Lactic Acidosis

New article from the New England Journal of Medicine:

Lactic Acidosis NEJM 2014

Key points for the trauma anesthesiologist…

1. The diagnosis of lactic acidosis is best made by the serum lactate level. Anion gap and decline in the serum HCO3 levels, although suggestive of lactic acidosis are non-specific and can be caused by other acid-base disorders.
2. Cardiogenic or hypovolemic shock, advanced heart failure, sepsis, and severe trauma account for the majority of lactic acidosis.
3. Treatment consists of restoring tissue perfusion with crystalloid, colloid, vasopressors, and inotropes, improving the microcirculation, initiating cause-specific measures (see the article), and base administration.
   • Vasopressors and inotropes are best avoided in trauma. They can lead to a false sense that bleeding has been controlled and that resuscitation is adequate when they are not.
   • In my opinion, colloids are best avoided. If a colloid is given, it should be albumin.
   • Normal saline is best avoided because it can generate or exacerbate metabolic acidosis whereas balanced salt solutions do not. PlasmaLyte is compatible with banked blood, lactated Ringer is not.
   • Dobutamine, acetylcholine, and nitroglycerin improve microvascular perfusion.
   • NaHCO3 administration is not benign. The CO2 produced/accumulated causes intracellular acidosis and the elevated pH causes a decrease in ionized calcium, which modulates cardiac contractility. THAM, another buffer, is approved for clinical use.
4. Goals of therapy include normal hemodynamics, HGB 7-10, pH > 7.2, O2 sat > 92, declining lactate.

More on the deleterious effect of “(ab)normal” saline

An interesting article and an editorial from Anesthesia Analgesia:

• Hyperchloremia After Noncardiac Surgery

• Should Normal Saline Be Our Usual Choice?

It is becoming more clear that the hyperchloremia associated with infusion of normal saline is not benign:

Hyperchloremic metabolic acidosis is not a benign, self-limiting, metabolic disturbance. We found that acute postoperative hyperchloremia in patients undergoing noncardiac surgery was associated with increased mortality, renal dysfunction, and length of hospital stay.

As the editorial points out, several things are clear:

1. hyperchloremia is more common with 0.9% saline than with balanced crystalloid solutions
2. hyperchloremia is associated with worse outcomes
3. there are better alternatives to 0.9% saline in most clinical situations (excluding hypochloremic metabolic alkalosis)
4. until an adequately powered randomized clinical trial proves us wrong, 0.9% saline will not be our crystalloid of choice for intravascular volume resuscitation in surgical patients.

Nice review of resuscitation fluids

This article appeared in the New England Journal of Medicine:

Resuscitation Fluids

Particularly important is the section on crystalloids.

Some important aspects are highlighted.

This manuscript helps us get closer to stopping the knee jerk use of so-called normal saline as the “resuscitation fluid of choice” and for the dilution of packed red blood cells.

The real indication for normal saline resuscitation is traumatic brain injury (TBI)  and hyponatremia/hypochloremia.

Except in cases of TBI and hyponatremia/hypochloremia, plasmalyte is a much better resuscitation fluid, as it does not cause hyperchloremic acidosis and it is compatible with the infusion of packed red blood cells.

The bottom lines:

Although the use of resuscitation fluids is one of the most common interventions in medicine, no currently available resuscitation fluid can be considered to be ideal.

In light of recent high quality evidence, a reappraisal of how resuscitation fluids are used in acutely ill patients is now required.

The selection, timing, and doses of intravenous fluids should be evaluated as carefully as they are in the case of any other intravenous drug, with the aim of maximizing efficacy and minimizing iatrogenic toxicity.

Clarification of Base Excess and the Need for NaHCO3 Infusion

Base Excess (BE) is a calculated value:

BE _(mEq/l) = HCO3 _(observed) + 10 [pH _(observed) -7.40] – 24

The BE has a range of normal of -4 to +4.

The reason for this is that the calculation is based on the pH and the  bicarbonate, each of which has its own normal range.

The normal range for HCO3 is 21-28 mEq/L, and that of  the pH is 7.35-7.45.

Remember that in trauma we deal almost exclusively with metabolic acidosis.

Therefore, we are concerned only with BEs that are MORE NEGATIVE than MINUS FOUR.

A BE less negative than -4 or less, does not need to be treated with sodium bicarbonate.

For example, a 70 Kg patient with a BE of -4 would appear to require ([0.3X70X-4]/50) or 1.7 amps of NaHCO3, when in fact (s)he requires no treatment.

Look also at the chloride and the lactate. When these are more than “mildly” elevated, and there is a BE more negative than -4, then NaHCO3 treatment is indicated.

Three Goals

Prevent the Lethal Triad (hypothermia, coagulopathy, acidosis)

• Temperature 37 degrees
  • Room temperature up
  • Active warming devices
  • Warm fluids
• INR 1.0, Platelet Count > 50K
  • Limit crystalloid to minimize clotting factor dilution
    • Tolerated Systolic BP 80-90 in healthy non-TBI injured patients
  • Transfuse plasma:PRBC:platelets in ratio of 1:1:1
  • Give tranexamic acid (1 gram) within three hours of injury, then 1 gram over next 8 hours
• Base Excess 0
  • Treat hyperchloremia
    • Stop transfusing normal saline
    • Use PlamaLyte (has no calcium, compatible with RBC transfusions)
    • Give NaHCO3 for hyperchloremia
  • Prevent lactic acidosis
    • Maintain adequate perfusion pressure

A Personal Campaign Against Iatrogenic Acidosis

Major Complications, Mortality, and Resource Utilization After
Open Abdominal Surgery

0.9% Saline Compared to Plasma-Lyte

Andrew D. Shaw, MB, FRCA, FCCM,∗ Sean M. Bagshaw, MD,† Stuart L. Goldstein, MD,‡ Lynette A. Scherer, MD,§
Michael Duan, MS, Carol R. Schermer, MD,¶ and John A. Kellum, MD#

Ann Surg 2012;255:821–829

Click this link to view the article: Saline versus plasmalyte

The purpose of this study was to evaluate adult patients undergoing major open abdominal surgery who received either 0.9% saline (30,994 patients) or a balanced crystalloid solution (926 patients).

The major findings of this study are:

1. The in-hospital mortality was 5.6% in the saline group and 2.9% in the balanced group (P < 0.001).
2. One or more major complications occurred in 33.7% of the saline group and 23% of the balanced group (P < 0.001).
3.  Treatment with balanced fluid was associated with fewer complications (odds ratio 0.79; 95% confidence interval 0.66–0.97).
4.  Postoperative infection (P = 0.006), renal failure requiring dialysis (P < 0.001), blood transfusion (P < 0.001), electrolyte disturbance (P = 0.046), acidosis investigation (P < 0.001), and intervention (P = 0.02) were all more frequent in patients receiving 0.9% saline.

The body defends its so-called milieu. Electrolytes are kept within a narrow range, as is the pH at 7.4. Temperature is also maintained at 37 degrees Celsius. Through evolution, this is the environment in which enzymes and metabolic processes work most efficiently. In fact, acidosis and hypothermia are two components of the triad of death (the third is coagulopathy).

During a trauma, we spend much of our time correcting hypothermia, hypovolemia, and coagulopathy, while the acidosis gets scant attention. This is probably because we believe that the acidosis is owing to hypoperfusion and once circulation is restored the body will correct the acidosis. Yet, isn’t it feasible that while we are fixing the hypovelemia, the acidosis will contribute to the coagulopathy by inhibiting the many enzymes of the clotting cascade?

More importantly the acidosis is iatrogenic in the majority of trauma. It is due to the administration of excessive amounts of normal saline (NS).  Actually “normal saline” is anything but normal and one speaker at a recent anesthesiology meeting referred to it as “AB-normal saline.” NS contains an excess of sodium and chloride. As little as two liters of NS is enough to cause hyperchloremic acidosis. Many physicians view hyperchlormic acidosis as inconsequential. However in a trauma where the pH is 7.0, it is anything but inconsequential and more often than not it is the greatest cause of acidosis.

In my practice, I find that the base excess in a traumatized healthy individual is nearly always [-1 X (chloride excess + lactic acid)]. In many cases it is the chloride excess, not the lactic acid,  that is the greatest contributor to the low pH (see blog on blood gas interpretation under categories, left side of screen). This acidosis owing to excess chloride is easily arrested by simply taking down all of the NS that is hanging and hanging Plama-Lyte in its place.

While the acidosis can be arrested in this way, the already present low pH will also need to be addressed and that is done by giving sodium bicarbonate or THAM.

A more appropriate solution to this problem would be to prevent developing the hyperchloremic acidosis at the outset by avoiding NS in the field, the emergency room, and operating room. Instead give Plasma-Lyte. Unlike Lactated Ringer’s solution, Plasma-Lyte contains no calcium and it is compatible with blood products.

Unfortunately, changing the trauma culture from NS to Plasma-Lyte will not be easy. But that is my “Personal Campaign Against Iatrogenic Acidosis.”

Hyperchloremic Acidosis

This post is unfinished

Hyperchloremic acidosis caused by large 0.9% saline infusions seems to be benign, unless it is confused with hypoperfusion. The pH values greater than 7.20 do not seem to have major pathophysiologic implications in the clinical setting we describe. Nevertheless, we believe that hyperchloremic acidosis caused by a 0.9% saline infusion should be treated to provide a BE close to zero at the end of surgery (or, alternatively, lactated Ringer’s solution should be used). In our experience in the early postoperative period, metabolic acidosis caused by hyperchloremia and respiratory acidosis caused by opiate analgesics may become additive and result in pH values much less than 7.20. A systematic analysis of this topic might provide valuable information. Scheingraber, et al

In trauma patients who respond to bolus crystalloid administration, hyperchloremic acidosis, is the most common cause of metabolic acidosis and it is often confused with an acidosis owing to hypoperfusion. It is obviously important to differentiate between the two, because hyperchloremic acidosis is relatively benign and that owing to hypoperfuison dangerous. These two types of acidosis are easily distinguished.

Hyperchloremic acidosis: Base Excess is negative, bicarbonate is low, chloride is elevated, lactic acid is normal.

Acidosis due to hypoperfusion: Base Excess is negative, bicarbonate is low, chloride is normal, lactic acid is elevated.

So don’t just look at the bicarbonate and assume that if it is low, the cause is hypoperfusion and lactic acidosis. Our ABG lab reports the Base Excess, bicarbonate, chloride, and lactic acid (if you ask for it). Look at them all to determine the cause of the acidosis. In the majority of cases an elevated chloride +/- an elevated lactate will account for nearly all of the negative Base Excess.

Hyperchloremic acidosis stems from giving too much 0.9% NaCl. Normal Saline is the solution given to trauma patients by paramedics and emergency room physicians. By the time these patients arrive in the operation room, they have been “flooded” with Normal Saline and already have a hyperchloremic acidosis.

Hyperchloremic acidosis can be mitigated/avoided by stopping all Normal Saline infusions and switching to Plasmalyte as soon as possible. Unlike Lactated Ringers, Plasmalyte contains no calcium and it is compatible with blood and blood product transfusions.

Hyperchloremic acidosis is also referred to as “dilutional acidosis.” I suspect this refers to dilution of plasma bicarbonate by volume administration. However the decline in the bicarbonate occurs only with volume administration of Normal Saline and not with Lactated Ringers or Plasmalyte. (see Figure 1 and Table 2, Scheingraber, et al)

The reader who wants more detail is referred to this treatise (Yearbook of Intensive Care and Emergency Medicine 2009, pp 221-232): hyperchloremic acidosis.

Briefly, strong cations predominate in the body leading to a net positive plasma charge that is described as the Strong Ion Difference (SID) by the following formula: SID (+40) = [Na+ + K+ + Ca2+ + Mg2+] – [Cl- + lactate-].

This net positive charge must be counterbalanced with an equal negative charge to satisfy the Law of Electrical Neutrality.

The balancing negative charge derives from nonvolatile weak acids is accounted for
as Atot (total weak acids). In plasma, these weak acids include albumin and inorganic phosphates.

Here is a simple question. If NS is so useful in the field and Emergency Room, why don’t we use it routinely in the operating room? Why do we use LR instead?

Solution	Na	K	Ca	Mg	Cl	Lactate	Acetate	Gluconate	Osmol	pH	pH range
LR	130	4	2.7	—	109	28	—	—	273	6.5	6.0-7.5
NS	154	—	—	—	154	—	—	—	308	5.0	4.5-7.0
Plasmalyte	140	5	—	3	98	—	27	23	294	7.4	6.5-8.0

Values are mEq/L

Solution	NaCl	KCl	CaCl2	MgCl	NaLactate	NaAcetate	NaGluconate	Osmol	pH	pH range
LR	600	30	20	—	310	—	—	273	6.5	6.0-7.5
NS	900	—	—	—	—	—	—	308	5.0	4.5-7.0
Plasmalyte	526	37	—	30	—	368	502	294	7.4	6.5-8.0

Values are mg/100mL

Text continues from here.

Interpretation of blood gases during trauma

Actual blood gases from a patient that I took care of two nights ago.

The first thing I look at is the Base Excess (BE). BE is a calculated value:

BE _(meq/l) = HCO3 _(observed) + 10 [pH _(observed) -7.40] – 24

If it is negative there is acidosis. If it is positive then there is alkalosis (rarely if ever seen in  a trauma patient). This patient arrived with a BE of -13, severe acidosis. In trauma, there are usually two contributors to this kind of BE, lactic acidosis and hyperchloremia. In the first ABG (far left) I would have expected the BE to be closer to -7. One unit owing to chloride 107 (upper limit of normal is 106) and 6 units owing to the lactate of 6. I can not explain the -13 unless the chloride is a lab error. The middle left and the middle right ABGs are more what I expect. The -12 (middle left ABG) is due to chloride 116 (ten units higher than normal) and the lactate of 3. The middle right ABG was after two amps of bicarb were given. This drove the chloride down to 108 (two units above normal) plus the lactate of 1.8 = BE -3.

If there are other unmeasured acids in the patient, this will be reflected in an elevated anion gap.

The other parameter to look at is the pCO2. Try to keep it around 40 by changing the ventilator tidal volume or frequency as necessary.

The pH doesn’t tell me much as it is the result of what is going on with ventilation AND metabolically. By itself, it does not point to the cause of the derangement the way that looking at the BE, Cl, and lactic acid do.

I pay little attention to the bicarbonate. It moves inversely to the Cl and the lactate. Surgeons used to follow the bicarbonate in a trauma reasoning that its decline was due to a rising lactate owing to poor perfusion and their response was to give more and more blood, which was diluted with normal saline, which in turn caused hyperchloremia and more bicarbonate excretion by the kidney. A viscous cycle. It is best to transfuse on the basis of the HGB instead of the bicarbonate.

A rising lactate is indicative of hypoperfusion and shock. This is treated by increasing perfusion (blood transfusion most often, inotropes rarely).

Hyperchloremia is treated with sodium bicarbonate. It can be prevented by diluting blood with Plasmalyte instead of with normal saline or giving sodium bicarbonate if normal saline is used to dilute blood.

CORRECTION OF ACIDOSIS with sodium bicarbonate:

0.3 X BE X Kg