Asynchrony EM: I'm All About That (Acid/) Base
New to Asynchrony EM? It's an asynchronous learning course in its third year at Brown EM. Digital resources and #FOAMed are curated and packaged by topic, following Brown EM's curricular calendar. In the spirit of #FOAMed, we've started putting it out there for the EM community at large. Check out the theme song, the 'extras', and the discussion questions, and other modules -- and leave us your thoughts in the comments section. Follow us on Twitter at @AsynchronyEM.
Note: Brown EM residents must complete the modules (including discussion/quiz) in Canvas to obtain credit hours.
Here we are, continuing in our endocrine/metabolic curricular block --
Holy moly, I CAN HEAR YOU GROANING FROM HERE!! Of course, you are not groaning about my punny Meghan Trainor reference, but about the topics: ACID-BASE estimations and HYPONATREMIA, which are dry and difficult and one of several reasons why you are not training to be nephrologists. I get it. But I'm going to try to make this as painless and relevant as possible.
There is LOTS of optional content listed, because there's a LOT more you could be reading about this if you're so inclined. Also, some references are not open access #FOAMed, but worth finding if you have institutional access to the New England Journal of Medicine (Brown residents can link to the e-library through Canvas). However, you'll get enough from the #FOAM content that you'll know what you're talking about, and I've also summarized some of the points from the NEJM below.
And you already know the theme song. "All About That Bass," Meghan Trainor:
"Yeah, my mama, she told me, don't worry about chlor-i-ide..." (#alternativelyrics)
ACID/BASE 'PARADIGM SHIFT': MEET STEWART AND SID
Just when you thought you had it all figured out, along comes a "paradigm shift" in acid/base teaching and thinking. If you haven't met them before, allow me to introduce you to Stewart and SID. They've been around a while, but are becoming more popular--they are the new poster children of a growing anti-normal-saline campaign. (Repeat after me, ad nauseum: "There's nothing normal about normal saline. There's nothing normal about normal saline. There's...")
1) Drs. Westafer and Faust take it away in their introductory-level discussion on the Stewart Ion Method, SID (Strong Ion Difference), Acid-Base and Sodium in FOAMCast (21:18). The first half is acid/base, the second is core content review of hyponatremia. Click the little 'POD' icon to the left of the title. (Their explanation of why normal saline causes acidosis is simplified--it's not just the chloride content, it's the SID of the solution itself that matters--read/listen on.)
2) Four points to learn on Integration of Acid-Base and Electrolyte Disorders (November 6, 2014; N Engl J Med 2014; 371:1821-1831), from that bastion of complexity, the New England Journal of Medicine. Reading the whole article is useful but OPTIONAL (and Brown residents can link to our e-library from Canvas-- sorry it isn't an open access article) but HERE are the main teaching points:
Read/learn the four excerpt points below (a through d) regarding the Stewart (physiochemical) approach to acid/base thinking {versus the traditionally-taught bicarbonate based method (Henderson-Hasselbach, etc.)}. The emphases are mine.
a) "Strong ions such as sodium and chloride are assumed to be completely dissociated in body water but can be lost or gained disproportionately. When the sum of all negatively charged ions (predominantly chloride) is subtracted from the sum of all positively charged strong ions, a value known as the strong ion difference (in millimoles per liter) is introduced. The strong ion difference is calculated as shown below:
strong ion difference=[Na+]+[K+]+[Ca2+]+[Mg2+]−[Cl−]
b) "Any developed difference in the ionic charge, or strong ion difference, determines the bicarbonate concentration. Essential to this argument is that any difference in an unbalanced charge will immediately result in the appearance or disappearance of bicarbonate formed from ubiquitous and neutral carbon dioxide and water.
c) "Since the normal concentration ratio of sodium to chloride in extracellular fluid is approximately 140:100, an increase in the sodium level, a decrease in the chloride level, or both will increase the strong ion difference and the bicarbonate concentration will increase (metabolic alkalosis), according to electroneutrality requirements. When the strong ion difference decreases, pH and the bicarbonate level will decrease (metabolic acidosis).
d) "...saline-induced acidosis...develops because the infusion of a proportionately high sodium chloride–containing solution, one with a sodium-to-chloride ratio of less than 140:100, will decrease the plasma strong ion difference and the bicarbonate concentration. The insufficient urinary excretion of the extra chloride as ammonium chloride leads to metabolic acidosis."
3) Put it all together. This one is tough going, but try to stick it out! "Stewart Acid-Base: A Simplified Bedside Approach" by Dr. David Story (2016). Courtesy of EM:Crit.
4) Another subscription access NEJM review (N Engl J Med 2014; 371:2309-2319) on lactic acidosis. Basically driving home the already-made point that we should probably be thinking more about what fluids we use (unless you're one of those ahead-of-the-curve types.)
An excerpt:
"Crystalloid and colloid solutions are both effective in restoring tissue perfusion in patients with sepsis or hypovolemia. However, reports of acute kidney injury, bleeding, and increased mortality in association with hydroxyethyl starch synthetic-colloid solutions provide evidence against their use. If a colloid solution is indicated, albumin should be used. Saline administration can generate or exacerbate a non–anion gap metabolic acidosis and reduce ionized calcium levels, factors that could depress cardiac function.Also, chloride-rich solutions have been linked to acute kidney injury. Crystalloids containing bicarbonate or its precursors (balanced salt solutions), such as Ringer’s solution with lactate and Plasma-Lyte (Baxter International) with acetate and gluconate, will not cause non–anion gap metabolic acidosis and may reduce the risk of acute kidney injury, but they can occasionally cause metabolic alkalosis.
A reduced need for renal replacement therapy has been reported in seriously ill patients receiving balanced salt solutions rather than saline, but opinions differ regarding which solution should be favored. Solutions containing a racemic mixture of -lactate and -lactate generate as much base as do solutions with an equimolar concentration of only -lactate. Infusion of large quantities of Ringer’s lactate can increase blood lactate levels, but the increment is often small in the absence of abnormalities in lactate clearance. Citrate-containing solutions can lead to the generation of microthrombi. Randomized, controlled studies are needed to determine the most effective and safe crystalloid."
RECAP:
SID (strong ion difference) can be estimated as the sodium level minus the chloride level. That difference determines the bicarbonate level and contributes to the pH level. In a normal state, the body will have a SID of about 38. A high SID indicates a metabolic alkalosis. A smaller SID signals a metabolic acidosis. Large amounts of infused normal saline will decrease the body's strong ion difference and thereby cause a metabolic acidosis. Saline administration can also reduce ionized calcium levels, depressing cardiac function; and also, normal saline use in patients with lactic acidosis and ICU patients has been linked to acute kidney injury and failure.
5) And now, an extra pinch of salt. An EMCrit podcast review of Severe Hyponatremia in the ED (21:25) Learn to not be afraid of hypertonic saline, how to order lots of labs, and how to sit on your hands. And more about electrolyte relationships: you know that sodium and chloride affects bicarb, and now potassium raises sodium, ergo...
THE OPTIONAL EXTRAS:
a) If you want MORE about SID and Stewart and the potential evils of normal saline, and you want to hear it in an Aussie accent (bonus!!), click through to the FOAMcast-cited original ICN lecture ("Is Chloride a Poison?"--July 2014) by Dr. Story, whose recent article is above.
b) And here is a link to the FOAMcast-mentioned 'life-changing' EM:Crit lectures on acid-base (there are actually 5 of them). Dr. Weingart's summary sheet is very helpful and goes a little further than we did here (calculating the SIG, or strong ion gap, for example.) OR, you can hear him do a shorter bit on SID in a slightly older EM:RAP from August 2013 (listen to the first 8 minutes--he goes into why the SID of the fluid itself matters.) (Remember, EMRA members can subscribe for free!)
2) Exercise induced hyponatremia, a slightly different beast from Grandma's hyponatremia--just driving home some points from the EMCrit podcast, and making the point that you can correct these folks more quickly. (LITFL, updated 8/15).
3) An uncommon cause of hyponatremia, in Emergency Medicine (10/1/14.) If a patient comes in seizing after their discharge from certain outpatient surgeries, better think about it.
THAT'S IT! Celebrate, but don't give yourself beer potomania-induced hyponatremia!
Discussion questions:
- Will you change anything about your fluid choices in given scenarios based on what you've read/heard here?
- On the hyponatremia portion: in the EM:Crit podcast, Dr. Weingart suggests a threshold for admission for hyponatremia at 130 mEq/L, saying others admit at 135 -- which seems high to me. What do you think of that guideline, and where do you draw the line for an asymptomatic patient without other reasons for admission? What have you seen in practice?
Leave us comments -- and see you next time!