The Clinical Problem Solvers
Episode 455 – Spaced Learning Series: Abdominal pain and distension
29 Apr 2026
Chapter 1: What is the main topic discussed in this episode?
Welcome back, Clinical Problem Solvers. Maddie and Yousef here. At CP Solvers, our mission is to make clinical reasoning accessible to learners worldwide. We invite you to join us for our live virtual morning reports, where we break down cases and sharpen our diagnostic reasoning together. Now over to you, Yousef.
Chapter 2: How does the team introduce the new member Anmol?
Thanks, Maddy. Just a quick reminder, this podcast is for educational purposes only and is not a substitute for medical advice. Patient details have been modified to protect their privacy and the views expressed here are our own, not those of our employers. Now, let's dive into the case.
Enjoy the show.
Welcome back, Kunkel Problem Slobbers. This is Jaz, one of the co-hosts of SLS. Today is a very exciting episode because I have the pleasure of introducing one of our newest members of the SLS crew, Anmolpreet Gurwal. I'm going to pause here and kind of give it over to Anmol to introduce herself.
Hello, everyone. I am very excited to be here at the SLS. My name is Anmol Preet. You can call me Anmol. And I'm a physician from India aiming for my internal medicine residency. Very excited to be here.
We're very excited to have you as well. Now to my other co-hosts today, Vale and Mukund. Vale, do you want to unmute and share our listening with you?
Yes. Hi, friends. I'm glad to be back. I'm Vale. I am an IMG from Peru, Lima, and I'm starting neurology residency soon. So I'm just working on that. That's what's new to me. How about you, Mukund?
Congrats, Vale. That's incredibly good news. I am about eight months ahead of you. I'm just finishing my first year of residency. I think while it's been difficult, it's also been one of the best years of my life. The learning curve is absolutely incredible, and every day is just filled with learning. Yeah, I'm having a blast.
For myself, I've just been busy as an attending and then also just trying to make sure that my 11-month-old doesn't harm himself in any way because he's a pretty mischievous kid. All right, with that, Mukund has a case today. I'm going to turn it over to him, and let's get this show on the road.
That sounds great. This was a really tough case and probably one of the more difficult clinical problem solving exercises I've run into an intern year so far. So good luck, you guys. But this is an 84 year old guy who was presenting to the hospital with sudden right upper quadrant pain, kind of sharp, stabbing, woke him up from his sleep and he classified it as a nine out of 10.
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Chapter 3: What clinical presentation does the patient have?
However, the imaging findings, as we can say, could be from the volume overload alone, and the leukocytosis should be interpreted in the context of him having a myeloproliferative neoplasm. So I would love to see the trend of his other cell lines to see if this is elevated for him or not, and also to trend them as he is hospitalized.
Now, if we combine both problems together, we get abdominal pain plus abdominal distension plus signs of possible inflammation. With this equation, my main concern is an intra-abdominal infection, specifically bacterial peritonitis. So I totally agree with the decision to start antibiotics while we wait for more clarity with some acidic fluid and more imaging.
That was amazing, Bale. I'm impressed by both you and Amol to dissect this very complex case into great teachable pearls. Question for the audience here, because I know there's a lot of information here, but let's kind of distill it down to see what you're thinking. Are we treating this as primarily heart, liver slash portal hypertension, infection, or are those categories misleading here?
I'll pause for a few seconds. So I would say the infection has to be treated now just because it can always progress and patients can have all sorts of complications, including death. But diagnostically, I don't think I'm ready to choose between the heart and liver just yet. The pleural effusions, the edema, the crackles, they definitely support congestion.
But the weight loss and the abdominal first presentation does make me worry that congestion is only part of the story. So I treat the infection empirically while using paracentesis and a liver portal vascular evaluation, such as Valet that she mentioned, evaluation to sort out whether this is portal hypertension, peritoneal inflammation, or rarely, but both can be involved as well.
Excellent. I think you guys are hitting on exactly the tensions that I was hoping for you to, namely, which organ system is involved? Is it multiple? Could it be all of them? I think the diagnosis is still very unclear at this point. So I'll give you some more data. Just for context, our hospital is very full right now.
So patients who are admitted to the hospital often need to stay in the emergency department for quite some time before they can be moved up into the wards for a hospital bed. So that's what happens to this patient. He's admitted as an ED boarder. So he is cared for by an inpatient team, but he lives in the emergency department.
And unfortunately, for a few days, he ends up living in the hallway of an emergency department. So the study that I'm really sure you're hoping for a paracentesis isn't done yet. It has to be done in a more protected environment than a hallway. So It's deferred to slightly later in the admission. So I'm sorry, you won't be getting that yet.
A HIDA scan is done, which shows non-visualization of the gallbladder. And the read is, this may reflect cholecystitis in the appropriate setting. However, the study was prematurely boarded due to patient tolerance. A second study is done, a right upper quadrant ultrasound with Doppler, which is completed and shows cirrhotic liver, no focal liver lesions.
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Chapter 4: How do the hosts differentiate between acute and subacute symptoms?
Or are we actually seeing portal hypertensive ascites that has been bled into, thereby contaminating the the ascites fluid albumin to serum albumin ratio and making it falsely appear as though it was a low sag ascites. This is the last aliquot and it involves some invasive data.
We got a liver biopsy because I think without tissue, it was impossible for us to decide whether this was cirrhotic ascites, whether this was non-cirrhotic ascites with a hemorrhaging component or whether this was some other diagnosis entirely. So We asked our colleagues in interventional radiology to do an IR-guided transjugular liver biopsy, and we asked for gradient measurements as well.
Radial pressure was measured at 10, and a normal value is less than 7 or 8. A hepatic venous free pressure was measured at 11. The hepatic venous wedged pressure was measured at 18. And therefore, the hepatic venous pressure gradient, or the wedged minus the free pressure, was 7. Technically, greater than 5 is defined as portal hypertension.
We also got a liver biopsy, benign hepatic parenchyma with a nodular contour.
Chapter 5: What initial assessments are made for the patient’s abdominal pain?
fibrous expansion of most portal tracts with patchy zone 1 and zone 3 perisinusoidal fibrosis, but without definitive bridging fibrosis appreciated. A reticulant stain highlights mild attenuation of the hepatic trabecula in the perivenular parenchyma, indicative of altered perfusion of the perivenular hepatocytes. A PAS stain is negative for intracytoplasmic alpha-1 antitrypsin.
And in summary, the pathologist says these findings are compatible with a chronic inflow-outflow impairment, and that given the presence of perisinusoidal fibrosis in the territory the biopsy was obtained, a diagnosis of nodular regenerative hyperplasia cannot be established on this particular biopsy sample. Anmol, I think you have the most difficult job of this episode so far.
Wow, amazing. What a case this has been. So now with the biopsy results in hand, we can finally bring everything together. But before we interpret the biopsy, let's take a step back and briefly review how it was obtained. a transjugular liver biopsy was performed which, unlike the percutaneous approach, accesses the liver via the internal jugular vein.
This route is particularly useful in patients with ascites or coagulopathy as it minimizes the bleeding risk by keeping any potential hemorrhage within the vascular system rather than in the peritoneal cavity. So I can pretty much understand why the transjugular approach was taken for this patient.
So in this process basically the catheter is advanced from the internal jugular vein into the superior vena cava and then through the right atrium into the inferior vena cava and ultimately into the hepatic vein. So the benefits of this technique is we can also measure the key hemodynamic parameters there.
The free hepatic venous pressure represents the pressure measured within a non-occluded freely draining hepatic vein and it reflects the systemic venous pressure. In contrast, the wedged hepatic pressure is obtained by occluding the hepatic vein and serves as an estimate of the portal venous pressure. Therefore, from these values, we can calculate the hepatic venous pressure gradient.
Portal hypertension is the elevation of the hepatic venous pressure gradient to more than 5 mmHg, while clinically significant portal hypertension is defined as a gradient of 10 mmHg or more. In this patient, the hepatic venous pressure gradient is only mildly elevated, and that is a critical pivot point in this case.
Because at first glance, with ascites and imaging suggestive of cirrhosis, it is tempting to attribute everything to portal hypertension from cirrhosis. However, this case requires us to move beyond that assumption. Now we have an important nuance here, which it's important to highlight that the hepatic venous pressure gradient primarily reflects sinusoidal portal hypertension.
So while an elevated gradient would clearly indicate portal hypertension at the sinusoidal level, A normal or mildly elevated gradient, as seen in this case, does not completely exclude portal hypertension, particularly in cases of presinusoidal diseases where the gradient can appear falsely normal.
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