Septic shock on front page of NY Times

[polarbebe]

Made the front page a few months ago... a young 12 y/o boy died from septic shock with a source from a simple superficial laceration on the arm (not even requiring sutures). Patient later developed fever, nausea and vomiting (and leg pain where no injury occurred previously), PMD and ER attending (per previous front page NY Times article) initially diagnosed as gastritis, sent home, returned several days in septic shock, died in ICU.

 

Initial article is quite one-sided... but does raise awareness of septic shock as a major cause of mortality.

 

http://www.nytimes.com/2012/12/21/nyregion/one-boys-death-moves-state-to-action-to-prevent-others.html?hpw&gwh=E1D855D4742317C0460B721BDC7B00CC

 

Working in both the ER and MICU and managing septic shock have learned a lot. Some ER providers may not be as familiar or look for sepsis as frequently as they possibly could. From what I recall at my PA program, MI management was really stressed, but septic shock management less so... Time is critical, an initial delay of antibiotics by every hour increases mortality by ~6%

 

Visit the surviving sepsis campaign to learn the international guidelines:

 

survivingsepsis.org

 

Be aware of SIRS criteria

Sepsis = SIRS plus suspected or known infection

Severe sepsis = Sepsis plus evidence of two organ dysfinction

Septic shock = severe sepsis not responsive to a physiologic bolus (20cc/kg or some people say 2L)... usually requiring pressors

 

Take the Fundamentals of Critical Care Support (FCCS) sponsored by SCCM and get 16 hours of CME I.

[Acebecker]

Would love more details on this case... Did he have the normal biochemical signs of sepsis? Abnormalities on CMP, elevated WBCs w/ L shift, etc?

[flyingsquirrel]

Yes...WBC 14.7, 53% bands

He was d/c home before the labs came back and there was no attempt to bring him back in.

 

http://www.nytimes.com/2012/07/12/nyregion/in-rory-stauntons-fight-for-his-life-signs-that-went-unheeded.html?pagewanted=all&_r=1&

[Kaepora]

I work in the MICU/CCU so sepsis is a very common diagnosis. However, all the ICUs in the hospital (plus the ED I'm pretty sure) cover the SIRS criteria with each pt every day.

[polarbebe]

I work in the MICU/CCU so sepsis is a very common diagnosis. However, all the ICUs in the hospital (plus the ED I'm pretty sure) cover the SIRS criteria with each pt every day.

 

Absolutely, septic shock is the "bread and butter" of the MICU, thus very common. I was posting this in the ER forum, because it is not always in the top differential. Per the surviving sepsis campaign, it is the 10th leading cause of death (over 235k per year) and some data to suggest outcomes for patients have only slightly improved or unchanged for a disease process that has a 28-50% risk of mortality. So, many initial contact providers are likely not following all the guidelines for early goal directed therapy.

 

There are PAs in urgent care clinics, fast tracks, PMD offices that don't do labs.

 

ER is scary (I read fast track disasters thread)... is it GERD or atypical MI? Flu or severe sepsis that may turn into septic shock with pneumonia as a source? Do I send the patient home?

 

The campaign is to raise awareness of sepsis and increase survival.

[EMEDPA]

when in doubt order a lactate, it's a great test. we had a guy recently we were on the fence about sending home with a cellulitis but otherwise young/healthy with no worrisome comorbidities, nonsmoker, etc. we were thinking IV abx now, po at home, recheck in 12 hrs.

a lactate of 7.5 bought him an admission and very aggressive tx.

[Timon]

I'm new to healthcare and I work in an ER. We have a sepsis screening we do for every patient (regardless of age or chief complaint) during triage regardless if they were a walkin or brought by ambulance. Is this not the case in most ERs?

[EMEDPA]

I'm new to healthcare and I work in an ER. We have a sepsis screening we do for every patient (regardless of age or chief complaint) during triage regardless if they were a walkin or brought by ambulance. Is this not the case in most ERs?

What is involved with this screen?

you can't do lactates and cbc's on every patient(?). full vitals, sure but that's nl triage.

we don't have a special sepsis screen. we have a sepsis panel that we can order but it isn't automatic.

[Timon]

What is involved with this screen?

you can't do lactates and cbc's on every patient(?). full vitals, sure but that's nl triage.

we don't have a special sepsis screen. we have a sepsis panel that we can order but it isn't automatic.

 

Theres a form we have almost like an algorithm that's filled out for everyone. From there the RN has standing orders to order labs or not or what the next step is.

[Acebecker]

Theres a form we have almost like an algorithm that's filled out for everyone. From there the RN has standing orders to order labs or not or what the next step is.

 

This sounds expensive. Have y'all done any research on cost and outcomes vs. the outcomes of clinical assessment by a trained provider?

 

ETA: Not to armchair quarterback - obviously something went amiss with this case. But I think anyone in their right mind would question serious infection in a kid with 53% bands. I'm sure the ER doc did question it, but the kid fell through the cracks. Major bummer. And this is the reason why I don't like to DC patients home (from urgent care) until labs have come back.

[Timon]

I'll ask the director of the ED when I see them next. The form is pretty straight forward and is just an 8.5 x 11" paper we include in the chart (were old school everything is pen and paper). Basically has 8 questions you answer yes and no to that checks if the patient is positive for SIRS and if so we do a sepsis work up including CBC and Lactate.

[EMEDPA]

seems inefficient

" I sprained my ankle"

"do you have a fever?", etc

suggest clinical correlation by an actual medical provider.

all the new "efficiency models" are getting rid of triage nurses and putting a pa or md up front

[Kaepora]

when in doubt order a lactate, it's a great test. we had a guy recently we were on the fence about sending home with a cellulitis but otherwise young/healthy with no worrisome comorbidities, nonsmoker, etc. we were thinking IV abx now, po at home, recheck in 12 hrs.

a lactate of 7.5 bought him an admission and very aggressive tx.

 

Awesome advice. My hospital system just had a rather large campaign to increase awareness about lactate and the usefulness of ordering a level on really any patient. They also handed out badge clips to everyone that say either "sepsis" crossed out or "got lactate".

[polarbebe]

Awesome advice. My hospital system just had a rather large campaign to increase awareness about lactate and the usefulness of ordering a level on really any patient. They also handed out badge clips to everyone that say either "sepsis" crossed out or "got lactate".

 

Definitely great advice. Also, if you didn't draw a lactate but wishing you did and already sent labs... there are some small things to remember to check which may point to a lactate metabolic acidosis (but also for many other etiologies):

 

Anion gap

Bicarb < 22 on the BMP

Tachycardia (part of SIRS criteria, since septic shock is a distributive shock, body increases HR to maintain adequate cardiac output with the increased vasodilatation)

RR > 20 (part of SIRS criteria, they may be blowing off pCO2 due to a metabolic acidosis and compensating with a respiratory alkalosis... or just anxious, pain, etc. :)

Warm skin (early on in septic shock, due to the vasodilatory effects of septic shock; later mottled and cool skin)

 

Drawing a lactate (or VBG/ABG which some labs include a lactate) is far more definitive.

[fuma102]

Its good to have a sepsis discussion based on this (extremely out of the ordinary & unfortunate) case. We here in NYC are more than a bit upset the physician's name was published in the original article. Thankfully it wasnt a PA that this happened to for our sake.

 

In sepsis though, its lactate, lactate, IVC sono, lactate. wbc elevation doesnt bother us, and normal vitals dont mean much if they present with a lactate >4 - they go to a unit. Im more scared of a lactate of 8 than a wbc of 38.

 

we have been housing our ICU patients for HOURS and if theyre in the ED, its ED management - no housestaff to place orders. Even with normal vitals & a CHF hx, were pushing fluids until they clear that lactate & have a normal IVC.

[polarbebe]

 

In sepsis though, its lactate, lactate, IVC sono, lactate. wbc elevation doesnt bother us, and normal vitals dont mean much if they present with a lactate >4 - they go to a unit. Im more scared of a lactate of 8 than a wbc of 38.

 

we have been housing our ICU patients for HOURS and if theyre in the ED, its ED management - no housestaff to place orders. Even with normal vitals & a CHF hx, were pushing fluids until they clear that lactate & have a normal IVC.

 

You're absolutely right on fluids to "fill up the tank" and replete intravascular volume that has greatly diminished due to the vasodilatory and "leaky" circulatory system in sepsis. I am unsure about the efficacy regarding IVC compression on U/S to assess intravascular volume status, the international guidelines and Manny Rivers trial use central venous pressure as a surrogate marker (and that has significant limitations). Remember to also include in your assessment of oxygen delivery signs of end organ perfusion such as menta status, urine output of at least .5cc/kg/hr. Other methods include checking for JVD, if a-line and CVL are placed may check try a leg lift (elevate both legs at least 45 degrees for 1 minute) to see if there is an increase in MAP, bolus the patient a liter and see if the tank is full (increase in MAP means you have farther to go, no change means you have filled the tank, decrease in MAP means you are on the wrong side of the Starling curve).

 

It is the initial management of the septic patient in the ED during the first 6 hours that is most critical and has the greatest effect on reducing mortality. We can briefly discuss initial management since many of us in the ED will be managing them until ICU consult arrives.

 

ABCs first then (should be occurring all simultaneously):

Increase oxygen delivery: get access and fluid rescuscitate aggressively to MAP generally at least 65. Measuring intravascular volume is based on many different things as mentioned above (CVP goal 8-10 and 14-16 in vented patients due to increased intrathoracic pressure with PEEP). Oxygen delivery = cardiac output (HRx stroke volume) x Hgb x SpO2 + (PaO2 x .003). Once you have determined you filled the tank (cardiac output is determinant on stroke volume, to increase stroke volume, preload is the principle determinant in a healthy compliant heart), and your central venous SpO2 < 70% (consider inotrope) or MAP < 65 you can consider to add a pressor - levophed is first line, can consider adding second or third agents and inotropes such as dobutamine (inotrope), neo (pressor) dopamine (inotrope with some pressor effects), epi (pressor/inotropy) or vaso (pressor effects). Transfuse to Hgb generally of at least 7 (not actively bleeding or in DIC) - higher Hgb has been shown to increase mortality, there is more oxygen carrying capacity but you increase afterload by high viscocity, pulmonary edema, TRALI, ARDS, etc.

 

Blood cultures before antibiotics but don't delay antibiotics

 

Antibiotics (usually broad spectrum initially), vanc and zosyn or cefepime, imipenem (many other combos used)

 

Get access: large bore IVs and probably central line (should never delay IVF) for pressors, foley to measure end organ perfusion

 

Vented patients limit tidal volume in ARDs patients, permissive hypercapnea - keep plateau pressure < 30, about 6cc/kg per ideal body weight (obese people don't have bigger lungs)

 

Bicarb gtt only recommended for pH < 7.1 generally (per ISS guidelines) but I have seen people use this much earlier

[Kaepora]

The ICU RNs that respond to codes also have to complete a quick sepsis worksheet on those Pts. Simple stuff like if they have a temp, elevated wbcs, hypotension, etc. and the number of "yes" checks escalates their care.

[CAdamsPAC]

You're absolutely right on fluids to "fill up the tank" and replete intravascular volume that has greatly diminished due to the vasodilatory and "leaky" circulatory system in sepsis. I am unsure about the efficacy regarding IVC compression on U/S to assess intravascular volume status, the international guidelines and Manny Rivers trial use central venous pressure as a surrogate marker (and that has significant limitations). Remember to also include in your assessment of oxygen delivery signs of end organ perfusion such as menta status, urine output of at least .5cc/kg/hr. Other methods include checking for JVD, if a-line and CVL are placed may check try a leg lift (elevate both legs at least 45 degrees for 1 minute) to see if there is an increase in MAP, bolus the patient a liter and see if the tank is full (increase in MAP means you have farther to go, no change means you have filled the tank, decrease in MAP means you are on the wrong side of the Starling curve).

 

It is the initial management of the septic patient in the ED during the first 6 hours that is most critical and has the greatest effect on reducing mortality. We can briefly discuss initial management since many of us in the ED will be managing them until ICU consult arrives.

 

ABCs first then (should be occurring all simultaneously):

Increase oxygen delivery: get access and fluid rescuscitate aggressively to MAP generally at least 65. Measuring intravascular volume is based on many different things as mentioned above (CVP goal 8-10 and 14-16 in vented patients due to increased intrathoracic pressure with PEEP). Oxygen delivery = cardiac output (HRx stroke volume) x Hgb x SpO2 + (PaO2 x .003). Once you have determined you filled the tank (cardiac output is determinant on stroke volume, to increase stroke volume, preload is the principle determinant in a healthy compliant heart), and your central venous SpO2 < 70% (consider inotrope) or MAP < 65 you can consider to add a pressor - levophed is first line, can consider adding second or third agents and inotropes such as dobutamine (inotrope), neo (pressor) dopamine (inotrope with some pressor effects), epi (pressor/inotropy) or vaso (pressor effects). Transfuse to Hgb generally of at least 7 (not actively bleeding or in DIC) - higher Hgb has been shown to increase mortality, there is more oxygen carrying capacity but you increase afterload by high viscocity, pulmonary edema, TRALI, ARDS, etc.

 

Blood cultures before antibiotics but don't delay antibiotics

 

Antibiotics (usually broad spectrum initially), vanc and zosyn or cefepime, imipenem (many other combos used)

 

Get access: large bore IVs and probably central line (should never delay IVF) for pressors, foley to measure end organ perfusion

 

Vented patients limit tidal volume in ARDs patients, permissive hypercapnea - keep plateau pressure < 30, about 6cc/kg per ideal body weight (obese people don't have bigger lungs)

 

 

 

Good stuff right on goal!