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Interesting case. ER gurus - was this patient in shock? If so, what kind?

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Heads up, long post.

I'm in my 8th rotation which happens to be EM. This was a patient that came through the ER with altered mental status, and my preceptor told me it'd be a good one to work up. Turns out this would be the most ill patient coming through the doors on my first week there.

My most pressing question (I didn't have a chance to ask my preceptor as things got crazy quick with this patient and the ER in general) is, was this patient in shock and if so what kind?

She was in a stupor, but could be aroused to her name and painful stimuli. She would also tell you her name if you asked. Important to note.

She was found lying on floor covered in feces by son who called EMS. EMS first BP reading was 62/40, they give 400cc of fluid. Second BP reading after bolus 70/44. We gave her 1L bolus in ER, BP now 74/50. Her heart rate this entire time stays in a narrow range between 70-76. This does not change during the entire course of ambulance ride, and her stay in ER before internal med takes over. We try multiple times to get a temp, but after 4 attempts on 2 different thermometers, (2 oral, 1 axillary, 1 rectal) they all error out. Patient also keeps screaming she is cold. We eventually place an indwelling rectal thermometer, which gave a reading of 34.0 celsius. Immediately started warming the patient.

Minus the heart rate and body temp, it's eerily similar to the septic shock patient we had 24 hours previous, I want to work her up for septic shock. Preceptor agrees. I order CBC, BMP, Lactic acid, Procalcitonin, ABGs, Blood cultures and Chest xray. Order abx Zosyn 4g-0.5g with vanc to follow

Now i'll jump to the good stuff. While waiting for stat labs patient continues to decomp, BP now 65/40.

Specific labs I remember. Lactic acid and procalcitonin were completely WNL. WBCs 22.3. BUN 140!!. Cr 11.8! The real kicker was her blood pH...6.9

She was in a state of complete anuresis. So it was clear she was in a state of uremic encephalopathy, acute on chronic kidney disease and all that good stuff. But I just cant figure out why we couldn't get her blood pressure up. We eventually placed a central line which gave a central venous pressure of 2. At this point internal med docs came down and started taking over. They asked for another 2L of fluid to be pushed, yet that BP never came up.

What was going on here?

 

 

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interesting case with broad initial differential with tox, metabolic, environmental, etc. Given that presentation a TSH and ammonia level could have been ordered as well to cover the ddx of hepatic encephalopathy and myxedema/hypothyroid coma. Did the pt end up on pressors? typically if someone has a map less than 65 or 70 after 2-3 L of crystalloid the next step is pressors and/or blood(if severely anemic for whatever reason). what did her lytes look like? na/k/ca/mg. in the setting of severe renal failure those are likely to be significantly abnormal as well and may require intervention. hyper-K can lead to sine-wave ekg, hypotension, and death. hypomag can cause serious fatigue and/or arrythmias. low CA can cause longggggggg QT. she certainly was in shock (remember the definition is poor tissue perfusion, which she certainly had given loc, temp, etc). hypothermic, and acidotic also generally implies coagulopathic, so look for pending DIC, check platelets, fibrinogen, etc

to call it sepsis you need SIRS criteria plus a source. I imagine this is probably a form of distributive/metabolic shock. she probably has enough fluid(maybe even too much given kidney failure), but can't shunt it to where it needs to be to maintain temp, bp, and mental status.

please post a follow up. great case.

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Off the top of my head with the hypotension and acidemia w/ pH 6.9>>very concerning

-couple amps of HCO3 stat (if no concern with ventilation, and assuming this is a metabolic acidosis/?AGMA (uremia, renal failure vs some toxic ingestion

-Central line placement>> and probably dialysis catheter for urgent/emergent dialysis

 

With a pH that low you can definitely have:

-vasoplegia/distributive shock

-also can have some element of cardiac dysfunction (ScvO2 off the central line/bedside echo)

 

Otherwise same as the above

-IVFs (barring physical exam findings c/w gross volume overload)

-vasopressors

-BS abx

-rewarming of the pt

 

 

 

Edited by jk5142

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Agree with Emed on all points. Lots of unknowns here to say what caused her shock, but definitely in shock. Still best to give her abx. I likely would have started her on norepi. Also don't see troponin, though this would likely be elevated anyway given her kidney function, but this could be ACS with shock, though agree with Emed likely metabolic. Would have thrown a US probe on her to look at heart function and IVC for fluid status. You couldn't get a temp because she can't even keep enough blood central to mount a core temp. 

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41 minutes ago, EMEDPA said:

interesting case with broad initial differential with tox, metabolic, environmental, etc. Given that presentation a TSH and ammonia level could have been ordered as well to cover the ddx of hepatic encephalopathy and myxedema/hypothyroid coma. Did the pt end up on pressors? typically if someone has a map less than 65 or 70 after 2-3 L of crystalloid the next step is pressors and/or blood(if severely anemic for whatever reason). what did her lytes look like? na/k/ca/mg. in the setting of severe renal failure those are likely to be significantly abnormal as well and may require intervention. hyper-K can lead to sine-wave ekg, hypotension, and death. hypomag can cause serious fatigue and/or arrythmias. low CA can cause longggggggg QT. she certainly was in shock (remember the definition is poor tissue perfusion, which she certainly had given loc, temp, etc). hypothermic, and acidotic also generally implies coagulopathic, so look for pending DIC, check platelets, fibrinogen, etc

to call it sepsis you need SIRS criteria plus a source. I imagine this is probably a form of distributive/metabolic shock. she probably has enough fluid(maybe even too much given kidney failure), but can't shunt it to where it needs to be to maintain temp, bp, and mental status.

please post a follow up. great case.

TSH honestly never occured to me. I haven't seen it ordered on any chart i've been in while in the ER (granted, i've been there for 4 days). I'm going to keep that in mind.

We were about to start her on pressors, but that is when Internal med came to ER bc patient was being admitted. I'm not sure if she ever got them, but it was certainly our next step as I had discussed it with my preceptor.

She was not critical anemic, I remember her HGB being low 11's.

Cant remember her electrolytes, however I remember sodium being mid 120's. It should be noted that the only *critical* labs, as noted by ER lab, were the BUN, Cr and blood pH.

I was thinking distributive shock, however her extremities were cold as well. IIRC, characteristic sign of DS is warm extremities d/t vasodilation.

 

Unfortunately, follow up will be tough. My preceptor is on vacay for a week, i'm not scheduled to be back in ER for 9 days. However i'm trying to pick up shifts w/ other docs because i love it so much. I'll update as I can.

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11 minutes ago, jk5142 said:

Off the top of my head with the hypotension and acidemia w/ pH 6.9>>very concerning

-couple amps of HCO3 stat (if no concern with ventilation, and assuming this is a metabolic acidosis/?AGMA (uremia, renal failure vs some toxic ingestion

-Central line placement>> and probably dialysis catheter for urgent/emergent dialysis

 

With a pH that low you can definitely have:

-vasoplegia/distributive shock

-also can have some element of cardiac dysfunction (ScvO2 off the central line/bedside echo)

 

Otherwise same as the above

-IVFs (barring physical exam findings c/w gross volume overload)

-vasopressors

-BS abx

-rewarming of the pt

 

 

 

Most of your questions I just addressed in Emed in my reply.

If i didnt state it in my original post, one of the last things we did was place IJ central line to get access for Vanc and CVP. As we were doing central line clinical pharms were setting up 2 amps of Bicarb.

 

Also, should be noted her EKG was normal. This case blew my mind. It seems the cases my preceptor is handing off to me are the crazy ones.

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11 minutes ago, LT_Oneal_PAC said:

Agree with Emed on all points. Lots of unknowns here to say what caused her shock, but definitely in shock. Still best to give her abx. I likely would have started her on norepi. Also don't see troponin, though this would likely be elevated anyway given her kidney function, but this could be ACS with shock, though agree with Emed likely metabolic. Would have thrown a US probe on her to look at heart function and IVC for fluid status. You couldn't get a temp because she can't even keep enough blood central to mount a core temp. 

Norepi was the pressor we were about to use. I guess the only reason we hadn't was because internal showed up and she had been admitted, even though still in ER.

 

I appreciate the replies everyone. This case, while stressful, has taught me a lot. Thanks to my preceptor as well for reinforcing my decision making. Great learning case.

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Patient was also placed in Bair Hugger warming system and still did not bring her temp up. However, seeing as we were continually intervening with her i'm not sure she was given much opportunity to warm up.

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Yeah definitely an interesting case!

 I'd want to see the pH and temp corrected to see if hypotension/shock improves. At least the lactate was not elevated which is somewhat reassuring. 

I think the only other thing that came to mind was considering intubation for this lady.

Sounds like she didn't need it (protecting her airway) etc, and the hx and scene you describe seems to imply her clinical condition was somewhat stable for the past 1-2hrs. (or at least somewhat responsive to interventions/not actively deteriorating).

But with a pH that low, and if was a metabolic acidosis: I would like to see her attempting to compensate respiratory wise with a low PCO2, if the the PCO2 was normal or elevated/or if there was any concern she was not stabilizing>>>intubation and hyperventilation at least to compensate and improve the pH somewhat.

 

 

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2 minutes ago, jk5142 said:

Yeah definitely an interesting case!

 I'd want to see the pH and temp corrected to see if hypotension/shock improves. At least the lactate was not elevated which is somewhat reassuring. 

I think the only other thing that came to mind was considering intubation for this lady.

Sounds like she didn't need it (protecting her airway) etc, and the hx and scene you describe seems to imply her clinical condition was somewhat stable for the past 1-2hrs. (or at least somewhat responsive to interventions/not actively deteriorating).

But with a pH that low, and if was a metabolic acidosis: I would like to see her attempting to compensate respiratory wise with a low PCO2, if the the PCO2 was normal or elevated/or if there was any concern she was not stabilizing>>>intubation and hyperventilation at least to compensate and improve the pH somewhat.

 

 

Again, I can't remember specific values, but I do remember everything on her ABGs being (L) or normal. I believe she was compensating. Her airway was fine, we did not think it needed to be protected. TBH, i'm not sure it even crossed our mind as she had good O2 sats, no labored breathing etc.

 

However, we do think she was lying on floor for much longer than 2 hours. Her condition did not occur suddenly. Also, take it as you may - for the entire time she was in our ER (~3 hours) the son who called EMS (or any other family for that matter)  showed up the the ER. It was our belief that she had been there for quite some time and was not cared after adequately. 

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5 minutes ago, MtoPA-S said:

Most of your questions I just addressed in Emed in my reply.

If i didnt state it in my original post, one of the last things we did was place IJ central line to get access for Vanc and CVP. As we were doing central line clinical pharms were setting up 2 amps of Bicarb.

 

Also, should be noted her EKG was normal. This case blew my mind. It seems the cases my preceptor is handing off to me are the crazy ones.

This is septic shock until proven otherwise. It smells of GNR sepsis. This is a relatively common presentation for someone with untreated sepsis for a while. Especially when found down.  would be willing to bet that the urine comes back dirty. 

A couple of things. When you have a pH like that and found down I would check a CK. You could have a superimposed rhabdo. It really wouldn't change management much except to go to dialysis early. 
On the subject of lack of tachycardia. Two answers either temp or the patient is on a beta blocker (fairly common depending on age). For that matter a certain subset of patients don't mount a tachycardic response no matter what. It probably has to do with the hyperdynamic nature of the heart in most sepsis. 

The way that I put this together is patient gets a UTI. Develops septic encephalopathy and shock. Goes down. Lays there an unknown amount of time and the goes into renal failure as well. 

The reason that the pressure didn't come up is you haven't filled up the tank yet. The CVP of 2 (while not generally used as a measurement any more) indicates the patient is profoundly intravascularly dry. It sometimes takes 5-6 liters until the patient is tanked up although this is controversial:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209309/

I generally give 30 ccs per kilo then put them on pressors. I also agree with dropping a probe to look at the IVC. That's a good way to guide further resuscitation. Also the Hgb is likely falsely high since the patient is probably hemoconcentrated. The patients BP is also probably artificially high due to temp. When you warm her up it will drop even more. 

I also disagree that you need SIRS plus a source to treat. In the new guidelines you have a QSOFA score of 2 which is enough to treat. Outside of known heart failure volume, pressors and early antibiotics are what improves survival. 

Overall it sounds like you did the right things. I would have gone to pressors earlier to get the pressure up while resuscitating but thats probably a style thing. 

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18 minutes ago, coloradopa said:

This is septic shock until proven otherwise. It smells of GNR sepsis. This is a relatively common presentation for someone with untreated sepsis for a while. Especially when found down.  would be willing to bet that the urine comes back dirty. 

A couple of things. When you have a pH like that and found down I would check a CK. You could have a superimposed rhabdo. It really wouldn't change management much except to go to dialysis early. 
On the subject of lack of tachycardia. Two answers either temp or the patient is on a beta blocker (fairly common depending on age). For that matter a certain subset of patients don't mount a tachycardic response no matter what. It probably has to do with the hyperdynamic nature of the heart in most sepsis. 

The way that I put this together is patient gets a UTI. Develops septic encephalopathy and shock. Goes down. Lays there an unknown amount of time and the goes into renal failure as well. 

The reason that the pressure didn't come up is you haven't filled up the tank yet. The CVP of 2 (while not generally used as a measurement any more) indicates the patient is profoundly intravascularly dry. It sometimes takes 5-6 liters until the patient is tanked up although this is controversial:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209309/

I generally give 30 ccs per kilo then put them on pressors. I also agree with dropping a probe to look at the IVC. That's a good way to guide further resuscitation. Also the Hgb is likely falsely high since the patient is probably hemoconcentrated. The patients BP is also probably artificially high due to temp. When you warm her up it will drop even more. 

I also disagree that you need SIRS plus a source to treat. In the new guidelines you have a QSOFA score of 2 which is enough to treat. Outside of known heart failure volume, pressors and early antibiotics are what improves survival. 

Overall it sounds like you did the right things. I would have gone to pressors earlier to get the pressure up while resuscitating but thats probably a style thing. 

Doing a CK was brought up, however not initially. I'm not sure if it was discussed during the consult between my preceptor and Internal, but after the consult my preceptor brought up to me that sometimes we would check a CK in these cases but there were more important things to worry about right now and it wouldn't change treatment plan (as you stated).

We were never able to get any urine while she was in our care. She literally had 0 urine to run. Nothing came out of catheter, she was then US'd, nothing in bladder. She wasn't producing a drop of urine.

As far as tachycardia - i brought your point up to my preceptor. I personally went through all her meds that came with her. There were no rate control meds in the grocery bag of ~8 scripts. It is possible that a blocker was left at home, however beta blockade as cause of her rate was on the radar.

Thanks for your points. Again, the case itself was a great learning experience as well as the stuff y'all are bringing up.

Edited by MtoPA-S

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TSH in the ER is helpful for 2 ddxs: thyroid storm presenting with ams, tachycardia, etc(these folks look like they are on meth) or the altered, poorly responsive , hypothermic pt who may have myxedema coma. I usually also get it for the worried well with "fatigue" just because it is in the ddx, but certainly less critical.

"lying on the floor for a long time" think rhabdo and get a CK.

great case. agree with the decision not to intubate if protecting her airway, gcs> 8 and Pco2< 50.

did the pt have a lot of peripheral edema , jvd, or other signs of fluid overload?

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22 minutes ago, coloradopa said:

I also disagree that you need SIRS plus a source to treat. In the new guidelines you have a QSOFA score of 2 which is enough to treat. Outside of known heart failure volume, pressors and early antibiotics are what improves survival. 

 

sorry if I was unclear. you don't need SIRS + a source to tx, you need it to make a final dx. I would have given abx and checked all the sepsis markers as well, but at the end of the day if they have neg sputum/urine/blood cultures, no cellulitis, nl diagnoistic studies (cxr, etc),  neg spinal fluid, etc then this is not sepsis. pretty hard to be this sick from sepsis with nl lactate and nl procalcitonin. remember , procalcitonin is fairly good for bacterial sepsis. lactate can be thrown off by lots of things like alcohol, dka, etc, but an elevated procalcitonin in the appropriate pt is hard to argue with.

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Possibly uremic pericarditis with tamponade as the reason for her low blood pressure, low heart rate and alter mental status. Remember any distended neck veins or friction rub? 

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I love your enthusiasm, but this format is more than just for torturing students, it can convey a lot of information succinctly.  For example, not one mention of her age, and you had a bag of meds but didn't tell us any history.

"a 22 y/o female with a history of..."

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5 hours ago, thinkertdm said:

I love your enthusiasm, but this format is more than just for torturing students, it can convey a lot of information succinctly.  For example, not one mention of her age, and you had a bag of meds but didn't tell us any history.

"a 22 y/o female with a history of..."

?

Initially I didn't read it closely and I thought it was a baby (my bias given I'm in peds), so I was thinking baby things in addition to sepsis.  I was thinking "why didn't the OP give me the birth history...".  I don't think whether the patient's mother was GBS positive matters at age 86 years :p.  It's funny how quickly you start thinking within your own box....

Edited by lkth487

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2 hours ago, thinkertdm said:

I love your enthusiasm, but this format is more than just for torturing students, it can convey a lot of information succinctly.  For example, not one mention of her age, and you had a bag of meds but didn't tell us any history.

"a 22 y/o female with a history of..."

Fair, I got a little excited and posted up quick before I had to leave.

69 year old AA female. I didn't list the meds because I personally did not right them down and I don't have access to the records at home. Ones I remember were lyrica 300, lisinopril 10, clonidine 0.1 and gabapentin 300. We didn't have PMH as this was the first time she was in our ER and there were no collateral to get any medical information from.

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5 minutes ago, MtoPA-S said:

Fair, I got a little excited and posted up quick before I had to leave.

69 year old AA female. I didn't list the meds because I personally did not right them down and I don't have access to the records at home. Ones I remember were lyrica 300, lisinopril 10, clonidine 0.1 and gabapentin 300. We didn't have PMH as this was the first time she was in our ER and there were no collateral to get any medical information from.

When you don't know, it's kind of a work in progress.  I'm going to guess (and this is a long shot): hypertension will be on there.  Neuropathy, possibly.  Both gabapentin AND lyrica?  Maybe...possible one was d/c and she didn't discard the bottle. 

Routine use of clonidine for bp drives me bonkers.

its on the beers list:

Beers Criteria: Clonidine is identified in the Beers Criteria as a potentially inappropriate medication in patients 65 years and older (independent of diagnosis or condition) due to high risk of CNS adverse effects and risk of bradycardia and orthostatic hypotension associated with central alpha blockers.

The  combination of both gabapentin and lyrica may increase the risk of cns depression, as will clonidine and the rest.

i am not an ed pa, so listen to those guys first.

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14 hours ago, EMEDPA said:

TSH in the ER is helpful for 2 ddxs: thyroid storm presenting with ams, tachycardia, etc(these folks look like they are on meth) or the altered, poorly responsive , hypothermic pt who may have myxedema coma. I usually also get it for the worried well with "fatigue" just because it is in the ddx, but certainly less critical.

"lying on the floor for a long time" think rhabdo and get a CK.

+1 for CK.

Also like TSH in new onset a-fib.

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22 hours ago, EMEDPA said:

sorry if I was unclear. you don't need SIRS + a source to tx, you need it to make a final dx. I would have given abx and checked all the sepsis markers as well, but at the end of the day if they have neg sputum/urine/blood cultures, no cellulitis, nl diagnoistic studies (cxr, etc),  neg spinal fluid, etc then this is not sepsis. pretty hard to be this sick from sepsis with nl lactate and nl procalcitonin. remember , procalcitonin is fairly good for bacterial sepsis. lactate can be thrown off by lots of things like alcohol, dka, etc, but an elevated procalcitonin in the appropriate pt is hard to argue with.

We don't have Procalcitonin so my experience with this is limited. However, 40% of sepsis is culture negative. The negative lactate is a bit of a puzzle but I have seen this in hypothermic patients. Once you resuscitate them and get them warmed up the lactate will probably go up. In our shop the patient would get 7 days of broad spectrum antibiotics unless they have something we could target. By the time the cultures come back negative the patient is either dead or getting better and nobody wants to stop abx. 

Edited by coloradopa
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Culture negative sepsis is the bane of my existence.  I hate it.  Not that I would do anything differently, but it's so unsatisfying.   We don't use procalcitonin as much in babies, though there are some studies that are coming out now showing it may be useful.  The problem is that oftentimes it's raised in things like RSV - I think it's made in the respiratory epithelium in times of stress? - so it can be elevated.  In Europe, they use procal as one of the criteria for working up a febrile infant.  But it hasn't really caught on here.

 

For the adults, do you guys use PCT to initiate abx or more to trend it to know when to stop abx?

Edited by lkth487

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CC PA here. I see these cases everyday. Just a couple of pearls for you:

 

this definitely wreaks of sepsis so definitely some fluids and ABX are warranted. However, Without better history and labs it’s hard to get a true sense of the differential. It sounds like she may have some comordities/chromic health issues (ESRD???) which would be helpful to know. Overdose? DKA? HHS? ACS unlikely without some EKG findings but agree that cardiac enzymes will be elevated regardless in a renal patient 

 

 With renal failure patients you should be resuscitating with balanced crystalloid as opposed to saline (SALT-ED and SMART trials) Also this patient needs dialysis ASAP. Call your local nephrologist!! A tip for obtaining central access in acute renal failure-put the Cvc in the left IJ or the femoral. Patient will likely need temp HD catheter placement and the catheters have better flow when placed in the right IJ.

 

also, I would have started this patient on pressor immediately when fluids werent doing much. “Filling the tank” only works when the tank isn’t leaking out everything you put in it into the interstitium. Give some fluid (30 cc/kg is COMPLETELY arbitrary and based no real data....also use ideal body weight) but if it’s isnt working start pressors! Pressors are not dangerous! Don’t keep pounding them with fluids. You can run pressor safely through a peripheral Line until you get central access so don’t delay. norepinephrine firstline followed by vasopressin and solucortef if she requires >15mcg/min norepinephrine.

 

as far as volume assessment, she is likely dry based on your description. However, looking at the IVC with US is essentially a coin flip when evaluating volume status. There are a ton of confounding physiologic variables that muddy your assessment. Also, a CVP of 2 is not abnormal and again is absolutely useless in managing shock.  A more valuable use of the ultrasound would be to look at the heart, kidneys, lungs and do a quick fast exam (rule out uremic pericarditis with effusion lol  ?)

 

Procalcitonin is useless in renal patients in my experience. Also, is it going to change your management of this patient? 

 

Agree with check a CK. Anyone found down needs a CK checked

 

Cultures only grow something out ~1/3 of the time so don’t stop ABX based on that. Also, qSOFA is garbage. It’s not very sensitive and wasn’t validated. The sepsis guidelines in general are useless.

 

Septic patients often have a mixed shock shock picture due to vasoplegia as well a cardiogenic component due septic cardiomyopathy...more common than you’d think!

 

a final thought on her airway. I would’ve have intubated this patient. If her pH is truly 6.9 and she’s not breathing hard or has a normal pCO2 that’s means she’s crapped out. Also when patients are in extremis work of breathing can use a significant chunk of your cardiac output. Alleviate that burden!! If you do decide to intubate, have pressors and fluids going when giving induction agents or you can write “death by glidescope” on her death certificate!

 

overall is an interesting case. Definitely enjoy managing these patients.

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On 10/6/2018 at 8:36 AM, newton9686 said:

Possibly uremic pericarditis with tamponade as the reason for her low blood pressure, low heart rate and alter mental status. Remember any distended neck veins or friction rub? 

HR 70s on presentation argues against acute pericardial tamponade or other causes of acute obstructive shock; however could have a chronic compensated obstructive process (quick POCUS to help evaluate undifferentiated shock may be helpful to r/o tamponade but studies shown that it doesn’t improve mortality...though there are many potential holes in this study)

https://journalfeed.org/article-a-day/2018/pocus-for-shock-dont-be-shoc-ed

Definitely agree given hypothermia (without environmental exposure factors) is most likely septic shock until proven otherwise.

TSH is extremely reasonable given hypothermia, hypotension, AMS... 

Procalcitonin has not been validated for screening for sepsis as it has a low sensitivity (~80%) in a pathology with a high mortality (~18-29% from the PROMISE , ARISE and PROCESS trials).  

It it has been validated for the de-escalation of antibiotics in patients that have a clinical picture not suggestive of a bacterial infection.  It also can be used to trend and can shorten the duration of inpatient antibiotics without mortality difference.  

In the inexperienced provider due to the low sensitivity it may sway clinical decision making against antibiotics which would be VERY worrisome.  

 

ICU/ER PA

Edited by polarbebe

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