No problem, Just a Lap Chole

[deleted171991]

There is nothing scary about bicarb

Uptodate:

"Potential harms of bicarbonate therapy — Rapid infusions of sodium bicarbonate have a number of potentially adverse effects:

●Increased arterial and tissue capillary PCO2

●Acceleration of lactate generation

●Reduced ionized calcium

●Hypernatremia

●Extracellular fluid (ECF) volume expansion"

"Even with adequate ventilation, the PCO2 is likely to rise at the local tissue level when bicarbonate is infused. Because CO2 readily penetrates cell membranes, this increase in tissue PCO2 may worsen intracellular acidosis even as arterial blood pH increases. This dissociation between tissue and systemic arterial acid-base parameters is magnified in patients with circulatory failure [13,14].

The cerebrospinal fluid (CSF) pH may also fall when bicarbonate is infused for two reasons: first, the mechanism described above increases the PCO2 locally in the brain and CSF; second, amelioration of systemic acidemia (ie, the rise in arterial blood pH) diminishes the drive for hyperventilation, causing the systemic PCO2 to increase. Any systemic and/or local increase in PCO2 will be quickly reflected within the CSF. In contrast, an increased blood bicarbonate concentration is only slowly transmitted to the CSF. Because CSF bicarbonate concentration does not rise as rapidly as the CSF PCO2, "paradoxical" CSF acidemia results and may be associated with neurologic deterioration [15,16]."

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[urge]

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:

None of that looks like strong evidence. I just don't see the harm, considering that co2 is low even during laparoscopy.

 

[deleted171991]

"SUMMARY AND RECOMMENDATIONS

●The role of exogenous bicarbonate therapy in patients with lactic acidosis is controversial. Most experts believe that it is appropriate to use bicarbonate in acutely ill patients with profound lactic acidosis and acidemia (arterial pH less than 7.1 and serum bicarbonate 6 meq/L or less). Such severe acidemia may produce hemodynamic instability as a result of reduced left ventricular contractility, arterial vasodilation, and impaired responsiveness to catecholamines. (See 'Introduction' above.)

●The following general approach applies to the use of bicarbonate therapy in patients with lactic acidosis (see 'Overview of therapy' above):

•The primary aim of therapy for lactic acidosis is reversal of the underlying disease(eg, shock). (See 'Therapeutic goal' above.)

•We suggest that patients with lactic acidosis and severe acidemia (pH less than 7.1 and serum bicarbonate 6 meq/L or less) receive sodium bicarbonate therapy. (See 'Which patients should receive bicarbonate therapy' above.)

•When using bicarbonate therapy in patients with lactic acidosis and severe acidemia, the aim is to maintain the arterial pH above 7.1 until the primary process causing the metabolic acidosis can be reversed. (See 'Therapeutic goal' above.)

•In adequately ventilated patients with lactic acidosis and severe acidemia, we give 1 to 2 meq/kg sodium bicarbonate as an intravenous bolus. We repeat this dose after 30 to 60 minutes if the pH is still less than 7.1. (See 'Approach' above.)

•Rapid infusions of sodium bicarbonate may increase the PCO2, accelerate the production of lactate, lower the ionized calcium, expand the extracellular space, and raise the serum sodium concentration. (See 'Potential harms of bicarbonate and alternative agents' above.)

•There is little evidence that any alternative buffering agents are superior to bicarbonate therapy. (See 'Potential harms of bicarbonate and alternative agents' above.)"

 

[Noyac]

There is nothing scary about bicarb

Actually there may be. The intracellular acidosis may worsen with biCarb administration.

There are definitely two camps when it comes to bicarb usage. I am in the "don't give it" camp. But I don't necessarily criticize those in the other camp. This debate has waged on for as long as I have been in this business. If you have a good reason for giving it then give it. Just remember, there are those out there that will disagree.


Ps: I was typing this response the same time FFP was typing his. It looks like we are both in the "don't give it" camp.

 

[urge]

Uptodate:

"Potential harms of bicarbonate therapy — Rapid infusions of sodium bicarbonate have a number of potentially adverse effects:

●Increased arterial and tissue capillary PCO2

●Acceleration of lactate generation

●Reduced ionized calcium

●Hypernatremia

●Extracellular fluid (ECF) volume expansion"

"Even with adequate ventilation, the PCO2 is likely to rise at the local tissue level when bicarbonate is infused. Because CO2 readily penetrates cell membranes, this increase in tissue PCO2 may worsen intracellular acidosis even as arterial blood pH increases. This dissociation between tissue and systemic arterial acid-base parameters is magnified in patients with circulatory failure [13,14].

The cerebrospinal fluid (CSF) pH may also fall when bicarbonate is infused for two reasons: first, the mechanism described above increases the PCO2 locally in the brain and CSF; second, amelioration of systemic acidemia (ie, the rise in arterial blood pH) diminishes the drive for hyperventilation, causing the systemic PCO2 to increase. Any systemic and/or local increase in PCO2 will be quickly reflected within the CSF. In contrast, an increased blood bicarbonate concentration is only slowly transmitted to the CSF. Because CSF bicarbonate concentration does not rise as rapidly as the CSF PCO2, "paradoxical" CSF acidemia results and may be associated with neurologic deterioration [15,16]."

Are those bad things? CO2 will be gone within a minute, so the csf effect well be short lived.

Your quote says maybe. We know what that means. Maybe yes, maybe no.

 

[Planktonmd]

All those pearls about how evil sodium bicarb is and how lactic acidosis should be treated by fixing the cause are fantastic... but when you have a patient in septic shock in the OR, your pressors are not working and you are watching the BP decline quickly, it's OK give a couple of amps of bicarb even if it pisses off the Gods of published articles.

 

[deleted171991]

Surviving Sepsis Campaign Guidelines (2012):
Recommend "Not using sodium bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidemia with pH≥7.15 (grade 2B)".

http://www.survivingsepsis.org/Guidelines/Documents/Other supportive therapy.pdf

 

[deleted171991]

All that stuff about how evil sodium bicarb is and how lactic acidosis should be treated by fixing the cause is fantastic... but when you have a patient in septic shock in the OR, your pressors are not working and you are watching the BP decline quickly, it's OK give a couple of amps of bicarb even if it pisses of the gods of published articles.

Sure. But you'll rarely have those pressors not working at a pH of 7.20. Also consider which pressors you are using (first two in sepsis should be norepi and low dose vaso).

 

[pd4emergence]

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?

Ok, So the second set of labs were sent while the case was still laparoscopic. The belly had not been opened.

 

[deleted162650]

get out of there before we get TRALI from all the blood products (that will need to be) given for hemostasis.

Our understanding of TRALI is evolving as well. I believe we have followed Europe's lead of not allowing multiperous women to donate plasma which has gone a long way to reducing the incidence. Additionally, TRALI rates in trauma have decreased since moving to 1:1:1 resuscitation and limiting crystalloid administration which is the opposite of what you would expect.

 

[deleted171991]

Ps: I was typing this response the same time FFP was typing his. It looks like we are both in the "don't give it" camp.

What's the reason to give it? It will correct the intravascular pH, while worsening intracellular acidosis? Where do those catecholamines act, and those myocytes contract? In the extracellular, or in the intracellular space?

Just wondering...

 

[Noyac]

Are those bad things? CO2 will be gone within a minute, so the csf effect well be short lived.

Your quote says maybe. We know what that means. Maybe yes, maybe no.

The intracellular and CSF CO2 will not decrease nearly as rapidly as the blood. So with bicarb, it is my opinion that people are just correcting numbers not physiologic states. Hopefully, they are not harming the pt in the process.

But look at it this way. There is more debate when trying to justify its use then when trying to justify not using it. The debate seems to hinge on, does it cause more harm?

Actually what they need is volume in this situation to improve perfusion. That is what will resolve the issue best.

 

[deleted171991]

Our understanding of TRALI is evolving as well. I believe we have followed Europe's lead of not allowing multiperous women to donate plasma which has gone a long way to reducing the incidence. Additionally, TRALI rates in trauma have decreased since moving to 1:1:1 resuscitation and limiting crystalloid administration which is the opposite of what you would expect.

Somewhat the opposite. Crystalloids have well-known pro-inflammatory effects.

 

[deleted171991]

Actually what they need is volume in this situation to improve perfusion. That is what will resolve the issue best.

They don't need volume, unless they lost volume. It's a septic patient, now also trending towards DIC. Leaky capillaries all around; hypervolemia is proven to worsen the leak (natriuretic peptides, blah-blah).

That laparoscopy probably did not help with hemodynamics/acidosis either.

 

[Planktonmd]

Sure. But you'll rarely have those pressors not working at a pH of 7.20. Also consider which pressors you are using (first two in sepsis should be norepi and low dose vaso).

Man... this is similar to people having long debates about giving steroids or not in a patient who is on steroid therapy and hypotensive... it' smuch easier to just give the damn thing

What's the reason to give it? It will correct the intravascular pH, while worsening intracellular acidosis? Where do those catecholamines act, and those myocytes contract? In the extracellular, or in the intracellular space?

Just wondering...

It does work and it does improve the hemodynamics when nothing else works.
It might be simply the sodium load... who knows? But it's a pretty harmless intervention and it does buy time.
I actually find it funny that you want to wait until the PH is 7.1 to give bicarb! Let's say that you last ABG showed a PH of 7.2 but now your patient has become unstable and not responding to what ever pressors you are giving, you would send a new ABG to see if the PH is now 7.1?

 

[deleted171991]

Man... this is similar to people having long debates about giving steroids or not in a patient who is on on steroid therapy and hypertensive...

It does work and it does improve the hemodynamics when nothing else works.
It might be simply the sodium load... who knows? But it's a pretty harmless intervention and it does buy time.
I actually find it funny that you want to wait until the PH is 7.1 to give bicarb! Let's say that you last ABG showed a PH of 7.2 but now your patient has become unstable and not responding to what ever pressors you are giving, you would send a new ABG to see if the PH is now 7.1?

Obviously not. But that just proves that bicarb is a last-resort measure.

You might improve hemodynamics and ABG temporarily with bicarb. The question is whether you improve the outcome, the intracellular physiology. And that's where there is no proof it helps. Patients die/survive during the first 30 days regardless of it.

 

[Noyac]

They don't need volume, unless they lost volume. It's a septic patient, now also trending towards DIC. Leaky capillaries all around; hypervolemia is proven to worsen the leak (natriuretic peptides, blah-blah).

That laparoscopy probably did not help with hemodynamics/acidosis either.

Volume is blood, FFP plts. This pt will need these.

 

[urge]

Obviously not. But that just proves that bicarb is a last-resort measure.

You might improve hemodynamics and ABG temporarily with bicarb. The question is whether you improve the outcome, the intracellular physiology. And that's where there is no proof it helps. Patients die/survive during the first 30 days regardless.

What do you (or Marik) have to say about nephrologists running bicarb drips all the time?

 

[deleted171991]

What do you (or Marik) have to say about nephrologists running bicarb drips all the time?

There are a few clear indications for bicarb. One is hyperchloremic metabolic acidosis iatrogenically induced by the abnormal saline given by one's dear doctor. With NS-induced hyperchloremic metabolic acidosis, the patient literally pees out his bicarb, never to see it again.

Another indication would be a bicarb-losing renal tubular acidosis. Another one is diarrhea. The hallmark is that the body is losing bicarb either in the urine or stool.

Plus metabolic acidosis in chronic kidney disease. Same story: the body loses bicarb.

P.S. I have only started reading the last edition of Marik's book.

 

[Planktonmd]

The way I see resuscitation of a patient in shock in the OR is that you give all you have even if the 30 days survival was not proven in a double blind controlled study

 

[ranvier]

How about giving tham?

 

[pd4emergence]

After the second set of labs, we started getting some products into the room. I did redraw the ABG as a fast way to determine the hemoglobin, it was 6. I also go a TEG and a fibrinogen at this time. TEG eventually showed what you would expect, a pretty coagulopathic picture. Fibrinogen was around 100. Also started a vasopressin infusion around this time. At this point they are just getting into the belly, surgeons say they haven't lost much blood. Starting Hct was 38.......

 

[Noyac]

Anyone ready to go my route and start giving products?

She was probably extremely hypovolemic and therefore the Hct was higher until you stared to resuscitate and now it's lower.

 

[Planktonmd]

If there was bleeding inside the abdomen your surgeon should have seen it on the laparoscopy, so if she is bleeding it's got to be retroperitoneal bleeding or hematoma with consumption, so is it a ruptured or leaking AAA???

 

[deleted171991]

There doesn't have to be necessarily bleeding. Hemolytic microangiopathic anemia, part of DIC, should be enough.

 

[Noyac]

How about giving tham?

• I likeTham. It works great. But this pt's pH isn't so low as to require it yet. She needs products.
• THAM is to be used instead of bicarb. Think pH under 7.2

 

[Planktonmd]

There doesn't have to be necessarily bleeding. Hemolytic microangiopathic anemia, part of DIC, should be enough.

The hemoglobin is dropping too quickly for just DIC

 

[risnwb]

I've read a few papers which suggest that bicarb doesn't even improve responsiveness to pressors.. Anyone have a paper that indicates it actually DOES improve this? Every time I've given it as an attempt to improve responsiveness I have not seen a response. So I am also in the no bicarb camp unless special circumstances dictate its use.

 

[OB1🤙]

I'll weigh in on bicarb, as another non-giver.

Aside from the issue of intracellular acidosis already pointed out, I think people lose sight of the fact that mild acidosis is actually good for you from an oxygen offloading perspective.

Yet you see people giving bicarb to mildly acidotic people all the time, *as if they think the acidosis itself is causing harm.* It isn't. If you have an ischemic tissue bed, you would much rather be acidotic than alkalotic so as to promote oxygen offloading, but you NEVER see people treat alkalosis.

So if you're going to give bicarb, you should be in the pH <7.2, escalating pressors, kitchen sink mode. Otherwise, even though you may feel better since you're doing something, what you're doing isn't helping and may be hurting.

THAM is OK, but again, only indicated if the acidosis itself is causing badness, which it usually isn't.

 

[OB1🤙]

Anyone ready to go my route and start giving products?

She was probably extremely hypovolemic and therefore the Hct was higher until you stared to resuscitate and now it's lower.

Yup.

 

[BLADEMDA]

Yup.

I've been invloved with hundreds of these cases. The O.R. is a war zone while the ICU is where the Generals pontificate about strategy. We must deal with acute, rapidly deteriorating hemodynamics which require URGENT action. This means we give FFP,Prbcs, Platelets along with lots of fluids. The pressors/Inotropes are utilized as well.

Again, the O.R. is not the ICU and while we can learn much from Critical Care the treatment of the case INTRAOP is not the same as when the patient arrives in the Unit.

As for overloading this patient with fluid I don't see that very often as most of the time in the PACU they end needing even more Fluids, Blood, etc.

 

[deleted171991]

I've been invloved with hundreds of these cases. The O.R. is a war zone while the ICU is where the Generals pontificate about strategy. We must deal with acute, rapidly deteriorating hemodynamics which require URGENT action. This means we give FFP,Prbcs, Platelets along with lots of fluids. The pressors/Inotropes are utilized as well.

Again, the O.R. is not the ICU and while we can learn much from Critical Care the treatment of the case INTRAOP is not the same as when the patient arrives in the Unit.

As for overloading this patient with fluid I don't see that very often as most of the time in the PACU they end needing even more Fluids, Blood, etc.

There is no shame in actually knowing and applying that critical care "strategy" in the OR. In the end, we are talking about medical science. Just because we are entombed in our old ways in the OR doesn't make them right. Whenever there is a chance to improve outcomes, we should take it.

For example, we don't do simple things that we could do with zero effort. We don't ventilate our patients with 6 ml/kg, and up to 14-18 breaths/min (as needed), which is much closer to physiologic. We don't use PEEP in every patient. We don't know that volume causes trauma, regardless of pressure, so we think it's fine to run 8-10 ml/kg on pressure control, as long as we do it at inspiratory pressures of less than 20-30. We use PACs when they are proven not to help except for right-sided issues. We don't take special care to run our patients on the dry side, using pressors instead of fluids, despite all the studies showing it leads to better outcomes (and that study was about intraop patients). Etc. I bet the list is long.

The Sun revolves around the Earth, and we'll be damned if we'll believe the opposite just because a pompous arse from the ICU thinks so.

 

[urge]

I'll weigh in on bicarb, as another non-giver.

Aside from the issue of intracellular acidosis already pointed out, I think people lose sight of the fact that mild acidosis is actually good for you from an oxygen offloading perspective.

Yet you see people giving bicarb to mildly acidotic people all the time, *as if they think the acidosis itself is causing harm.* It isn't. If you have an ischemic tissue bed, you would much rather be acidotic than alkalotic so as to promote oxygen offloading, but you NEVER see people treat alkalosis.

So if you're going to give bicarb, you should be in the pH <7.2, escalating pressors, kitchen sink mode. Otherwise, even though you may feel better since you're doing something, what you're doing isn't helping and may be hurting.

THAM is OK, but again, only indicated if the acidosis itself is causing badness, which it usually isn't.

I see a fair number of people getting acetazolamide in the ICU for metabolic alkalosis. Have seen a handful get ammonium chloride. Plus, a lot of them are only treated with fluids. So, I wouldn't say alkalosis is NEVER treated.

We can agree to disagree on the bicarb until higher quality evidence is available. Until then this conversation will end with a MAYBE.

May we continue with the thread, since it looks like this bicarb discussion is going nowhere?

 

[Noyac]

We don't ventilate our patients with 6 ml/kg, and up to 14-18 breaths/min (as needed), which is much closer to physiologic. We don't use PEEP in every patient.

Um, that's exactly how I ventilate pts.

 

[BLADEMDA]

Um, that's exactly how I ventilate pts.

This discussion is going nowhere. We can pontificate about extrapolating studies from the ICU or elective Bowel Surgery to this unstable, rapidly deteriorating patient or most us can use good, common sense judgment to provide adequate resuscitation to this patient. From my years of doing this the vast majority of patients are under-resuscitated in the Operating room and their ongoing condition requires even more volume, products in the PACU. Of course, my care has changed over the years to include SVV, SV, TEE, Blood gases, etc to better gauge volume requirements but this hasn't altered the fact that these types of cases are very challenging and require lots of volume, blood, products, etc. Better monitoring doesn't mean we lose our common sense.

As for the VENTILATION mode in the O.R. many of us are aware of the reduced tidal volume, increased resp. rate with PEEP Strategy. Again, we would be extrapolating the data to make it fit in this type of case where recruitment manuevers may NOT Be occurring on a regular basis due to the acute nature of the case. So, are we doing more harm than good if we miss or skip the recruitment maneuver here? Some would say yes. Please don't confuse my statements about Ventilation to mean that I'm not in favor of the strategy but rather that strategy comes with strings attached as well as less than definitive proof it actually changes outcome in these types of cases.

 

[sevoflurane]

This is a discussion. It's all good y'all.

I don't think people are saying to drop a couple of amps of bicarb for a ph of 7.2. Saying otherwise is just crazy. Metabolic acidosis that is not due to hypovolemia in the 6.8 range? then HELL yeah... Give it. No questions. Little harm and big up potential in some patients. If you are sure it's due to hypovolemia or a heme issue... then fix that first, but you should correct the acidosis in the meantime... going up on your pressors cuz they don't work will just exacerbate the situation via the splanchnic circ and vasoconstriction. This is all really simple stuff peeps.

 

[pd4emergence]

At this point we are giving products, her hemodynamics are not too bad considering. She's on some levo and vasopressin. We give her 4 or so of cell, ffp, cryo, platelets. Surgeons are working in the belly, it's open, no major vessel bleeding, no obvious bowel ischemia or pathology. The room kinda stinks though. Second read of the CT, shows a couple of gas containing abscesses in the right abdomen, one large one on the right. After getting past the bowel, they find some nastiness that looks like a tuboovarian abscess. The gyneciatrists are called and confirm that this is the case. We get more labs, they don't really look any better. Hemoglobin is like 7. Even after the 4 units....

 

[Ignatius J]

Curiously, what did her urine look like? If she had hemolysis on this level with DIC, there should be some pink tinge starting to show I would think. In that case, maybe sodium bicarb ain't such a bad idea after all.

 

[Planktonmd]

At this point we are giving products, her hemodynamics are not too bad considering. She's on some levo and vasopressin. We give her 4 or so of cell, ffp, cryo, platelets. Surgeons are working in the belly, it's open, no major vessel bleeding, no obvious bowel ischemia or pathology. The room kinda stinks though. Second read of the CT, shows a couple of gas containing abscesses in the right abdomen, one large one on the right. After getting past the bowel, they find some nastiness that looks like a tuboovarian abscess. The gyneciatrists are called and confirm that this is the case. We get more labs, they don't really look any better. Hemoglobin is like 7. Even after the 4 units....

This is starting to look very strange

 

[urge]

At this point we are giving products, her hemodynamics are not too bad considering. She's on some levo and vasopressin. We give her 4 or so of cell, ffp, cryo, platelets. Surgeons are working in the belly, it's open, no major vessel bleeding, no obvious bowel ischemia or pathology. The room kinda stinks though. Second read of the CT, shows a couple of gas containing abscesses in the right abdomen, one large one on the right. After getting past the bowel, they find some nastiness that looks like a tuboovarian abscess. The gyneciatrists are called and confirm that this is the case. We get more labs, they don't really look any better. Hemoglobin is like 7. Even after the 4 units....

So what's the surgical plan?

I would just keep replacing blood until something good or bad happens.

Can the surgeons assess for retroperitoneal bleeding?

 

[Noyac]

So what's the surgical plan?

I would just keep replacing blood until something good or bad happens.

Can the surgeons assess for retroperitoneal bleeding?

Just to be Devils advocate, why would there be a retroperitoneal bleed? I know crazy **** happens but! Is there anything besides the free air, which I don't think would fit the picture anyway since the air should not come from an aneurysm or should not be intraperitoneal if the bleed is retroperitoneal.

So why are you going there, urge? What am I missing?

 

[jwk]

Just to be Devils advocate, why would there be a retroperitoneal bleed? I know crazy **** happens but! Is there anything besides the free air, which I don't think would fit the picture anyway since the air should not come from an aneurysm or should not be intraperitoneal if the bleed is retroperitoneal.

So why are you going there, urge? What am I missing?

Somebody tear something with aggressive retraction?

 

[urge]

Just to be Devils advocate, why would there be a retroperitoneal bleed? I know crazy **** happens but! Is there anything besides the free air, which I don't think would fit the picture anyway since the air should not come from an aneurysm or should not be intraperitoneal if the bleed is retroperitoneal.

So why are you going there, urge? What am I missing?

Aren't the fallopian tubes retroperitoneal?

Just brainstorming. The thread seems to have stalled.

This thread needs some bicarb to get it going again.

 

[Noyac]

Aren't the fallopian tubes retroperitoneal?

Just brainstorming. The thread seems to have stalled.

This thread needs some bicarb to get it going again.

I see your bicarb and I raise you some pitocin.

 

[Planktonmd]

Just to be Devils advocate, why would there be a retroperitoneal bleed? I know crazy **** happens but! Is there anything besides the free air, which I don't think would fit the picture anyway since the air should not come from an aneurysm or should not be intraperitoneal if the bleed is retroperitoneal.

So why are you going there, urge? What am I missing?

If you suspect bleeding and you don't see blood inside the abdominal cavity you should always suspect a retro peritoneal bleed.
I have seen it a few times and it requires a high index of suspicion.
I had a patient in labor who almost died of a ruptured renal artery aneurysm with an abdomen that had no blood in it.

 

[Noyac]

If you suspect bleeding and you don't see blood inside the abdominal cavity you should always suspect a retro peritoneal bleed.
I have seen it a few times and it requires a high index of suspicion.

Ok. Where is it coming from?

 

[Planktonmd]

Ok. Where is it coming from?

Renal arteries? adrenals? big traumatic hematoma?

 

[Noyac]

Renal arteries? adrenals? big traumatic hematoma?

But this is an open case. Maybe if laparoscopic. I could see someone putting a trochar into something but not in an open case. Or was this laproscopic in the beginning?

 

[Planktonmd]

But this is an open case. Maybe if laparoscopic. I could see someone putting a trochar into something but not in an open case. Or was this laproscopic in the beginning?

It started laparoscopic

 

[Noyac]

It started laparoscopic

My short term memory at its best.