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