My answer to the poll. And an apology.

Sorry for the delay. Let’s start by going through the simple intervention that brought down the patient’s EWS from the last post, and then in the next post I’ll talk through how I attempted to apply the NICE guidelines to an MI that I was left pretty much alone to sort out.

The patient from the previous post met the criteria for SIRS, as her respiratory rate was 23 and her temperature was 39. I realised that I didn’t give enough information to allow you to call this sepsis, as I did not mention that she was being treated for a presumed UTI (nitrites positive, leukocytes positive.) Sepsis is defined as SIRS plus a source of infection. The Venn diagram and resources at emedicine are incredibly helpful for clarifying the difference between simple bacterial infections, SIRS, sepsis, septic shock and severe sepsis.

I only recently appreciated that severe sepsis has a mortality rate of 35%, whereas acute coronary syndrome has a mortality of 5%. You won’t find a doctor hanging around when someone presents with ACS, and severe sepsis should prompt the same degree of urgency.

Just a quick aside about nitrites and leukocytes on the dipstick. A positive test for leukocyte esterase is 57-96% sensitive and 94-98% specific for identifying pyuria. Pyuria means more than 10 white cells per mm^3. Pyuria is found in most cases of UTI, but can also be seen in other infections such as STIs and TB (especially for for MCQs). It can also be found in sepsis even when the urinary tract was not the original source of the infection. Stones, urinary tract cancers and papillary necrosis are amongst the commoner non infectious causes.

Leukocyte esterase is 48%-86% sensitive and 17 %-93% specific for identifying UTIs, which reflects the fact that most but not all UTIs cause pyuria (which makes it a bit less sensitive for UTIs) and that there are many cause of pyuria that are not UTIs (which makes it lot less specific for UTIs).

Nitrites are produced by the breakdown of nitrates to nitrites by bacteria, usually gram negative urea splitting bugs like Proteus and E Coli. It is less sensitive than leukocyte esterase (45 %-60% in most situations) with higher levels of specificity (85 %-98%).

Anyway, the patient had a positive dipstick for nitrites and leukocyte esterase.

The management of an unwell patient does of course start with ABC, but there are specific treatments on the way that we should give to optimise the ABCs. For example, we are taught all about airway manoeuvres and all sorts of exciting tubes under airway. However, in an anaphylactic patient the treatment that most non-anesthetists can do that makes the biggest difference to the airway is adrenaline. This tackles the underlying root cause of the airway compromise. You should of course do the manoeuvres and use adjuncts as needed, but without the specific treatment the patient will deteriorate in front of you, just at a slower rate thanks to your interventions. (And the earlier you call the anaesthetist the better, as intubation becomes harder the more tissue swelling develops.)

In a similar way, although we are rightly taught about the importance of fluids under C, in the case of sepsis (or any distributive shock like anaphylactic or neurogenic), you have to also treat the cause of the distributive problem. This means following the Survive Sepsis guidelines. Even though this patient has a likely fluid deficit, treating just with fluids in a septic patient is not sufficient. Septic shock is more severe than severe sepsis, and is defined as systolic blood pressure less than 90 mHg despite adequate fluid resuscitation. This implies that treatment beyond fluids and more fluids is required to fix the low blood pressure. On the ward, immediate IV antibiotics are the first step.   The patient may need pressors in ITU if they go into septic shock.

Now to be a hypocrite. All we did initially was give 500ml of Normal Saline, stat. We started another 500ml over 1 hour whilst we reassessed the patient. We made sure the rest of the Survive Sepsis plan was done whilst reassessing. 2 days later the patient was discharged.

Is there a right answer to the poll? Is this not just a mash up of the most popular two answer? Probably. The point of the poll was to get us thinking about what we prioritise, even if what we do in reality is a mash of a few options. If the situation arose again, I think my priority would be an initial 500ml stat bag of pretty much any fluid other than 5% glucose whilst working through the Sepsis Six. The importance of early antibiotics must be stressed, as there is plenty of evidence that the delay in starting antibiotics in sepsis is associated with increased mortality. The target is 3 hours from A&E presentation to the first dose of antibiotics. How much more seriously do we take an ACS target of 90 minutes ‘door to needle’, the thrombolysis in stroke of 3 hours or even ‘4 hours till they breach’ in A&E despite the mortality of septic shock being 50%.

The difference in how the patient looked subjectively and objectively with just 500ml of fluid is something I will not forget. But the fact that giving the fluid and seeing such a dramatic response does not mean job done is something I must make sure I remember.


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