Necessity of Lactate for every person with a potential infection

[thegenius]

I've been thinking about this a lot over the past several months.

Where I work, if a patient has an infection or potentially an infection, it's almost reflexive to order a lactate. This is irrespective of the patient history, vital signs, or physical exam.

For instance, we (meaning the ER docs) get lactates on the following
- routine leg cellulitis of a middle aged patient with no PMH and normal vitals signs.
- cough with temp 99.6, everything else on H&P is OK
- a butt abscess and HR 110, BP is 140/90.

we get lactates all the time. I think it's terrible

What good is an elevated lactate if someone's blood pressure is normal or high?
Is there a belief that the patient with a wound infection and a BP of 150/90, who has a lactate of 3.6, will benefit from getting 30 ml / kg? Or even any fluid? Is the idea that we should perfuse the organs even more than what a MAP of 100 is already doing?

My understanding of CC medicine and treatment of true septic shock is you give fluids and vasopressors until you have a normalish MAP and maybe optimize a few other things like UOP, CVP, pO2. Then, after that...if the lactate is still elevated and not coming down, there isn't much else to do. Perhaps there is microcirculatory dysfunction at the organ cellular level which cannot be fixed. You can perfuse organs all you want, but if there is organ dysfunction at a cellular level in the capillaries, then well I guess you just have to wait for the body to heal.

I get so many patients with normal vital signs, or maybe a HR 108 and BP 145/80, who have lactates between 2-4. Maybe they have a leukocytosis, maybe not. But it doesn't matter...

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[Rekt]

Sounds like an incredibly poor practice decision with no utility being ordered like that.

 

[thegenius]

Yea what I meant from

I get so many patients with normal vital signs, or maybe a HR 108 and BP 145/80, who have lactates between 2-4. Maybe they have a leukocytosis, maybe not. But it doesn't matter...

is that initial orders are placed usually by mid-level, sometimes even an MD, and I have to deal with these lactates. Sometimes the hospitalist wants it well after the pt has been in the ED, received treatment and prior to admission. So frustrating

 

[gamerEMdoc]

Indication creep. These definitions of sepsis sound good, but there's in the end they just are too broad. And on top of that, no one can agree on a definition for sepsis, and people use different definitions, which make all of this way more difficult. The older definition of if you met SIRS + Source back in the day, you were supposed to screen with a lactate if you met that, which was pretty simple. Which sounds good until you realize you could order a lactate on every strep throat you seen. I actually had an attending in residency that made me get a lactate 10 years ago on a strep throat. Not kidding.

Sepsis 3 definitions/recommendations state the ED should use a QSOFA score to determine who needs to get screened for tissue hyperperfusion. If you have 2 out of 3 of RR > 22, GCS < 15, or SBP < 100, then you are qsofa positive. Which is much harder to hit, so that would mean you would do less "screening lactates". I like that. But common sense would have to prevail. I mean if I had a 35 year old with a SBP of 70 and a fever of 104, but their RR was 16 and their GCS was 15, I'd still get a lactate and admit them to the unit.

 

[southerndoc]

Have you never seen a patient with a BP of 160 and a lactate of 5? They tank precipitously when they start to decompensate.

A person with a lactate of 3.6 and a BP of 150 doesn't need a 30 mL/kg bolus. You don't understand the severe sepsis guidelines. A patient meeting severe sepsis just needs cultures, repeat lactate, and broad spectrum antibiotics according to SEP-1 (they need some fluid according to MIPS, but that's at the discretion of the provider). Severe sepsis only needs a bolus if they have a SBP <90 or MAP <65 at any time (including pre-hospital).

Septic shock is refractory hypotension after 30 mL/kg bolus OR lactate >4. You can have septic shock with a normal blood pressure. These people almost always tank if they don't get fluids fast enough.

Whether fluids help or harm is another question. CMS believes in the sink or swim philosophy. Either sink your way to the grave or swim like a madman trying to keep from drowning. One academic center is currently randomizing hypotensive septic patients to 30 mL/kg or 70 mL/kg bolus to see if they can keep patients off pressors. Sometimes pressors are not a bad thing.

We have coupled our blood cultures with lactate orders. Meaning you cannot order blood cultures without a lactate q6 hrs x 3 being reflexively added. The nurse can cancel remaining lactates once a lactate is <2. We have identified a ton of septic patients with this, but like anything, we have also identified many patients who did not have sepsis but who received aggressive treatment.

Missing sepsis has major consequences for the provider (MIPS quality data) and the hospital (lost revenue). A DRG for a pneumonia admission may reimburse the hospital $6,500 for the entire admission (whether the stay is 24 hours or 30 days) while a sepsis DRG would reimburse at $25,000. This isn't even mentioning the fact that poor SEP-1 performance will cost hospitals Medicare revenue by reduced reimbursements for all admissions and not just sepsis admissions.

Early identification of sepsis saves lives. Like with our trauma system, you have to allow an overtriage. The 30 mL/kg bolus is overkill IMO, but unfortunately it's here to stay.

 

[GonnaBeADoc2222]

The utility of a lactic acid in a normotensive well appearing patient is so that the hospitalist can refuse admission.

 

[GeneralVeers]

I see my midlevels (and most docs) ordering lactic and full septic workup on every febrile young person who comes in with a bit of tachycardia. I usually give them tylenol/motrin, treat any appropriate infection with PO antibiotics and send them home. Seriously, what is the incidence of true blood culture positive sepsis in healthy patients under 40? My guess is close to zero.

 

[RoyBasch]

We have a similar situation, any patient that flags for sepsis requires a lactate be ordered as part of a "sepsis bundle" and failure to do so is recorded in separate sepsis metrics.

I have long accepted that in the majority of these cases the lactate is not helpful and does not guide management in any meaningful way. However, I am a mere rank and file physician, it is not up to me to make these policy level decisions. Thus I toe the line.

I think the there are some situations where a lactate can be helpful.

I think for patient's who are frankly in shock (lets say HR 130, BP 70/40) the first lactate is not very helpful (you know the patient is in shock already); however, a repeat lactate ordered by the inpatient team can give them an idea how the patient is responding to resuscitation and can help guide downstream decision making. The trend can be helpful and giving the critical care team a starting point I think is good form.

Another situation is a patient with compensated shock who is on the precipice of hemodynamic collapse. This is usually younger patients without too many comorbidities who may be severely septic but appear well at the initial evaluation. They may be tachycardic but normotensive. A low lactate can be somewhat reassuring. A high lactate can be an important warning sign which can help guide disposition and trigger further fluid resuscitation.

 

[deleted547339]

We have a similar situation, any patient that flags for sepsis requires a lactate be ordered as part of a "sepsis bundle" and failure to do so is recorded in separate sepsis metrics.

I have long accepted that in the majority of these cases the lactate is not helpful and does not guide management in any meaningful way. However, I am a mere rank and file physician, it is not up to me to make these policy level decisions. Thus I toe the line.

I think the there are some situations where a lactate can be helpful.

I think for patient's who are frankly in shock (lets say HR 130, BP 70/40) the first lactate is not very helpful (you know the patient is in shock already); however, a repeat lactate ordered by the inpatient team can give them an idea how the patient is responding to resuscitation and can help guide downstream decision making. The trend can be helpful and giving the critical care team a starting point I think is good form.

Another situation is a patient with compensated shock who is on the precipice of hemodynamic collapse. This is usually younger patients without too many comorbidities who may be severely septic but appear well at the initial evaluation. They may be tachycardic but normotensive. A low lactate can be somewhat reassuring. A high lactate can be an important warning sign which can help guide disposition and trigger further fluid resuscitation.

Great username. That is all.

 

[RoyBasch]

Great username. That is all.

Thanks, I was surprised it wasn't already taken.

 

[lymphocyte]

no one can agree on a definition for sepsis, and people use different definitions, which make all of this way more difficult.

Sepsis 3 definitions/recommendations state the ED should use a QSOFA score to determine who needs to get screened for tissue hyperperfusion.

1. A lot of people agree on a definition of sepsis. That's the whole point of Sepsis 3, which is a widely-adopted consensus definition. People who disagree with it are on the margin of medicine (for better or for worse).

2. qSOFA is NOT meant to be used as a screening tool. It is a prognostic tool validated in the ED setting only.

3. Lactate is generally not a marker of tissue perfusion (except in extremis.) This is a myth that needs to die. It's much more often a product of accelerated glycolysis from an endogenous catecholamine response to stress or shock. Hence, people can have occult shock with a "normal blood pressure" that is only sustained by a very robust endogenous response -- these people can crump pretty quick, especially the young ones.

4. Getting a lactate based on SIRS has been studied, and there's a well-established mortality risk independent of the associated vital signs. I think it's a very fair thing to get in a protocolized fashion.

Freund Y, et al. Prognostic Accuracy of Sepsis-3 Criteria for In-Hospital Mortality Among Patients With Suspected Infection Presenting to the Emergency Department. JAMA. 2017;317(3):301-308.

Garcia-Alvarez, Marik PE, Bellomo R. Sepsis-associated hyperlactatemia. Critical Care. 2014; 18: 503.

Shetty AL, Thompson K, Byth K, et al. Serum lactate cut-offs as risk stratification tool for in-hospital adverse outcomes in emergency department patients screened for suspected sepsis. BMJ Open. 2018;8(1):e015492.

 

[gamerEMdoc]

1. A lot of people agree on a definition of sepsis. That's the whole point of Sepsis 3, which is a widely-adopted consensus definition. People who disagree with it are on the margin of medicine (for better or for worse).

2. qSOFA is NOT meant to be used as a screening tool. It is a prognostic tool validated in the ED setting only.

3. Lactate is generally not a marker of tissue perfusion (except in extremis.) This is a myth that needs to die. It's much more often a product of accelerated glycolysis from an endogenous catecholamine response to stress or shock. Hence, people can have occult shock with a "normal blood pressure" that is only sustained by a very robust endogenous response -- these people can crump pretty quick, especially the young ones.

4. Getting a lactate based on SIRS has been studied, and there's a well-established mortality risk independent of the associated vital signs. I think it's a very fair thing to get in a protocolized fashion.

Freund Y, et al. Prognostic Accuracy of Sepsis-3 Criteria for In-Hospital Mortality Among Patients With Suspected Infection Presenting to the Emergency Department. JAMA. 2017;317(3):301-308.

Garcia-Alvarez, Marik PE, Bellomo R. Sepsis-associated hyperlactatemia. Critical Care. 2014; 18: 503.

Shetty AL, Thompson K, Byth K, et al. Serum lactate cut-offs as risk stratification tool for in-hospital adverse outcomes in emergency department patients screened for suspected sepsis. BMJ Open. 2018;8(1):e015492.

Yeah my wording wasn't the best.

What I meant by no one can agree on the definition, I guess I meant that the definition is ever evolving and I still hear admitting docs refer to SIRS + source as sepsis. The Sepsis 3 recommendations specificly cited too many definitions of sepsis, and stated it as one of their reasons for a new definition. They basically said SIRS/source definition was useless in defining sepsis. So yes, they did clarify one definition of sepsis now which is nice. However, their definition is vague and doesn't exactly define what sepsis is in the ED. The Sepsis 3 definition may be widely adopted, but it isn't clear at all on how sespsis is definited anywhere but in the ICU. They define sepsis "as life-threatening organ dysfunction caused by a dysregulated host response to infection. For clinical operationalization, organ dysfunction can be represented by an increase in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with an in-hospital mortality greater than 10%". Ok. But they say that the SOFA score is to be used in patients admitted to the ICU and that the all the data in the score may not be available in the ED (and we should use qsofa as a predictor of who will get worse, but don't say we are to use qSOFA to define sepsis). Ok. So if we don't use SOFA scores in the ED, and that's how you are to determine organ dysfunction which is the definition of sepsis, so then we can't diagnose sepsis in the ED?

I don't know, I just think the definition in Sepsis 3 is too vague. I get that they recommended against using the SIRS/Source definition, which I agree was too easy to hit. But now its so vague everyone gets sepsis screening with a sepsis bundle because no one knows precisely how Sepsis is defined in the ED setting.

I definitely misspoke in calling qSOFA a screening tool, I didn't mean it that way. I meant its a score to screen who is at risk for higher mortality, but you are correct, its not meant to guide who is or isn't supposed to be screened for sepsis. It just prognosticates who is going to have a bad outcome. Logically too me, that would mean those are the ones who should have sepsis bundles applied, but I realize that isn't the point of the qSOFA, it's merely meant to predict who is at highest risk to die.

This is all just so ambiguous to me. When you look at the surviving sepsis recommendations, their entire section on screening for sepsis doesn't even mention who to screen. It's all about having bundles for screening and why bundles are useful. But nowhere do they address the basic question of who we should be screening. Maybe that should be the SIRS/Source group that was previously defined as sepsis, which Sepsis 3 says isn't sepsis. Maybe that should be called the "maybe sepsis?" or "sepsis screening" group in the Sepsis 4 definitions. Haha.

 

[jdh71]

The bundles too often make us all do the wrong things at times but I think there is a lot of utility in getting the lactate. But it’s clearly not some kind of “if this, then THAT” phenomenon and requires us to THINK about the value and the clinical context. I know letting physicians think keeps administrators up at night . . .

I liked the joke that it allowed hospitalists to block. That is funny. Because it’s true. Though I’m a guy who generally sides on better safe than sorry and I’ll do that “soft ICU” admit with 60 year old four chronic problems and cellulitis with a lactic of 3.8 and a normal range BP.

 

[RoyBasch]

The bundles too often make us all do the wrong things at times but I think there is a lot of utility in getting the lactate. But it’s clearly not some kind of “if this, then THAT” phenomenon and requires us to THINK about the value and the clinical context. I know letting physicians think keeps administrators up at night . . .

I agree with this. Lactates are like d dimers, can be helpful; however, require quite a bit of interpretation of the lab value and the clinical context to be maximally effective.

Unfortunately this part of it has been completely steam-rolled by the clip-board nurses and their metric mania mandate laid out by administration.

 

[jdh71]

I agree with this. Lactates are like d dimers, can be helpful; however, require quite a bit of interpretation of the lab value and the clinical context to be maximally effective.

Unfortunately this part of it has been completely steam-rolled by the clip-board nurses and their metric mania mandate laid out by administration.

****ing suits.

We’ve taken to documenting our rationale for not dumping in 30ccs/kg right after we’ve talked about it during the admit conversation. Both myself and the EP. So far this has been deemed acceptable.

 

[SamtheWise]

Effect on Septic Shock Mortality of Resuscitation Targeting Peripheral Perfusion vs Serum Lactate Levels

This randomized trial compares the effects of resuscitation strategies targeting normalization of capillary refill time vs normalization or decrease of serum lactate levels on 28-day mortality among patients with septic shock.

jamanetwork.com

Lactates are dumb because they lead to us blindly giving 30 ml/Kg of cold coagulopathic respiratory distress in a bag.

Edit: To expand, yes I order them because it's what we do, but if a patient is mentating, urinating, has a normal BP/HR and has appropriate antibiotic coverage for their infectious source, does it matter in any way what the lactate is?

 

[deleted109597]

This argument is remarkably similar to the door to antibiotics argument for pneumonia that was had decades ago. The government is incredibly poor at what they choose to use as a stick, but they do it in a reactionary manner due to public outcry. And because doctors don't fight back hard enough, everyone suffers.
Be an advocate. Tell your rep, not a sympathetic group of doctors.

 

[TooMuchResearch]

Me: "D*MN it, who ordered a lactate on this guy with DKA?"

 

[emergentmd]

Lactic, Sepsis order sets and protocols are a bunch of Crock. Whoever shows me another study that exalts how many lives they save can pound sand.

Do you think the hospitals care about patient outcome/morbidity? The only thing they care about is $$$$ which is why sepsis, Door to greet, wait times, patient satisfaction, pain control are harped on. Do you remember how vigilant they were with Pneumonia and early IV abx 5 yrs ago? Ever wonder why this metric doesn't matter any more; follow the money.

If insurance companies paid 10 times more for door to sutures placed under 60 minutes, I bet there would be a SUTURE alert, Suture team.
If insurance paid 10x more for PICC lines, I bet there would be 20 PICC line teams doing all IV access.
If insurance paid 10X more for ER docs to intubate surgery patients, I bet all intubation would be done by the ER docs

We do more harm putting everything that walks around with a fever and tachycardia into the sepsis protocols than help the sliver that really needs early ABX and IV fluids.

We all talk about the risking cost of healthcare and then turn around Putting IVs, starting broad spectrum ABX, starting IV fluids when all they need is a dose of motrin.

How on earth can anyone justify the same patient going to their PCPs office and getting a note for work with a diagnosis of viral syndrome while the same patient gets a 10K septic ER workup?

Its a wonderful world where we put 99% of viral syndrome patients into a septic workup to possible improve the outcome of 1% when the MD would have given them fluids, early ABX b/c we can tell who really is septic.

 

[southerndoc]

When comparing US and Australia data (where there is not so much emphasis on IV fluid resuscitation), mortality rates have improved more in Australia than the US. The real benefit to sepsis alerts is earlier antibiotics, which have been shown definitively that earlier administration improves mortality.

One large academic center is about to start (or perhaps already has started) randomizing patients to receive a 30 mL/kg bolus or a 70 mL/kg bolus in order to keep patients off pressors. Sometimes pressors are not a bad thing. I'm sure the intubation rate for those receiving a 70 mL/kg bolus over an hour will be significantly higher than their controls. Which is more harmful? Pressors or inducing respiratory failure?

 

[RoyBasch]

70 mL/kg bolus in order to keep patients off pressors. Sometimes pressors are not a bad thing.

I don't understand how even a patient without contraindication to volume (no heart failure, liver failure, renal failure, etc.) can tolerate that much volume. You are going to be intubating people with normal hearts and kidneys.

I think if a patient really needs 7L of fluid to maintain blood pressure, its not purely a volume problem, there must be a component of vasodilatation and capilary leak. Sure you gotta fill the tank before you step on the gas, but I think if you are just dumping fluid into leaky capilary beds, you aren't really targeting the actual etiology of the pathology at it's core. I think pressors are a more physiologically sound treatment here as you are directing your treatment a the pathology.

That being said, there are many things that "make sense" physiologically that don't pan out clinically for some underlying reason not yet known. So maybe they are right to give 7L and we'll see the result of their study. That being said, it sounds nuts.

 

[emergentmd]

Bunch of Crock. Blah Blah Sepsis. Blah Blah 30ml/kg or you will fall out. Blah Blah Sepsis protocol with 30ml/kg order or the sepsis RN will come down on you.

Blah Blah We don't care if you give it as a bolus or run it over hours

Me: 30ml/kg run at 150/hr. Great Job Doc

WTF

 

[TooMuchResearch]

Me: "But I wrote in my note that I didn't suspect infection."

Sepsis administrator: "Provider, the patient had an infection as identified by the hospitalist three days after admission."

 

[thegenius]

Lactic, Sepsis order sets and protocols are a bunch of Crock. Whoever shows me another study that exalts how many lives they save can pound sand.

Do you think the hospitals care about patient outcome/morbidity? The only thing they care about is $$$$ which is why sepsis, Door to greet, wait times, patient satisfaction, pain control are harped on. Do you remember how vigilant they were with Pneumonia and early IV abx 5 yrs ago? Ever wonder why this metric doesn't matter any more; follow the money.

If insurance companies paid 10 times more for door to sutures placed under 60 minutes, I bet there would be a SUTURE alert, Suture team.
If insurance paid 10x more for PICC lines, I bet there would be 20 PICC line teams doing all IV access.
If insurance paid 10X more for ER docs to intubate surgery patients, I bet all intubation would be done by the ER docs

We do more harm putting everything that walks around with a fever and tachycardia into the sepsis protocols than help the sliver that really needs early ABX and IV fluids.

We all talk about the risking cost of healthcare and then turn around Putting IVs, starting broad spectrum ABX, starting IV fluids when all they need is a dose of motrin.

How on earth can anyone justify the same patient going to their PCPs office and getting a note for work with a diagnosis of viral syndrome while the same patient gets a 10K septic ER workup?

Its a wonderful world where we put 99% of viral syndrome patients into a septic workup to possible improve the outcome of 1% when the MD would have given them fluids, early ABX b/c we can tell who really is septic.

Love it! Need more pithy comments like this

 

[SpacemanSpifff]

I don't understand how even a patient without contraindication to volume (no heart failure, liver failure, renal failure, etc.) can tolerate that much volume. You are going to be intubating people with normal hearts and kidneys.

I think if a patient really needs 7L of fluid to maintain blood pressure, its not purely a volume problem, there must be a component of vasodilatation and capilary leak. Sure you gotta fill the tank before you step on the gas, but I think if you are just dumping fluid into leaky capilary beds, you aren't really targeting the actual etiology of the pathology at it's core. I think pressors are a more physiologically sound treatment here as you are directing your treatment a the pathology.

That being said, there are many things that "make sense" physiologically that don't pan out clinically for some underlying reason not yet known. So maybe they are right to give 7L and we'll see the result of their study. That being said, it sounds nuts.

Agreed. We already know what happens when you flood these patients -- this was sepsis care prior to 2010 when people routinely got 5L+ in the ED alone

One large academic center is about to start (or perhaps already has started) randomizing patients to receive a 30 mL/kg bolus or a 70 mL/kg bolus in order to keep patients off pressors. Sometimes pressors are not a bad thing. I'm sure the intubation rate for those receiving a 70 mL/kg bolus over an hour will be significantly higher than their controls. Which is more harmful? Pressors or inducing respiratory failure?

I hear some intensivists say, "I would much rather deal with a vent than a patient who is in shock from under-resuscitation". I'm not sure the tradeoff is that simple. Extravascular lung water outside of respiratory failure, renal failure from venous congestion - there are other issues with over aggressive fluid resuscitation. I'm much more interested in the CLOVERS results, which looks at a fluid restrictive strategy with early vasopressors versus a more standardized fluids with pressors if needed route. If the underlying process of septic shock is vasoplegia, fluids don't address that.

 

[MechEDoc]

I see my midlevels (and most docs) ordering lactic and full septic workup on every febrile young person who comes in with a bit of tachycardia. I usually give them tylenol/motrin, treat any appropriate infection with PO antibiotics and send them home. Seriously, what is the incidence of true blood culture positive sepsis in healthy patients under 40? My guess is close to zero.

Close but not zero. But I don't think that lactate alone will find those patients. Good gestalt, repeat evaluation, luck, and more luck. I know of a young healthy physician who died of strep septicemia that was missed at a "good" ER.

I think it's mostly BS. But if the gov't wants to ram a bunch of BS down my throat, I'm happy to return the favor. If I'm planning on admitting them, I'll chart the patient as meeting CMS sepsis guidelines and bill for critical care time.

 

[thegenius]

We all know the problem with starting pressors early in these septic patients is the time it takes to place a central line. If we could start pressors peripherally and let them run for hours, and not have the hospital get mad at us, not potentially violating hospital policy, not hearing the wrath of our lazy intensivists who don't want to put one in either....we would run press all the time.

We have all been in this situation. Your 75 yo frail man with urosepsis, initial BP 88/50, lactate 4.2. You give him 2L, zosyn and just pray his SBP > 90 or MAP > 65.

Initially his BP goes to 100/70. Disaster averted. But 1.5 hours later, after 2L and zosyn are in, his BP is 81/53. He doesn't need to be intubated, but is squirming around and it would be a real pain in the arse to put a central line in. You may have to give him ketamine just to sedate him to put one in.

So you pray that the 3L of fluid keeps his MAP just high enough to sent to the ICU.

 

[southerndoc]

We give peripheral pressors (low dose) for a short period of time (<30 minutes). We place CVL's like crazy though. Usually we give pressors peripherally as we're inserting the CVL.

 

[TooMuchResearch]

We run peripheral pressors and call the PICC team to place in the ED or ICU.

Or if I'm rural, I run peripheral and ship unless it's a) slow as **** and b) the receiving center tells me to hold them for awhile because the "bed" isn't ready yet.

 

[Siggy]

We all know the problem with starting pressors early in these septic patients is the time it takes to place a central line. If we could start pressors peripherally and let them run for hours, and not have the hospital get mad at us, not potentially violating hospital policy, not hearing the wrath of our lazy intensivists who don't want to put one in either....we would run press all the time.

Did you really just call intensivists lazy while justifying not providing the care the patient needs for an emergent condition who is in an emergency department while being cared for by an emergency physician?

 

[MechEDoc]

Did you really just call intensivists lazy while justifying not providing the care the patient needs for an emergent condition who is in an emergency department while being cared for by an emergency physician?

Yes, but sometimes they are. A patient who doesn't yet need a line (and likely won't for several hours) won't be accepted into the ICU until a central line is placed. Meanwhile you're single coverage and the department is blowing up. The idea that a hospital would come together to take care of patients doesn't always happen. Everyone knows about the hospitalist that one can't admit without one or more delaying (and unindicated) interventions or studies that put the patient's disposition well beyond the end of the hospitalist's shift.

 

[GeneralVeers]

We have all been in this situation. Your 75 yo frail man with urosepsis, initial BP 88/50, lactate 4.2. You give him 2L, zosyn and just pray his SBP > 90 or MAP > 65.

Initially his BP goes to 100/70. Disaster averted. But 1.5 hours later, after 2L and zosyn are in, his BP is 81/53. He doesn't need to be intubated, but is squirming around and it would be a real pain in the arse to put a central line i

Yes, but sometimes they are. A patient who doesn't yet need a line (and likely won't for several hours) won't be accepted into the ICU until a central line is placed. Meanwhile you're single coverage and the department is blowing up. The idea that a hospital would come together to take care of patients doesn't always happen. Everyone knows about the hospitalist that one can't admit without one or more delaying (and unindicated) interventions or studies that put the patient's disposition well beyond the end of the hospitalist's shift.

I agree with you. I generally work mid/night and am often single coverage. I don't put in lines on stable patients. It's not a life-saving procedure, and can wait until morning for a PICC. I've seen ED docs allow their departments to grind to a halt because they are single coverage and putting in lines on patients who really don't need them. Just because a patient is going to the ICU doesn't mean they need a line. If they don't have refractory hypotension, and have good IV access this really can wait.

 

[deleted109597]

If they don't have refractory hypotension, and have good IV access this really can wait.

Even if they do have refractory hypotension, an 18 ga is better than a TLC.

Notwithstanding the fact that I've had the ICU tell me that a patient was too unstable for the ICU. Whatever that means.

 

[TooMuchResearch]

Even if they do have refractory hypotension, an 18 ga is better than a TLC.

Notwithstanding the fact that I've had the ICU tell me that a patient was too unstable for the ICU. Whatever that means.

What in the fork does that mean? Hopefully you then offered to transfer to another hospital...

 

[Apollyon]

Even if they do have refractory hypotension, an 18 ga is better than a TLC.

Why do you say this? Is it because of the time needed to put in the line? Because a TLC has one 16g and two 18g channels.

 

[SpacemanSpifff]

Why do you say this? Is it because of the time needed to put in the line? Because a TLC has one 16g and two 18g channels.

Assuming this is a comment on the flow rate, as a central line is longer and thus has higher resistance. That said, in refractory hypotension you need vasopressors, stress dose steroids, etc., not more fluid. Single coverage folks are in a tough spot in these cases.

 

[TooMuchResearch]

Assuming this is a comment on the flow rate, as a central line is longer and thus has higher resistance. That said, in refractory hypotension you need vasopressors, stress dose steroids, etc., not more fluid. Single coverage folks are in a tough spot in these cases.

Eh, patients have peripheral veins and bones.

 

[SpacemanSpifff]

Eh, patients have peripheral veins and bones.

Neither of which is an answer to refractory shock that will require vasopressors for more than 4 hours. If they’re going to be out of the ED in 1 hr, then fine. But if not, a line is worth the 15 extra minutes in my mind.

 

[Siggy]

I agree with you. I generally work mid/night and am often single coverage. I don't put in lines on stable patients. It's not a life-saving procedure, and can wait until morning for a PICC. I've seen ED docs allow their departments to grind to a halt because they are single coverage and putting in lines on patients who really don't need them. Just because a patient is going to the ICU doesn't mean they need a line. If they don't have refractory hypotension, and have good IV access this really can wait.

The scenario is specifically a patient in septic shock on pressors. That's not "stable." Also, the ICU often has single coverage overnight... which includes covering rapids and codes on the inpatient side.

I agree that not every patient in the unit needs a line. However the patients that do need a line... need a line and shouldn't have to wait hours for the patient to be moved upstairs before they get one.

 

[Siggy]

Notwithstanding the fact that I've had the ICU tell me that a patient was too unstable for the ICU. Whatever that means.

I've had emergency departments say the same thing... and I feel the same way when a patient has too much emergency for the emergency department.

 

[CCM-MD]

The scenario is specifically a patient in septic shock on pressors. That's not "stable." Also, the ICU often has single coverage overnight... which includes covering rapids and codes on the inpatient side.

I agree that not every patient in the unit needs a line. However the patients that do need a line... need a line and shouldn't have to wait hours for the patient to be moved upstairs before they get one.

This discussion is quite "academic" considering many community hospitals don't have an intensivist physically present at night and the ER doc comes up to the unit to put the line in anyway...

 

[GeneralVeers]

This discussion is quite "academic" considering many community hospitals don't have an intensivist physically present at night and the ER doc comes up to the unit to put the line in anyway...

Hah hah no. Would never work in a place I had to up and put central lines in ICU patients.

 

[CCM-MD]

Hah hah no. Would never work in a place I had to up and put central lines in ICU patients.

Good for you.

But these places exist.

 

[GeneralVeers]

Good for you.

But these places exist.

They shouldn't. Can't imagine having to drop what I'm doing to go to the ICU to place a line. Intubations are at least potentially life-saving. No one died because they went 6-8 hours without a central line.

 

[CCM-MD]

They shouldn't. Can't imagine having to drop what I'm doing to go to the ICU to place a line. Intubations are at least potentially life-saving. No one died because they went 6-8 hours without a central line.

I get where you are coming from but sometimes there isn't an alternative. I cover some places at night via eICU telemedicine that have intensivists during the day but none physically present at night. Usually low acuity, non-PCI, non-stroke centers, sometimes even without hemodialysis capability and nobody needs procedures at night. Anyone sick enough gets transferred to the flag ship in the city that has intensivists in house.

But from time to time there is a patient in shock that needs a line - extravasation isn't pretty so running peripherally at moderate doses isn't a great option. Lots of different set ups but many of these places have ER docs putting in lines when necessary. Some have intensivists on "home call" who come in for procedures.

 

[TooMuchResearch]

They shouldn't. Can't imagine having to drop what I'm doing to go to the ICU to place a line. Intubations are at least potentially life-saving. No one died because they went 6-8 hours without a central line.

I go to the floor for stuff in rural/critical access hospitals, but if they need a CVL the hospitalist probably already transferred them or they will as soon as they call in to see what's going on.

 

[deleted109597]

I've had emergency departments say the same thing... and I feel the same way when a patient has too much emergency for the emergency department.

Except, that is the ICU's job.
The ER's job is to identify the problem and send the patient to the right place. Whether it be the ICU, the OR, the floor, the IR suite, etc.
The ER's job is not to manage the patient indefinitely. The patient to physician ratios for ICU vs ER are immense.

 

[deleted109597]

Why do you say this? Is it because of the time needed to put in the line? Because a TLC has one 16g and two 18g channels.

If they need volume, the peripheral is faster.
If they need pressors, the data shows it's perfectly safe to use it for extended periods of time. And it's easier to place than a central line.
Don't even get me started on the ICUs not letting IOs come upstairs.

 

[deleted547339]

We run peripheral pressors and call the PICC team to place in the ED or ICU.

Or if I'm rural, I run peripheral and ship unless it's a) slow as **** and b) the receiving center tells me to hold them for awhile because the "bed" isn't ready yet.

Why is bed in quotes???

 

[deleted547339]

Except, that is the ICU's job.
The ER's job is to identify the problem and send the patient to the right place. Whether it be the ICU, the OR, the floor, the IR suite, etc.
The ER's job is not to manage the patient indefinitely. The patient to physician ratios for ICU vs ER are immense.

Not really. I have more patients in the icu than in the ER- it’s just that I know the patients in the icu and the ER patients are new.