72: Total Effusion of the Heart

She recently successfully completed the ID match process and will be starting her ID fellowship at UT Southwestern in July.

It is to the extent that he's unable to ambulate around his home without feeling significantly short of breath. His cough started about two weeks ago and it was initially dry though in the past two days, he's been coughing up a small amount of clear sputum. On further history, he shares that his breathing has been worse when laying down and he has to sleep with the head of his bed elevated. He denies any other preceding or concomitant symptoms including nausea, diarrhea, rash, or fever.

The patient's only prescribed medication is losartan, though he admits that he is been out of this medication for over a month and has not been taking it. He lives at home with his wife. He has two adult sons, both of whom live in the area. He's originally from Honduras and moved to this country four years ago to be closer to his family. He previously worked in construction but has not worked for the last 10. He denies a history of smoking, drinking, or drug use. There's no pets in the home.

He denies any sick contacts or historical contacts with people known to have tuberculosis. Upon presentation to the emergency department, he was tachycardic, normotensive, afebrile. He was saturating 94% on room air with respiratory rate of 16 to 18. Physical exam documented in the ED notes a prominent JVD to 13 centimeters, crackles in the bilateral lung fields, irregularly irregular heart rate with no notable murmurs or extra heart sounds, and two plus pitting edema in the lower extremities.

He underwent E K G and was noted to be in new onset atrial fibrillation with rapid ventricular response to the 160s. Chest X-ray in the emergency department showed pulmonary edema and massive cardiomegaly. He was started on diltiazem for rate control. He was admitted and shortly after admission was started on a apixaban for anticoagulation. While admitted, he undergoes diuresis and on hospital day two, he undergoes an echocardiogram as part of routine workup for new onset AFib.

It shows a large circumferential pericardial effusion. We can pause here Dr. Polk and can you talk about your differential in this?

And you know, classically for a pericardial effusion or what is described is a water bottle sign of an enlarged cardiac silhouette. And so I just wonder about that appearance of cardiomegaly on the chest x-ray and whether there were just some of those subtle clues to the presence of the effusion be before we got the echo.

But since we're talking about differential, the next question really would be, Were there any signs or symptoms of an acute inflammatory syndrome or acute pericarditis, and we're really not given any here. So in the H P I, you talked about there really wasn't fever or chest pain or ST elevations on the EKG, suggestive of pericarditis. He does have a cough, but it sounds like it might just be more from his pulmonary edema.

If he did have some of these acute inflammatory symptoms, then I might be more concerned for an infectious etiology, particularly for a pathogenic bacterial infection like Staph aureus, pneumococcus, or other streptococci diseases. NNeisseria, Legionella, Mycoplasma. In my experience, patients with those typical bacterial pathogens generally are fairly ill appearing and, and come in sick with if they have acute pericarditis.

In the absence of that, might think about viral pathogens, coxsackievirus, adenovirus, the one we see in adults is usually H I V, uh, which is something to think about. Fungal pathogens might be on our differential, especially the endemic fungi. Blastomycosis, Cocci(dioides), histoplasma.

And then of course we can't forget about tb, tuberculosis, and it's really possible for, uh, effusions from TB to really be more indolent with fewer acute inflammatory symptoms, although maybe patients might have weight loss or night sweats. So thinking through some of the infectious etiologies of a pericardial effusion, I would think through that set of possibilities. And then I would also think about non-infectious etiologies, especially given his lack of acute inflammatory symptoms.

You know, as ID clinicians, we are often asked to kind of act as a master diagnostician and really consider non-infectious etiologies, and I just often find it particularly satisfying to make a non-infectious diagnosis. But just sort of thinking through those possibilities here. You know, what might they be?

Well, he was recently initiated on anticoagulation, so I think we have to think about bleed a little bit, although on this echo he had, there's really no mention of an aortic dissection or leakage into the pericardial sac. You know, always think about MI, which might have a complication of pericardial effusion at some point, although presumably maybe he had some cardiac enzymes done or was assessed for that given his new onset atrial fibrillation.

You know, we think about uremia in our adult patients as in etiology in this. Then for this patient, he does have a history of malignancy and malignant effusions might be a consideration. Although usually malignant effusions would complicate lung or breast cancer, leukemia, lymphoma, probably not as an isolated recurrence of prior gastric cancer.

That would seem to be unusual, but just sort of thinking through that, uh, mixed edema might cause a pericardial effusion, although, if anything with, new onset atrial fibrillation with rapid ventricular rate. You might think he's hyperthyroid. And then always think about connective tissue disorders too in our differential, right? Lupus, rheumatoid arthritis, granulomatosis with polyangiitis.

Sarcoid, maybe even familiar Mediterranean fever, all of which I would think would have systemic manifestations, uh, rather than an isolated effusion, but just sort of thinking through a full differential would consider those. And then that sometimes medications or drugs can cause effusions such as hydralazine, but he really doesn't appear to be on those. So that's a really big differential to both infectious and non-infectious etiologies.

But the truth is, a lot of times these effusions are idiopathic and we don't find a good answer and maybe that's the answer here too. So with that differential, Annie, Do you have some more information so that we can maybe narrow it down or focus on where we're going with this case?

He went to another hospital about a week ago and was told that he had pneumonia. He was prescribed an oral antibiotic. He isn't sure which one, and he didn't have improvement. Further history revealed that he's had chest pain and hemoptysis for two weeks leading up to his current presentation. The chest pain is sharp in nature. Anterior in location and exacerbated by inspiration and cough. His cough is productive of white frothy sputum. He also notes feeling febrile at home with night sweats.

Over the past two weeks though, he is been unable to take his temperature. He has no other focal symptoms. His vitals at presentation show sinus tachycardia, 110 to 120 beats per minute with a blood pressure within normal range. He's febrile to 103.1 Fahrenheit. He's tachypnic to 24 breaths per minute, but satting well on RA, he's ill appearing in diaphoretic. Physical exam is significant for the tachycardia and soft heart sounds. There's no murmurs, rubs, or gallops.

He's using accessory muscles for respiration with subcostal re retractions. There's no notable rashes and no lower extremity edema. He has palpable lymphadenopathy. Mental status was intact. On the initial assessment. Labs showed elevated sedimentation rate of 124 millimeters per hour. His chest x-ray shows blunted costophrenic angles with massive cardiomegaly. Ekg showed sinus tachycardia with classical electrical alternans.

Point-of-care ultrasound confirms a massive pericardial effusion with RV collapse. With this initial presentation, what are your initial thoughts, Dr. Polk? How is this similar and different than our patient in North Carolina and how does your patient's differential change with this specific history?

But I think we have to stop and really do due diligence and consider the the full infectious differential and think about staphylococcal disease, pneumococcal disease, meningococcal disease, all of which are certainly quite possible here. Of note, where Chogoria is in Kenya is not in the meningitis belt. It's a little south of that, but you know, certainly would remain a consideration. Uh, histoplasma also can occur in Africa, so might consider that as well.

I also wanna comment briefly on this patient having cardiac tamponade, which I think is interesting and we didn't really discuss so much in the first case, still was reported to have a large effusion, but is obviously a very important diagnosis to make and assess for.

And you know, in tamponade, maybe more related to the rapidity of fluid accumulation than the size, and maybe we suspected when there's J V D in the presence of hypotension, which the second patient really didn't have described interestingly, we might also suspect that if there's electrical alternans on the ekg, but if you don't have a handy point of care ultrasound to look for tamponade, the other quick bedside test you can do is a pulses paradoxus so here you check the patient's blood pressure doing inspiration and expiration and

systolic blood pressure drops at least 10 millimeters of mercury. That's a concern and, and I will just briefly comment, the only time I was ever reprimanded as a resident is when I didn't do this, when admitting a patient and the program director came in the next morning and the patient was in tamponade. So it's a quick, easy bedside test you can do that. I'll certainly never forget if you don't have that point of care ultrasound.

Um, so are, are we going to find out more about either of these patients, Annie?

His C B C showed a white count of 12,000 with a hemoglobin of 10 and platelets of 400. His electrolytes were all within normal limits, a Cr of one and normal BUN. His a s t and a l t were unremarkabe. He did undergo a CT chest in the emergency department. The circumferential effusion is again noted, and he had no lesions in the lung parenchyma, cavitary, or otherwise. He had trace plural, effusions, far too small to consider tapping.

It was actually at this point in the hospital course that infectious diseases was consulted. As the ID consultant, what would you suggest in terms of diagnostics in this patient at this point in his hospital?

Were there any experiences with incarceration or homelessness or other risk factors we can tease out? Uh, we might think about that in the context of risk factors for endemic fungi as well of. He was here in Charlotte, where we have a little bit of Histoplasma from time to time, but he was from Central America where there's sort of increasing rates of histoplasma. So we might think about that. We might ask about family history of rheumatologic illness, which might.

Provide some clues and, and then we would really wanna embark on a further workup. We really have some basic labs here, which is great. He probably doesn't have a uremic effusion. We know that now. But what about an H I V test?

You know, just looking at some case series from tuberculous peritonitis, a positive igra has a sensitivity and specificity of around 85%. So that's a positive predictive value, about 90% negative predictive value, 70%. So it might raise your suspicion for tuberculosis, um, if it's positive, but again, Really excluded from the diagnosis, either if it's negative. Other things we might do really boil down to obtaining fluid or tissue for diagnosis here. Right?

And pericardial fluid, while helpful is only diagnostic and about 40% of the time pericardial effusion with from tb. So something to keep in mind and we can't really use lights criteria on pericardial fluid the way we can for pleural effusions. That's part is not helpful. But what we can send, obviously our AFB smears and cultures, and then an adenosine deaminase test. Which maybe is worth talking a little bit about.

In addition to TB pcr, adenosine deaminase is part of purine metabolism that is elevated in TB and given off by lymphocytes. It's not exclusive to tuberculosis, but is helpful to make a diagnosis of a ppleurall or pericardial effusion from tb. So I think it might be really helpful here to send that. The other gold standard we can think about is doing a pericardial biopsy, and we classically think about this as increasing yield for making a diagnosis of TB from in the pericardial space.

Unfortunately, it's maybe a little less sensitive than we like to think of it as. So an AFB smear from pericardial fluid, fluid is only about 5% sensitive, culture is about 50%, and a pericardial biopsy does increase your sensitivity, but only to about 65%.

So making the diagnosis here is a little bit of a challenge no matter what modality you use, but you probably do wanna obtain some fluid and try and think through sending some of those tests again, particularly the adenosine deaminase or the TB pcr, which may have a sensitivity of up to 90%. And then finally, you could also think you about sending a T-SPOT from your fluid, which also is pretty sensitive, but about 90%.

So that's some of the things I would sort of think through in workup of the patient from the us What, what about that patient in Kenya?

One liter of dark bloody fluid was drained in the first 30 minutes after placement. The patient's hemodynamics improved. Soon thereafter, the patient was started on empiric RIPE therapy. Over the next three days, a total of three and a half liters of fluid was drained from the pericardial drain throughout the hospital course, the patient clinically improved with a complete resolution of that altered mental status.

Gene expert testing of the pericardial fluid did confirm a diagnosis of tuberculosis. Dr. Polk, what are your thoughts about this?

Alternatively, from South Africa, a case series published on pericardial effusions identified TB as the most common cause. So epidemiology always matters.

What treatments, if any, are you starting on this patient at this point in the hospital course and at what point did we consider empiric tuberculosis therapy in this patient in the United States?

So we're down to thinking about cancer or tb and we've already talked about how it would be unusual for gastric cancer to recur just in the pericardium and from the chest imaging we have. We don't see a suggestion of other chest cavity malignancy that might go with a malignant effusion. So we're down to thinking about tuberculosis again, and the fact that he did have a prior residence in a country with higher endemicity of tb.

I'd also say we previously talked about sending an interferon gamma release assay here, and I'm guessing that's still not back yet.

Yes, we are working on it. Mm-hmm.

He had a negative A f B sputum smears. Three were collected, specifically negative blood cultures, but his QuantiFERON did return. The pleural fluid was sent for analysis and the ADA was elevated at 55 milliliters. What do we make of diagnosis at this point?

But just thinking about TB pericardial disease in general, since we have these two cases, it's interesting because it's really rare. It's less than 5% of cases of TB present this way and unfortunately, Classically, it had a fairly high mortality rate prior to sort of modern, effective therapy, and still we worry about the complication of constrictive pericarditis because in the later stages of pericardial.

Uh, TB disease, the fluid gets reabsorbed, and then there's scarring of the pericardium, granuloma formation, and constrictive heart physiology can occur. So that's a concern. Certainly treatment, uh, with ripe is indicated there. And then sometimes steroids have been given and the, this is maybe a little controversial, and the, the data. Inconclusive, but they might be helpful early.

Although studies really haven't completely demonstrated definitive benefit in preventing constrictive pericarditis, but it is a concern. And if there's progression in some patient, they may need surgical pericardiectomy for constructive pericarditis, but two really interesting cases in different locales leading to the same diagnosis.

Stay safe and I'll see you next time.