Complicated Cholecystitis - SD

Introduction to Complicated Cholecystitis

Hello, I'm Dr. Brooke Jeffrey from Stanford University, where I'm professor Radiology and chief of Abdominal Imaging.

My topic today is complicated cholecystitis. My topic today is complicated cholecystitis, and let's begin by defining that term.

This is a series of entities really that are at the end of the pathologic continuum of acute cholecystitis. And while it's certainly fair to say that all of these entities funnel into a final common pathway, histologically characterized by mucosal ischemia, mural inflammation, hemorrhage, transmural, necrosis, and perforation, all of these have distinctive features that it's worth reviewing them.

And my intention is that at the end of this talk, you will note that even though it's complicated, you'll hopefully feel a little bit more like Alec Baldwin and a little bit less like Meryl Streep.

So along the way, what I'd like to do is review the pathophysiology of these entities emphasizing the gallbladder findings, and we're going, we are going to work our way from inside out, from the gallbladder lumen, moving on to the wall, and then finally into the spaces around the gallbladder of the Peric cystic space.

And I would like to emphasize the complimentary roles of sonography with ct. And finally, to discuss some of the mimics of complicated cholecystitis such as carcinoma.

Clinical Overview

Well, just in terms of a broad clinical overview, in general, most surgical series report that complications of cholecystitis occur in about 15 to 25%.

But there is no question that these patients have an overall increased morbidity and mortality, which in some series is up to 15%.

In many cases, the clinical signs and symptoms are fairly non-specific with fever and sepsis. Being the most common right upper quadrant pain is variable.

And as we'll see in patients with gangrenous cholecystitis, perhaps up to a third do not have a sonographic Murphy sign.

Now the treatment options do vary between open and laparoscopic cholecystectomy or even percutaneous chole cystostomy.

So once we'll make the diagnosis, we'll often go on to stage the degree of inflammation using ct.

Pathophysiology

Now, in terms of the pathophysiology, it's been known from experimental studies. If you perform external ligation of the cystic duct, it merely results in atrophy and not cholecystitis.

However, if there is internal obstruction of the cystic duct by stones, this leads in turn to distension mucosal ischemia and submucosal inflammation.

And in most cases, this is of course going to be due to calculus obstruction of the neck or cystic duct by a stone leading to prolonged distension, raised intraluminal pressure and ultimately bile stasis.

Now, once there's mucosal ischemia and sloughing of the mucosa, then intramural hemorrhage and edema ensue.

And here we can see a normal histologic section of the gallbladder wall, the luminar epithelium with the lanar propria deep to it, the muscular elements of the wall and the loose connective tissue.

And all of this is obliterated. Once we get gangrenous and hemorrhagic cholecystitis, the mucosal surface is denuded. We recognize no luminar epithelium, and instead what we see are areas of hemorrhage and intense inflammation extending all the way to the wall.

Now in addition to that prolonged distension contributing to ischemia, there are a number of biochemical factors that are at play as well.

And ethin and prostaglandin, particularly prostaglandin e, have been implicated in mucosal ischemia.

And once that mosa is denuded, then the phospholipids in concentrated bile salts act directly on the submucosa to incite intense intramural inflammation.

Now, within the first 48 hours, this is largely a sterile inflammation, the only exception to that being emphysematous cholecystitis.

And with increasing transmural inflammation, we ultimately get complicated cholecystitis.

Imaging Findings

So let's now look at the imaging findings working our way from inside out, starting with the lumen, proceeding with the gallbladder wall, and then the peric cystic spaces.

Gallbladder Lumen

So let's first take this quiz. What do these four different patients have in common? A sludge B, no sludge C carcinoma or D plus?

Well, in fact, what they have in common is that none of these patients have sludge. All the internal echoes in the lumen are related to in this patient cancer, this patient puss, this patient blood, and another patient with puss.

So the first point to be made is that do not assume with intraluminal findings that there's sludge and keep in mind the differential of blood puss or cells.

And if we see very echogenic material in the gallbladder lumen, we should suspect that that's blood. And confirm that with a non-contrast ct.

If we see linear echoes within the gallbladder, think of slough mucosa or fibrin strands.

And if there are linear high amplitude echoes, casting dirty shadows, we'll be thinking of gas bubbles.

And we'll talk also about the contribution of colored doppler and not mistaking sludge for carcinoma as well.

So here's an example where we have very echogenic material filling the gallbladder lumen, and the next thing to do is obtain a non-contrast ct.

And if the hounsfield units are 30 and above, we can make a diagnosis of hemorrhagic cholecystitis.

Similarly, in this patient with increased echogenicity within the gallbladder lumen, the non-contrast CT confirms hemorrhagic cholecystitis.

Now, low level echoes have an overlap between sludge and puss.

And here's a patient with a clear cut, gallbladder perforation. This individual happened to have a calculus cholecystitis, and we can see focal A of neural necrosis in surrounding this very similar to the low level echoes in the gallbladders, this pus.

And this is a patient with, in, in essence an empyema with perforation and surrounding pus.

So there's an overlap between puss and just sludge. So keep that in mind.

Now, one of the very important things that we need to do on all patients with gallbladder disease as use colored doppler, we'll see that it certainly has limitations.

But in this patient, if unless you use colored doppler, you might incorrectly assume that there's just a stone floating here and this sea of sludge within the gallbladder.

But in fact, we can see that the lumen has internal echoes with internal flow, and that's the key to making the diagnosis of gallbladder carcinoma.

Now, linear, intraluminal echoes are critical because they often indicate fibrin strands, necrotic debris, slough mucosa.

And here in this past slide, you can see in addition to the hemorrhage, these linear white strands of dead necrotic tissue as well as the fibrin strands of clot.

And what that's gonna look like graphically, again, are these linear internal membranes, floating in the lumen of the gallbladder.

And that should always prompt you con skitter, complicated cholecystitis, particularly gangrenous cholecystitis.

Now ultrasound is superior to CT in this regard.

And here's a patient with SL mucosa that is clearly evident, graphically but very difficult to assess on ct.

On the other hand, we do get the sense of the areas of focal loss of mucosal enhancement and areas of peric cystic inflammation, and we'll have much more to say about that in just a moment.

But whenever you see these linear echoes within the gallbladder, think of complicated or gangrenous cholecystitis.

This is a patient in fact, who had a combination of slough mucosa and hemorrhage where the increased echoes represented blood clot and these linear echoes were slough mucosa.

Now, once we identify high amplitude linear echoes within either the lumen or the wall, we should go on to do CT because I want to introduce the concept of staging, the degree of inflammatory change.

And here we can see in the corresponding ct, not only is there, gas within the lumen, but very importantly this patient is perforated emphysematous cholecystitis, and now has, gas bubbles would we can see in the sub phrenic space.

And so why this is important is that a simple percutaneous chole cystostomy is not gonna be indicated here. This patient's already perforated and na a lavage of the peritoneal cavity.

So it's very important to, stage the patient correctly and CT is much more, accurate in this regard.

Gallbladder Wall

So let's transition now from the lumen to the actual gallbladder wall and make the point that one of the important findings is loss of the normal sonar reflectivity.

Again, something that's not there is often very difficult to recognize. On sonography, what has been emphasized in the literature is gallbladder wall thickening, of course, and there have been articles that are looked at the so-called striated appearance where we have the multiple linear echoes.

It's important to emphasize that this is a non-specific finding, can be seen in hepatitis as well as gang mens cystitis in these two patients.

On the other hand, what is much more specific are areas of focal and asymmetric thickening of the gallbladder wall, either due to ulcerations, intramural abscess or intramural hemorrhage.

And you can see two patients with gang MaRous cystitis with vary asymmetric gallbladder, wall thickening with focal hypo coic areas. And that's very important to identify.

And you can see in the corresponding ct, this patient has intramural abscesses as well as perforation and abscesses in the Morrison's pouch.

Now here's a patient that, let's just look at as a little quiz here and we can see, selected images of the gallbladder. So what is missing in this patient?

Well, what's missing is any evidence of the sonar, reflectivity of the gallbladder wall. Remember, the gallbladder should have a very well defined sonar reflectivity of the gallbladder wall.

And what this patient had was gang cholecystitis with complete absence of the gallbladder wall. And what's enhancing on CT is the sort of fibro capillary rim of a huge abscess.

And this patient had had surgery, no really visible gallbladder wall intact at all, just a contained abscess in the pericole cystic space.

So not infrequently, this focal loss of reflectivity occurs primarily at the fundus, which due to the area of the greatest wall tension of the porous blood supply is the first area of the gallbladder undergo necrosis.

So that's what this looks like. Here we can see, normal reflectivity of the gallbladder wall and loss of reflectivity, empiric chole cystic fluid.

And this is a patient with gang cholecystitis with perforation of the fundus. And much of the anterior wall here is all necrotic.

So pay attention to that finding, particularly at the fundus.

And here's a patient with extensive loss of sonar reflectivity of the fundus. A little bit is preserved here. Large areas of the gallbladder wall are absent.

Notice the increased echogenicity and notice that this extends in the pericole cystic space.

This patient had a combination of puffs and hemorrhage, and actually expired from sepsis from this, perforated gangrenous cholecystitis, another patient with focal loss of reflectivity in the fundus, the surrounding peric cystic abscess.

This is what this looks like on the corresponding ct. You can see the, focal loss that's right here and then the surrounding abscess.

And when you have multiple abscesses like this, which CT is really critical to determine this, patient's often not going to respond well just to a single tube placed in the peric cystic space.

And the sooner you operate on these patients, and drain the abscess, the better off they'll be.

And once the surgeon is forewarned, generally this is an open cholecystectomy as opposed to a laparoscopic approach.

Here's another patient with focal mural loss of reflectivity and adjacent to, the gallbladder fundus. We see these multiple abscesses as we do here, and this is a case where there's more focal loss of reflectivity in the surrounding ct showing the peric cystic abscess.

Again, this is important in terms of staging and, at least at our institution, once there are prominent pericole cystic gapes, that's an indication for surgical drainage.

Now, when we look at the wall with colored doppler, it's important to recognize that there are clear limitations to this.

And what's normal with high resolution modern equipment is that we can visualize the cystic artery, particular, it's a dorsal branch, and sometimes it's ventral branch as well. In the proximal half of the gallbladder.

What's abnormal is to see flow in the fundus. That's generally an abnormal finding. We'll talk about some phos positives in a moment.

But in the setting of acute inflammation, this would be considered to be within the range of normal. But, as this patient had a calculus cholecystitis proven surgically, so there are clear limitations to this, because cold doppler is really a late finding. It's not all that sensitive for the early diagnosis.

Now here's an example where there's a true positive with flow in the distal half of the gallbladder, the patient who did have a calculus cholecystitis.

But here's a false positive in a patient with cirrhosis. And when you diminish portal flow, there's in compensatory increase in hepatic arterial flow.

So in patients, with, diminished portal flow, don't be surprised if you see a fair amount of flow in the gallbladder. This merely reflects the increased flow in the hepatic artery.

Now, when we define the mural abnormalities that we wanna look in patients with complicated cholecystitis, we've made the point that the striated wall lacks specificity and has an overlap with many benign entities such as hepatitis, asymmetric wall thickening is a key point that I want to emphasize, as well as the loss of sonar reflectivity.

We've seen the normal and abnormal, flow patterns and be sure, to focus specifically on the fundus.

Pericholecystic Spaces

Now let's turn to series of findings around the gallbladder in the pericole cystic space. And here I wanna emphasize the inflamed echogenic mentum as a surrogate for transmural inflammation.

And what we're going to look for are complex fluid collections or gas bubbles that indicate pericole cystic abscesses. We'll look for fluid and we'll look for this inflamed echogenic fat that relates to either, edematous fat from either the omentum or the hepato de ligament.

Now, pericole cystic fluid has been known for a long time to be seen in conjunction with gangrenous or complicated cholecystitis as it was in this case.

But it's important to recognize that this is a, again, a non-specific finding. And can these are two patients with hepatitis that have marked gallbladder wall thickening and peric cystic fluid and, do not have, cholecystitis at all.

So keep in mind that this is a non-specific fluid, finding, pericystic fluids also seen in other acute entities.

Here's a patient with pancreatitis. Here's a patient with peptic ulcer disease. So with fluid, both in marson's pouch and around the gallbladder.

So we have to be a little bit circumspect about this finding.

There's another example of peric cystic fluid and HIV aids and two different patients. They often have marked gallbladder wall thickening, and it's not uncommon to see a little bit of fluid around the gallbladder.

Now the inflamed echogenic fat that's around the gallbladder in the peric cystic space, is inflamed fat from the omentum.

The omentum is the policeman of the abdomen. Its job is to wall off perforations and abscesses.

And what we're seeing in this case is actually a mental flow. This is not in the wall of the gallbladder. This is hyperemia with in the omentum.

And this patient has gang cholecystitis. Notice the marked asymmetric wall thickening and the inflamed a adjacent fat.

Here's another patient with, linear echoes in the gallbladder gang cystitis. And this thick wad of echogenic tissue is the inflamed omentum, this gang cholecystitis.

This is not within the wall that's in the inflamed omentum.

So the mentum gets inflamed when there's transmural inflammation. And this is an important secondary clue, the fact that you're dealing with complicated cholecystitis.

And here we can have this echogenic inflamed fatty tissue that's walling off a peric cystic abscess.

Here we can see the site of perforation and some surgeons will attempt to do these via laparoscopic approach. You can see that the mentum is just plastered all over the gallbladder. You can't even recognize any normal structures here.

And so I think in general, there's a growing tendency to do these casings open rather than f laparoscopic approach.

Acalculous Cholecystitis

Now I wanna just make a few points about a calculus cholecystitis in particular, and to emphasize this is a very difficult diagnosis to make. We make many false negative and false positive diagnoses.

I want to emphasize in particular, looking for progressive gallbladder wall edema and looking for CT findings.

So while this is, really a distinct minority of patients with acute cholecystitis, because this is occurs in patients are critically ill of many comorbidities or in the ICU from trauma or burns or major surgery, there's a very high mortality with this and perforation in the setting, with bile peritonitis is often the terminal event.

So it's less common a patient just right off the street, but occasionally in diabetic patients and patients without the sclerotic disease, it's been reported and it should make the, finding that, traditionally ultrasound and nuclear medicine have a very low, reported sensitivity for this disease.

Now, instead of cystic duct obstruction being the primary disposing factor as it was with calculus cholecystitis, usually a low flow state producing mucosal ischemia is the precipitating event.

And there are a number of other biochemical factors that come into play, such as prostaglandin e bile salts, platelet activating factor have all been implicated in causing intense mural inflammation and hemorrhage.

There's some thought that there is a degree of cystic duct, obstruction from viscous sludge.

In any event, the final common pathway is loss of the, mucosal area, areas of hemorrhage, neutrophilic infiltration into the wall.

Now the problem is that critically ill patients all have thickened gallbladder walls and sludge. You take the portal equipment up to the ICU, it's hard to find somebody who doesn't have sludge in a thick and gallbladder wall.

So how do you really know who's got ocular cholecystitis?

We've already made the point that collar doppler isn't really all that helpful. And in a patient who's ventilated, it's impossible to elicit a sonographic Murphy sign.

So not too surprisingly, sonography has a relatively poor sensitivity for this.

So let me pass along a few things that I've learned the hard way over the years.

And one is, if you start out in a, in a patient who has the clinical demographics, ICU patient who's fevered sepsis, right upper quad pain, you're suspicious that this patient has potentially a calculus cholecystitis.

And if you start from a relatively normal gallbladder wall thickness, just slightly thickened, the thing to do is get a followup ultrasound in 12 hours, maybe even 24 hours.

And if there's progressive gallbladder wall edema in the absence of congestive heart failure or fluid overload, that's probably a pretty good bet that the patient has, a calculus chole cystitis.

And, our group wrote this up, a number of years ago, but that has stood the test of time.

And we do this routinely on patients who start out with, relatively normal gallbladder wall.

But what if you start out with a very thickened wall right off the bat if your baseline is thickened?

Well, we've reported that CT in these patients is really the way to go. And what you're looking for are areas of mucosal ischemia.

Here's the normal enhancing mucosa. The wall's very thickened, but there are large regional areas of mucosal ischemia.

And look at the perico cystic inflammatory changes. Those findings are very specific, a calculus cholecystitis.

And at that point, depending upon whether there are abscesses around the gallbladder, your options are cholecystectomy or percutaneous chole cystostomy.

Mimics of Complicated Cholecystitis

Gallbladder Carcinoma

Now I wanna just conclude by talking about some mimics of complicated cholecystitis. And the first one we'll talk about is carcinoma.

And here is where color doppler plays a very important role. Gray scale alone is often very confusing, but I would say if you see rounded areas that are nice and spherical and rounded, don't just conclude that that's tomb effect of sludge.

You really should think about going on and getting a contrast ct.

And sometimes, what you'll see is really quite striking because ultrasound is very poor for identifying these areas adjacent to the gallbladder.

And here you can see the enhancing mass within the gallbladder lumen that's nice and spherical and rounded, and there's already direct extension into the liver.

And here is an example of, pseudo sludge where the gallbladder is infiltrated. There is cancer within the wall and the lumen, and you really do need CT to confirm this.

The other thing that you need, CT four is staging. And here we can see there's extension of the gallbladder cancer, to the hepatic flexor.

Pyogenic Liver Abscesses

The final mimic that I want you to keep aware of, are seen in these four patients, what do they have in common?

And all these patients have abscesses and there's very highly variable appearance, iso, coic, echogenic, multis, SubT, cystic.

And so any focal liver lesion in the right demographic, focal, right upper quadrant pain and abscess is very important.

Keep in mind that pleural fluid is a very important sign. So if you see pleural fluid, you need to carefully inspect the sub phrenic spaces, and the patient's got fever and right upper quadrant pain.

And here we can see by turning the patient and examining the sub phrenic spaces, we can see an abscess.

And if you go back, the original image there is where the abscess happens to be. It's just our focal zone is not optimized for the near field.

So biogenic liver disease clinically mimic complicated cholecystitis and they have incredibly varied clinical, and imaging features.

We'll just point out a few things that they can look solid, they can look multi septated.

Here's a patient with a solid abscess, just very subtle areas of hypo echogenicity. Again, notice the pleural fluid. That means you've got inspect the, the NIC space and CT shows this.

The classic cluster sign of biogenic abscesses here is a more echogenic one that has a hypo coic, rim around it.

This was a, a patient who has another clue of a space occupying mass. The right hepatic vein is monophasic and the middle hepatic veins a normal phasic flow.

That means there's a space occupying mass within the right lobe.

Here's an epigenic abscess, that was related to Klebsiella and here is a multi septated abscess. That was an e coli abscess as well.

Here's one where that mimics metastatic disease, multiple HypoChlor kalos, our friend, the right pleural effusion is there.

And here we can see the CT showing us the cauliflower appearance of multi septated gas.

In the snic space, can produce a gas forming abscess as we see here.

And in the liver transplant population. Patients presenting with fluid collections and fever always in addition to, finding this abnormality is to make sure the patient doesn't have hepatic artery stenosis. Go on to get a CTA.

Here's another patient with an infected myeloma. That should trigger careful Doppler interrogation.

And here we can see on the CT angio the occlusion in the hepatic artery.