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.

The hypoxic drive myth

It was difficult to go through any single month in medical school without being reminded that giving oxygen to chronic CO2 retainers abolishes their respiratory drive (which in these patients is apparently dependent on hypoxia).

This is taught with similar vigour in nursing schools.

There is one small problem with this elegant concept. To quote Blackadder; “it is complete bollocks”.

The concept was developed in 1949 and we have held onto it with fervour ever since. I would not wish to minimise the efforts of physicians who precede us, but for context the year 1949 predates the invention of CPR.

co2

This graph (1) from 1980 shows what happens when patients with COPD and acute respiratory failure are given uncontrolled high flow oxygen for 15 minutes. The first thing to note is that the ventilatory drive (minute ventilation – VE) is supranormal to begin with (normal is about 5L/min). The graph is produced here with no permission whatsoever.

The second thing is that after a brief, not particularly significant, drop in the minute ventilation in the first few minutes, it pretty much returns to baseline. The last is the lack of correlation between minute ventilation and the rise in CO2 (which has been confirmed in subsequent studies).

So how does uncontrolled oxygen result in worsening hypercapnia in chronic CO2 retainers? It seems two main mechanisms are at play. The first is that oxygen displaces CO2 off of haemoglobin- the Haldane effect. The second is that usually the blood flow in the lungs is directed away from crappy hypoxic alveoli to healthy alveoli where the CO2 can be properly eliminated (hypoxic pulmonary vasoconstriction). Supplying crappy alveoli with excess oxygen reverses this process.

So, yes, uncontrolled oxygen can make respiratory failure worse, but it will not make your patient stop breathing. Which is important to know. If the patient has a respiratory arrest it is likely because they were tiring out and heading there anyway, not because you weren’t stingy enough with the oxygen.

It is also important to realise that the patient saturations give a good indication of how much oxygen their alveoli are seeing (it is this that determines how much hypoxic pulmonary vasoconstriction goes on). People obsess about the flow rate on the wall, but really the flow rate does not tell you how much oxygen is getting into crappy alveoli. As long as you are hitting a more conservative oxygen saturation target of 88-92%, you are fine.

References:

  1. Crit Care. 2012; 16(5): 323. Published online 2012 Oct 29. doi: 10.1186/cc11475. PMCID: PMC3682248 PMID: 23106947. Oxygen-induced hypercapnia in COPD: myths and facts. Wilson F Abdo  and Leo MA Heunks

Why it’s important to question authority, even in medicine

Last night I was watching one of those air crash disaster shows. For 60 minutes it followed the case of Comair flight 3272, which crashed in 1997 on its approach to the airport, killing all 29 aboard. While I get bored of the constant analogies drawn between medicine and the aviation industry, I found that this case imparted a powerful lesson.

For those of you who are regular readers (hopefully there are some!) you may have noticed a pattern in my blog posts- they often advocate challenging commonly held wisdom that may come from your seniors. It has not escaped my attention that this is one of those ‘easier said than done situations’. Comair flight 3272 will help me expound why I think this is important, and how to go about it.

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