In this podcast, Dr. Harrison with Paul Shiu, DO, on interpreting arterial blood gases, including calculating a high anion gap metabolic acidosis (HAGMA), a normal anion gap metabolic acidosis (NAGMA), a urinary anion gap, renal tubular acidosis, and their possible causes.
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Anil Harrison, MD, is the associate program director of the internal medicine residency program and the ambulatory care director of Touro University and St Joseph’s Medical Center-Dignity Health (Stockton, CA). Dr. Harrison is board certified in India and the United States.
Paul Shiu, DO, is a sophomore internist at St Joseph’s Medical Center (Stockton, CA).
Dharminder Singh, M.D., is chief of internal medicine at St Joseph’s Medical Center (Stockton, CA).
Moderator: Hello all. And welcome to Multidisciplinary Dialogue: Clinical Rounds and Case Reviews with your host, Dr. Anil Harrison, who is the Associate Program Director for the Internal Medicine Residency Program and the Ambulatory Care Director at Toro University and St. Joseph’s Medical Center, Dignity Health in Stockton, California.
Today we have a case review that Dr. Harrison and Dr. Paul Shiu will analyze and provide treatment insights. dr. Shiu is a sophomore internist at St. Joseph’s Medical Center in Stockton, California. In this episode we discuss HAGMA and NAGMA. The views expressed by the speakers are their own and do not reflect the views of their respective institutions or the views of Consultant 360.
Dr Paul Shiu: dr. Harrison, how are you this morning?
Dr Anil Harrison: I’m fine, Paul. It is a beautiful day. Very good morning to you.
Dr Paul Shiu: Very good morning to you. For our new listeners, you may not know this, but Dr. Harrison and I like to start our podcast with a joke. And in this case, it’s not so much a joke, but an observation. People say I can’t eat late at night for many reasons, but if there’s a problem with dinner, why do they have lightbulbs in the fridge, Dr. Harrison?
Dr Anil Harrison: Find me, Paul.
Dr Paul Shiu: So today we are going to talk about metabolic acidosis, high and normal anion gap. So this is the third part of a series on arterial blood gases. We build the foundation to interpret arterial blood gases. The subject here is HAGMA and NAGMA. And I actually had a case, Dr. Harrison, and I was wondering if you could help me with that.
Dr Anil Harrison: You’re welcome, Paul.
Dr Paul Shiu: We have a 40-year-old who found the following labs after evaluating the history of recurrent kidney stones. Sodium was 133. Potassium is 3.2. Chloride is 110. Bio carb is 15. A blood sugar of 100. A BUN of 20. A creatinine of 1. Its serum osmolality measured by the lab is 280. And then if we calculate the serum osmolality, which is sodium times two, plus glucose divided by 18, plus BUN divided by 2.8, we get a calculated serum osmolality of 278. This tells us that there is a metabolic acidosis and there is no osmolar gap.
Dr Anil Harrison: Yes you’re right about that. So we have someone with metabolic acidosis and no osmolar gap. So if you think about it, Paul, if there’s no osmolar gap, we can probably rule out methanol and ethylene glycol. Right? There is no osmolar gap.
Dr Paul Shiu: Right.
Dr Anil Harrison: So our patient also meets the criteria for metabolic acidosis with a bicarb of 15. Normal bicarb is between 22 and 28. So what we need to do next is determine if this person has an anion gap, which is sodium minus chloride minus bicarbonate. Our patient has an anion gap of eight, confirming that this is normal anion gap metabolic acidosis.
So you think about it, what are the etiologies for normal anion gap metabolic acidosis? And it’s a simple mnemonic called HARD UP. H stands for hyperalimentation, A for acetazolamide and other carbonic anhydrase inhibitors, such as topiramate, renal tubular acidosis Type I, IV and II, ureterosigmoid fistulas and pancreatic fistulas because you lose bicarbonate. All these should be entertained in the differential. However, if you think about it, our patient didn’t get hyperalimentation. This patient is on no medication, has no previous surgery and has no history of diarrhoea. Therefore, I have a feeling that this could indicate renal tubal acidosis.
Dr Paul Shiu: So if you notice, at least in our patients’ labs, the bicarb is low, the chloride high. I believe another term for this would be hyperchloremic metabolic acidosis.
Dr Anil Harrison: You’re right, Paul. Yes. So what is the pathophysiology for what actually happens with a normal anion gap metabolic acidosis is there acidosis or retention of hydrogen ions or there could be a loss of bicarbonate which is alkaline. And while the bicarbonate is lost, there is retention of chloride. Acid in the blood, in the form of hydrogen ions, is excreted in the kidneys. Similar to an acid load, there is an increased production of ammonium by the nephrons, which combine with the hydrogen ions to form NH4. It is this NH4 that binds with chloride and is then excreted.
Since ammonia in the urine is difficult to measure, it is a surrogate, which measures chloride instead. The urinary anion gap, which is urine sodium plus urine potassium minus urine chloride, is usually zero or has a slightly negative number. Remember that instead of measuring ammonia, we are going to measure the surrogate, which is urine chloride. If the urine anion gap, which is urine sodium plus potassium minus chloride, if it has a negative value, if it has a negative value, then you think you have a gut problem.
Dr Paul Shiu: Haha. This just happens to be the gut just fits in negative.
Dr Anil Harrison: Kind of.
Dr Paul Shiu: Very easy to remember. Thank you, Dr. Harrison.
Dr Anil Harrison: Absolute. But another reason for a negative urine anion gap could be proximal renal tubular acidosis, which is a Type II. What happens if the urine anion gap is positive? This mainly points to the kidneys, it is either a distal Type I or a Type IV renal tubular acidosis. If you remember that with proximal type II and distal type I renal tubular acidosis the serum potassium is low, but in type IV renal tubular acidosis, due to aldoster deficiency or resistance, the serum potassium is elevated. Paul, if you agree, in another presentation we can discuss renal tubular acidosis and go into the details of the different abnormalities seen with the different types of RTAs.
Dr Paul Shiu: It’s funny, we had a morning report today and we were talking about a really good case of renal tubular acidosis or a discussion of renal tubular acidosis. And for the audience that tuned in, who weren’t lucky enough to join us on the morning report, why do we have renal tubular acidosis, 1, 2, and 4? What happened to three? I have a feeling that renal tubular acidosis 3 resembles Pluto. It’s kicked off. So hopefully if Dr Harrison agrees maybe we can talk more about renal tubular acidosis and also what happened to 3.
Dr Anil Harrison: Yes, poor little 3.
Dr Paul Shiu: Poor little 3. As a refresher, our patient has a urine anion gap that was positive, a urine pH that was 6.2. He had low serum potassium. Therefore, his diagnosis points to a type I distal tubular acidosis of the kidney.
Dr Anil Harrison: On the spot. Look at that, Paul. So to summarize, a 40-year-old patient with a history of recurrent kidney stones and labs suggesting normal anion gap metabolic acidosis, who also had a positive urine anion gap, a urine pH of 6.2, I think would lead to believe he has a distal type I renal tubular acidosis, sometimes associated with kidney stones.
Dr Paul Shiu: This whole thing with recurring kidney stones, can you explain the connection between Type I RTA and kidney stones, please?
Dr Anil Harrison: Absolutely, Paul. This occurs due to a lack of urinary acidification by the distal nephron and a lack of urinary citrate. And that’s why the treatment is potassium because these people have hypokalemia and you give them citrate. So potassium citrate is a treatment to replenish both potassium and citrate and citrate is converted to bicarbonate.
Dr Paul Shiu: A brilliance, folks. Well, Dr. Harrison, we’re very lucky to have you on board to help us understand NAGMA and HAGMA and very helpful reminders about it. Last time we talked about CAT-MUDPILES. Today we talked about HARD UP. I don’t know what acronym we’re talking about next, but since we’re on the subject of kidney stones, I do know we’re steps away from our next podcast.
Dr Anil Harrison: That’s a good one, Paul.
Dr Paul Shiu: I tried, Dr. Harrison, I was trying to keep up with you. So folks, thank you so much for tuning in to another podcast with Dr. Harrison and me, and we hope you keep tuning in. And for those just joining us, we invite you to listen to podcast one and two, because this is a long-term series on understanding arterial blood gases and acid base. And we beg you to listen, give us feedback and we’ll get back to you. And if you ask a really, really, really hard question and really scratch our heads, Dr. Harrison will send you a personal message via email. Thanks people. Really appreciate you.
Dr Anil Harrison: Thanks everyone.