June 16, 2026 VMR with Ravi & Khashayar - Fever and Generalized Body Pain for 3 Days

[00:00:03]Hello, welcome everybody to Tuesday VMR.

[00:00:06]It's my pleasure to discuss a case. We have a first-time case presenter, Sudarian, who's currently down at George Washington University doing a GI rotation in the heart of DC, Foggy Bottom, if anybody knows where that is.

[00:00:22]Um but before we get underway, I want to introduce one of our um academy members who's going to be co-discussing this case with us. So Kasher, how you want to unmute and just uh say hello and tell us how things are?

[00:00:38]>> Hi everyone, I'm Kasher, longtime academy member and a medical student in Iran. Currently doing my final year of internship here. Very excited to be here. It's been such a long time since I discussed case.

[00:00:53]>> Yeah, it's just wonderful. We're truly international. So, um, and then we have Sudashan who is a first-time case presenter. You want to unmute and just say hello?

[00:01:04]>> Yeah. Oh my god, it's um it's a long time um in the wait. I've just I've been following CPS for at least two years now and uh yeah, I'm just so happy to be here presenting today. Absolutely wonderful to have you. Excited to to have you featured today. And then we have Lucas who's going to help us with scribing. You following the Germany national team closely, I hope in the World Cup.

[00:01:31]>> No, I I played so much football in my my youth. That's enough football in my life, I guess. So, I'm Lucas. I'm scribing. And um yeah, back Mike, back to you, Robbie.

[00:01:43]>> Sorry. Thank you. And we have Julia probably probably following the Brazilian national team who's also play.

[00:01:50]I'll try to make it a World Cup edition of CPS.

[00:01:54]>> Hi everyone. Yes, I'm Julia. I'm following today. We will watch the Argentina and we have Brazil again on Friday.

[00:02:02]>> Absolutely. Yeah. Wonderful. And uh let's uh start with the first Aliquad and Kashier you take first step at the first Alad.

[00:02:14]Awesome. What's good?

[00:02:18]>> Um, awesome. So, we have a 28-year-old male who comes to the ED with complaints of fever and generalized body pain for 3 days.

[00:02:30]Um, so he was in his uh usual state of health until 3 days prior when he developed severe fatigue requiring him to leave work. Um this was followed by um intense generalized body pain and two episodes of vomiting. Um he's had poor oral intake since his symptom onset and intermittent high-grade fevers with a T-max of 103 um which he just measured at home. Yeah. Stop here.

[00:03:04]So, uh, the current presentation is pretty unspecific while looking very severe at first. We need to further take a look at the patient and gain more info. My first thought is nothing really specific. The initial complaint sounds like a viral illness, but I want to take a look at the severity of the severity of things, especially the intense generalized body pain is worrying to me.

[00:03:32]And just to take a general approach at an unspecific fever, we need to look for a source of infection first and then work up to see if we don't get an answer from that initial workup. So yeah, these are my thoughts.

[00:03:48]I want to take a look at the patients, see how ill they are and go from there.

[00:03:54]>> Yeah, absolutely.

[00:03:56]>> Yeah, Kure. I I absolutely agree. Yeah, I think a wonderful starting point in this journey of this case. So, first of all, Sadashan, great um groundwork that you've you've laid down for us for this case. You set the stage young person.

[00:04:12]I'm very worried about this young person. Usually, somebody this age wouldn't come to the emergency room with this sort of these constitutional s signs and symptoms. So 3 days pretty acute and then vomiting could that signal something in the GI tract but then there's this whole body sort of manifestation of a condition which you mentioned could be infection I would be worried about and maybe there's a signature of inflammation in the body and the fevers is in is an indicator of either of these conditions. So you know while while we are discussing this first aloquat I also want to mention to people if if you haven't presented a case and if you're planning on doing any sort of rotations in the United States or planning residency in the United States is a great way to practice presentation.

[00:05:04]So presenting your case I'm going to be doing actually an orientation for new interns all across the the US. New interns are starting next week, this week and one of the things we have to teach them is how to present a case and getting repetitions in with CPS is a great way to practice that. So on day one you are off to a flying start in medical residency. So so Dashan this is a great way to to get acquainted with the style of presentations in the US. So with this first aloquat I think we we have set the horizon of inflammation slash infection.

[00:05:41]There was this kind of saying that we've used I think um Stephanie has mentioned this. I really like this approach to young patients, right? So young patients will not epidemiologically have conditions that maybe older patients may have. So you you have to consider maybe bad environment, bad genes, um bad habits, things like that in such a presentation as well. So beyond just the usual infection, inflammation and 28 year olds shouldn't unless they have some sort of immuno compromised status.

[00:06:18]So I think it will be important to at least get some background in this patient like is are they immuno competent? Are they imunocmpromised? Is there any genetic predisposition to any sort of condition? Could they have maybe at this age autoimmune condition also that could be potentially contributing to this presentation? So uh I think at this stage this should be enough just to also add to what you've mentioned cashier and we'll move on to the next article unless you have anything else to say cashier right anything come to mind >> no amazing discussion so far awesome case let's see what happens next >> awesome discussion um so just a brief review of systems he has uh no history of shortness of breath chest pain cough rhoria diarrhea, uh, dysura, headache, or neck stiffness. Um, there are no similar complaints in any of his family members. He's had no similar episodes in the past. Um, no sick contacts and no recent travel history as well.

[00:07:26]Um, so his past medical history is significant for eczema and major depressive disorder and he's currently on certuline. Um family history is significant per eczema and allergic rhinitis in his father and nasal polyps in his paternal aunt. Um social history, he drinks alcohol socially. He is a software engineer. It's just a desk job basically. He is not sexually active and has no history of uh IV drug use. Um allergies, he has no known drug allergies. Um and just prior to presenting to the ED he took estim um okay so uh I'll just give the physical exam vital signs as well before um yeah so his his temperature was 99 in presentation his heart rate was 93 uh BP was 124 by 82 respiratory rate was 20.

[00:08:34]His um oxygen saturation was 99% on room air and his BMI is 25. Um on physical exam, he appears weak and in mild distress. Um his lips and oral mucosa indicated mild dehydration.

[00:08:52]Um CVSr normal. Um his abdominal examination was significant for uh mild poorly localized right-sided tenderness but no paronial signs. Um his neuro exam um showed that he was slightly lethargic uh but no overt focal deficits but we were unable to complete a full neuro exam. Um, his capillary refill time was uh 2 seconds. Extremities were slightly cold and there was a blanching macular rash over his abdomen.

[00:09:29]I'll stop there.

[00:09:32]>> Again, wonderful. Now, very broad uh second aloquot. So, uh wonderful case of subversion. So what I'll do cashier I'll tackle the additional information HPI to the health related related behaviors and I'll have you tackle the exam. Okay. So um so with some more additional information, you know what's interesting with this with this young person, the disease manifestations usually uh are less intense because at this age if you have a robust compensatory mechanism, your physiology is intact. So younger patients tend to mask or hide manifestations of conditions or disease.

[00:10:17]So, you know, I'm just sort of I'm leaving the exam, but I was just couldn't help but look at the hemodynamics here. But the check engine light on this patient is the fever. The fever is quite quite uh large um in in um in its severity. So, and the and the manifestations also patient is very weak that I that I'm ascertaining from Sadashian's um presentation so far. So the review systems is very helpful at least there that there's negative like we we can maybe pivot away from various conditions if we initially when you have a patient like this initially you can't help but have to consider infection right we see a lot of infectious disease in the hospital setting and we have to at least with this fever we don't have a white count yet but those would have a very powerful pre-est probability for an infection. So my mind will start thinking about infections in this patient. The most common infections that we likely see in the hospital setting.

[00:11:23]One would be respiratory urinary and here there's no shortness of breath. But does the shortness of breath mean that there's no pneumonia. So pneumonia is quite common. It's one of the top two infections. Not necessarily because this patient is on a trajectory maybe early in his course in say if there is a pneumonia and there is a phenomena of blossoming pneumonia. So the shortness of breath may not set in until maybe the next day. So this patient is never going to be static. There's always they're always going to be dynamic. Dura that could be a good indicator for uni tract infection but again disura may manifest or set in one or two days in the hospital setting. So you want to ask usual complaints to sharia frequency urgency and so on. Headache. Does headache indicate menitis?

[00:12:12]Likely not. You can have headache-free menitis, nucal rigidity, neck stiffness and so on. But it kind of does lessen the likelihood of these conditions. But still I I must think of these as well.

[00:12:24]Cough, chest pain, uri. So the top infections I was going through GI, respiratory, urinary, bacteria, skin, soft tissue, CNS and a while back um with a student we made a pneummonic grubs grubs C with CNS um and it's uh and it sounds like bugs, right? So those are the areas of domains I look at for identifying an infection.

[00:12:53]So right now there I don't have anything that is moving my infectious disease needle or compass towards an infection at this point. So I'm still going to be thinking broadly in the history. We're going to we're going to look for any pre-existing disorders. Maybe a previous infectious disorder that is reoccurring.

[00:13:15]Maybe there's imunocmpromised status.

[00:13:17]I'm not really seeing anything. But you know this eczema is interesting right?

[00:13:20]So eczema could be an indicating indicator of an inflammatory priinflammatory condition maybe aig cell associated condition maybe there's an pre-existing allergic imunologic disorder that's happening in this patient as well looking at the medications I looked at Hans's pneummonic I made so drugs are also part of the equation so certrilline what could that maybe serotonin syndrome but here I'm not getting any signal for serotonin syndrome but that can give you rip roaring fever as well and then found the history what do we see again we see eczema then we see allergic rhinitis we see nasopolyp is a formula for some sort of mel IG associated condition so should we really pay heed to this condition I'm not sure but I'm going to put a pin in it and maybe follow it up in the laboratory section as uh social history, nothing there. Health related issues, nothing there really uh that could contribute. Now I'll turn it over to Kashia to go through the physical exam. Over to you.

[00:14:35]>> Thank you. Uh amazing points so far. We have we have cleared a lot of things up.

[00:14:40]But there are two things in the physical exam that kind of changed how I approached the case. There is the abdominal pain and there is the rash.

[00:14:50]I'm gonna start with the rash because fever and rash is a completely different thinking ground than fever alone. And I just finished up a pediatrics rotation and I we saw a lot of fever and rash in the pediatrics population. But this particular pattern of macular blanching macular rash over the abdomen of all places doesn't bring anything specific to mind.

[00:15:18]Most of them the most of the rashes that I'm familiar with always have a pattern that they go from. For example, if we're thinking something like Marcella, there is a pattern that goes with the dermats. If we're thinking uh for example cellulitis, there is a different kind of rash. So I'm keeping the rash in mind. Maybe I need to give the rash some time for it to develop.

[00:15:46]Maybe I need to look at other places and see other uh on his body and see different manifestations of the same rash so it becomes more specific. But I'm keeping that in mind and specifically because we were thinking about infections.

[00:16:01]Uh, one thing in the history that was interesting to me was that no one else is sick in his family, which makes me think about either this is not an infection, but we still need to rule it out, or if it is, it's not a viral infection because we usually see those spread fast between the families. But that's just a general thought I had.

[00:16:26]Now, let's approach the abdominal pain.

[00:16:28]Here we have a poorly localized right-sided tenderness without perton peronial signs. So the poor localization makes me think if we think about it anatomically we can't uh say that this is a generalized pain because we're clearly seeing it on the right side. But the poor localization makes me think of the bowels and probably the colon first. But we need to move systematically for approaching abdominal pain. If this was more localized, I would I would think about something like choleiccyitis in the right upper quadrant. But right now, it doesn't really give me anything.

[00:17:14]It just brings out the severity of the case for me because we have something that is localizing for us alongside with the vomiting that maybe point to a source in the abdomen.

[00:17:27]Thinking about next steps, we want to get imaging on the abdomen probably aside from the regular things.

[00:17:36]And I would love to see the rash if it's available. Maybe we can gain more information from that. So these are my thoughts so far.

[00:17:48]>> Yeah, just to to add to that, this this rash is very interesting. You're right.

[00:17:52]Yeah, fever and rash. I get worried because there's some conditions when you try and solve this problem, you will divide this into is it a rash that is blanchable or non-blanchable and then non-blanchable rashes and fever and toxicity. you start thinking about various things like um extravisation of blood into into the subcut tissue or is it a rash due to something like dress uh could it be toxic shock syndrome although the vital signs are are stable at this point is it something like nerium menidities uh give a young patient you get peticial rash things like this but here was described as being blanchable And usually you do something called a glass test. You take the glass, you put it over and you push and you see in the glass the extra the the um rash start blanching. And to me when I see a blanchable rash I start thinking about uh a abnormal vessel or vasculitis of the skin. So maybe something like gluccoylastic vasculitis. So certain vasculitis can be that can be associated with abdominal pain and so on so so on you you start thinking about something like HSP but here was interesting with the nasal polyps I'm going to do a early like a type one thinking nasal polyp upper respiratory issues maybe vasculitis could this be something on the lines of EGPA GPA but usually EGPA has that associ association where you have autotopi eczema allergic rhinitis it has that association so that's something I am sort of formulating or it's sort of percolating in my mind I can't be sure at this point but my pet's probability is is hedging towards a higher level so this would warrant testing I think we we when we do testing we would look at the CBC uh chemistries and also then start doing autoimmune tests testing as well. But um anything else? This could also be a manifestation of infection like Cashier mentioned. So we would be entertaining.

[00:20:13]I would get a blood culture definitely to see if something is moving within the body causing such a presentation. Any other thoughts cashier before we turn the mic over to Sasha?

[00:20:23]>> I just wanted to make sure we have the rash as blanchable rash. I want to just make sure I heard it right.

[00:20:32]>> Yeah.

[00:20:39]Okay. Um I guess we can move to the next part. Um this is it's pretty heavy.

[00:20:46]There's a lot of details. Um so we did do imaging. Um so we did a chest X-ray that showed clear lungs and a normal cardiac silhouette. We did a bedside ultrasound which showed uh mild hepattoomegali and trace rightsided plural eusion. Um, an EKG was done which showed normal sinus rhythm. Um, so as far as labs go, um, his CBC showed a WBC was normal at 5,600 with a normal differential. His hemoglobin was 14.2.

[00:21:20]His hematocrit was 49%.

[00:21:24]His platelets were 124,000.

[00:21:29]Um his chemistry uh showed a sodium level of 140, potassium of 4.2, uh chloride of 101, by carb of 24, a pH of 7.44.

[00:21:45]Um his creatinin was 1.2 and B was 30.

[00:21:50]Um glucose was 102. Calcium and magnesium were with the normal limits.

[00:21:56]Um his A was 340, his ALT was 232, his ABFOS was 104, his TBI was 1.2.

[00:22:09]Um with direct being um direct was 1. Um serum albamin was 3.5, total protein was 7.4, um ESR was 34, CRP was 2, lactate was 2.8. date. Um so at this point um I think we decided that the patient was just um really sick and he was transferred to the ICU started on IV fluids. Blood cultures were obtained he was empirically started on um antibiotics septin and aithroyc and he was being closely monitored.

[00:22:47]That's the end of the salad.

[00:22:56]What do you think cashier?

[00:22:59]>> I'm thinking beautiful case. Thank you for bringing it.

[00:23:04]Uh, okay. So, the problem with approaching labs for me is always to pick the signal from the noise and I just want to mention a few things and then maybe something dawns on me. So we have a heptogle which again changes the picture plus a right-sided plural eusion. Then we have a little bit of tromocytoenia, a rise in the LFTs which seem to have a hepoiler pattern, not that much rise in the belly but still we're seeing a rise. We have direct berenemia a lowered albiman and we didn't have a coagulation testing I believe so far. So uh we are getting a picture of liver injury and if we get a pt INR rise up to more than pro one and a half or changes in thementation of the patient we have to approach it as a liver failure but so far we're seeing liver injury which com which changes the picture for me but the only presentation being fever combined with liver injury uh makes thinking about a specific infection. So, uh a little bit hard for me so far, but uh I can't point to any specific uh organisms that I'm thinking of, but um here it's kind of pointing to a systemic response. So, cancers and especially liquid cancers come into play as well. So, I would like to see a PBS probably on the next step.

[00:24:53]He has started on antibiotics and I'm going to need help with that.

[00:24:59]I'm I'm just getting a general picture here. I'm understanding how to approach the case. But going forward, which which infections to think about, what antibiotics choice I have in front of me is a little bit difficult for me. So I would love to hear your thoughts, Dr. Robbie.

[00:25:14]>> Absolutely wonderful, Kajier. You you laid a very nice starting point. I actually would agree with this. Again, I think a patient like this before we jump to more esoteric or rare conditions, we do still have to do our due diligence, get cultures, patients now in ICU getting worse. And then you see now the labs are showing a much broader involvement or sort of a multi-system condition. And when you get to multi-system associated conditions, you have to start opening the book on could this be sepsis can could manifest like this, right? the lactate is elevated. Uh sometimes with hypotension your your liver does suffer injury, congestion and so on. Um the other thing I can't help but early on you mentioned viruses, right? So viruses viral phenomena can cause some liver issue can disturb the the the c the WBC the bone marrow and everything and cause rashes, abdominal pain, fevers like this and the white count. It's not a very what do you call it a very exciting white count. If the white count was abnormal, we could say okay maybe likely bacterial infection or predominantly there were lymphosytes this could be a viral infection. But here this is a kind of a sneaky thing without a signal on the white count. So I have to start thinking if it's not bacterial or early bacterial maybe move to viral infection.

[00:26:42]So viral infections around this age range, CMV can manifest like this. EBV, you have to think about uh early HIV I would get in HIV. So I would do my due diligence. I don't know which one of these may be causing it, but I would cast a wide net like last week said cast a wide net and try and grab anything test for them and see what comes back.

[00:27:04]Right? So really we can't put our finger on it's this right now. There's no really pivot point to really move to a single diagnosis. So many diagnosis and last week we had a a nice case of anoplasmosis.

[00:27:19]So the platelets a little low fever rash and you have to start thinking you where is this patient? If this patient is I I I'm thinking maybe this patient is in the US and if they're in this area northeast you have to start thinking about conditions anoplasmosis uh Lyme disease and then I less likely rocky mounted spotted fever. Then we have bunnies and ericchiosis. Could this be is there a reticular endothelial flavor to this as well? I'm not sure.

[00:27:56]But again, cast a wide net start looking for clues. Are we still going to think about autoimmune? I think so as well. Uh we can be very sneaky. GPA, especially with those nasal polyps. I had a case we had somebody present a case like this a while back and it was it was moving along this sort of course and the nasal polyp you have to start thinking upper respiratory vasculitis egpa does come to mind as well. So that definitely is a wide net. I'm sure I missed a few things. Any other before we turn the mic over, any other conditions come to mind or would you want to test for customer?

[00:28:35]>> Uh, nothing. No specific conditions. I just want to get an explanation on some of the other findings we're seeing which I think could be interesting going forward. First one is a plural fusion.

[00:28:47]As some people in the chat mentioned, these could lead to thinking about maybe dangi fever. But also the plus the plural eusion could be explained by the liver injury itself or maybe we should take a look at the heart. Uh although I don't see any specific risk factors.

[00:29:05]Then we have the direct rubinia which is reassuring that I'm not probably not seeing any uh hemalyis right now with combined with this picture explaining that it may just be the liver failing for me. But I still would like to get a look at the um oh I forgot the words. The things that come out of the liver.

[00:29:35]>> Oh liver liver enzymes or >> no no no the things that carry the bile.

[00:29:45]>> Oh the tubes. Right Dave. The >> Yeah. Yeah.

[00:29:48]>> The bile ducts.

[00:29:49]>> The bile ducts. Yeah. Um yeah, you really I I there's a lot to digest here, right? So I I didn't really entertain.

[00:29:57]You're right. So this plusion is interesting. Could that also be a a disturbance from the liver and inflammation across the diaphragm into the into the lung or is the lung causing the reverse sequence? So at this point, I'm not sure, but I'm kind of move that over a bit, but concentrate on the liver. So liver is uh enlarged, right?

[00:30:18]And the pattern of liver enzymes is very interesting, right? So if you have mainly a parcellular damage, the ALT should be higher than A. But here we have the opposite. So the A is higher than the ALT. ALP is normal. So we we kind of gravitate away from colistatic associated conditions. And um so it's it's kind of very odd, right? we do jump to it's not twice like A two times higher than ALT but in some conditions that do cause that um yeah I guess yellow fever deni may do that too I'm wondering also leptosperosis could that that's something that could also manifest in this in this way but again casting a wide net I'm sure has some tests for us so at least we can start moving away from some diagnosis like HIV and so on and moving towards other diagnosis that we've been entertaining. Back to you, Sadashi.

[00:31:16]>> Um, amazing discussion. I've never been on this side of things and it's so much fun. Um, but anyway, moving on to the next alopod. Um, so his uh, UA was done, which was within normal limits. Uh, a repeat hematocrit was done and it was now 54. Um, his urine output um was decreased. His platelet count was repeated and it was also decreased to 89,000.

[00:31:44]His lactate levels had increased to 3.2.

[00:31:48]Um his liver enzymes were now um so uh his A was 2860 and his ALT was uh 1400.

[00:31:59]His coagulation profile showed a PTT of uh 48.2 2 seconds, a PT of 18 seconds, and an INR of 1.9. His LDH was 450. His fibbrinogen levels were 180. His feritin was within normal limits. Um, and serum albamin was uh 3 g per deciliter.

[00:32:24]Um so we also did a couple of repeat imaging which included an ultrasound um which showed asites bilateral plural of eusion um the right side greater than the left there's also heptogalier and some gallbladder wall edema um a chest x-ray was also repeated they showed bilateral plural eusion without pulmonary edema or infiltrates um a respiratory viral panel was done and this was negative for COVID, for RSV, for influenza and MS1 antigen. Um, his EBV and CMV cerologies were negative. His hepatitis and HIV cerology was also negative.

[00:33:06]Um, yeah, the next quad will reveal the diagnosis.

[00:33:11]>> Oh, wow. We're down down to the wire, Kashia. So, it looks like the plot thickens here.

[00:33:19]And to me it's it's almost getting more nebulous because this instead of getting answers we're getting more disturbance in in this patient right so the liver let me just take we we ended on the last allebot on the discussion of liver enzymes and liver enzymes have really gone through the roof then once you're in this domain of like thousands um if it is the liver you have to start thinking about is this something patients taking is it toxins is it like severe acute choleiccyitis is um we' mentioned drug induced liver injury is there hepatitis so I don't see viral oh hepatitis was done HIV was done so good at least we kind of move away from that as well and then shock liver I don't get a sense that this patient although the patient went to ICU I don't see any disturbance in the hemody parameters but it would something to consider and again if you look at the the ratio A is much higher than ALT. So in these instances you may have to move to is the is the is it a muscle associated condition. Usually you have a 4:1 I'm not seeing the 4 to one there but you just have to sort of wonder and think about it. Could it also be homoysis? homolysis the A will always be higher. If this is a true liver injury at some point the liver the ALT will start taking over and the A will start lagging behind but we still have that A way ahead of ALT. So you do have to wonder the PTT I don't remember uh what was normal with me. Um but if you look at the LDH the LDH is a little high.

[00:35:08]Yeah. Well, if if this is homolysis, the LDH is going to be through the roof as well. It's going to rise in association with A. We're not getting that right here. So, where else can you get LDH?

[00:35:20]Any sort of liver uh the my my second sort of line of thinking with LDH elevation. I start thinking of solid organ disturbance. So, things like liver injury, renal injury, cardiac injury, and then also lung injury like PJP. If if you remember for PJP infection, ALDH tends to be elevated as well. If it if this is not the fact, you have to wonder about my third line of thinking usually will be lymph lymph node disturbance, leukemia and vasculitis.

[00:35:55]Kind of going back to the vasculitis condition there. But um let's see chest X-ray showing um oh sorry was Sasha was it bilateral infiltrates now?

[00:36:12]>> Yes.

[00:36:13]>> All right. So so bilateral infiltrates >> it wasn't infiltrates. It was bilateral plural eusions.

[00:36:20]>> Oh plural diffusions. So b now now the polar fusions is that significant? It's interesting going from one side to both sides. Usually both sides is is uh associated with like maybe cardiac conditions. You have to wonder uh I don't see any tension in the hydro uh sorry encotic pressure lymphatic clearance anything like that causing plural eusions because usually it's a battle between onotic pressure hydrostatic pressure lymphatic clearance and this can can um be associated with either transitative exodative conditions transitative being more associated with maybe cardiac um conditions here. So where do we go with this?

[00:37:07]You know, one one thing I was wondering like could could we now be dealing with maybe a multi-istic disorder. So what kind of multi-ymic disorders do we have?

[00:37:18]We have conditions. We have all these sorts of conditions. I don't see anything here like you know poem syndrome and so on.

[00:37:25]um there's no hematologic signature although the hemoglobin the hematocrit is higher if I remember uh it's 54% and so the patient I I thought this was likely due to hemocentration but the matquate rising uh more could this be associated with polyythemeia or polyythemia associated condition so um that would hinge on getting an EPO test and if The EPO is elevated. This is secondary. If the EPO is low, then we're in the domain of polyythemia.

[00:38:01]Am I still have I am I still kind of bought into the autoimmune phenomena?

[00:38:06]Yeah, I would still get testing for autoimmune associated conditions. And um at this point, I'll turn the mic over to you, Cashier. I'm still thinking. So, I'm going to think of what you have to say and I'll come back after you to see what we can come up with.

[00:38:23]Well, I love your thoughts and one thing that I want to add is the mention of ASD being unspecific to the liver and nonspecific to liver and maybe we are seeing signature from the muscles disturbing the picture which uh kind of fits well with the generalized body pain that the patient was mentioning. I have seen this picture of shockike liver with patients taking opiums. I had actually a patient last week with a similar presentation who had taken opium was bound down. But this doesn't fit our picture here. So I'm thinking what are other things available to us that could reveal a diagnosis. So we have an ascites, we have a plural fusion, both of which are going to need tapping probably the definitely almost the plural eusion maybe. And and one thing that is interesting to me is that the plural eusion on initial pocus was right-sided only. Now it has developed to a bilateral picture.

[00:39:31]The assitis is going to be helpful here because it can show us uh how are the cinosoids of the of the liver are doing here because if we get a depending on what kind of a serum albamin and societies ratio we gradient we get we are going to get an answer of whether we have portal hypertension here or we are dealing with protein in the acidic fluid which could lead to cancerous pathology, some autoimmune pathology. On the other hand, if we get a portal hypertension, some of the infections can lead to that.

[00:40:13]I'm thinking about maybe leptosperosis causing portal hypertension, but maybe I'm remembering incorrectly. I remember the cysts producing precinidal cyst producing portal hypertension, but maybe I'm thinking of the wrong infection here.

[00:40:30]Uh so yeah, these are the first thing that I'm thinking about. Another thing is that it's a good thing that we got the virals out of the way. So I'm thinking maybe the cultures will reveal something in the next step and yeah not much else to add.

[00:40:52]>> Yeah.

[00:40:54]>> Yeah, it definitely is complicated. But you know what was interesting? We we we remember we classed the bide net and maybe you had mentioned deni as well right and if you if you try and follow the patent with fluid with thro worse so the hematocrit got worse uh actually no the hematocrit got higher right so concentrated thrombocytoenia fluid everywhere could this be the the severe form of dangi manifesting is this patient from India Sudashian or >> yes the person >> oh okay what do you think Kashir you you you take it from here >> I'm actually not familiar with dangi fever because we never we almost never see it here so if this is dangi fever I would love to learn >> yeah so we've had several cases again I've not seen deni before but we've had cases of it here with this is this is a very one of the like severe presentations of it. Right? So dangi with the the hemorrhagic or the um vessel associated issues where you a lot of fluid seeping you can sometimes um also have the hypobalummia platelets decrease increasing and then the liver enzymes having this pattern. I definitely yeah I think the chat is also very strongly in favor of deni they're on fire. I definitely would start with that and then go down the line with the rest of the other tests that we were thinking about.

[00:42:38]Any thoughts cashier? Are you on board team deni fever?

[00:42:44]>> Oh yeah I'm always on board with [laughter] your opinion Dr. Robbie.

[00:42:49]Let's see what happens next.

[00:42:54]Okay, awesome. Um, so we so the typhoid cerology was done which came back negative. His blood cultures came back negative. Um, autoimmune markers like AMA and RF were done which were also negative. His uh malaria smear was negative. Leptospir and scrapiferology was also negative. Um his so his denucleus uh came back positive for IGM and IGG. Um and so at this point antibiotics were discontinued and a diagnosis of severe deni uh was established. Um and so yeah basically the the patient was kind of managed in the ICU with like fluid therapy um with serial management of um yeah that was >> wow unbelievable it's interesting we were like on this journey and then I guess just knowing that the patients in India that increases the likelihood of these kind of conditions we're not you know, in in say that you're in the US, you're in the heart of DC, you have this patient. It could be a patient that just traveled, right? Just came into IAD, flew in and has deni. However, we're starting to see deni in the lower states that are more in the southern hemisphere, Florida. So, it is a with what we call climate change and climate change medicine, we're seeing more and more these conditions now rearing its head uh in the northern hemisphere. So that'll be vital um to learn about this even more. Kashia, your first case of deni fever, really really devastating, right? Very very complicated. How do you feel?

[00:44:41]>> This was an beautiful case. And what is interesting to me is how subtle the presenting symptoms were. We start with just three days of fevers and generalized body pain. If the patient wasn't so ill, this maybe could have been just a cold.

[00:44:58]It started as a picture that was we thought was just maybe it's a cold, but to for it to become so severe is so interesting. My hats off to chat. They solved this one.

[00:45:13]And thank you for bringing us such a great case. It was really enjoyable.

[00:45:18]>> Yeah, absolutely. and patients getting sicker and I think that the clues Sadashian was giving us the clues with with all of these findings. Sadashian any any what did you learn from this case or what was uh really the defining point for you for this case?

[00:45:34]>> Yeah, I think a few things that I wanted to mention. Um so the NS1 antigen is is what we do for Deni in India. I'm not sure if this exists in the US or if it's even done. Um, so I just wanted to sort of put that out there. And it has uh a decent sensitivity which I mean it's not great basically which is which is what I wanted to also um um talk about that it turned out to be negative here but very often um it's it's the cerologies that come back positive and that's kind of what we need to rely on. NS1 is a pretty rapid test. if if there's a high suspicion that's kind of when um it should be done. Um and this also is a pretty typical course for deni and and like a breadandbut case in India it's a lot of people uh present this way and just like in this patient he was treated in the ICU for a bit given fluids and he improved and he was discharged in a week and he was back to normal and that's just the typical way that deni works.

[00:46:41]Um, I've seen patients do this myself.

[00:46:43]I've had friends who've gone through the same thing, been in the ICU come out.

[00:46:47]So, it's it's uh um it's not the scariest thing. It's uh but but definitely something to to be aware of.

[00:46:55]Um and um a lot of the the dilemma in in India in India that we have is is really differentiating um the uh shock caused by deni which is like a hypoalmic shock versus like septic shock because he had fever and all of the things that would necessitate a diagnosis of septic shock. But um the management is very different. you you only give fluids in in the case of deni, but it's also important to not overload them with fluids because then it'll just like seep out. Um so that was that was an interesting um thing to note and um vasopressor should generally be avoided um which is the management for septic shock and again steroids should be avoided um and blood transfusions should not be given. Um yeah so so this this is kind of what I learned and sort of reiterated through this case. So yeah >> wonderful wonderful teaching points.

[00:47:56]Thank you. Thank you so for educating us today. So um hopefully if uh a patient does I come across a patient with this I will do better in di trying to diagnose this. Uh great job cashier or co- discussing yeah difficult case because we don't see this often but now even better. That's why CPS uh helps us to learn even more. And we'll turn it over to to Julia to take us home with the teaching points.

[00:48:25]>> Uh congratulations for this amazing case. Thank you everyone for being here.

[00:48:30]So I'll try to summarize uh the learning from from it. So first we started with the fever that indicates inflammation/infection.

[00:48:41]uh we had a pneummonic IMA that indicates some causes of uh fever. So infection, malignancy, autoimmune drugs and everything else that is like a uh another disease that can came with fever. Uh the most common infections that we deal in a daily basis are respiratory, urinary and less common neurologic and young patients tend to hide severe conditions because of uh cardiovascular and uh all of the compensations that they have. Second, we learn about abdominal pain and tenderness that when we have a poor localization as in this case generalized tenderness, we should think about bal or colon um localization of this pain. Uh third we learn about the rash uh the differentiation between non-blanchable versus blanchable. non-blendable indicate extravisation of blood under the the skin and indicate severe conditions such as maningo cocoitis.

[00:49:54]Um in the other hand blanchable rash blanchable rash indicate infection or maybe eczema.

[00:50:03]Uh we also uh see the motor system involvement in this case with the high lactate levels elevated liver function test and with this motor system involvement without an elevated white blood cell we should think about viral infection especially EBV and CMV.

[00:50:25]Another cases of mood system involvement are rock mountain spotted fever and an anoplasmosis.

[00:50:34]This patient also had a very elevated um liver function test that indicated a cholestatic injury p pattern when the ag is greater than the alt. Uh some common infection that could appear as this case are deni and leptosperosis.

[00:50:54]And when the liver function test increase to a thousand we should think about toxins, acute viral infection such as hepatitis, emolsis or uh muscle weakness. And we in the end we learn about the severe deni that cames with all of this symptoms of fluid extravisation, liver injury, low platelets and even shock is a tropical disease and NS1 is a test with a high sensitive but maybe can be negative if it it is too early or too late on the disease course. So that's the uh resume of this case. Thank you everyone.

[00:51:37]Thank you Julia. Wonderful teaching points. You grabbed every really important feature about this case. Uh thank you again Sadashan. Wonderful case. Please come back do some more get some more reps in with cases. Thank you Kashier also come back. Wonderful wonderful discussion. You had lots to say and we learned we we learned together right. So this was this was uh very amazing and thank you everybody for joining and uh hopefully see you back tomorrow for another session of CPS for you tomorrow. Take care. Have a wonderful rest of your Tuesday. Bye.