Surreptitious Vomiting, Primary Hyperaldosteronism
In this episode, Dr Harrison speaks with Dharminder Singh, MD, about metabolic alkalosis, a patient with surreptitious vomiting, and a patient with primary hyperaldosteronism.
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Anil Harrison, MD, is the Associate Program Director of the Internal Medicine Residency Program and the Ambulatory Care Director at 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 second-year internal medicine resident at St Joseph's Medical Center (Stockton, CA).
Dharminder Singh, MD, is an internal medicine chief resident at St Joseph’s Medical Center (Stockton, CA).
TRANSCRIPTION:
Hello, everyone 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 Touro University in St Joseph's Medical Center, Dignity Health in Stockton, California. Today, we have case presentations that Dr Harrison and Dr Dharminder Singh will analyze and provide treatment insights. Dr Singh is a second-year internal medicine resident at St. Joseph's Medical Center in Stockton, California. In this episode, we'll discuss metabolic alkalosis, a patient with surreptitious vomiting, and a patient with primary hyperaldosteronism. The views of the speakers are their own and do not reflect the views of their respective institutions or the views of Consultant360.
Dr Anil Harrison: Good afternoon, Dr Singh.
Dr Dharminder Singh: Good afternoon, Dr Harrison. How are you doing today?
Dr Anil Harrison: I am doing well. And I think we're at the conclusion of The “Evaluation of Arterial Blood Gases” series, and I am open to any cases that you might have that we can discuss?
Dr Dharminder Singh: Sure. I have this one, very interesting one. A 20-year-old female with BMI of 18 presents with fatigue. Her blood pressure is 90/70, sodium 138, potassium 3, chloride 94, bicarb of 35. Urine chloride is less than 10. ABG shows pH of 7.47 with a PCO2 of 47.
Dr Anil Harrison: Okay. The choices that you have given me are: could this be a surreptitious laxative use, or could this be surreptitious vomiting, could this be surreptitious active diuretic use, could this be Bartter syndrome, or could this be primary hyperaldosteronism? Okay, so let's take a look at the pH. The pH is 7.47, which tells us that this patient has alkalemia. And the next thing we do is we take a look at the PCO2, and the PCO2 is trending in the same direction as the pH. Hence, this tells me that this is primarily a metabolic problem. And with a serum bicarb of 35, the patient has metabolic alkalosis. Then, the next thing to do is to check what is the patient's volume status and what is a person's blood pressure? In our case, the volume status and the blood pressure are low normal, right?
Okay. Then, the next thing you do is what is the potassium doing? Her potassium is low. Therefore, the etiologies for metabolic alkalosis with normal to low blood pressure and low potassium would be contraction alkalosis, vomiting, diuretic use, Bartter or Gitelman syndrome, or NG suctioning. In our case, it probably is not NG suctioning, because we don't get that from a history or an exam. The next thing we do is metabolic alkalosis with low normal blood pressure, low potassium, and with a urine chloride that is less than 10, rules out recent diuretic use, Bartter syndrome, and Gitelman syndrome. The etiology for this patient's metabolic alkalosis with low normal blood pressure, low potassium, and a urine chloride less than 10, is possibly surreptitious vomiting.
Therefore, recapping the evaluation of metabolic alkalosis. The first thing to do is to assess the volume status. And if the volume status is low normal, consider contraction alkalosis, vomiting, NG suctioning, diuretics, Bartter and Gitelman syndrome. But if the volume status is normal or high normal, check the blood pressure and potassium. And if the blood pressure and potassium are both elevated, it probably represents mineralocorticoid excess. And in that scenario, you check aldosterone and renin levels. If the aldosterone is elevated and the renin is not, and the aldosterone to renin ratio is greater than 20, this represents primary hyperaldosteronism. If both renin and aldosterone are elevated and the aldosterone to renin ratio is less than 20, this represents secondary hyperaldosteronism. If both renin and aldosterone are normal, this possibly represents Cushing syndrome. But if both aldosterone and renin are low, this could represent exogenous steroids, licorice intake, or Liddle syndrome. Also, remember, if both blood pressure and potassium are normal, consider milk-alkali syndrome. If the blood pressure is normal and the potassium is low, consider severe hypokalemia as the etiology. This is my take on this patient.
Dr Dharminder Singh: Well, thank you so much, Dr Harrison. How about another joke?
Dr Anil Harrison: Okay. How do you throw a space party? You planet.
Dr Dharminder Singh: Well, I think I have another interesting case to discuss with you, if that's okay?
Dr Anil Harrison: Absolutely, Dr Singh.
Dr Dharminder Singh: This is a 38-year-old male with blood pressure of more than 160/100 for the last six months. Sodium of 140, potassium of 3.3, chloride of 108, bicarb of 32, magnesium of 2, and urine chloride is more than 15.
Dr Anil Harrison: The choices, Dr Singh, you've given are: surreptitious vomiting, or is it Gitelman syndrome, could it be a surreptitious thiazide use, or could this be primary hyperaldosteronism? If you look at the pH, which is more than 7.45, and the serum bicarb, if it is more than 28, this represents metabolic alkalosis. Now, in our patient, the bicarb is 32. Hence, he or she satisfies a diagnosis of metabolic alkalosis. The next step is what is the volume status and blood pressure? Our patient's blood pressure is elevated. The next thing is our patient with metabolic alkalosis and hypertension. You got to see what is the potassium doing? And in our patient, the potassium is low. Therefore, the next step would be what is the chloride in the urine doing? And with our patient's urine chloride being greater than 15, this suggests that our patient has an excess of mineralocorticoid in the system, and therefore the next step would be to check serum renin and aldosterone.
In our patient, the serum aldosterone was elevated, but the renin was normal, suggesting primary hyperaldosteronism. And what do I think would be the next step? I would probably confirm with a salt loading test. And if positive, I would go straight to an MRI of the adrenal gland. Once again, if aldosterone is elevated and the renin is not, and the ratio of aldosterone to renin is greater than 20, this is primary hyperaldosteronism. If the ratio of aldosterone to renin is less than 20, this is secondary hyperaldosteronism. If both renin and aldo are normal, this possibly could represent Cushing syndrome. If both aldosterone and renin are low, this could represent exogenous steroids or licorice or Liddle syndrome. However, if both blood pressure and potassium are normal, consider milk-alkali syndrome. If the blood pressure is normal and the potassium is low, consider severe hypokalemia as the etiology. This is my take on our patient.
Dr Dharminder Singh: Well, thank you so much, Dr Harrison. I have another question. What do you call a fake noodle?
Dr Anil Harrison: A fake noodle? I don't know.
Dr Dharminder Singh: An impasta.
Dr Anil Harrison: That's a good one.
Dr Dharminder Singh: Well, thank you so much for your help today.
Dr Anil Harrison: Absolutely, Dr Singh. And everybody, keep tuning in. I hope you enjoyed our series on evaluation of arterial blood gases with Dr Singh and Dr Shiu. And we'll be joining in soon with some other podcast with other very interesting cases or case reports and other things that are going to be interesting for all of us. Anyways, have a great day. Bye.
Dr Dharminder Singh: Goodbye