Clinical Cycles and Case Reviews, Ep. 3

In this podcast, Dr. Harrison talks with Paul Shiu, DO, about interpreting arterial blood gases, including the calculation of high anion gap metabolic acidosis (HAGMA), high anion gap metabolic acidosis, normal anion (NAGMA), urinary anion gap, renal tubular acidosis, and their possible causes.

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Anil Harrison, MD, is Associate Director of the Internal Medicine Residency Program and Director of Ambulatory Care at Touro University and St Joseph’s Medical Center-Dignity Health (Stockton, CA). Dr. Harrison is board certified in India and USA.

Paul Shiu, MD
Paul Shiu, DO, is a second-year internal medicine resident at St Joseph’s Medical Center (Stockton, CA).

Dharminder Singh, MD

Dharminder Singh, MD, is Chief Internal Medicine Resident at St Joseph’s Medical Center (Stockton, CA).

Moderator: Hi there. And welcome to the multidisciplinary dialogue: clinical rounds and case reviews with your host, Dr. Anil Harrison, who is Associate Program Director for the Internal Medicine Residency Program and Director of Ambulatory Care at Toro University and St. Joseph, Dignity Health in Stockton, Calif.

Today we have a case review that Dr. Harrison and Dr. Paul Shiu will analyze and provide treatment information. Dr. Shiu is a second-year internal medicine resident at St. Joseph’s Medical Center in Stockton, California. In this episode, we will discuss HAGMA and NAGMA. The views of the speakers are their own and do not reflect the views of their respective institutions or the views of the 360 ​​Consultant.

Dr. Paul Shiu: Dr. Harrison, how are you this morning?

Dr Anil Harrison: I’m fine, Paul. It’s 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 as that, it’s an observation. People tell me not to eat late at night for many reasons, but if there’s a problem with eating at night, why do they have blisters in the fridge, Dr Harrison?

Dr Anil Harrison: Look for me, Paul.

Dr. Paul Shiu: So today we are going to talk about metabolic acidosis, high and normal anion gap. So here is the third part of a long series on arterial blood gases. We are building the foundation for interpreting arterial blood gases. The subject here is HAGMA and NAGMA. And I had a case, Dr. Harrison, and I was wondering if you could help me.

Dr Anil Harrison: I would be delighted, Paul.

Dr. Paul Shiu: We have a 40-year-old man found to have the following labs when evaluating a history of recurrent kidney stones. Sodium was 133. Potassium is 3.2. Chloride is 110. Biofuel is 15. Blood sugar is 100. BUN is 20. Creatinine is 1. His lab measured serum osmolality is 280. And then if we calculate serum osmolality, that 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 metabolic acidosis and there is no osmolar hole.

Dr Anil Harrison: Yes you are right. 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: To correct.

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 normal anion gap metabolic acidosis.

So think about it, what are the etiologies of normal anion gap metabolic acidosis? And it’s a simple mnemonic, which is called HARD UP. H stands for hypereating, A for acetazolamide and other carbonic anhydrase inhibitors, such as topiramate, type I, IV and II renal tubular acidosis, ureterosigmoid fistula and pancreatic fistulas because you lose bicarbonate. All this must be entertained in the differential. However, if you think about it, our patient was not hypereating. This patient is not on any medication, has had no previous surgery, and gives us no history of diarrhea. Therefore, I have a feeling this might indicate renal tubal acidosis.

Dr. Paul Shiu: So if you notice, at least with our patient labs, though, bicarb is low, chloride is high. I believe another term for this would be hyperchloremic metabolic acidosis.

Dr Anil Harrison: You are right Paul. Yes. So what’s the pathophysiology of what’s really going on with normal anion gap metabolic acidosis is that there’s acidosis or retention of hydrogen ions, or there could be loss of bicarbonate, which is alkaline. And by losing the bicarbonate, there is chloride retention. The acid in the blood, in the form of hydrogen ions, is excreted in the kidneys. As with an acid charge, there is an increased production of ammonium by the nephrons, which combine with hydrogen ions to form NH4. It is this NH4 that binds to chloride and is then excreted.

Because ammonia in urine is difficult to measure, it is a surrogate, i.e. chloride is therefore measured instead. The urine 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 its substitute, which is urinary chloride. If the urine anion gap, i.e. urine sodium plus potassium minus chloride, if it has a negative value, if it has a negative gut value, you are thinking of a bowel problem.

Dr. Paul Shiu: Ha-ha. It is a coincidence that the intestine just fits in the negative.

Dr Anil Harrison: Type of.

Dr. Paul Shiu: Very easy to remember. Thank you, Dr. Harrison.

Dr Anil Harrison: Absolutely. But another reason for a negative urinary anion gap could be proximal renal tubular acidosis, which is type II. Now, what if the urine anion gap is positive? This points to the kidneys, specifically, it’s either distal renal tubular acidosis type I or renal tubular acidosis type IV. If you recall type II proximal and type I distal renal tubular acidosis, serum potassium is low, but with type IV renal tubular acidosis, due to a deficiency or resistance to aldosterone, serum potassium is elevated. Paul, if that’s okay, in another presentation we could discuss renal tubular acidosis and we could go into detail about the various abnormalities that are seen with the different types of RTA.

Dr. Paul Shiu: It’s funny, we had a morning report just today and we were talking, we had a very good case on renal tubular acidosis or a discussion rather on renal tubular acidosis. And for the listening public, who didn’t get a chance to join us on the Morning Report here, why do we have renal tubular acidosis, 1, 2 and 4? What happened to three? I feel like Renal Tubular Acidosis 3 is like Pluto. It was launched. So hopefully if Dr. Harrison agrees, maybe we can talk more about renal tubular acidosis as well as what happened to 3.

Dr Anil Harrison: Yeah, poor kid 3.

Dr. Paul Shiu: Poor little 3. As a reminder, our patient has a urinary anion gap which was positive, a urinary pH which was 6.2. He had low serum potassium. Therefore, his diagnosis points to type I distal renal tubular acidosis.

Dr Anil Harrison: Perfect. Perfect, Paul. So to summarize, a 40-year-old patient with a history of recurrent kidney stones and lab work to suggest normal anion gap metabolic acidosis, who also had a positive urinary anion gap, urinary pH of 6.2, I think, would lead us to believe that he has type I distal renal tubular acidosis, which is sometimes associated with kidney stones.

Dr. Paul Shiu: This whole recurring kidney stone business, could you elucidate the connection between type I RTA and kidney stones, please?

Dr Anil Harrison: Absolutely, Paul. This occurs due to a lack of acidification of urine by the distal nephron and due to a lack of urinary citrate. And that’s why the treatment is potassium because these people have hypokalemia and you give them citrate. Potassium citrate is therefore a treatment to replenish potassium as well as citrate and citrate is converted into bicarbonate.

Dr. Paul Shiu: A stroke of genius, people. Well Dr Harrison we are very lucky to have you here to help us understand NAGMA and HAGMA and some very useful mnemonics for that. Last time we talked about CAT-MUDPILES. Today we talked about HARD UP. I don’t know what acronym we have coming up, but I know because we’re talking about kidney stones that we’re just a stone’s throw away from our next podcast.

Dr Anil Harrison: That’s a good one, Paul.

Dr. Paul Shiu: I tried, Dr. Harrison, just to try to follow you. So folks, thank you so much for listening to another podcast with Dr. Harrison and I, and we hope you keep tuning in. And for those who have just joined, we invite you to listen to podcast one and two, as this is a long-running series on understanding arterial blood gases and the acid base. And we implore you to listen, give us your feedback, and we’ll get back to you. And if you have a really, really, really difficult question and we’re really racking our brains, Dr. Harrison will send you a personal message via email. Thank you friends. I really appreciate you.

Dr Anil Harrison: Thank you everyone.

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