Good morning. And we need to start on time. So, I'm going to read a little bit of the rules that we have to follow to make sure we're on time and we don't run over time. So I would thank the presenter for coming and attending and presenting. We're very happy to have you. And please do not forget to read your disclosure slides, or if you don't have a disclosure slide, to out loud say that you have no disclosures. Each presentation is limited to eight minutes. We will give you a one-minute warning, and we will not let you go over time. And we'll leave a little bit of time for one or two questions in between the presentation. The first presentation is Dr. Mahoney from NYU, and thank you. Thank you. We have one minute left. Okay, perfect. Thank you. Good morning, everybody. So I'm here to present a case report on the development of a slow-growing, large pleural-based mast after a top pleurodesis. My name's Ian Mahoney. My co-authors are Dr. Schaefer, Ruland, and Tsai. I'm a fellow at New York University in New York. I have nothing to disclose. So the lesson objectives for us today are to identify talc granuloma formation as a potential complication of talc pleurodesis, and to understand the radiographic and histopathologic findings associated with talc granulomas. Our current presentation, a 75-year-old female with a history of endometriosis, lupus, prior pneumothorax, presented to clinic with a few months of mild dyspnea and chest discomfort. Her story starts all the way back in 2004 in Jamaica. She underwent a talc pleurodesis after having recurrent ketamanial pneumothoraxes. The procedure went well. She actually never had another recurrence of the pneumothorax. In 2006, she moved to the United States and started following with an outside pulmonary clinic, not associated with my university, who did serial computed tomography imaging. Notably, the patient had no respiratory symptoms at the time. So here are two of her CT scans. The first in the top part of the screen is from December of 2006. So you can see in the right side hemithorax, there are some pleural plaques. You can note an anterior and a posterior pleural plaque, which can be commonly seen in talc after talc insulation. Fast forward to May of 2013, and you can see here that particularly the posterior pleural plaque is much enlarged and developed a central hypodensity. The anterior pleural plaque is also enlarged. There is also central hypodensity, but it's not well appreciated in this picture. Given these concerning findings on her CAT scan, she underwent needle aspiration, which showed histiocytes and benign mesothelial cells. Notably, it was negative for malignancy. In 2014, she was diagnosed with lupus. She was started on prednisone, mycophenolate, mofetil, and hydroxychloroquine. The pleural-based masses continued to grow. In 2021, due to the continued growth, she actually underwent a pleural biopsy that had chronic granulomatous inflammation and polarized crystals. In 2022, she developed shortness of breath and chest tightness. Then she was referred to Bellevue Hospital for a resection. So here's her CT scan when she came to our clinic in November of 2022. Let me see if I can play the video. Oh, I'm sorry. Okay, here. Okay. So in this CT scan, you can appreciate that these pleural-based masses have dramatically enlarged. Now comes in a significant portion of her right hemithorax, with mass effect on the surrounding structures including her heart. On PET-CT scan, you can see that the periphery of the masses are highly FDG avid, whereas the interior of the masses are not FDG avid. Given her symptoms and the dramatically increasing size of the masses, in a differential diagnosis which included malignancy, surgical resection was pursued. The surgery was very difficult. The surgeons were unable to dissect the posterior mass from the surrounding pleura due to plastering from her prior talc pleurodesis. The mass was found to have a necrotic center which was debulked. There was significant intraoperative bleeding. They needed to give a massive transfusion protocol during the case and she became hypotensive. So due to the difficulty of the operation, no intervention was performed on the anterior mass. Here I'd like to present pathology from the case. So on the left side, the left-sided image, you can see a low-power image. In this image on the very left side is lung parenchyma with both chronic and active inflammation. On the right side is fibrose pleura, which you would expect to see after talc pleurodesis. In the middle there are crystals. The crystals can actually be seen on the right-sided image. This is actually an identical view, just under polarized light. So you can see these crystals are polarizable. What is interesting about these crystals is you can actually see some have migrated into the lung tissue as well and surrounded with inflammation. So here is a high-power view. So here you can see crystals of varying sizes surrounded by granulomatous inflammation. And then on the right side is, again, identical view under polarized light and you see these crystals are polarizable. It should be noted that there are also giant cells seen on microscopy, which are not included on these pathology pictures. The final pathology slide I would like to share is another high or another low-power view, low-power image. On the very right side is the wall of the pleural mass. This is made up of crystals with chronic inflammation and fibrosis. And on the left side, you can see the necrotic center, which is made up of necrotic cellular debris. Her postoperative course was complicated by prolonged air leak and deconditioning. She was admitted for an entire month. Shortly after discharge, she developed a pneumonia, which required admission. She had a lung consolidation, which you can see in the image here, with a loculated pleural fusion. She was given a six-week antibiotic course. It was actually improving in her symptoms. And actually, by the time I saw her again after the antibiotic course, she said she felt better than before the surgery. So for the discussion, the goal of pleuradesis is to create a permanent synthesis between the visceral and parietal pleura through formation of fibrin adhesions. Chemical sclerosins promote inflammation, which releases cytokines and adhesion molecules and activates a coagulation cascade to promote fibrinogenesis. TALK installation into the pleural space initially induces migration neutrophils, followed by an accumulation of mononuclear histiocytes and giant cells that can form into granulomatous inflammation. Typically, the inflammation after TALK is localized and limited, being replaced by fibrosis after months. Rarely, a persistent granulomatous inflammation can occur, with formation of a mass or a granuloma that mimics a malignancy, with increased metabolic activity on PET due to the inflammation, the active inflammation. There is a positive data describing incidence or risk factors through the development of persistent TALK granulomas, though they are rare and case-reportable. Pathology, as in this case, shows polarizing crystals of various sizes, with presence of mononuclear and giant cells that form into granulomas. So most likely diagnosed in this case is a TALK granuloma or a TALKoma. TALKomas should be on the differential and pleural-based masses after TALK pleurodesis. The malignancy and infection should also be considered. While TALKomas have been previously described before, the impressive size in this case is unique. Surgical resection may be needed for symptom relief, as was what happened in this case. Thank you. All right, next speaker is Andre Schwartz. Perfect. Assuming I did this right. All right. Got it. Good. All right. Thank you. I'll let you have one minute, okay? Hi, everybody. So my name is Andre Schwartz, and I will present a case of hemothorax and cardiac arrest after chest tube removal. So again, I'm one of the fellows at the University of Iowa Hospitals and Clinics. I'm a pulmonary care fellow. And my lesson objectives today are to discuss the complications of chest tube placement and how to avoid them or decrease them, and then to discuss a rare presentation that we had here, which occurred at the time of the chest tube removal. So my case is a 16-year-old guy that had a history of mesothelioma. He was admitted with left-sided chest pain, dyspnea. He had like mild fevers. He had a history of left-sided pleurofusion, and he's had three or four thoracic diseases in the two or three months prior to the presentation to our hospital. And then one month prior to seeing us, he had a thoracic disease that showed purulent fluid and cultures that were positive for enterobacter. So he's treated with six weeks of levofloxacin orally. So when he came to us, we had concern for partially treating him because of the symptoms and the continued fevers. So we, our department placed a 16 French chest tube percutaneously, and this was uneventfully, this was done in the mid-axillary line. And the fluid analysis was consistent with a paranormonic, complicated paranormonic effusion with a low glucose, a very high LDH, and a pH that was 7.16. He did have negative cultures at this point. So that was kind of consistent with our thought about a partially treating behemoth. And we wanted to try to facilitate the drainage, so we treated him with intrapleural TPA and Dorne's alpha. He had no issues with bleeding throughout all of this. And then on kind of, on a morning after we finished the drainage, we decided that it was about time to take the chest tube out. But unfortunately, immediately after the removal of the chest tube, he developed significant bleeding and was pulsatile. So this was concerning for arterial injury. He was immediately taken, even without kind of new imaging, to the IR suite. And then he had a short cardiac arrest there. He had chest compressions done, and we were able to achieve a return of spondylic circulation. So at the IR suite, after the cardiac arrest, he underwent thoracic angiography, and he had gel foam embolization of the eighth and the ninth left intercostal arteries. And they tried doing embolization of the tenth intercostal artery as well, but it had vasospasm, so they couldn't access it. So they were not able to embolize that artery. These are coronal and sagittal images of the chest tube prior to the removal. And as you can see, and I'll point it here in case you can't, it is kind of really abutting the inferior margin of the rib, which is kind of probably what unfortunately caused this complication of the arterial bleed. So aftermath of this event, he had a long, complicated hospitalization. He had, with the cardiac arrest, he had both a ischemic stroke and a subarachnoid hemorrhage that resulted in hemiparesis that kind of slowly improved during hospitalization. He had intermittent hemoptysis, but also at the same time, he had DVTs of both upper and lower extremities. So with all the kind of bleeding and clotting complications, there was a lot of issues with how to manage his anticoagulation, obviously. He was ultimately discharged to acute rehab center probably around one month after his hospitalization. And he was able to receive one cycle of immunotherapy, but unfortunately due to the progression of his mesothelioma, he pursued hospice and died a few months later. So for discussion, obviously you guys know that chest tube insertion is a common procedure that a lot of us do, and it's usually to drain either air or fluid, which can be either pus or blood from the pleural cavity. And this is often done with the Seldinger technique, which you can see kind of an example of a kit down here, or the blunt dissection technique, which you kind of probably use less often these days. And then regardless of the approach, the tube must be placed on the superior rib margin or as close as we can to it to avoid injury to the intercostal neurovascular bundle that you can see here. This is an article that one of our interventional pulmonary staff shares with every fellow as we come into the program, and I think it's a very good one. So this is a cadaver study that was done probably 10 or 15 years ago, 10 years ago. So on the left-hand side here, you can see kind of the average of how much the artery is basically hiding beneath or behind the rib. So as you get more lateral, and kind of the magic number is six centimeters from the spine, you can see that most of the arteries are hiding in between or behind the rib. So it kind of makes the procedure like thoracentesis or chest tube placement safer. This is another graph from the same article that kind of looks at the same data, but based on the intercostal artery. So this is kind of the 11th intercostal artery and 10th, 9th, 8th, 7th. So kind of the more caudal you go, the safer it is, and you can see that more of the arteries are hiding behind the rib compared to like more superior arteries or ribs. So obviously following this, recommendations would be to prefer lateral placement. So again, kind of the magic number that we often discuss is six centimeters from the spine. This chest tube was done in the mid-axillary line, so obviously well within that space. And then as much as you can, placement in more caudal rib spaces is preferred. Same for thoracentesis. The more caudal you can go, the better. And then other risk factors for injury to the bundle that were seen in different studies are old age, obesity, rushed chest tube insertion obviously, and then in trauma, multiple rib fractures or hematomas that can result in this complication. So our conclusions are that unfortunately hemorrhage from intercostal artery is a potentially life-threatening complication of this procedure that we often do. And then as in this case, the bleeding can rarely occur during the chest tube removal and not without any warning signs during the placement, even despite TPA or donorase. And this is thought to be because of the tube tamponading the injured artery and preventing bleeding until its removal or kind of the friction of the artery while the chest tube is removed. All right. Hi. My name is Esther. I am a second-year Palmcret fellow at the University of Minnesota, and I will be presenting a rare case of rapidly progressive gastroplural fistula formation in a patient with prior bariatric surgery. I have no financial disclosures. So this is a 74-year-old male. He has a history of aortic stenosis with the TAVR, history of GI bleed, Barrett's esophagus, Roux-en-Y bypass about 20 years ago, some mood disorder and heavy alcohol use. He was a former smoker, like I said, a heavy alcohol user for the past 15 years and has significantly worsened since his wife passed away with multiple recurrent admissions for alcohol intoxication. He presents to our ED with a chief complaint of one month of fatigue and three days of melanin. His vitals overall were very stable, except for a little bit of a mild tachycardia. EKG shows sinus tach. BMP was also pretty within normal limits. The sodium is at his baseline. He was mildly hyperglycemic. He had an elevated white count that was neutrophil predominant. He was treated with fluids, IVPPI, and then admitted overnight for further management. After he was admitted overnight, he was complaining of pretty significant chest pain on the left side, and at that time, he revealed that he fell a couple weeks ago. So at that time, the overnight cross-cover got a chest X-ray that showed a left lower lobe of pacification. And then the next day, the day team ended up getting a chest CT to just better delineate what that lower lobe of pacification was. And as you can see here, there is a large pleural fusion on the left side with compression analectasis. So he was sent down to IR, and he received a large volume diagnostic and therapeutic thoracentesis. Pleural studies were very positive. Biolyzed criteria, less than 5 glucose, 1600 LDH, 79,000 WBCs, 64,000 RBCs, and the gram stain was polymicrobial as well. So then the next day, we were consulted for this management of this infected pleural space. We placed a 14 French chest tube for him at the bedside, and immediately, this very incredibly foul-smelling brown liquid with debris came out. My attending said it was the worst pleural fluid she's ever done, and it was very dark brown. And then so we also told them to start the patient on antibiotics, which they haven't done up until this point. That night, the pleural cultures came back, and as you can see, it's polymicrobial gram-negatives. So then over the next two days, the patient continued to have about 2.3 liters of amber output, but despite the chest tube and the antibiotics, his white count persistently went up from 11 all the way to 19. During this time, he remained pretty hemodynamically stable. He just had that persistent myotachycardia and all his other labs besides the white count were pretty within normal limits. Then on hospital day six, the chest tube stopped draining and so we re-imaged him to see if we can pull the tube out and to our surprise, if you can see here, there is gas tracking inferiorly from the stomach along into the diaphragm right here and you can see from the chest, with the chest tube out, there's debris here and then there's this pocket, right, sorry, is there no pointer? Oh, let's try again. Sorry about that. Fantastic. Round two. All right. Oh gosh. Okay. Pointer. All right. So there is gas tracking along the diaphragm and this was, this is his stomach cavity and then as you get more posterior, it'll come back, you can see that this cavity is well off and there is this like fluid filled collection that seems to be communicating with the thoracic space over here. So this is his current, this is the prior from admission. So there is definitely a huge concern for a fistula tract going from the abdominal cavity into the pleural space and so thoracic surgery, GI, and general surgery recalled. He got an upper GI series and as you can see here, there's going to be extravasation up through the diaphragm. It's very subtle, but it's going, the contrast is going up into the diaphragm. And so what we think happened is that this patient had impaired perfusion due to multiple factors. When he had the ruminant bypass about a decade, two decades ago, a few years later, he had a staple line breakdown that required a revision and then more recently, he had a he had a massive GI bleed with gastric artery embolization and then this altogether impaired with his, together with his heavy drinking probably led to mucosal ischemia and gastric ulcers ultimately leading to a perforation of fistulas formation. So he was taken into the operating room that night by the minimally invasive bariatric surgeons and they did a multiple laparoscopic procedures on him. Before I go into the findings, just a reminder about the Roux-en-Y bypass. You have your gastric pouch, you have the bypass portion, gastric, you have your normal stomach and from this you create a little pouch. You take the degenerum and connect it to that pouch and then you have a portion of the bypass stomach and the bypass duomno. And they had multiple findings. What they found was that there was perforation of the gastric pouch and gastric ruminant and both of these were communicating with the chest wall and that there were multiple ulcers without bleeding. And then in addition, that really big abscess that we saw posteriorly on that CT was a large chronic food filled abscess that was communicating with both the stomach and also the chest cavity. So essentially we were draining his gastric contents and the debris was probably a sandwich he ate like a day ago. So because of the degree of adhesions and how messy the abdomen is and how much inflammation and the chronicity of this ongoing fistulas formation, they didn't do any surgical removal. They opted for conservative management. So as a result, they put in a large 22 French JG tube. The G2 portion actually went into the gastric remnant right here to drain and the J portion went into the thoracic space. And then both of these connected exteriorly with a JP drain that was draining into it. In addition, the chest tube that we put in was upsized by thoracic surgery to a 36 French and the idea was to wait for the inflammation to die down and the tracts to mature before we were able to go in. So he remained on TPN for a month and with strict NBL. And a month later he had multiple stage procedures done on several different days. So first he had a closure of this tract between the pouch and the left pleural space. Then they took the J tube that was originally in the pleural space and put it into the roux limb, which was the jejunum, and the G tube remained in the gastric pouch remnant. And he was started on trickle fees and gradually advanced. And then also he just got downsized his pigtail catheter for his chest tube and he got prolon antibiotics because this effusion just took a very long time to go away. During this time they did a repeat GI series and after these procedures there was no longer formation at least between the stomach and the thorax. Two months later he was discharged to rehab. He completed his antibiotics and chest tube removal. Five months later he had the GJ tube removed and then he just had a PEG tube in his gastric pouch. He was tolerating feeds well. And then ten months later the J tube was completely removed and he's a hundred percent oral dependent again. So a few takeaway points for this. Gastropoietic fistulas are a really rare complication of bariatric surgeries. Up until my case there's only been nine reported ever that I can find. Typically they happen because of an asthmatic breakdown causing ulcer formation causing abscess and fistulas. Sometimes ulcers can also cause this phenomenon as well. They can occur anytime post procedure usually within the first year but anytime for three months to 13 years. Up until our case 13 years was the longest time period to go. And then there are no formal guidelines to the management because of its rarity. Usually it's just a step-up approach. First conservative management with antibiotics and then with non-invasive percutaneous drainage and stents and then more aggressively surgical resection. And then these are my resources and that's my presentation. Good morning everyone my name is Ayman Mohammed. I'm a third year internal medicine resident at St. John Hospital in Michigan. And today I'll be presenting a case of right-sided pleural diffusion. I'm secondary to pleural pleurotonia leaks from peritoneal fluids and I have no financial disclosures. So these are the lessons objectives to recognize the pleural effusions as a potential complication of CAPD and to distinguish the various diagnostic methods to detect the pleural pleurotonia leaks and also determine the appropriate treatment methods for the recurrent pleural effusions. So my patient was 64 year old female with a history of ESRD. She came to our facility for evaluation of dyspnea. She experienced dyspnea mainly with light activity and her symptoms started three days prior to her presentation. She reported dry cough for the same time period but no fevers chills or chest pain. She has been started the peritoneal dialysis approximately two months prior to her presentation. When she presented she was tachycardic at 128 beats per minute. Physical exam was only significant for reduced breath sounds on the right side. Chest x-ray showed a large right-sided pleural effusions. Labs on presentation were mostly unremarkable. CBC the creatinine was 4.18 which was around her baseline. Potassium 3.9, glucose 112, LDH 347 and total protein of 6.4. An ultrasound guided thoracentesis was done and we had 2.2 liters of pleural fluid drained, light straw colored and the analysis of the fluid was consistent with transdentive fluids with very high glucose levels. So this is the pleural effusion analysis. The RBC led in 2000, white blood cell 15, PMN of 7%, lymphocytes of 78%, the glucose 441, LDH of 40, protein of 0.3 and pH of 8. She then two days later experienced worsening of her respiratory status again was increasing oxygen requirements. A chest x-ray done at that time showed reaccumulation of her right-sided pleural effusion. A decision was made at that time to hold the peritoneal dialysis and place a hemodialysis catheter and then she underwent video-assisted thoracoscopy with pleurodesis where we had one about one liter of peritoneal fluid drained. There was no malignancy found and the lung was in good shape and she was eventually switched to hemodialysis. Follow-up x-ray, chest x-ray done a month later didn't show any reaccumulation of her pleural fluids and her respiratory status has been stable ever since. So for the pleural peritoneal leaks it's an infrequent complication of CAPD. Incidence about 1.6% involves the escape of the dialysate from the peritoneal cavity to the pleural space. Etiology is mainly because of the increased intra-abdominal pressure and the pleural peritoneal pressure gradient from all the dialysis fluids as well as congenital or acquired diaphragmatic defects including either fistulas or diaphragmatic blebs. Most cases are on the right side and unilateral. You suspect it when you have a patient on CAPD who develops acutely dyspnea with pleuritic chest pain or cough with the formation of the right-sided pleural infusion and analysis of the pleural fluid usually will yield a translucent fluid with low cell count and elevated glucose fluids, glucose levels. For the diagnosis in addition to the chest x-ray and ultrasound to just localize the pleural infusion and the thoracitis as well you can do a CT peritoneography which involve putting a small amount of contrast material about 100 cc's in two liters of the dialysis fluids and then it's used over 30 minutes prior to obtaining the imaging. It's useful for detection of the large pleural peritoneal communication but not as sensitive for the smaller ones and it also has a disadvantage of having anaphylaxis reactions and nephrotoxicity and of course exposure to ionizing radiation. Similarly to a MR peritoneography similar to it is just limited by the cost and availability in the institution and in this case the MRI obviously will detect the water signals from the dialysis fluid and then the peritoneal scintigraphy it has a slightly higher sensitivity than the CT peritoneography about 40 to 50 percent less exposure to radiation as well as less allergic reaction and it can use can be used with the single photon emission tomography to detect smaller leaks and then finally the methylene blue you just put some drops of methylene blue dialysate has low sensitivity and can irritate the peritoneum and cause peritonitis. As well for the management involves for smaller leaks you can stop the CAPD could be from six to three months or permanently and switch to hemodialysis during that time. In case of if you need to continue the COPD you can use smaller exchange volumes. For video assistive thoracoscopy you can do pleurodesis or you can also do the direct repair of the diaphragm which has success rates of up to 90 percent in some reports and then finally surgical repair of the diaphragm has been done as well. And that's all. Thank you. Good morning everyone. My name is Ashmal Husna. I'm one of the third-year internal medicine resident at Mercy Health St. Elizabeth Youngstown Hospital and I have no disclosure today. So with our case we are trying to explain the causes of the extra thoracic causes of chylothorax, mostly like in the right in the thyroid. So we have a patient, 67-year-old male, who presented to the emergency department who was referred from the primary care physician's office due to worsening dyspnea along with the decreased appetite for last two months. Patient has no recent travel history, does not have any exotic pet, turtle, any birds, or any history of tuberculosis or any tuberculosis exposure. There was no asbestosis or silicosis exposure and at the same time patient had no occupational exposures including coal, foundry, or cotton mill. So on patient's past medical history, patient had hypertension, hyperlipidemia, CKD, gout, and benign prostatic hyperplasia for which patient was taking Losartan, Amlodipine, Terazosin, Phenofibrate, and Finasteride. Patient has never been a smoker before, drinks alcohol occasionally, does not have any history of illicit drug use, and family history wise, father had coronary artery disease and mother had a stroke and no allergy history. So from the objective data we found the patient was having only loss of appetite, dry cough, and shortness of breath. On initial presentation in the ED, patient was saturating 96% with 5 liter nasal cannula and tachypneic with a respiratory rate of 26 but remained hemodynamically stable that time. On physical exam, there was decreased right-sided breath sound and but there was no wheezing, rills, or anything else found. Rest of the physical examination was not significantly remarkable that time. On the lab work wise, patient had mild AKI from loss of appetite, creatinine was 1.7 and BUN 27, but other than that, rest of the lab work has been unremarkable. So this is patient's initial chest x-ray that showed the complete opacification of the right lung with a large right-sided pleural effusion. So initially a pulmonology was consulted and thoracentesis was performed and a right-sided chest tube was placed and connected to negative 20 suction. 700 cc of YOLO creamy pleural fluid was obtained from the pleural area and it was it was diagnosed as chylothorax at that point, but STAT page was 7.43 which was less likely for infection. So initial plan was to drain 2 liter fluid at once and then clamp the chest tube and reopen it after 6 hours to continue the drainage to avoid rapid fluid shifting. So this is initial chest x-ray after one day of chest tube presentation. This is after two days and this is after three days. So we started having the lung back and that was the time the second day the CAT scan was done that showed a moderate to large right-sided pneumothorax and a pleural fluid on the chylothorax per history. So initial fluid analysis was exudative, triglyceride level was 443, but it was negative for any malignancy. Initial CT scan also showed a 3-5 centimeter lung mass with anterior visceral pleura, but CT guided biopsy was negative for that mass. So patient underwent two VATs and pleurodosis and a pleural catheter placement. So after this, there was a concern that if this is a primary or secondary chylothorax. So patient was discharged and outpatient PET-CT actually showed a tracer uptake in the right lobe of thyroid gland and a concern of 1 centimeter thyroid nodule. So initial FNA of the nodule was suspicious for papillary carcinoma of the thyroid gland and patient underwent to the thyroid activity and isthmus activity. And the biopsy result was consistent with the papillary thyroid carcinoma as well. So patient after that had a follow-up PET scan that was negative for any tracer uptake and pulmonary nodule that was initially found at a 3 centimeter has remained unchanged in the follow-up PET scans as well. So this is the CAT scan of the patient. So you can see the capsule of the thyroid gland and this is the normal thyroid tissue, the colloid, and this is the papillary thyroid carcinoma. And at the same time, this is the histological changes with nuclear enlargement and elongation and overlapping chromatin changes that was also found in the patient's thyroid gland. So a chylothorax is an infrequent and potentially life-threatening complication that can be associated with thyroid surgery. So usually when the patients have thyroid activity, later they develop this chylothorax. But before even having any intervention with the thyroid and having only right-sided chylothorax make this case unique in this situation. So initial symptoms of thyroid cancer can range from the painless lump to a local compression symptoms. But our patient only presented with the shortness of breath, no symptoms that can be concerning for thyroid cancer at this point. So the presentation of chylothorax due to compression of the thoracic duct is rare and it mainly happens after the modified radical neck dissection of the thyroid carcinoma. So for our knowledge, when I was doing the literature review, I just found only one case in the Egyptian Journal that was also a chylothorax that was caused by follicular carcinoma of the thyroid gland. But other than that, this would be the first case of chylothorax that is caused by the papillary thyroid cancer. And these are my references. Thank you.

dyspnea

chylothorax

thyroid carcinoma

pleural effusion

biopsy

PET-CT scan

thoracic duct