SPEAKER_00: 0:00

Welcome back to the deep dive. Today we're tackling a topic that's, well, it's foundational for anyone in clinical practice. And it's frankly one of the most painful things a patient can go through: nephrolithiasis, kidney stones. We're going to get into the history, the diagnostics, and the management pathways you really have to master.

SPEAKER_01: 0:16

It's incredibly high yield content. And we've structured this entire deep dive around those critical clinical task areas you need to know. From that first patient chat all the way to long-term prevention. At its core, you know, stone formation is just a chemistry problem, a really painful one. Think of it like making rock candy. If you have too much salute, too much sugar, and too little water, well, you end up growing a solid rock.

SPEAKER_00: 0:40

Okay, that rock candy analogy is perfect. Let's start with the scale of the problem. The sources suggest this is becoming much, much more common.

SPEAKER_01: 0:48

Oh, it is. We're talking about something like one in ten Americans being affected. It's huge.

SPEAKER_00: 0:52

One in ten, wow.

SPEAKER_01: 0:53

Exactly. And the epidemiology here, it really tells a story about our broader public health. It used to be seen as you know overwhelmingly a male problem, but the prevalence in women has just skyrocketed. We're talking a 45% increase.

SPEAKER_00: 1:07

45%? What's driving that?

SPEAKER_01: 1:09

It's directly linked to rising rates of obesity and metabolic syndrome. The very same things that cause heart disease, diabetes, high salt, high animal protein, not enough water. Those are the exact things that are supersaturating our urine.

SPEAKER_00: 1:22

That's a critical link. It's amazing how this presents as a renal crisis, but it's really a systemic metabolic issue. But you know, when a patient walks in, they're not thinking about epidemiology, they're thinking about the pain. Tell us about that classic presentation.

SPEAKER_01: 1:35

It is. Uh it's acute, it's severe, and the key descriptor you'll always hear is unremitting colic. This pain just hits them. Often it's so abrupt it wakes them up from a deep sleep. And it's almost always associated with really profound nausea and vomiting. That's because the kidney and the gut share some autonomic pathways.

SPEAKER_00: 1:53

I've always found that word fascinating. Unremitting. Does that mean the pain meds just don't touch it? Or is it more about the stone itself constantly causing irritation?

SPEAKER_01: 2:02

It's a bit of both, actually. The pain is from the sudden blockage, the obstruction, which stretches the renal capsule or the ureter. And that doesn't really resolve until the stone moves or is removed. The movement of the stone, of course, that just changes where the agony is located.

SPEAKER_00: 2:19

Okay, so where does it start and where does it go?

SPEAKER_01: 2:21

Typically it's flank pain radiating forward across the abdomen. But here's the real diagnostic nugget you need for the history. As that stone travels down the ureter, especially when it gets close to the bladder, the pain refers distally.

SPEAKER_00: 2:37

Distally to where, exactly, because that really helps narrow things down.

SPEAKER_01: 2:40

It classically refers to the ipsilateral groin, or sometimes, in man, right to the tip of the penis. When it gets to that point, the patient might also start complaining of things like urgency, frequency, dysuria, can really mimic a UTI, which can be confusing for them.

SPEAKER_00: 2:54

So on physical exam, how do we lock this in? How do we distinguish it from, say, appendicitis or another acute abdomen?

SPEAKER_01: 3:02

This is such a crucial clinical distinction. A patient with peritonitis, they're in agony, but they lie perfectly still because any movement makes it worse. Your kidney stone patient is the exact opposite. They are pacing, they are writhing. They cannot find a comfortable position.

SPEAKER_00: 3:18

They can't get still.

SPEAKER_01: 3:19

They cannot get still. They're the one tearing up the floor in the waiting room.

SPEAKER_00: 3:22

That clinical picture, the writhing patient versus the still patient, that can save you so much time in the ED.

SPEAKER_01: 3:28

Absolutely. Yeah. And this brings us to our emergency alert moment. You have to get vitals immediately. If you see a fever, tachycardia, or god forbid, hypotension with an obstructing stone, that screams concurrent infection, pylonephritis, and that is a non-negotiable medical emergency.

SPEAKER_00: 3:44

Okay, so the clinical suspicion is sky high. Now let's pivot to the diagnostics. We need to confirm it, find the stone, and figure out what kind of rot candy we're dealing with.

SPEAKER_01: 3:53

Aaron Powell Right. The workup always starts with a urinalysis, a UA. You'll see blood, either microscopic or gross hematuria in about 90% of cases. But, and this is key, its absence doesn't rule a stone out, so don't get faked out. The real nugget in the lab work, though, is the urine pH.

SPEAKER_00: 4:10

The pH. So that's the key to figuring out the stone's composition.

SPEAKER_01: 4:13

It's a critical chemical fingerprint. If you see a persistent urine pH of less than 5.5, you should be thinking uric acid stones. They love acidic environments. On the flip side, a persistent pH greater than 7.2 points you toward either struvite stones, which are always from bacteria like proteus, or sometimes calcium phosphate stones.

SPEAKER_00: 4:34

That's fantastic. So pH tells us the what. How do we find the where and the how big? What's the gold standard imaging?

SPEAKER_01: 4:40

The gold standard is without a doubt the non-contrast CT scan of the abdomen and pelvis. It's the most accurate. The sources sometimes even mention this specific technique of doing it in the prone position.

SPEAKER_00: 4:50

Prone? Why is that?

SPEAKER_01: 4:51

It can help you differentiate a stone that's still stuck in the distal ureter from one that's already passed into the bladder. A nice little trick. Now, a quick caveat on imaging. We often use ultrasound, right? Especially for pregnant patients. It's safer. But you have to remember that a KUB, a plain X-ray, is way less sensitive, and it will completely miss those radiolucent uric acid stones.

SPEAKER_00: 5:13

Good. That's a crucial point. So once we know the stones there, we need to formulate the diagnosis, which often means looking for a systemic driver.

SPEAKER_01: 5:21

Precisely. This isn't just an acute event. For anyone who's a recurrent stone former or even a high-risk first timer, you need metabolic testing. That means a 24-hour urine collection. It's the only way to get a personalized look at their unique rock candy recipe. We measure volume, calcium citrate, oxalate, uric acid. The works.

SPEAKER_00: 5:42

And are there systemic diseases we should be looking for?

SPEAKER_01: 5:45

Two big ones jump out. If you see elevated serum calcium and elevated parathyroid hormone, you have to suspect primary hyperparathyroidism.

SPEAKER_00: 5:52

Right, because the PTH is just dumping calcium into the blood, which then spills into the urine. What's the other one?

SPEAKER_01: 5:57

The other one is renal tubular acidosis or RTA. You'd suspect that if you see an elevated serum chloride, low bicarb and hypokalemia, it just means the kidney can't regulate acid properly, which creates a perfect environment for crystallization.

SPEAKER_00: 6:11

Okay, we've got the diagnosis, but that patient is still in terrible pain. What does acute management look like?

SPEAKER_01: 6:18

First things first, analgesia. Get them comfortable. NSA80s are highly effective here, like 600 milligrams of ibuprofen. For smaller stones, let's say less than five or six millimeters, we can usually manage them conservatively, just observation for up to four weeks. They often pass.

SPEAKER_00: 6:35

Let's tackle the biggest clinical myth right now, the one you see in movies. They always hook the patient up to a huge IV bag and try to blast the stone out with fluids. Is that right?

SPEAKER_01: 6:44

That is the single most common and dangerous misconception. We have to drill this in. Yeah. Forced intravenous fluids or forced diuresis is counterproductive. It often makes the pain exponentially worse.

SPEAKER_00: 6:54

Why is that? What's the mechanism?

SPEAKER_01: 6:56

Well, think about it. You're pushing fluid into a blocked system. You're just increasing the pressure behind that stuck stone, which stretches an already distended renal capsule, just aggravates the pain. We hydrate them, of course, but we do not flood the system.

SPEAKER_00: 7:09

Got it. No forced fluids. So if we aren't using IV fluids to move it, what about meds? What is medical expulsive therapy?

SPEAKER_01: 7:17

For distal stones, especially those a bit bigger than five millimeters, we use medical expulsive therapy or met. This usually involves alpha blockers, specifically TAMsillosin, 0.4 milligrams a day. It relaxes the smooth muscle in the ureter and helps it pass.

SPEAKER_00: 7:32

And when does this stop being about observation and meds and become a surgical issue?

SPEAKER_01: 7:37

There are a few non-negotiables. First, that emergency we mentioned, an obstructing stone with an infection that needs immediate decompression. Other reasons would be intractable pain, persistent vomiting, if the patient only has one kidney that's obstructed, or if the stone just fails to pass after four weeks.

SPEAKER_00: 7:53

So what are our main surgical tools?

SPEAKER_01: 7:55

We have three main options. Ereteroscopy is great for mid and distal stones. We go up with a scope and either basket it out or break it up with a laser. Then there's shockwave lithotripsy or SWL. It's non-invasive, uses external shock waves to fragment the stone. Best for renal stones under two centimeters.

SPEAKER_00: 8:13

Any contraindications for SWL we should know?

SPEAKER_01: 8:15

Definitely. Pregnancy, an untreated UTI, and bleeding disorders are all absolute contraindications. And finally, for the big stuff stones over two centimeters, or those big branching staghorn calculi, the treatment of choice is percutaneous nephrilithotomy or PCNL.

SPEAKER_00: 8:31

And just to hammer home that infection point one more time, an infected obstructing stone requires urgent drainage with a stent or nephrostomy tube before you even think about removing the stone itself.

SPEAKER_01: 8:42

Absolutely. Drainage is lifesaving. Relieve the infection first.

SPEAKER_00: 8:45

All right, let's shift to the long game. This is where health maintenance and patient education become so critical. How do we change that recipe so they never make rock candy again?

SPEAKER_01: 8:54

It starts with the single most important intervention for every single stone type, no matter what it's made of. Fluid intake. We tell patients they need to be voiding more than 2.5 liters of urine per day. To do that, they'll probably need to drink close to three liters of total fluid daily. It's all about dilution.

SPEAKER_00: 9:11

Now let's bust the biggest dietary myth. Every patient with a calcium stone is terrified of this. I have to cut all calcium out of my diet. Is that true?

SPEAKER_01: 9:20

It's a common and very dangerous misconception. Patients should not restrict dietary calcium. A normal intake, a thousand to twelve hundred milligrams a day, is necessary. It's counterintuitive, but restricting dietary calcium actually increases how much free oxalate you absorb from your gut. And since most stones are calcium oxalate, that paradoxically makes your stone risk worse.

SPEAKER_00: 9:39

That is a crucial distinction. So if they shouldn't cut calcium, what should they restrict?

SPEAKER_01: 9:44

Two main things. First, sodium. Keep it under 3,500 milligrams a day. Excess sodium makes you excrete more calcium in your urine. And second, animal protein, limited to about one gram per kilogram per day. Too much protein lowers urinary citrate, which is a natural stone inhibitor.

SPEAKER_00: 10:00

And finally, let's talk targeted medications based on that 24-hour urine collection.

SPEAKER_01: 10:04

For recurrent calcium stones with high urine calcium, the first line MED is a thiazide diuretic, like chlorphalidone. It's another one of those counterintuitive renal tricks. Thiazides make the kidney reabsorb more calcium, so less of it ends up in the urine. For uric acid stones, we do the opposite of what formed them. We use alkalinization with potassium citrate to get the urine pH above 6.0. And for shruvite stones, it's all about aggressive antibiotics.

SPEAKER_00: 10:32

This has been a fantastic deep dive. We've really covered all the task areas for kidney stones, from spotting that classic writhing patient to ordering the non-contrast CT, managing the acute pain, and remembering no forced fluids all the way to a targeted prevention strategy.

SPEAKER_01: 10:47

At the end of the day, stone prevention is just about changing that crystallization recipe. You adjust the hydration, the diet, the medications to make it chemically impossible for that rock to form in the first place. You have to understand the chemistry to master it.

SPEAKER_00: 11:00

Right. And thinking about those rising rates, that clear link to obesity, hypertension, insulin resistance, here's a final thought for you to chew on. If we know a patient's first kidney stone is often a metabolic alarm bell, how should our standard screening for these other issues change? When a young patient presents with their very first stone, should that automatically trigger a more aggressive metabolic workup beyond just the stone analysis? Something to consider about the deep overlap between the renal system and general internal medicine.