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Sepsis I: why lactate is like a Pap smear.

This is the start of a series of posts on sepsis, I hope to cover the following topics in the coming weeks:

  • I :  Sepsis: screening and diagnosis
  • II : Antibiotics – what and when
  • III : Identify the source and control it if you can
  • IV :  Fluid and inotropes in sepsis

So here is the case for discussion – this is a real ED case from Broome last month.

39 yo woman with type-2 DM on insulin and metformin.  Presents to ED with fever, vomiting and vague (L) lower abdo pain for 12 hours.  States she feels thirsty, looks uncomfortable. No cough, URTI, no diarrhea.  Recently treated for UTI by GP, no urinary sxs since.

Triage obs @ 08:45 am : p=135/min,  BP = 119/73, T = 39.5, RR = 20.

Physical exam = tender (L) lower abdo, ENT / chest clear.   U/A = 2+leuks, 2+ blood.   BSL 8.4

Seen by RMO who recognised she was sick, IV access bloods and 2 L of normal saline.  Bloods sent:

  • FBP – mild lymphopenia
  • CRP = 19
  • UEcr / LFTs  all normal.  Bicarb 26
  • VBG – pH 7.27; pCO2 56; BE 1.9;  HCO3  28;  lactate 4.7
  • Blood cultures sent

On review a few hours later – patient feeling a bit better.  USS of abdo /pelvis – no findings to explain LIF tenderness.

Remained unwell with headaches, fever, tachycardia.  Repeat bloods for VBG were done – now looking more normal, acidosis corrected and lactate down = 1.9.  (What does “lactate clearance mean?” in this scenario)  So what happened?  Case D/W senior docs and…

Discharged home….  then represented later that night with same symptoms, rigors.  Admitted and commenced on IV ceftriaxone and gentamicin @ 22:00 (~13 hrs post triage).  This is not Broome ED’s finest moment, a possible near miss.  So how could we do better?

This is where I compare screening for sepsis to a Pap smear (hang in there, it is a weird comparison but stay with me).  As GPs we look at women’s cervixes all the time and we screen them for cervical neoplasia using Pap smears.  However, there was a time before Pap smears when we just looked at women with a symptom – eg. PV bleeding and did a spec to look for cervical changes / cancer etc.  I am sure most of the referrals to the Gynae yielded a positive result – but a lot of women with subtle changes / CIN were missed in the asymptomatic early stage of disease when intervention would have helped.  This is the basis of any screening tool: screen an “at risk” population with a sensitive test to find those who potentially have pre-clinical disease.   So back to sepsis:

Screening at triage uses a set of criteria to define the “at risk” group of patients.  The following criteria are used in other centres:

  • Fever (>38) OR suspected infection
  • pulse > 90
  • RR > 20
  • systolic BP < 90
  • Any change in mental status
  • SpO2 < 92 % on RA
  • Immunocompromised: steroids, chemo, uncontrolled diabetes
  • Invasive devices, surgery or procedures recently

So if you have 3 or more of these criteria you are into the high risk group and you automatically get the screening tool = bloods including a venous or arterial lactate sample, cultures, FBP, CRP, UECr, LFTs, Coag profile.  Lactate is either <2   OR  > 2.  (If > 4 then resuscitation should be commenced ASAP.)

You then get early review by a senior doctor to commence septic source identification workup: cultures, urine, CXR, any other pus, LP if indicated.

The goal is to expedite this process so that empirical or directed anitbiotic therapy can be delivered ASAP (door-to- ABs time minimised)

So that is screening in a nutshell.  Identify the “at risk” patients, do basic bloods + lactate then decide on appropriate therapy / Investigation.  The plan is to remove idiosyncratic decision making around the sick patient and streamline the process from triage to diagnosis / treatment.

I imagine that the “at risk” group will be in the 100 per month in my ED, then the lactate + patients will be ~5 % of those, ie. I am happy with a 1 in 20 pick up to maximise sensitivity and not miss any true positives.

Let me know if this sounds crazy…. evidence to follow

 

Comments

  1. Minh Le Cong says:

    Hi Casey et al
    Point of care lactate for sepsis screening is analagous to point of care troponin for ACS. If its positive , the patient should get admitted for 24 hrs of observation and serial labs, incl lactate.

    Case in point she had a positive lactate of >4, yet sent home because it was clearing..sounds reasonable but imagine would we send someone home if troponin was positive and their CK was decreasing on next lab?

    Also I think you got to be careful sending someone home without diagnosing a source for their sepsis.

    Not sure about the analogy with Pap Smear, Casey..bit of a long bow to draw!

  2. Casey Parker says:

    Hi Minh
    Thanks for the feedback (my wife agrees – a long bow!) So I have posted another analogy, maybe a shorter bow to draw.
    Also I have updated the Sepsis 1 post to point to a paper on Lactate clearance and its prognostic implication.

    I think it is fair to say that the diagnosis and management of early / occult sepsis in the average ED is somewhat idiosyncratic and in need of some more structured protocols – it is a bit like where ‘chest pain’ was back in the days before we got good at risk-stratification, now everybody gets it and we miss fewer MIs.

    Maybe you work in a better place than me, but I see a lot of random decision-making when it comes to these types of patients – as evidenced by the case I presented. And if you look at the stats on her 30-day morality with a lactate of 4+, it is much worse than sending home a small non-STEMI! What happened here: 2 L of saline, no ABs and home is probably akin to the non-STEMI getting oxygen, GTN and feeling better/pain free then being discharged despite a raised troponin.

    As for diagnosing a source – yep, that is coming up in the next post on Sepsis.

    Thanks for the feedback – always helpful
    Casey

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