Clinical Case 036: Silent, sitting sepsis
This case is part of my “Sepsis week” at Broome Docs. Lets say this case happpens in January, just after the first big rain for the wet season.
58 yo Aboriginal man, presents to triage at ED complaining of “cold sick” [flu] symptoms. Has been feeling hot, sweating and had a non-productive cough intermittently for a week. No good localising symptoms.
Obs: P= 110, temp = 38.9, RR = 20, BP 110/50, SpO2 = 97% RA BGL = 17.7 mmol
PMHx: type 2 DM, untreated. Hypertension, gout and recently investigated for PR bleeding = diverticulosis, old rheumatic heart disease – mild MR on ECHO. “Drinks a bit”
Meds = perindopril / hydrocholothiazide, allopurinol, aspirin.
Examination: Sitting up, smiling. ENT – normal, chest clear, systolic murmur c/w MR, abdomen soft, though mildly tender in the RUQ. No loin tenderness. No skin lesions. Alert and quiet, happy to sit… Urinalysis = gluc 3+, protein 2+, blood +
This man gets a triage score of 3 – which means he should be seen within 30 minutes. So after waiting his allotted 30 minutes he collapses in the ED waiting room and gets carried into the Resus bay….
Obs: pulse = 150 thready, BP = 70/30, RR = 35 shallow, Spo2 unrecordable, GCS = 8ish. Groaning, localising to pain. A bedside BSL = 20.3 mmol.
A portable CXR is done, and an ABG is drawn on 15L via NRB
PaO2 = 84
PaCO2 = 29
HCO3 = 12
Lactate = 6.3
BE – 14
Here are the questions? I will give it a day or two for answers to come in from the readers…
Q1: What is your next move?
Q2: What bugs do you need to cover to ensure you give adequate early empirical antibiotics?
Q3: If you chose to intubate this man – what ventilator settings would you go for?
1) Get IV access, 500ml-1l cristalloid bolus. If consciousness and hemodynamic not improving quickly and dramatically, then intubate (preoxygentae with CPAP), EtCO2, CVC, arterial line, bladder cath, get all the specimen you need for culture and start antibiotics as soon as possible. Insulin bolus and continuous infusion if needed. Bedside echo, continue fluid loading according to echographic criteria of fluid-responsivness. Get ScvO2, check lactate level evolution. I personally couldn’t care less about CVP. Start noradrenaline and/or dobutamine if needed. PRBC if Hb <8gr%. IV thiamine.
2) I guess the bugs would differ if you are in Broome or in Belgium… S. Pneumoniae of course, atypical pathogens and whatever nasty tropical bugs are running amok in your neck of the wood… Depending on the time since he was explored for his bleeding, I would also cover hospital-acquired gram negative and consider covering staph aureus. Anyway, the empirical therapy would be broad-spectrum and possibly a combination therapy
3) Analgesia, sedation and volume control mode until things are sorted out. 6-8ml/kg tidal volume, PEEP 3-5cmH20 then titrated to FiO2 and hemodynamic response. Recruitment maneuvers if severely hypoxaemic. Other parameter according to patient physiology and response (auto-PEEP, thoraco-pulmonary compliance, blood gases and so on).
Thank you for your great blog.
Hi Casey – great case!
1. Simultaneous assessment and resucitation with attention to airway, breathing, and circulation etc. etc.
Practically, sepsis resuscitation often comes down to “fill the tank”, “fix the pipes”, and “optimise the pump” – EMCrit has a great podcast discussion on this.
2. The Australian indigenous population is special in regards to its comorbidities and susceptibility to nasty bugs. In the diabetic patient who lives in a tropical/sub-tropical (or even arid zone), Burkholderia pseudomallei (Melioidosis) should be high on the list of differentials – treatment should take this into consideration. Empiric Meropenem 1g TDS for at least 14 days should be initiated – this will also cover the usual pneumonia suspects other than MRSA.
3. Ventilation settings should be based on what you are familiar with using, while taking into account such strategies as ARDSNet with low Vt (6mL/kg) and open-lung ventilation with appropriate PEEP.
Casey great case.
Summary: Septic Shock = If in small hospital with limited resource urgent early retrieval and call to retrieval services.
A: Start simple
A/B- Start SImple NRB or Bipap (Trail Ketamine if fighting Bipap). Bipap not needed at this stage. As interim Measure to intubation. Optimisation of Sats.
He will Need ventilation for two reason at least.
1: Likely impending Respiratory Failure
2: Large metabolic Reserve taken up by the patient spontaneously breathing. Intubation will take this metabolic demand away.
Intubation: Ketamine likely agent with paralytic of choice.
Optional: Consider using ventilator (Settings Pressure control 15 (decreases gastric insufflatio ) as BVM to give pressure controlled breaths during apenia to reduce the worsening acid base at this stgae and maintain sats. B
C: Two lines large bore. Fluid resus. Will need central line if possible (local resources dependent)
Bloods- (FBC/EUC/LFT/Blood Cultures x2) Venous Gas-Lactate etc
500ml Fluid bolus multiple this patient is behind in the fluid resus he will need large amounts of fluids. Art Line if technology is available. Early use of inotropes (whatever is available – Adrenalin/norad/Metarminol etc)
D: GCS
EFG; Insulin infusion aim for high normal bsl except 7-10 glucose. NG Tube
Ultrasound: RUSH exam- pipes/pump/tank
B: ANTIBIOTICS ANTIBIOTICS ANTIBIOTICS
Usual suspects + as everyone has stated meliodosis: Especially in diabetic aboriginal male in tropical Australia. Therefore Meliodosis may consider stat dose of gentimicin. Important that this patient may get worse at the 3-4 hour mark after the antibiotics go in. Early use of inotropes (whatever is available – Adrenalin/norad/Metarminol etc). Additional coverage of Swine flu (instigate tamiflu via NG).
c: Vent Settings (depends on my machine)
Tidal Volume 6-8ml per KG ideal body weight
Rate: 12
PEEP/FiO2: as per ARDS net or local. Initally start PEEP 5 and FiO2 100%. Titrate fi02 and peep to sats aiming for at least 92%.
Wot the above lot said.
This guy needs a tube but it could get a little hairy (ie we could kill him.) I’d pour in fluids and have some aramine drawn up before attempting the intubation. He has a metabolic acidosis with partial compensation (RR 35 and shallow; PaCO2 29) which is going to get worse if we don’t tube him. On the other hand if / when we paralyse him, his CO2 will climb, his pH get worse and he could arrest. Even after the tube has been successfully placed, (using our shinny new King Vision – free plug) we will need to bag him at a fast rate and continue to closely watch his CO2. I’ve heard some people argue that with a severe metabolic acidosis you should bag at about the same rate as they were spontaneously breathing. I don’t think that is necessary in this case as we will generate better TV’s than the patient was so maybe start at around 20 breaths a minute and watch the end tidal CO2 closely. (aggressive bagging may also decrease his venous return and contribute to the likely decreasel in BP during intubation or the post-intubation period ) Some people give such patients a shot of bicarbonate prior to intubation but I’m not sure that it really helps. He will likely need a faster RR on the vent than most of us usually start with as well.
Hi folks
this case gives me flashbacks of the remote patient I saw right after lunch at a Cape York clinic at the height of the h1n1 pandemic . It was memorable because I contracted swine flu from the very patient and was the sickest I have been in decades..thank God for Tamiflu!I still got pneumonia though!
This guy needs fluids then Adrenaline infusion ASaP. We had no noradrenaline in the clinic and a dodgy old infusion pump so made up 1mg adrenaline into 1000mls saline and ran that in at around 300mls per hour to start with ..his BP improved to 100systolic and never dropped during the rest of the resus, including the RSI.
Thanks for all your plans – I think we are all in agreement – this man is sick, and has to be intubated to ensure his oxygen supply and demand remain in check!
However, intubating could lead to his demise – so we need a careful approach. Look no further than Scott Weingart at Emcrit – listen to his podcast on intubating the severe acidosis patient
In terms of Microbiology – well, all the usual suspects, pneumococci, Klebsiella, pseudomonas…. but the big one in tropical Australia is Melioidosis (Burkholderia pseudomallei). This is a nasty bug that can cause pretty much every type of infection you can think of and can kill quickly. It tends to pop up in epidemics in the wet season, especially if you disturb the soil. The communities to the north of Broome are infamous in Micro circles for its presence. So you need to cover this – which means giving meropenem in most cases, this is the time to bring out the big guns!
Ventilation could be tricky – the basic plan is a “lung-protective” strategy. Around 6 – 7 mls / kg (IBW) tidal volume, with a high RR to continue the respiratory compensation he is requiring to keep his pH in check. PEEP titrated to oxygenation, likely to be highish value needed – and maybe position him good side down, or even prone if you are able.
As for the rest – well, see previous posts on the current sepsis strategies out there.
Casey
I missed the early bit and have never seen meliodosis! Though I was always told that Legionella is more prevalent following heavy rainfall so maybe it needs to be in there too