils down to is that I’m more likely to win the lottery than a 90 year old is to have “normal” renal function with a Cr of 90. This, at least, is commonly accepted, although commonly ignored, probably because we all have a habit of only looking at the exact number if it appears in red.

The nephron deepens

There are more interesting conclusions we can come to just from looking at the Cr clearance formula. Consider the graph that plots the function y = 1/x (CrCl being proportional to 1 / Cr)

inverse

If the y axis is Cr clearance and the x axis is Cr, what you can see is that

  • On the first part of the graph a fairly significant fall in Cr clearance is accompanied by only a small increase in Cr
  • Towards the end of the graph a fairly small drop off in Cr clearance is accompanied by a large increase in Cr

Continue reading

Tricky gut ischemia, the uselessness of lactate, and the importance of clinical suspicion

You are called to see Ms A, an 80 year old woman on the surgical ward, due to worsening abdominal pain and tachycardia. She was admitted 8 hours ago with the same abdominal pain and diarrhea and had a CT abdomen, which the radiology registrar has provisionally reported as showing non-specific pericolonic fat stranding. She has been treated as an infectious colitis. She has a history of ischemic heart disease, atrial fibrillation and claudication. Examination of her abdomen shows diffuse tenderness but no peritonism.

You call the surgical registrar to express your concern this lady might have ischemic gut. He informs you he is reassured by the CT findings, the lack of peritonism and the normal lactate, which you had decided to check because you have recently heard about the association between gut ischemia and elevated lactate. When you arrive at work the next morning you discover that overnight she had become septic, spiked her lactate to 8 and been taken for a laparotomy, where extensively necrotic bowel was found. She was palliated.

Ischemic gut is one of those diagnoses that is always tricky to make, as there is no lab test to help you and the examination findings can be non-specific, although “pain out of proportion to the exam” is what you might find in the textbooks.  Age confers an exponentially increasing risk, and past the age of 75 it becomes more likely than appendicitis or ruptured AAA (1). This is a fact which I certainly hadn’t appreciated and I suspect many people don’t, given the frequency with which we query the latter two on CT requests and the infrequency with which we query ischemic gut.

The first point to make abundantly clear is that peritonism is a late sign of extensive bowel necrosis so is not reassuring. The same applies to the finding of portal venous gas on an abdominal Xray, pictured below (2). The whole point is to diagnose the condition early enough that you can do something about it (either open or endovascular revacularisation). By the time these signs develop, the proverbial train has left the station.

portal venous gas

Continue reading

The Hb in acute bleeding

bleeding

Imagine you are called to review a patient who has started vomiting blood an hour ago. You arrive to find them tachycardic with a heart rate of 110. Amongst all the other stuff you would do for this patient, you check an Hb. Its 130, unchanged from baseline. What does this tell you about the severity of the bleed?

The answer is nothing at all. Zilch. De nada.

The reason for this is explained brilliantly in the chapter on acute blood loss anemia in the book Clinical Haematology: Theory and Procedures (1) and supported by more recent articles (2).

When blood is lost from vessels, it is both plasma and red cells that are lost in equal numbers. Therefore acutely the haemoglobin concentration will not change. What is responsible for the haemoglobin dropping is shift of fluid from the extravascular space to the intravascular space in response to reduced intravascular volume, thus diluting haemoglobin.  It can take 48 hours for the full effect of this to be seen.

The earliest haematological findings that are seen are actually an increase in the platelet count which can take place in as little as an hour. Soon after a neutrophilia with left shift of white cells develops. The latter can take 2-4 days to resolve.

So in the above example, don’t be reassured by the fact that the Hb is normal, even though many times even your seniors will try and tell you “the patient can’t be bleeding significantly because there is no haemoglobin drop”.  In fact, the presence of a resting tachycardia, as in the above example, indicates fairly significant blood loss, potentially consistent with greater than 750ml if the classification of shock systems are to be believed.

The other corollary to this is that you don’t base the decision to transfuse blood on the Hb level, but rather on the patient’s clinical progress/your assessment. The full ins and outs of this are something that is difficult to discuss in a blog post. Additionally, the presence of thrombocytosis or neutrophilia/left shift can give you clues to the presence of bleeding when you are unsure, as they develop quite early.

References:

  1. Clinical Hematology: Theory and Procedures, Volume 936. Mary Louise Turgeon. Lippincott Williams & Wilkins, 1999. Pages 116-119.
  2. Clinical review: Hemorrhagic shock. Guillermo Gutierrez, David Reines and Marian E Wulf-Gutierrez. Critical Care2004(8):373