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Code Blue: Just Trying Figure Out What Happened?

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by Binz Binz (New) New Nurse

Binz specializes in Med/Surg.

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PeakRN specializes in Adult and pediatric emergency and critical care.

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16 minutes ago, Susie2310 said:

The patient was diagnosed with sepsis/pneumonia  - the patient was severely hypotensive - BP was 70's systolic 50's diastolic at the start of care, with a fever, elevated lactate, elevated WBC, respiratory retractions, and the MD diagnosed pneumonia/sepsis from the CXR and the presenting symptoms and labs.  It also appears the patient had serious pre-existing heart problems, possibly heart failure.  There was a point raised earlier on the thread that it is not possible to know how much of the hypotension is sepsis related and how much is related to the presumed pre-existing cardiac problem.  

For me the questions are, given the patient's diagnosis of pneumonia/sepsis and what we know about the patient:  1) Why was the lasix given to this particular patient?  2) Why was fluid resuscitation apparently not given to this patient?

 

If the patient was hypotensive from their cardiac history then norepi is the wrong choice.

If the patient was hypotensive from septic shock then norepi is the wrong choice.

If a patient is in cardiac failure, giving lasix is not going to improve blood pressure.

If a patient is in septic shock, giving lasix is not going to improve blood pressure.

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MunoRN has 10 years experience as a RN and specializes in Critical Care.

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38 minutes ago, Susie2310 said:

The patient was diagnosed with sepsis/pneumonia  - the patient was severely hypotensive - BP was 70's systolic 50's diastolic at the start of care, with a fever, elevated lactate, elevated WBC, respiratory retractions, and the MD diagnosed pneumonia/sepsis from the CXR and the presenting symptoms and labs.  It also appears the patient had serious pre-existing heart problems, possibly heart failure.  There was a point raised earlier on the thread that it is not possible to know how much of the hypotension is sepsis related and how much is related to the presumed pre-existing cardiac problem.  

For me the questions are, given the patient's diagnosis of pneumonia/sepsis and what we know about the patient:  1) Why was the lasix given to this particular patient?  2) Why was fluid resuscitation apparently not given to this patient?

 

I think you added the fever part, that certainly would have contributed to a more clearly defined dx of sepsis.  The findings given aren't necessarily specific to sepsis, and most could also be explained by aseptic decompensated heart failure.  Although it does become a little trivial, since one of the main components of sepsis is circulating negative inotropes, so in the end what you're dealing with is fairly similar.  

If Norepi is being given, then it's very important that the patient have sufficient intravascular volume for the Norepi to work, which usually requires a volume status more on the fluid overloaded side.  Once-upon-a-time, Norephinephrine, ie levophed, was referred to as "leave-'em-dead" since it wasn't found to be all that effective, until it became more commonly understood that Norepi doesn't do much in a hypovolemic or even normovolemic patient.  So to diurese a patient on Norepi would mean the patient would have to have so much excessive intravascular volume that diuresing would still leave them somewhat fluid overloaded, the only obvious indication for that would be fulminant pulmonary edema, otherwise you're going to need that fluid volume to stay in there for the time being.  It may also have been that the patient was hyperkalemic, in which case lasix would be a good option but may requiring replacing the diuresed volume with IV fluids. 

A better option for dealing with fluid overload in this patient would be to look at cardiac output vs metabolic demand, either directly or by indirect indicators like an ScVO2, and give an inotrope if indicated, if that works sufficiently then the kidneys will get rid of that extra fluid volume when they deem it appropriate.  

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9 hours ago, MunoRN said:

I think you added the fever part, that certainly would have contributed to a more clearly defined dx of sepsis.  The findings given aren't necessarily specific to sepsis, and most could also be explained by aseptic decompensated heart failure.  Although it does become a little trivial, since one of the main components of sepsis is circulating negative inotropes, so in the end what you're dealing with is fairly similar.  

If Norepi is being given, then it's very important that the patient have sufficient intravascular volume for the Norepi to work, which usually requires a volume status more on the fluid overloaded side.  Once-upon-a-time, Norephinephrine, ie levophed, was referred to as "leave-'em-dead" since it wasn't found to be all that effective, until it became more commonly understood that Norepi doesn't do much in a hypovolemic or even normovolemic patient.  So to diurese a patient on Norepi would mean the patient would have to have so much excessive intravascular volume that diuresing would still leave them somewhat fluid overloaded, the only obvious indication for that would be fulminant pulmonary edema, otherwise you're going to need that fluid volume to stay in there for the time being.  It may also have been that the patient was hyperkalemic, in which case lasix would be a good option but may requiring replacing the diuresed volume with IV fluids. 

A better option for dealing with fluid overload in this patient would be to look at cardiac output vs metabolic demand, either directly or by indirect indicators like an ScVO2, and give an inotrope if indicated, if that works sufficiently then the kidneys will get rid of that extra fluid volume when they deem it appropriate.  

Muno, I didn't add the fever part.  It's right there on page 3 - a comment by the OP.  Here's the OP's quote from page 3 of the thread:

"She also had a fever. I'm sorry, I keep leaving details out. Initially when she started sweating, we thought it was either due to her fever breaking or BG being low but it may  have a sign of impending cardiac arrest??"

So pneumonia/sepsis is a clearly legitimate diagnosis based on the CXR, elevated lactate, elevated WBC, severe hypotension, FEVER, respiratory retractions.  We know that elevated lactate by itself is not a specific indication of sepsis.

Your explanation about the use of Norepinephrine makes sense if we presume the patient was so fluid overloaded that using Lasix would still leave them somewhat fluid overloaded.  Am I correctly understanding you are saying that fluid resuscitation for sepsis/severe sepsis would not be necessary in this situation and that norepinephrine could be given without prior fluid resuscitation?

Your last paragraph re the ScVO2 monitoring may be appropriate to the ICU but the patient was in the ED.  Also, a patient with serious heart problems is likely to have renal problems also so I don't see that we can say that the kidneys will just get rid of the extra fluid when they deem it appropriate.

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MunoRN has 10 years experience as a RN and specializes in Critical Care.

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7 hours ago, Susie2310 said:

Muno, I didn't add the fever part.  It's right there on page 3 - a comment by the OP.  Here's the OP's quote from page 3 of the thread:

"She also had a fever. I'm sorry, I keep leaving details out. Initially when she started sweating, we thought it was either due to her fever breaking or BG being low but it may  have a sign of impending cardiac arrest??"

So pneumonia/sepsis is a clearly legitimate diagnosis based on the CXR, elevated lactate, elevated WBC, severe hypotension, FEVER, respiratory retractions.  We know that elevated lactate by itself is not a specific indication of sepsis.

Your explanation about the use of Norepinephrine makes sense if we presume the patient was so fluid overloaded that using Lasix would still leave them somewhat fluid overloaded.  Am I correctly understanding you are saying that fluid resuscitation for sepsis/severe sepsis would not be necessary in this situation and that norepinephrine could be given without prior fluid resuscitation?

Your last paragraph re the ScVO2 monitoring may be appropriate to the ICU but the patient was in the ED.  Also, a patient with serious heart problems is likely to have renal problems also so I don't see that we can say that the kidneys will just get rid of the extra fluid when they deem it appropriate.

Yes, I apologize.

If the patient already has more than sufficient intravascular volume to facilitate treatment, ie if the tank is already overflowing, then there wouldn't be much benefit to additional fluids.  Most patients require fluid resuscitation to adequately fill the tank, in other patients their chronic fluid overload becomes therapeutic.  If the fluids there but it's mainly third spaced, then albumin or other osmotic could pull that fluid into the intravascular space.

Central lines are not uncommon in the ED, and an ScVO2 can be run off of a sample from a central line as a venous gas.  

If the patient is a completely anuric dialysis patient then no, a boost in CO wouldn't do anything, but poorly perfused kidneys can still respond to the normal feedback mechanisms for maintaining fluid balance to at least some degree.

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AN Admin Team has 50+ years experience.

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Please note posts have been edited and/or removed.

Please do not engage on a personal level as this derails the topic.

Thank you.

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Were antibiotics started? 

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Binz specializes in Med/Surg.

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*UPDATE*

I went back and looked at the labs from the day this happened. Her WBC was 8 and lactate was 2.5. ANC was also not elevated. Creatinine was over 6.

She eventually had to be started on CRRT and is still on an epi drip in the ICU. 

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MunoRN has 10 years experience as a RN and specializes in Critical Care.

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1 hour ago, Binz said:

*UPDATE*

I went back and looked at the labs from the day this happened. Her WBC was 8 and lactate was 2.5. ANC was also not elevated. Creatinine was over 6.

She eventually had to be started on CRRT and is still on an epi drip in the ICU. 

That's a normal WBC level, a lactate of 2.5 is mildly elevated but not necessarily abnormal in a patient in acute renal failure since the kidneys play an important role in lactic acid excretion which accounts for about a quarter of total lactate removal.  

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1 hour ago, MunoRN said:

That's a normal WBC level, a lactate of 2.5 is mildly elevated but not necessarily abnormal in a patient in acute renal failure since the kidneys play an important role in lactic acid excretion which accounts for about a quarter of total lactate removal.  

I don't know that I would go so far as to say that an elevated lactic acid level is normal for patients in renal failure. Metabolic acidosis driven by decreased bicarb production or buildup of other acids, sure. But the numbers I've read normally attribute only 10% to 15% of lactic acid clearance to the kidneys; and more offhand, I've treated a ton of patients in renal failure, sometimes quite severe, and I haven't observed an elevated lactate level to be a normal part of the presentation.

Just saying that if a patient in my care who presented with uncomplicated renal failure was found also to have an elevated lactic acid level, I'd be looking for additional problems/causes to explain it. Attributing it to the loss of maybe 10% or 15% of a patient's normal clearance (even at only 2.5) seems a likely way to miss a part of the clinical picture.

Hope my nitpicking doesn't offend. 

Edited by Cowboyardee
Clarity

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MunoRN has 10 years experience as a RN and specializes in Critical Care.

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31 minutes ago, Cowboyardee said:

I don't know that I would go so far as to say that an elevated lactic acid level is normal for patients in renal failure. Metabolic acidosis driven by decreased bicarb production or buildup of other acids, sure. But the numbers I've read normally attribute only 10% to 15% of lactic acid clearance to the kidneys; and more offhand, I've treated a ton of patients in renal failure, sometimes quite severe, and I haven't observed an elevated lactate level to be a normal part of the presentation.

Just saying that if a patient in my care who presented with uncomplicated renal failure was found also to have an elevated lactic acid level, I'd be looking for additional problems/causes to explain it. Attributing it to the loss of maybe 10% or 15% of a patient's normal clearance (even at only 2.5) seems a likely way to miss a part of the clinical picture.

Hope my nitpicking doesn't offend. 

That's a fair point since renal metabolism accounts for about 15% of total lactate removal, although the kidneys both metabolize and directly excrete lactate.  While the rate of lactate metabolism is fairly stead at around 15%, the rate of excretion varies based on the level of circulating lactate, and you're right that at a level that low, the rate of excretion likely doesn't reach 10-15% so it wouldn't result in a total removal rate of 25-30%.  From what I can find, that level of renal lactate removal only occurs at significantly higher levels. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC137458/

You would certainly still look for explanations for a mildly elevated lactate level in a renal patient, although it should be considered that an impaired ability to clear lactic acid is magnified by an increase in lactic acid production, such in the setting of an EF of 20%.

Not offended at all, you make a good point.

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The patient was diagnosed with pneumonia/sepsis from the CXR and symptoms which were tachycardia, fever, severe hypotension with systolic BP in the 70's, diastolic BP in the 50's, elevated lactate which we were just told was 2.5, elevated WBC which we were just told was 8 which was in the normal range but we don't know what the differential was.  This still looks like the original diagnosis of sepsis (severe) to me which resulted in acute renal failure (we're not told the patient had any pre-existing kidney problems, although the pre-existing EF of 20 appears to indicate that pre-existing renal problems are likely and it appears the patient had serious heart problems - pre-existing EF of 20 and history of A-Fib).  So to me since the OP's update it looks like the patient has severe sepsis/septic shock with acute on chronic renal failure, possibly complicated by heart failure.  As I'm seeing it, the elevated lactate is due to the sepsis.

Edited by Susie2310

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kbrn2002 has 25 years experience as a ADN, RN and specializes in Geriatrics.

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My first though when you said the sudden change happened on the toilet is the patient had a vaso-vagal response.  With an already compromised cardiopulmonary system it wouldn't take as much to trigger that while toileting. 

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