Name:
A 21-Year-Old with Nausea and Vomiting
Description:
A 21-Year-Old with Nausea and Vomiting
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T00H07M14S
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Upload Date:
2025-07-17T00:00:00.0000000
Transcript:
Language: EN.
Segment:0 .
♪ (music) ♪
CATHY: Hi, welcome to Harrison's Podclass where we discuss important concepts in internal medicine. I'm Cathy Handy. And I'm Charlie Wiener, and we're coming to you from the Johns Hopkins School of Medicine. ♪ (music) ♪ Welcome to Episode 18, A 21-year-old with Nausea and Vomiting. I'll start with the case. A 21-year-old woman with a history of type 1 diabetes mellitus is brought to the Emergency Department with nausea, vomiting, lethargy, and dehydration.
CATHY: This sounds like it might become a case of DKA or diabetic ketoacidosis. Unfortunately, that's a common complication of type 1 diabetes.
CHARLIE: Well, in fact, her mother does note that she stopped taking her insulin one day before presentation.
CATHY: I can tell where this is headed, so, let's go over the basics of type 1 diabetes. It's the result of complete or near total insulin deficiency due to autoimmune destruction of beta cells in the pancreas. Usually, clinical diabetes doesn't result until about 70%-80% of beta cells are destroyed. And this happens most commonly in younger people, but can occur in older adults. And insulin is required basically for survival in type 1 diabetics. So, skipping it even for a day can have devastating consequences, like in this case.
CHARLIE: So, tell me more about what happens in diabetic ketoacidosis, or DKA.
CATHY: There are two major requirements for DKA to develop. The first is insulin deficiency, in this case it's because she didn't take her insulin, and the second is glucagon excess-- the prime manifestations or hyperglycemia, and a shift to fatty acid metabolism which causes the ketoacidosis. The decreased ratio of insulin to glucagon shifts the handling of pyruvate towards glucose synthesis. and away from glycolysis. So, the result is that glucose isn't being broken down.
CATHY: You also get glycogenolysis, or a breakdown of glycogen which gives you even higher levels of circulating glucose. And the ketosis results from an increase in release of free fatty acids from adipocytes.
CHARLIE: What are the typical precipitating factors for DKA? Is it only just stopping your insulin?
CATHY: Stopping insulin is one way that you can precipitate DKA, but it's certainly not the only way. Other acute illnesses like an infection, even a mild one, or a pancreatitis, or a myocardial infarction can also increase the insulin requirements. So, you end up with a relative insulin deficiency, which can also trigger this process. Typically patients with type 2 diabetes, which has a totally different path of physiology and is characterized more by insulin resistance rather than insulin deficiency, those patients don't develop DKA.
CHARLIE: Okay, so let's go more into this case. The patient is a thin woman in mild respiratory distress with a respiratory rate of 28 per minute. Her blood pressure is 80 over 40. Her heart rate is 112 per minute. Her heart sounds are normal, lungs are clear, the abdomen is soft and there's no organomegaly. She's responsive and oriented times three, but she's somnolent and diffusely weak. Her mucous membranes are dry everywhere.
CATHY: Those are all common symptoms of DKA.
CHARLIE: What labnormalities would you expect in this case, if she does have DKA?
CATHY: As I mentioned before, you'd expect a hyperglycemia and acidemia. Typically, total body sodium, potassium, and magnesium are usually depleted, but it's not always accurately reflected by their measurement because of the hyperglycemia, acidosis and hypovolemia. Sometimes there can also be evidence of acute kidney injury from volume depletion, but we'll have to see what we have in this case.
CHARLIE: Alright, so let's review her labs. Her serum sodium is 126, her potassium is 4.3, her magnesium is 1.2, blood urea nitrogen, or BUN, is 76, creatinine is 2.2, her bicarbonate is 10, her chloride is 88, her serum glucose is 720. What do you think of those labs? That's a lot to throw at you at one time.
CATHY: Yeah, so let's start with the glucose. So, her serum glucose, in this case, is 720 mg/dl, and that's actually a bit higher than what I was expecting. In type 1 diabetes, you can get DKA with much lower serum glucoses even in the high 100s or low 200s. I think of the really high glucose levels to cause complications in type 2 diabetes, but these aren't absolutes. And, honestly, the degree of hyperglycemia doesn't really correlate well with the complications or development of DKA.
CATHY: So, some of the other labs that you mentioned-- the serum sodium of 126 mEq/L is technically low, but you have to correct for the serum glucose. I usually do this just on an app or on the web. And when you do that, you see that the serum sodium level is actually around 140 which is within normal. Next, she gave me the potassium of 4.3, and that's on the lower end of what you would expect, but with insulin deficiency and the acidosis, there's an extracellular shift in potassium.
CATHY: And when you start treating with IV insulin, the potassium will be shifted back into cells. So, it's important to watch that frequently and replace with IV potassium. Next, you had magnesium of 1.2, that's low and very common in DKA, and should be replaced with IV magnesium. The bicarb of 10 is also low, but that just reflects the acidosis, and the hypochloremia is not unexpected given the volume depletion from vomiting and the osmotic diuresis.
CATHY: Essentially, all patients with DKA will require volume resuscitation, which often requires liters of fluid.
CHARLIE: Wow, I'll also point out that her anion gap is 28, which is elevated and typical of DKA also. I also wanted to say, as a generational thing, it's interesting that now we don't have to memorize sodium correction formulas anymore--
CATHY: [laughs]
CHARLIE: we can just go to our phones or to the tablet computer and get the correction, which I think is fantastic!
CATHY: Yeah, and it's so much easier.
CHARLIE: Alright, so finally we get to the question, and the question asks: All of the following are appropriate management steps, except: a) 3% sodium solution; b) arterial blood gas; c) IV insulin; d) IV potassium; e) IV fluids. Four of those are appropriate interventions. Which of those is not an appropriate intervention, Cathy?
CATHY: So, the answer here in the intervention that isn't indicated is a 3% sodium solution. When you correct for the sodium glucose, like I mentioned before, the serum sodium is actually within normal. So, you don't need to give hypertonic saline. You will want to be giving IV fluids which will have sodium in it to replace the volume, but the 3% sodium isn't indicated. Treatment really centers on the replacement of insulin because that will stop the formation of keto acids, normalize the pH, restore normal glycemia, and eventually, you'll get a normal volemia as well.
CATHY: An ABG or VBG can help with the assessment of the level of acidosis, so you do almost always want to do that. And usually, despite the severe acidosis, bicarb administration isn't indicated or really beneficial at all. IV potassium is indicated because the serum potassium will rapidly fall once insulin is started. So, don't forget to do that.
CHARLIE: Okay, so the teaching point here is that decay is common in type 1 diabetics and can be precipitated by nonadherence to insulin therapy, or any sort of mild infection. Treatment is with insulin, fluids, and electrolyte repletion. But don't get fooled by pseudohyponatremia.
CATHY: And you can read more about this in the Harrison's chapter on Diabetes Mellitus. ♪ (music) ♪
