Critical Care, Improving Outcomes, Mythbusting, Neurology

Compazine… for infectious disease?

Today’s article’s (1, 23 ) are a break from the usual trials that are typically discussed and a bit more “benchside medicine” than bedside medicine.  In fact, let’s look at this as an early request for one of the 12 trials of Christmas.

Phenothiazines have demonstrated in vitro (as well as some in vivo) activity for gram positive cocci, mycobacteria, amoeba (4; 5), and some gram negative rods.

It should be noted that Klebsiellae, pseudomonads and acenetobacters were highly resistant to almost all of these drugs.

The MIC for phenothiazines are usually not reached with conventionally used doses, but these compounds do enhance the activity of various antibiotics to which various bacteria are susceptible (including vancomycin), and even decrease the MIC of resistant organisms.

So where am I going with all of this? For starters, lets look at some common causes of meningitis, in no specific order:

Strep pneumo (gram positive); group B strep (gram positive); staph aureus (gram positive); Listeria (gram positive); Neisseria meningitidis (gram neg diplococci); H flu (gram neg)

All things phenothiazines are thought to have activity against.

You’re likely to be giving patients with potential meningitis something for pain (I hope?), so why not go with compazine?  Likewise, patients whom you may suspect bacteremia from a cellulitis, why not give compazine to, ummm, “counteract the nausea” associated with the opiates you gave for pain control?

I think this falls into the unlikely to harm, might help category, and is seemingly a ripe area for research.  Is this practice changing?  Nope, not at all.  Food for thought, but until compazine is proven unsafe in an infectious process, I will continue my love affair with compazine for headaches, nausea, and vomiting (regardless of suspected etiology).

Standard
Critical Care, Improving Outcomes, Mythbusting

1 in 10 EGLS saves a life.

Do current sepsis guidelines go far enough?

That was my first thought when I read today’s article. This single center ICU study looked at 220 patients divided into two categories- one category in which patients that were managed in adherence with the 2012 surviving sepsis guidelines – 20-49 ml / kg initial IV fluid bolus, continued fluid challenges until CVP of 8-12, with more given based on treating team. Noradrenaline until MAP of 65, and dobutamine for cvSO2 <70% in combination with either lactate >2 or urine output <0.5 ml / kg / hr). The other 110 patients had treatment guided by limited echo:

Treatment options looked like this:

1) IVC fluctuation <15% & normal LV function= give pressors only (discontinue IV fluid)

2) IVC fluctuation >15% & normal LV function = 20-40 ml /kg IV fluid given

3) IVC fluctuation >15% & mod/severe LV function = 10-20ml/kg IV fluid given AND initiate dobutamine 5ug/kg/min

4) IVC fluctuation <15% & mod/severe LV function = discontinue IV fluid and initiate dobutamine 5 ug/kg/min

 

These patients were pretty sick- all patients were mechanically ventilated and on noradrenaline. Limited echo was performed within 24 hours of presentation to ICU and within 36 hours of presentation to the ED (actual times were within 7-15 hours in the ICU, on average, 11 hours). Patient characteristics were pretty similar in terms of age, APACHE scores, and labs (similar ESRD/CHF percentage as well ~20% of both patient arms). Surprisingly, patients received a ridiculous amount of IV fluid from the ED – 68 (55-70) ml / kg in the echo group vs 65 (55-72) ml / kg in the standard of care arm. Yes, even with 20% of patients having ESRD / CHF – the least amount of IVF given was 55 ml / kg !

Results?

Despite all of this IV fluid given in the ED, 35% of patients still have >15% IVC collapse (!). 65% of patients had their fluid restricted, and 22% in the echo arm vs 12% in the standard of care were started on dobutamine. On Day 1 in the ICU, patients received less IVF in the echo arm (49 (33-74) ml / kg, vs 66 (42=100) ml / kg) – but still a significant amount if IVF.

28 day survival was 56% vs 66% in favor of the echo arm, with significantly less acute kidney injury (65% vs 88% for all AKI, and 19% vs 36% for stage 3 AKI).

So your NNT to save a life is 10, and 4 to reduce incidence of any AKI.

So, is this really an ED paper? Well, it depends on your area of practice. The local flavor of the authors is such that their local policy was to initiate dobutamine in the ICU and not in the ED. Are you boarding ICU players? Are your hospitalists ultrasono savvy? How involved are your intensivists in patient care while patients are awaiting an ICU bed? Are you okay with administering at least 40 ml /kg IV fluid and starting pressors on your septic shock patients? If the answer is no or “not really” to any of these questions, then the answer is yes.

Standard
Improving Outcomes, Improving Throughput, Mythbusting

Albuterol: Sepsis Mimic

In today’s day and age of overtesting, some providers will not send home a patient with an abnormal lactic acid at all, regardless of etiology. So let’s examine what can possibly cause abnormalities of the current apple of our sepsis eye.

Here, 28 healthy subjects were randomized to placebo or 10 mg of nebulized albuterol over an hour. This is what many of us would consider “an hour long treatment” – or about 4 of those plastic neb vials. Serum lactate (and serum potassium as well) was measured prior to treatment, and at 30 minutes and 70 minutes after the start of treatment.

In the 14 patients receiving albuterol, their lactate went up on average 0.77 mmol/L vs a decrease of 0.15 mmol/L for the placebo group, while serum potassium levels went down by 0.5 mEq/L in the treatment arm vs no change in the placebo arm.

In our current overdiagnosis induced sepsis frenzy, if you must order a lactic acid, do it before giving albuterol, or better yet, if there is clearly some other reason for dyspnea aside from an infectious etiology (asthma or COPD that require immediate albuterol) – don’t order a lactic at all and document that an infectious etiology is not the cause of today’s abnormal vital signs.

Standard