No problem, Just a Lap Chole

[pd4emergence]

60ish year old lady in ED with abd pain, fever, nausea, vomiting, and increased bilirubin. No other significant past medical history. CT shows free air around the gallbladder, right sided abscesses. Tachy, bp in the low 100's. Other than the increased bili, no other significant labs, Hct is 38, coags are normal. Pt is brought to OR by a particularly slow surgeon (even slow for academics). Go......

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[BLADEMDA]

Emphysematous cholecystitis, known less commonly as clostridial cholecystitis, is an acute infection of the gallbladder wall caused by gas-forming organisms (eg, Clostridium or Escherichia coli) that is generally considered a surgical emergency. An infrequent, insidious, and rapidly progressive form of acute cholecystitis, emphysematous cholecystitis is characterized by early gangrene, perforation of the gallbladder and high mortality. Although this condition develops in approximately 1% of all cases of acute cholecystitis, compared with typical acute cholecystitis, emphysematous cholecystitis is associated with much higher rates of gangrene and perforation of the gallbladder and significantly increased rates of mortality (15-25%).

 

[deleted171991]

60ish year old lady in ED with abd pain, fever, nausea, vomiting, and increased bilirubin. No other significant past medical history. CT shows free air around the gallbladder, right sided abscesses. Tachy, bp in the low 100's. Other than the increased bili, no other significant labs, Hct is 38, coags are normal. Pt is brought to OR by a particularly slow surgeon (even slow for academics). Go......

I would treat this one as a septic patient. Have a helper around if possible. Two large bore IV's, Foley, LR bolus up to 30 ml/kg or until decent urine output, A-line, central line, pressors ready. That's before we do anything else. (Maybe the central line +/- post induction, depending how she behaves during induction.) Wide spectrum antibiotics, including anaerobes. NG tube, continuous suction. Preoxygenation. If concerned about cardiovascular/sympathetic reserve and crash on induction (most probable, how high are the fever, WBC and tachycardia?), controlled induction with fentanyl, touch of versed, propofol and pressors, sux; otherwise, I would just bring the SBP to 160 pre-induction and RSI with same meds. Tube. (All these assuming airway looks easy.)

I would try to convince the surgeon that this is a disaster waiting to happen, and to be assisted/replaced by the fastest surgeon around.

There is also the question of open vs lap chole. I don't think this lady would do well with laparoscopy (given both her anesthetic and surgical status), so I would encourage the surgeon to do it open. Question for surgeon whether this could be temporized by IR and perc cholecystostomy and abscess evacuation, at least until SIRS/sepsis is under control.

Intraop, continue fluids and pressors as needed (try to keep on dry side). Also consider stress steroids if pressor resistance. Monitor ScvO2, ABGs.

What am I missing? (Haven't done one of these in almost 3 years.)

 

[pd4emergence]

I would treat this one as a septic patient. Have a helper around if possible. Two large bore IV's, Foley, LR bolus up to 30 ml/kg or until decent urine output, A-line, central line, pressors ready. That's before we do anything else. (Maybe the central line +/- post induction, depending how she behaves during induction.) Wide spectrum antibiotics, including anaerobes. NG tube, continuous suction. Preoxygenation. If concerned about cardiovascular/sympathetic reserve and crash on induction (most probable, how high are the fever, WBC and tachycardia?), controlled induction with fentanyl, touch of versed, propofol and pressors, sux; otherwise, I would just bring the SBP to 160 pre-induction and RSI with same meds. Tube. (All these assuming airway looks easy.)

I would try to convince the surgeon that this is a disaster waiting to happen, and to be assisted/replaced by the fastest surgeon around.

There is also the question of open vs lap chole. I don't think this lady would do well with laparoscopy (given both her anesthetic and surgical status), so I would encourage the surgeon to do it open. Question for surgeon whether this could be temporized by IR and perc cholecystostomy and abscess evacuation, at least until SIRS/sepsis is under control.

Intraop, continue fluids and pressors as needed (try to keep on dry side). Also consider stress steroids if pressor resistance. Monitor ScvO2, ABGs.

What am I missing? (Haven't done one of these in almost 3 years.)

We don't monitor SvO2 all that often where I am. It seems to have fallen out of favor over the past few years. It's a good thought. It's also a great point. Whats the latest data? I ask cause I haven't looked at it in a while and was hoping somebody would know.

So to me this lady looked like she was well on the septic/sirs downslope but not quite there. She was not on any pressors. HR was 105 or so. BP's low 100's. If you were presented with this case, would you really go straight to a central line if she had good peripheral access? I find myself not doing these near as often as I used to. Do you really have to have a CVL for pressors? I know in these theoretical situations we usually go for the most conservative option but in the real world what would the board have done?

By the way, I have to admit, I didn't know about the CT. This was billed as a routine regular old lap chole.

 

[urge]

1 liter fluid before induction. +/- Awake a line. Pent sux tube with some pressors.

Send intubated, on phenylephrine, to icu 6 hrs later after the surgeon is done causing more harm than good.

 

[BLADEMDA]

1 liter fluid before induction. +/- Awake a line. Pent sux tube with some pressors.

Send intubated, on phenylephrine, to icu 6 hrs later after the surgeon is done causing more harm than good.

You still have Pentothal avail?

 

[urge]

You still have Pentothal avail?

No. It's a figure of speech. I have fond memories of it.

 

[cchoukal]

Lots of people adopted ScvO2 after the Rivers trial, but the subsequent literature has not supported its use. A handful of retrospective analysis attempting to examine which pieces of the "bundle" were the most effective did not support ScvO2 in the regression modeling (including one trial by the Surviving Sepsis Campaign; I think the lead author was Levy). Furthermore, recent trials of early goal directed therapy bundles (including ScvO2) have not shown better outcomes than standard care (but keep in mind standard care has gotten better over time). Look for the PROCESS trial and the ARISE trial.

In my own practice, I do use it in septic patients, along with SVV, and lactate. I find the ScvO2 is really only helpful when low (in early sepsis, it's often normal or high).

For this patient, I anticipate she will get worse before she gets better and I'd probably put a central line in, both for pressors and for ScvO2.

 

[deleted171991]

We don't monitor SvO2 all that often where I am. It seems to have fallen out of favor over the past few years. It's a good thought. It's also a great point. Whats the latest data? I ask cause I haven't looked at it in a while and was hoping somebody would know.

So to me this lady looked like she was well on the septic/sirs downslope but not quite there. She was not on any pressors. HR was 105 or so. BP's low 100's. If you were presented with this case, would you really go straight to a central line if she had good peripheral access? I find myself not doing these near as often as I used to. Do you really have to have a CVL for pressors? I know in these theoretical situations we usually go for the most conservative option but in the real world what would the board have done?

By the way, I have to admit, I didn't know about the CT. This was billed as a routine regular old lap chole.

I wouldn't have gone to central line for those numbers either, had I not known about the CT. I think you can also argue that, at this point, she doesn't really need one.

I wouldn't put in a CVL just for SvO2, but if I have one...

 

[pd4emergence]

Heh...are you at my hospital?

This story sounds familiar and with a bad ending.



You could try IR but for bad emphysematous cholecystitis from my (limited) experience you need better source control than what IR will buy you.

I wouldn't even consider laparoscopy - skip straight to an open chole.

With the elevated bill I would let GI mess with the common duct endoscopically when/if she's more stable. Not touching the common duct operatively in that setting.

I'd probably be asking the anesthesiologist for everything you mentioned if they didn't explicitly state their plan ahead of time; I've seen these patients sink fast. Emphysematous cholecystitis is bad news bears.

I'd also be willing to do a damage control partial cholecystectomy and lay drains rather than mess around for too long if it looks too bad in there.

It's terrifying that this came billed from a surgeon as "just a lap chole"

This is a case where the clock definitely matters. For the slow surgeon - there should be no shame in asking for help.

Thank you for you input. It's always nice to get a surgeon's point of view. It's something I find myself more and more clarifying as I get farther into my career. I agree with you. I think this lady needed to be in the OR. I don't think that IR would have done her much good. Especially in hindsight. Unfortunately, this surgeon was the one to do the case. This is the surgeon on call. The only one there. This person was not a technically bad surgeon, just slow. Hindsight also makes me question the initial surgical approach but initially, a laparoscopic chole seemed reasonable.

 

[BLADEMDA]

I do a lot of sick elderly patients. I mean they are septic and near death but the surgeon still wants to operate.

Hence, I know the drill quite well:

1. Arterial line
2. Careful induction (low dose ketamine plus low dose propofol)
3. Central line
4. SVV if not in A fib
5. TEE if needed and no contraindications.

Inotropic support ready to go: Epi, Norepi and vasopressin 0.03 IU per min
Volume blouses and maintain Hgb above 8. I use around 9 most of the time.

Lab work in OR to include Hgb, ABG, lactate level. Follow acidosis and treat if needed.

 

[BLADEMDA]

Lots of people adopted ScvO2 after the Rivers trial, but the subsequent literature has not supported its use. A handful of retrospective analysis attempting to examine which pieces of the "bundle" were the most effective did not support ScvO2 in the regression modeling (including one trial by the Surviving Sepsis Campaign; I think the lead author was Levy). Furthermore, recent trials of early goal directed therapy bundles (including ScvO2) have not shown better outcomes than standard care (but keep in mind standard care has gotten better over time). Look for the PROCESS trial and the ARISE trial.

In my own practice, I do use it in septic patients, along with SVV, and lactate. I find the ScvO2 is really only helpful when low (in early sepsis, it's often normal or high).

For this patient, I anticipate she will get worse before she gets better and I'd probably put a central line in, both for pressors and for ScvO2.

I am up to date on all this literature. That said, in the OR we must be more aggressive than the ER or ICU. This means the Process and Arise trials aren't our standard of care. We must stabilize the patient who is likely to Be hypotensive with decreased CO under general anesthesia. Inotropic support and volume repletion are often times required by the patient under our care.

http://www.survivingsepsis.org/SiteCollectionDocuments/ProCESS-ARISE.pdf

 

[pd4emergence]

So, I see this lady in the holding area and she has the look of somebody on the way to getting sicker. She has a 20g. IV and it looks like the ER was lucky to get that. BP's and HR are as above and stable. We open up her fluids and head to the OR, induce (gently), RSI, and she did ok with induction. Place an aline and CVL. With two good IV's I might have tried it but she just didn't have any other viable possibilities and she looked like she needed a CVL. I ask the resident in the room to draw an abg, coags, cbc, lactic acid and step out to put out other fires. They get started. It takes awhile to get the gallbladder exposed. In the mean time the labs come back with the expected septic looking picture ph of about 7.28, be around -5, LA around 2, hgb of 10, INR 1.2 and a PTT that was a little bit above normal. Also, when they get to the gallbladder, it does not look infected, it's not ruptured, it looks pristine. What do you think of the labs? What should be done next?

 

[Noyac]

I dont use CVL as often as I used to whither but this is the type of person I routinely put one in, the ones that will go to ICU and might be there for a few days. PIVs just don't last and it makes their job much easier.

I think those labs are survivable but they need intervening. You could give IVF's or PRBC's. Both are fine in my opinion but I know others feel differently. If you want to wait till the Hct is below some magic number before giving PRBCs , then fine. If you think the coats will continue to worsen then give some FFP as well. Won't hurt.

What's the plt count?

 

[urge]

So, I see this lady in the holding area and she has the look of somebody on the way to getting sicker. She has a 20g. IV and it looks like the ER was lucky to get that. BP's and HR are as above and stable. We open up her fluids and head to the OR, induce (gently), RSI, and she did ok with induction. Place an aline and CVL. With two good IV's I might have tried it but she just didn't have any other viable possibilities and she looked like she needed a CVL. I ask the resident in the room to draw an abg, coags, cbc, lactic acid and step out to put out other fires. They get started. It takes awhile to get the gallbladder exposed. In the mean time the labs come back with the expected septic looking picture ph of about 7.28, be around -5, LA around 2, hgb of 10, INR 1.2 and a PTT that was a little bit above normal. Also, when they get to the gallbladder, it does not look infected, it's not ruptured, it looks pristine. What do you think of the labs? What should be done next?

Slight acidosis. Not bad for someone who "wouldn't tolerate" laparoscopy. Bicarb can't hurt, although it might not help either. I wouldn't treat it. I would like to see a trend develop.

As to what next, don't know. That's a surgical question. They should probably discuss the CT with radiology for starters. Diagnostic laparoscopy, or exploratory laparotomy will likely follow if they have no clue of what's going on.

 

[deleted171991]

Those labs are pretty benign. I was expecting worse.

Hgb is 10. I would not correct that anemia. I would maintain hemodynamics, give fluids if fluid-responsive, and get another set of labs in one hour.

No bicarb at that pH.

 

[Noyac]

No bicarb in my opinion either.

 

[BLADEMDA]

So, I see this lady in the holding area and she has the look of somebody on the way to getting sicker. She has a 20g. IV and it looks like the ER was lucky to get that. BP's and HR are as above and stable. We open up her fluids and head to the OR, induce (gently), RSI, and she did ok with induction. Place an aline and CVL. With two good IV's I might have tried it but she just didn't have any other viable possibilities and she looked like she needed a CVL. I ask the resident in the room to draw an abg, coags, cbc, lactic acid and step out to put out other fires. They get started. It takes awhile to get the gallbladder exposed. In the mean time the labs come back with the expected septic looking picture ph of about 7.28, be around -5, LA around 2, hgb of 10, INR 1.2 and a PTT that was a little bit above normal. Also, when they get to the gallbladder, it does not look infected, it's not ruptured, it looks pristine. What do you think of the labs? What should be done next?

Mild metabolic acidosis. Asses volume status as you likely need more fluid. Most experts say a Hgb at or above 9 is more than adequate here. So, check urine output and SVV for adequate volume status. Sodium bicarbonate is not indicated for this metabolic acidosis as the ph Is above 7.20.

 

[BLADEMDA]

utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis.

http://jasn.asnjournals.org/content/20/4/692.full

 

[deleted171991]

There is no discussion about bicarb at pH of 7.28. Only around 7.10-7.15.

Careful with fluids in sepsis: excess of fluids increases mortality, and paradoxically AKI.

P.S. As you can see, I started reading more recent literature.

 

[Noyac]

Mild metabolic acidosis. Asses volume status as you likely need more fluid. Most experts say a Hgb at or above 9 is more than adequate here. So, check urine output and SVV for adequate volume status. Sodium bicarbonate is not indicated for this metabolic acidosis as the ph Is above 7.20.

Agreed but as we all know, we give volume as needed here and the next thing that happens is the hct is 8. I wouldnt criticize giving blood here. 2 units would be acceptable to me. But would probably just give the IVF at the start and see where this case goes.

 

[BLADEMDA]

There is no discussion about bicarb at pH of 7.28. Only around 7.10-7.15.

Careful with fluids in sepsis: excess of fluids increases mortality, and paradoxically AKI.

2.3. Sodium Bicarbonate Therapy in Patients with Septic Shock
In patients diagnosed with septic shock, sodium bicarbonate therapy has not been associated with improvement of hemodynamic variables or mortality rate in retrospective [38] and prospective [39] studies. Accordingly, the 2008 update of the Surviving Sepsis Campaign guidelines recommends against the use of sodium bicarbonate in patients with hypoperfusion-induced lactic acidosis and a ph greater than 7.15 [40].

2.4. Sodium Bicarbonate Therapy in Patients with Intraoperative Metabolic Acidosis
A negative impact on mortality has been reported following the use of sodium bicarbonate in a retrospective cohort study of severely acidotic (arterial ) trauma patients who underwent emergency surgery [14]. No benefit from bicarbonate therapy has been found either in a small prospective randomized trial of patients who developed intraoperative mild metabolic acidosis in the absence of hypoxemia [41].

2.5. Sodium Bicarbonate Therapy in Patients with Cardiac Arrest
Sodium bicarbonate therapy has long been removed from guidelines for advanced cardiac life support, as a review of the medical literature shows no beneficial effect of sodium bicarbonate on survival rates in this setting [13].

 

[BLADEMDA]

There is no discussion about bicarb at pH of 7.28. Only around 7.10-7.15.

Careful with fluids in sepsis: excess of fluids increases mortality, and paradoxically AKI.

Third spacing and volume loss are occurring in the O.R. That said, I utilize SVV and urine output to guide my fluid therapy.

 

[deleted171991]

Third spacing and volume loss are occurring in the O.R. That said, I utilize SVV and urine output to guide my fluid therapy.

It's OK to replace volume loss. It's not OK to replace third-spacing with fluids, especially if the patient is not hypotensive. Beyond 20 ml/kg, it's better to use pressors (unless one sees fluid-responsiveness, as measured by echo preferably or SVV, not BP). Urine output should not guide your fluid therapy in sepsis; it can result in fluid overload. Hypervolemia produces increase in natriuretic peptides, which are proven to increase endothelial permeability by affecting the endothelial glycocalyx.

Oh, and it seems that now norepi can be safely used on a PIV until 0.2 mcg/kg/min. Also 10 mg of phentolamine can be added to each liter of solution containing norepi without affecting the pressor effect.

Also, definitely no transfusion at Hgb of 10 (recommended only under 7). It seems that transfusions impair microcapillary flow and tissue oxygenation in septic patients.

P.S. I am quoting the latest Dr. Marik "Evidence-based critical care" book here. If you have SpringerLink at work, you can read/download it for free online.

 

[BLADEMDA]

It's OK to replace volume loss. It's not OK to replace third-spacing with fluids, especially if the patient is not hypotensive. Beyond 20 ml/kg, it's better to use pressors (unless one sees fluid-responsiveness, as measured by echo preferably or SVV, not BP). Urine output should not guide your fluid therapy in sepsis; it can result in fluid overload. Hypervolemia produces increase in natriuretic peptides, which are proven to increase endothelial permeability by affecting the endothelial glycocalyx.

Oh, and it seems that now norepi can be safely used on a PIV until 0.2 mcg/kg/min. Also 10 mg of phentolamine can be added to each liter of solution containing norepi without affecting the pressor effect.

Also, definitely no transfusion at Hgb of 10 (recommended only under 7). It seems that transfusions impair microcapillary flow and tissue oxygenation in septic patients.

P.S. I am quoting the latest Dr. Marik "Evidence-based critical care" book here.

In the operstimg room 7.0 is probably too low. Most experts in our field recommend 8.0. The latest data shows SURGERY is different than the ICU.

http://anesthesiology.pubs.asahq.org/article.aspx?articleid=2043033

Surgery patients with cancer benefit from a Hgb of 9.0 while the remainder of our sicker patients should be kept in the 8.0-9.0 range. Evidence suggests 7.0 may be too low for our sickest OR patients.

The vast majority of O.R. patients are under resuscitated by CRNAs which is why I utilize SVV and urine output.

 

[deleted171991]

The patient can be in the OR, it's still sepsis. It's reasonable to replace surgical losses but, beyond that, the body responds the same way. And it seems that blood transfusions are not beneficial at a Hgb over 7, in sepsis.

In sepsis (per Dr. Marik):
- transfusions do not acutely increase tissue oxygen uptake
- they have been demonstrated to impair microcapillary flow and tissue oxygenation
- the release of cell-free Hgb from banked blood may be particularly deleterious
- transfusion of PRBCs was associated with worsened clinical outcomes in patients with septic shock treated with EGDT
- blood transfusions are associated with an increased risk of secondary infections, MODS and death, and should be only considered at a Hgb <7
- 100% of a crystalloid bolus will end up in the interstitium after 3h

The way I see it, what we do in the OR is:
- give fluids, while chasing urine output
- give blood, while chasing Hgb
- the result is exactly that hypervolemia which has been proven to worsen outcomes both in sepsis and surgical patients (even in trauma). There are actually some new suggestions to aim for a CVP lower (!) than 8 in sepsis.

Btw, the entire fluid management chapter in Dr. Marik's book will ROCK your world!

 

[BLADEMDA]

1. Is this patient meeting SIRS criteria?
2. Does the patient have a suspected / documented infection?
3. A Give an IV fluid bolus of 30 cc/kg over the next hour
B. Give antibiotics
4. Check to see if this patient meets criteria for severe sepsis? (organ dysfunction, lactate, etc)
5. What happens with this patient when I give fluids?
6 A Gets better (BP, urine output, cardiac output, color, mental status, etc) – give more fluids
B No better – start pressors and admit to ICU (Early Advanced Care)
C. If unsure, give more fluids and call for help – (i.e. ICU or a colleague/ second opinion)
D. Worse with fluids – call for help/ consider wrong diagnosis.
7. Congratulations! (and THANK YOU for not mucking around to much!)

 

[deleted171991]

1. Is this patient meeting SIRS criteria?
2. Does the patient have a suspected / documented infection?
3. A Give an IV fluid bolus of 30 cc/kg over the next hour
B. Give antibiotics
4. Check to see if this patient meets criteria for severe sepsis? (organ dysfunction, lactate, etc)
5. What happens with this patient when I give fluids?
6 A Gets better (BP, urine output, cardiac output, color, mental status, etc) – give more fluids
B No better – start pressors and admit to ICU (Early Advanced Care)
C. If unsure, give more fluids and call for help – (i.e. ICU or a colleague/ second opinion)
D. Worse with fluids – call for help/ consider wrong diagnosis.
7. Congratulations! (and THANK YOU for not mucking around to much!)

1. Probably (I would bet her fever and WBC levels will qualify).
2. Absolutely. Look at those abscesses.
3. It's not 30 cc/kg anymore. That was an EGDT number. It should be less than that, and only if fluid-responsive, as measured by the increase in stroke volume.
4. Not meeting criteria.
5. That should be monitored by echo, or at least A-line (SVV/PPV).
6.
A. The only thing that should guide your fluid input is fluid responsiveness, preferably measured by echo. Urine output should not, for septic patients.
B. If not objectively fluid-responsive and hypotensive, give pressors. Can give norepi on PIV up to 0.2 mcg/kg/min. Consider adding vaso 0.03U/min. Forget EGDT.
C. Don't give more fluids, unless evidence of fluid loss. Hypovolemia is better than hypervolemia, and normovolemia is better than both.
D. Too late. Now you have a lot of fluids in the interstitia, which will be removed only by lymphatics, which are also inhibited by exactly the same natriuretic peptides that were stimulated by hypervolemia and which worsened endothelial permeability in the first place.
7. tl;dr Conservative fluid therapy results in better outcomes.

 

[BLADEMDA]

The patient can be in the OR, it's still sepsis. It's reasonable to replace surgical losses but, beyond that, the body responds the same way. And it seems that blood transfusions are not beneficial at a Hgb over 7, in sepsis.

In sepsis (per Dr. Marik):
- transfusions do not acutely increase tissue oxygen uptake
- they have been demonstrated to impair microcapillary flow and tissue oxygenation
- the release of cell-free Hgb from banked blood may be particularly deleterious
- transfusion of PRBCs was associated with worsened clinical outcomes in patients with septic shock treated with EGDT
- blood transfusions are associated with an increased risk of secondary infections, MODS and death, and should be only considered at a Hgb <7
- 100% of a crystalloid bolus will end up in the interstitium after 3h

The way I see it, what we do in the OR is:
- give fluids, while chasing urine output
- give blood, while chasing Hgb
- the result is exactly that hypervolemia which has been proven to worsen outcomes both in sepsis and surgical patients (even in trauma). There are actually some new suggestions to aim for a CVP lower (!) than 8 in sepsis.

Btw, the entire fluid management chapter in Dr. Marik's book will ROCK your world!

There is no evidence to suggest the patient discussed in this thread has severe sepsis. Hence, the evidence from the Recent trials disproving EGDT should be taken into consideration here. The patient responded to fluid boluses and Inotropic support was not needed so urine output can be a measure of adequate volume status in this patient.

Evidence from our literature suggests a Hgb of 8.0 is better than 7.0 for our sicker, older patient population. The Hgb of 7.0 is best reserved for the ICU and ASA1-2 patients. In the operating room we may suspect early sepsis but the diagnosis isn't always clear.

Fluid balance can be tricky so the use of SVV, CO, Urine output, etc can be quite helpful in fluid replacement therapy.

The operating room is not the ICU as we are giving anesthetics which affect preload, after load and contractility just to name a few.

 

[deleted171991]

There is no evidence to suggest the patient discussed in this thread has severe sepsis. Hence, the evidence from the Recent trials disproving EGDT should be taken into consideration here. The patient responded to fluid boluses and Inotropic support was not needed so urine output can be a measure of adequate volume status in this patient.

Evidence from our literature suggests a Hgb of 8.0 is better than 7.0 for our sicker, older patient population. The Hgb of 7.0 is best reserved for the ICU and ASA1-2 patients. In the operating room we may suspect early sepsis but the diagnosis isn't always clear.

Fluid balance can be tricky so the use of SVV, CO, Urine output, etc can be quite helpful in fluid replacement therapy.

The operating room is not the ICU as we are giving anesthetics which affect preload, after load and contractility just to name a few.

Not severe sepsis. Just sepsis.

The evidence for Hgb of 9 better than 7 was in advanced cancer patients. Different pathophysiology from sepsis. Explained why transfusions harmful in sepsis, above.

Again, urine output is not a good target in sepsis (anymore).

If you affect preload, afterload and contractility, why do you give fluids instead of pressors and inotropes?

P.S. Thank you for making me catch up with my reading.

 

[deleted171991]

So, as I said, the fluid management chapter in Dr. Marik's latest book will ROCK your world. Here comes the part about PPV/SVV in predicting fluid responsiveness.

"Conditions which need to be met (ALL) to ensure accuracy of PPV/SVV:
- Sinus rhythm
- Volume cycled ventilation with Vt of at least 8 ml/kg IBW
- No ventilator-patient dyssynchrony
- Heart rate/respiratory ratio > 3.6
- Normal chest wall compliance (change in intrapleural pressure)
- No evidence of cor pulmonale - pulmonary hypertension
- Normal intra-abdominal pressure
- Normal pulmonary compliance

In a cohort of cardiac surgical patients Lansdorp and colleagues demonstrated that PPV/SVV did not predict volume responsiveness in routine clinical practice [46]. Multiple studies have now confirmed these findings [47, 48]. In the largest study to date, Canneson and colleagues demonstrated that despite a strong predictive value, the PPV was inconclusive in predicting fluid responsiveness in 25 % of patients during general anesthesia [49]. The utility of the PPV/SVV in the ICU appears significantly worse [47, 48]. In a multicenter, point prevalence study Mahjoub and colleagues demonstrate that only 2 % of ICU patients met the validity criteria for using the PPV to assess fluid responsiveness [50]. Furthermore, only 3 % of patients with an arterial line in place satisfied all the validly criteria. These data suggest that due to the frequency of confounding factors the PPV/SVV should not be used as the primary technique for directing fluid management in the OR and ICU.

Nevertheless intravascular volume depletion should be suspected in patients who demonstrate marked PPV evident on either an arterial pressure waveform or pulse oximetric waveform. However, in these situations other tests should be performed to confirm fluid responsiveness (see below)."

"Ultimately only two techniques are currently available which can be used to determine fluid responsiveness with a high degree of accuracy, namely the passive leg raising maneuver (PLR) and the fluid challenge [17, 40, 59, 60]. These techniques are best coupled with minimally invasive cardiac output monitors (see Chap. 10) which can track changes in SV and cardiac output dynamically and in real time [17, 40]. Changes in carotid artery flow measured by Doppler is another method to assess the response to either a fluid challenge of PLR maneuver [48, 61]. For obvious technical reasons the fluid challenge technique is preferred during anesthesia while the PLR is preferred in the ICU and post-operatively. The various methods to assess fluid responsiveness, grouped by diagnostic accuracy are listed in Table 9.1.

Table 9.1 Techniques for assessing fluid responsiveness [my comment: listed from worse to better]

Static pressure and volume parameters (ROC ~ 0.5–0.6)
Central venous pressure (CVP)
Pulmonary artery occlusion pressure (PAOP)
Inferior vena cava (IVC)/superior vena caval (SVC) diameter
Flow corrected time (FTc)
Right ventricular end-diastolic volume (RVEDV)
Left ventricular end-diastolic volume (LVEDV)
SVC/IVC variation during mechanical ventilation

Dynamic techniques based on heart-lung interactions (ROC ~ 0.7–0.8)
Pulse pressure variation (PPV)
Stroke volume variation (SVV)
Pleth variability index (PVI)
Aortic blood flow (Doppler or echocardiography)

Techniques based on real or virtual fluid challenge (ROC ~ 0.9)
Passive leg raising (PLR)
Rapid fluid challenge (200–300 cm3)

ROC area under receiver operator characteristic curve"

tl;dr PPV/SVV during a respiratory cycle has much lower predictive value for fluid responsiveness than SVV or CO changes with passive leg raising or rapid fluid challenge (200-300 ml), as measured by minimally invasive cardiac output monitors.

 

[BLADEMDA]

Not severe sepsis. Just sepsis.

The evidence for Hgb of 9 better than 7 was in advanced cancer patients. Different pathophysiology from sepsis. Explained why transfusions harmful in sepsis, above.

Again, urine output is not a good target in sepsis (anymore).

If you affect preload, afterload and contractility, why do you give fluids instead of pressors and inotropes?

P.S. Thank you for making me catch up with my reading.

The OR is not the ICU. I don't believe 7.0 is the correct target for our sickest patients. The best available evidence suggests a slightly more liberal approach like 8.0 for our ASA3-4 patients should strongly be considered. Until the evidence shows otherwise I use that target number (8.0-8.5).

I utilize SVV and SVI along with CI more than anyone in my group. I believe the evidence strongly suggests the use of TEE and SVV are superior estimators of volume status for patients. (We Agree here).

Several of older studies show fluid boluses can correct the diminished preload and CI in anesthetized patients. Most patients only need a fluid bolus to correct hypotension and restore urine output. That said, if the response to the fluid bolus isn't occuring then other interventions like pressors or Inotropes may be needed. This is when the TEE and CI/SV become part of the data for best treatment.

I am aware of the limitations of urine output as a measure for volume status and adequate renal perfusion. That said, most of the time when inotropes or pressors Are not needed the urine output is a way to measure adequate volume status in most patients. I agree that in sepsis that a low urine output doesn't equate with the need for more volume. But, is the reverse true? If the patient in this thread had a urine output of 400 mls per hour wouldn't the Anesthesiologist think volume status is at least adequate?

 

[BLADEMDA]

So, as I said, the fluid management chapter in Dr. Marik's latest book will ROCK your world. Here comes the part about PPV/SVV in predicting fluid responsiveness.

"Conditions which need to be met (ALL) to ensure accuracy of PPV/SVV:
- Sinus rhythm
- Volume cycled ventilation with Vt of at least 8 ml/kg IBW
- No ventilator-patient dyssynchrony
- Heart rate/respiratory ratio > 3.6
- Normal chest wall compliance (change in intrapleural pressure)
- No evidence of cor pulmonale - pulmonary hypertension
- Normal intra-abdominal pressure
- Normal pulmonary compliance

In a cohort of cardiac surgical patients Lansdorp and colleagues demonstrated that PPV/SVV did not predict volume responsiveness in routine clinical practice [46]. Multiple studies have now confirmed these findings [47, 48]. In the largest study to date, Canneson and colleagues demonstrated that despite a strong predictive value, the PPV was inconclusive in predicting fluid responsiveness in 25 % of patients during general anesthesia [49]. The utility of the PPV/SVV in the ICU appears significantly worse [47, 48]. In a multicenter, point prevalence study Mahjoub and colleagues demonstrate that only 2 % of ICU patients met the validity criteria for using the PPV to assess fluid responsiveness [50]. Furthermore, only 3 % of patients with an arterial line in place satisfied all the validly criteria. These data suggest that due to the frequency of confounding factors the PPV/SVV should not be used as the primary technique for directing fluid management in the OR and ICU.

Nevertheless intravascular volume depletion should be suspected in patients who demonstrate marked PPV evident on either an arterial pressure waveform or pulse oximetric waveform. However, in these situations other tests should be performed to confirm fluid responsiveness (see below)."

"Ultimately only two techniques are currently available which can be used to determine fluid responsiveness with a high degree of accuracy, namely the passive leg raising maneuver (PLR) and the fluid challenge [17, 40, 59, 60]. These techniques are best coupled with minimally invasive cardiac output monitors (see Chap. 10) which can track changes in SV and cardiac output dynamically and in real time [17, 40]. Changes in carotid artery flow measured by Doppler is another method to assess the response to either a fluid challenge of PLR maneuver [48, 61]. For obvious technical reasons the fluid challenge technique is preferred during anesthesia while the PLR is preferred in the ICU and post-operatively. The various methods to assess fluid responsiveness, grouped by diagnostic accuracy are listed in Table 9.1.

Table 9.1 Techniques for assessing fluid responsiveness [my comment: listed from worse to better]

Static pressure and volume parameters (ROC ~ 0.5–0.6):
Central venous pressure (CVP)
Pulmonary artery occlusion pressure (PAOP)
Inferior vena cava (IVC)/superior vena caval (SVC) diameter
Flow corrected time (FTc)
Right ventricular end-diastolic volume (RVEDV)
Left ventricular end-diastolic volume (LVEDV)
SVC/IVC variation during mechanical ventilation

Dynamic techniques based on heart-lung interactions (ROC ~ 0.7–0.8):
Pulse pressure variation (PPV)
Stroke volume variation (SVV)
Pleth variability index (PVI)
Aortic blood flow (Doppler or echocardiography)

Techniques based on real or virtual fluid challenge (ROC ~ 0.9):
Passive leg raising (PLR)
Rapid fluid challenge (200–300 cm3)

ROC area under receiver operator characteristic curve"

I've read all this my friend. The critical care blog I follow has this and much more. In the OR I use a fluid challenge and SV along with other measures like urine output to assess adequate volume status. My goal in the OR is KISS which means I Strive to obtain adequate volume status which results in good hemodynamics and hopefully good urine output.

Again, I am aware of the limitations of urine output especially in severe sepsis.

 

[deleted171991]

I love Dr. Marik. Guys, do yourself a favor and get his latest book (I have the PDF from Springer through my workplace).

"NOT all patients who are fluid responsive require a fluid bolus. Normal healthy people are fluid responsive (have preload reserve). In patients who are fluid responsive and are hypotensive or have signs of poor organ perfusion a fluid bolus (500 cm3) should be strongly considered. However, this decision should be based on the patient’s clinical status, overall fluid balance and oxygenation. Repeat fluid boluses in fluid responsive patients should be based on the same ongoing assessment. Low dose norepinephrine should be considered in hypotensive patients who are fluid-non responders (or poor responders), those with acute lung injury and those with severe sepsis (see Chap. 12). Fluid boluses should not be given to patients who are non-responders. The CXR is a poor indicator of pulmonary edema (lung water) and the measurement of extra-vascular lung water (EVLW) by transpulmonary thermodilution is recommended in those patients in whom the management of fluids and pressors is particularly troublesome (see Chap. 10)… and when all else fails consult Dr. Harry Potter."

 

[pd4emergence]

So based on her first gas, we gave some fluid (1L of LR and a bottle of 25% albumin). I held off on the cells. During the time that the surgeons were getting to the gallbladder, her BP's were slowly trending down. I had a pretty low threshold for starting some levophed and thats eventually what happened. At this point, We redrew another set of labs. 7.21/p02 normal/pco2 35ish, BE -9, LA was 3.5 or so, wbc's 21k, plt's 95k (down from 150), hgb 7, INR now 1.8 and PTT was headed out. These labs were drawn about 40 minutes minutes after the initial gas.

After consulting with radiology, procedure was changed to an exlap.

 

[deleted171991]

Hgb 10 -> 7, INR 1.2 -> 1.8, Plt 150 -> 95 in one hour? And you gave only 1L of LR and a bottle of albumin 25% in the meanwhile?

 

[urge]

I love Dr. Marik.

Get a room!

 

[urge]

So based on her first gas, we gave some fluid (1L of LR and a bottle of 25% albumin). I held off on the cells. During the time that the surgeons were getting to the gallbladder, her BP's were slowly trending down. I had a pretty low threshold for starting some levophed and thats eventually what happened. At this point, We redrew another set of labs. 7.21/p02 normal/pco2 35ish, BE -9, LA was 3.5 or so, wbc's 21k, plt's 95k (down from 150), hgb 7, INR now 1.8 and PTT was headed out. These labs were drawn about 40 minutes minutes after the initial gas.

After consulting with radiology, procedure was changed to an exlap.

1 Why is it that base deficit gets translated into needing more volume? I have never understood that.

2 She is getting more acidotic quickly. I would probably give some bicarb and transfuse her. Is she in DIC? Get some D dimers or a TEG. Probably need to order ffp and platelets , even if you don't use them.

3 I must be a master surgeon.

 

[deleted171991]

Get a room!

I rarely see such a clear, opinionated but still rational, voice, when reading a medical book. He could have written an evidence-based book a la "Pocket Medicine", dry and unenjoyable.

I love truly good medical books, and I count their authors among my great teachers.

 

[deleted171991]

1 Why is it that base deficit gets translated into needing more volume? I have never understood that.

Me neither. I would have expected that from base excess ("contraction alkalosis"), not deficit. I guess the logic is that acidosis means hypoperfusion, which used to be treated with fluids.

2 She is getting more acidotic quickly. I would probably give some bicarb and transfuse her.

One doesn't give bicarb at a pH of 7.21 unless one is more interested in good-looking numbers, not the patient.

Is she in DIC? Get some D dimers or a TEG. Probably need to order ffp and platelets , even if you don't use them.

That's a very good hypothesis, given how fast the sky is falling. I think the best treatment is finishing the surgery ASAP.

3 I must be a master surgeon.

Did they teach you about bicarb during your surgical internship? Or was it cardiac anesthesia?

 

[urge]

One doesn't give bicarb at a pH of 7.21 unless one is more interested in good-looking numbers, not the patient.

Or was it cardiac anesthesia?

I'm not aware of bicarb causing harm. At the speed things are moving I don't see it being a choice. I'm aware is not standard of care.

My cardiac attendings were never in the room. They couldn't teach me anything, either good or bad.

 

[Noyac]

This is why we can't rely on strict numbers to treat. When she entered the OR her Hct was low. You know you are going to give fluids and start some blood letting so why not just give the blood? Your next ABG would have shown better resuscitation if this were the approach. I used to do exactly what was done here. Then I found myself chasing numbers and not pt physiology. If this were the end of the case then this approach would have been acceptable IMO. But not at the beginning.

These comments are not to critisie at all. They are meant to stimulate thought and discussion. The approach here is completely acceptable.

 

[Planktonmd]

This is probably ischemic bowel with perforation and sepsis that was left untreated too long, probably at the hepatic flexure with infection extending to the liver which explains the high bili abd now heading toward DIC.
It's not rocket science: Fluids, Pressors (maybe some vasopressin), blood products as needed...
Just keep fixing the hemodynamics while the surgeon cleans her up

 

[deleted171991]

I'm not aware of bicarb causing harm. At the speed things are moving I don't see it being a choice. I'm aware is not standard of care.

My cardiac attendings were never in the room. They couldn't teach me anything, either good or bad.

I found some cardiac anesthesiologists chasing pH numbers with bicarb to make the last ABG look good for the ICU.

Let me quote Marik again:

Except in specific circumstances (outlined below), there is no scientific evidence to support treating a metabolic or respiratory acidosis with sodium-bicarbonate [23]. Furthermore, it is the intracellular pH which is of importance in determining cellular function. The intracellular buffering system is much more effective in restoring pH to normal than the extracellular buffers. Consequently, patients have tolerated a pH as low as 7.0 during sustained hypercapnia without obvious adverse effects. Paradoxically, sodium-bicarbonate can decrease intra-cellular pH (in circumstances where CO2 elimination is fixed). The infusion of bicarbonate can lead to a variety of problems in patients with acidosis, including fluid overload, a post-recovery metabolic alkalosis and hypernatremia. Furthermore, studies in both animals and humans suggest that alkali therapy may only transiently raise the plasma bicarbonate concentration. This finding appears to be related in part to the carbon dioxide generated as the administered bicarbonate buffers excess hydrogen ions. Unless the minute ventilation is increased (in ventilated patients) CO2 elimination will not be increased and this will paradoxically worsen the intracellular acidosis. Currently, there is no data to support the use of bicarbonate in patients with an acidosis associated with an increased lactate concentration [23, 24].

 

[deleted171991]

This is why we can't rely on strict numbers to treat. When she entered the OR her Hct was low. You know you are going to give fluids and start some blood letting so why not just give the blood? Your next ABG would have shown better resuscitation if this were the approach. I used to do exactly what was done here. Then I found myself chasing numbers and not pt physiology. If this were the end of the case then this approach would have been acceptable IMO. But not at the beginning.

These comments are not to critisie at all. They are meant to stimulate thought and discussion. The approach here is completely acceptable.

I don't think this was just acidosis related to blood loss/hemodilution (if they only gave 1L of LR plus 1 bottle of albumin 25%). I am afraid this is DIC, with all the bad rheology in the microcirculation.

The surgeon needs to clean her up well and fast (at least compared to his usual speed), and get out of there before we get TRALI from all the blood products (that will need to be) given for hemostasis.

 

[Noyac]

I don't think this was just acidosis related to blood loss/hemodilution (if they only gave 1L of LR plus 1 bottle of albumin 25%). I am afraid this is DIC, with all the bad rheology in the microcirculation.

The surgeon needs to clean her up well and fast (at least compared to his usual speed), and get out of there before we get TRALI from all the blood products (that will need to be) given for hemostasis.

TRALI is a concern but we can't hold off on these products for fear of it occurring. Which I'm sure you aren't proposing.

You may be correct about DIC but in my experience she would have presented sicker. She may be headed this way but I don't think she is there yet. Howevere, plts are dropping and coats are rising. Time to start thinking about it and addressing the issues.

 

[sevoflurane]

Doesn't metabolic acidosis inhibit the ability of indogenous and exogenous catecholamines from working maximally? Doesn't acidosis inhibit myocardial performance?

 

[Planktonmd]

Doesn't metabolic acidosis inhibit the ability of indogenous and exogenous catecholamines from working maximally? Doesn't acidosis inhibit myocardial performance?

Absolutely!
And this is why you should not be afraid to give sodium bicarb when your pressors don't seem to work as expected.
It might be a temporary fix but it buys you time.

 

[deleted171991]

Doesn't metabolic acidosis inhibit the ability of indogenous and exogenous catecholamines from working maximally? Doesn't acidosis inhibit myocardial performance?

Only in severe acidosis (pH under 7.10). That's why one doesn't give bicarb routinely during CPR.

Here's the link to the specific Uptodate article: Bicarbonate therapy in lactic acidosis.

However, we do not recommend bicarbonate therapy in patients with less severe acidosis (pH 7.1 or greater). Two randomized trials failed to find a benefit of bicarbonate therapy in critically ill patients with lactic acidosis and pH values greater than 7.1:

 

[Planktonmd]

Only in severe acidosis (pH under 7.10). That's why one doesn't give bicarb routinely during CPR.

There is nothing scary about bicarb