New article from the New England Journal of Medicine:
Key points for the trauma anesthesiologist…
- 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.
- Cardiogenic or hypovolemic shock, advanced heart failure, sepsis, and severe trauma account for the majority of lactic acidosis.
- 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.
- Goals of therapy include normal hemodynamics, HGB 7-10, pH > 7.2, O2 sat > 92, declining lactate.