Good day. I'm Stephanie Levine. I'm a professor of medicine in the Division of Pulmonary Diseases and Critical Care Medicine at UT Health San Antonio and the South Texas Veterans Health System in San Antonio, Texas. And today we'll be going through several SEEK questions. I have no conflicts of interest as it relates to this topic, but I am on the SEEK editorial board. So let's start with our first case, question one. A 45-year-old woman is referred for mild shortness of breath and the constellation of findings seen here, her chest and abdominal CT. I'll let you look at that for a moment. And the question is, which of the following statements is correct regarding this disease process? A, lung tissue will stay positive with S100. B, a cholesterol pleural effusion develops in one third of patients. C, the disease does not recur following lung transplantation. D, rapamycin or serolimus may be therapeutic. So I'll give you a few seconds to think about this. And the correct answer here is D, rapamycin or serolimus may be therapeutic. So let's talk about this topic. So this patient has lymphangial leiomyomatosis or LAM. It's rare, affected about one to two per million, premenopausal women, 36 years mean age, and it's due to atypical smooth muscle proliferation. We'll talk a little bit more about the pathogenesis. The majority of cases are due to a sporadic mutation, 85% of cases, and patients present with nonspecific findings, dyspnea, cough, may have scantum opticis. There may be crackles on exam and pulmonary function testing may be mixed, may be obstructive, or early on may actually be normal. So the pathogenesis is due to atypical smooth muscle proliferation and really all compartments of the lung. It can affect the bronchovasculature, the lymphatics, and the interstitium. And you can see this indicated with the arrows on the top panel. The tissue stains positive for HMB45, smooth muscle cells, melanocytic differentiation. And the disease is characterized by extensive cysts and we know that estrogens play a major role. On imaging, on CT, you can see thin-walled, round cysts. They can be small or actually quite large. There are no nodules with LAM as opposed to LCH, which we'll talk about in just a moment. These patients get chylis, true chylis effusions with triglyceride elevation. And they can get pneumothoraces when these cysts form on the edge of the pleura, the edge of the lung but in the pleura. And pneumothoraces recur in up to 60 to 70% of cases. These patients also get angiomyolipomas as the name sounds, angioblood, myomuscle, lipomas fat. And these often form in the kidneys but can also form in other pelvic organs. The tissue, as we said, stains positive for HMB45. And an elevation in VEGFD in the serum greater than 800 picograms per ml is diagnostic and supportive in the right clinical context for a diagnosis of LAM. 10-year survival is quite variable. The most common cause of death is respiratory failure. And as we discussed in the question, treatment is with serolimus or rapamycin. And studies have shown that this provides beneficial effects both on the volume and size of the angiomyolipomas. And it also slows the deterioration in pulmonary function. Other treatments that have been tried, oophorectomy, progesterone, octreotide depoform may be used for treatment of chylothoraces in the refractory setting. And these patients can undergo lung transplantation, but it is one of the diseases that can recur following transplantation. So again, let's look back at the imaging. On your left, you can see the CT and you see rounded, thin-walled cysts. And notice they can be a various size, but round in configuration. On your right, you can see that there's a right angiomyolipoma on the right kidney. So let's compare LAM to pulmonary lung graham cell histiocytosis. So epidemiologic wise, LAM, as we said, premenopausal, women, LCH, male more common than female. They tend to be young and they're almost all smokers. Radiographically in LAM, we talked about round multiple cysts of different sizes without nodules. They're diffuse. In LCH, the cysts are described as eccentric. They are predominantly found in the mid to upper lung fields, and you do have nodules. Both diseases can be associated with pneumothoraces. In LAM, serum VEGFD greater than 800 is important, smooth muscles in the pathogenesis and HMB45 staining. In LCH, Langerhans cells are found. It stains positive for CD1a and S100. And complications with LAM, chylis effusions, chylis ascites, angiomyolipomas. And with LCH, they can get bony lesions and diabetes insipidus can occur when the hypothalamic access is involved. The treatment for LAM is serolimus and transplantation. For LCH, there's really no clear treatment, but stopping tobacco use is important. Sometimes steroids are tried and sometimes off-label cladribine has been tried. LCH can also be treated with lung transplantation. It too may recur following transplantation. So back to our question, A is incorrect. No, it's not S100, it's HMB45. B is incorrect because it's a true chylis triglyceride effusion, not a cholesterol or pseudokylis effusion. C is incorrect because yes, it does recur following transplantation. Okay, next question. This is a 64-year-old man who presents with complaints of a 20-pound weight loss, night sweats, fevers, and productive cough with scant hemoptysis for four weeks. Past medical history, 40-pack year tobacco use. He's thin, temperature 38.3, vital signs otherwise stable. He has poor dentition. Lung exam reveals right upper lobe agophany and scattered wheezes. White count is 10,000, hemoglobin is 11.5. Sputum for AFB is negative times three. He undergoes bronchoscopy. The material is AFB negative. Here is the imaging, and I'll let you look at this for a moment. On your left, a plain film. On your right, two representative images of the CT. Here we see some of the path results, cytologic results, an H&E stain on your left and a GMS or silver stain on your right. These are from the bronchoscopy. The question is, the appropriate treatment for the most likely diagnosis in this patient is A, penicillin IV for four to six weeks and PO for six to 12 months. B, imipenem IV for six weeks. C, trimethoprim sulfa PO for six months. Or D, penicillin PO for three months. I'll give you a little time to think about the answer here. The correct answer here is A, penicillin IV for four to six weeks and PO for six to 12 months. This patient has actinomycosis. It can be cervical, facial, abdominal, and thoracic disease in terms of the clinical findings. Thoracic involvement occurs when there's aspiration from the oropharynx. Actino is a gram-positive filamentous anaerobic bacteria. It does have sulfur granules, and it's AFB negative, as opposed to neocardia, which is weakly acid-fast, and one treats these with the sulfonamides. Here again is our pathology. On the left, you see the H&E with necrosis. On the right, you see sulfur granules on the silver stain. For thoracic actino as in our patient, it presents with subacute to chronic pneumonia, fevers, chills, cough, systemic findings, weight loss, or maybe chest pain, hemoptysis, anemia. Radiographically, the x-ray shows a mass or infiltrate. There may be cavitation as in our case, and pleural disease is often seen. In fact, you'll sometimes hear the term empyema necessitans because the organism can cross the fissures and can also invade bone, but pleural disease is quite common. The diagnosis can be made with a fine needle aspirate, bronchoscopy, or biopsy, and culture. Again, here we have our imaging. One can see a large right upper lobe area of cavitation, and the treatment for actino, thoracic actino, is penicillin IV for four to six weeks, then oral for six to 12 months. Other agents that can be used include ceftriaxone or amoxicillin. If the patient is penilegic, one could consider doxycycline, the macrolides, possibly clindamycin, although we certainly worry about C. diff, and then the carbapenems can also be used, and in isolated cases, surgery may be required. So here we'll compare and contrast actino and neocardia. They're both gram positive. Actino, anaerobe, neocardia, aero. Clinically, actino presents with pulmonary pelvic and cervical facial disease, neocardia, pulmonary CNS, and skin disease. Generally, actino occurs in immunocompetent hosts, although it can also occur in immunocompromised. Neocardia more often occurs in immunocompromised hosts. AFB is negative in actino and weakly positive in neocardia. Actino has the sulfur granules. Neocardia does not. And radiographically, actino infiltrates cavities, pleural involvement, and neocardia nodules and infiltrates. And the treatment in general for actino, the penicillins, and for neocardia, sulfonamides. So back to our question. B, imipenem is incorrect. It does cover this, but it's not needed at this point, and that duration is too short for this type of involvement. C is incorrect. It's the wrong choice of drug. That is what we would use for neocardia. And D is incorrect because it's both the wrong route and wrong duration of treatment. Question three. A 55-year-old woman is admitted for six weeks of intermittent fevers, progressive shortness of breath, night sweats, a 10-pound weight loss, and a dry cough. Her past medical history is unremarkable. She takes no meds. She's an office secretary, no history of tobacco use, and she drinks alcohol only occasionally. There has been no recent travel. On exam, she's a mild respiratory distress with a rate of 24 per minute, a pulse of 88, temperature 38.5. On exam, she has no cervical adenopathy. Lung exam reveals scattered crackles without wheezes. The remainder of the exam is unremarkable, and she has no clubbing. Lab studies reveal a white count of 14,000 with 20% eosinophils. Serum chemistry results are normal. And here is her imaging. I'll give you a moment to look at that. And the question is, which of the following statements regarding this patient's condition is correct? A, relapses are uncommon. B, progression to respiratory failure is typical. C, a history of asthma is present in nearly 50% of patients. D, transbronchial biopsy may show stages of diffuse alveolar damage. And I'll give you a few seconds to think about the answer. And the correct answer here is C, a history of asthma is present in nearly 50% of patients. This patient has chronic eosinophilic pneumonia. Women are affected more often than men. Most cases, actually 90% occur in nonsmokers. And clinical features include the subacute onset of cough, shortness of breath, and constitutional findings of fever, weight loss, and sweats. Patients often have wheezing, and a history of asthma is present in close to 50% of patients. And progression to respiratory failure is uncommon. Lab findings include peripheral eosinophilia, as in our patient. They may have anemia. There are elevated IgE levels often. And BAL eosinophil counts exceed 20% to 40%. The pathology is comprised of interstitial and intraalveolar eosinophils and histiocytes with minimal fibrosis. There may be a component of bronchiolitis obliterans with or without organization, but there is no diffuse alveolar damage. Here again, we have our radiology. One can see the peripheral opacities, often described as the photographic negative of pulmonary edema. And this is present, this classic finding is present in about one third of cases. But it's not specific for a CEP diagnosis. Treatment is with steroids, usually with an excellent response in days to weeks. Spontaneous resolution is rare, but you have to taper your steroids slowly, because patients often relapse in more than half of cases. So you usually taper over three to six months. Maintenance treatment may be needed with low dose oral steroids or inhaled corticosteroids. This is in contrast to AEP, which is acute. AEP is associated with new onset smoking, resumption of smoking, or dust exposure. Respiratory failure is common in AEP. Men are affected more than women. And x-ray in AEP shows ground glass opacities, alveolar filling disease, and occasionally pleural effusions. And the pathology, especially if severe, will show diffuse alveolar damage with eosinophils present. Of interest, BAL eosinophils are common with AEP, but early on peripheral eosinophilia is not present. And here I have these compared and contrasted acuity. AEP is acute and severe. CEP, as we saw, chronic milder weeks to months. Asthma, not a feature of AEP, but often seen with CEP. Blood eos early on are absent in AEP, always present in CEP. Both have BAL eosinophilia. AEP, the radiograph is diffuse, GGO. They may have effusions. It may look like ARDS. CEP classically is the peripheral consolidation or the photographic negative of pulmonary edema. Treatment for both is steroids. In AEP, relapse is rare. However, in CEP, as we discussed, relapse is common. So back to our question, relapses are uncommon. No, that's incorrect. They're frequent in CEP. Progression to respiratory failure is typical. No, it's unusual in CEP. And transbronchial biopsy may show DAD. No, that's true for AEP, but not CEP. Question four. This is a 20-year-old patient. She had AML, has AML, received an autologous stem cell transplantation 16 days prior. During the past several days, she's developed a nonproductive cough, dyspnea, and fever. Her oxygen saturation has fallen, and she now requires supplemental oxygen. A chest radiograph and imaging will be shown, and she subsequently requires intubation and mechanical ventilation. She undergoes bronchoscopy and serial left to right aliquots of BAL will be shown. The BAL fluid I'll show you recovered from several other segments has a similar appearance. Bacterial, fungal, and acid-fast smears of the fluid are negative, and cytology of BAL fluid is negative for infectious agents. Here is what her imaging looks like prior to intubation, her radiograph on the left and her CT on the right. I'll let you look at that for a moment. Here is our serial BAL with aliquots one, two, three, four consecutively obtained. Here's the question. Which of the following statements regarding this condition is true? A, associated mortality may be greater than or equal to 60 to 80 percent. B, the condition is more common in allogeneic than autologous stem cell transplantation. C, hemoptysis occurs in about 50 percent of patients with this condition. D, transbronchial biopsy is often necessary to confirm the diagnosis. So I'll let you think about that for a few seconds. And the correct answer here is A, associated mortality may exceed 60 to 80 percent. This patient has DAH in the setting of stem cell transplantation. It complicates hematopoietic stem cell transplantation, rarely less than one to two percent in most series, up to five percent in others. And of interest of all the BMT complications, DAH is one that is at least equal or perhaps greater in the autologous than the allogeneic recipients. Risk factors include pre-transplant intensive chemotherapy, total body thoracic radiation, renal dysfunction. There's only a weak association of DAH with thrombocytopenia. And in the thrombocytopenic situation, it does is not clearly corrected with platelet transfusion. It can be also seen in the setting of acute GBHD. The pathogenesis is likely multifactorial, a combination of underlying lung injury, microvascular damage, microthrombi, acute inflammation, and cytokine release. Infection may also be associated. We mentioned acute GBHD. And DAH often develops during the time of white blood cell recovery. One does not perform transbronchial biopsy in this situation, given that they're almost always thrombocytopenic and perhaps coagulopathic. But DAD would be found on biopsy. Clinically, patients present with dyspnea, cough, fever, hypoxemia, diffuse infiltrates. Hemoptysis is actually uncommon, only occurring in about 15% of cases. It's an early complication following BMT, usually within the first 30 days and often during the engraftment period. On radiology, one sees interstitial and alveolar infiltrates, bilateral areas of GGO and consolidation on CT. The diagnosis is made with BAL with progressively bloody return on serial BAL and greater than or equal to 20% hemosiderin-laden macrophages. In addition, one wants to rule out infection. As we mentioned, transbronchial biopsy would be not necessary, may lead to increased bleeding, but if performed, would show DAD. The treatment you would treat underlying risk factors such as infection or acute GVHD. Generally, these patients are treated with systemic corticosteroids at moderate to high doses, although there are not adequate prospective randomized trials for this. Other things that have been tried, factor VIIa, plasmapheresis has been tried, and more recently, tranexamic acid. Many patients, as did our patient, require mechanical ventilatory support. There's certainly an increased risk for secondary infections and other complications, and the prognosis of DAH in stem cell transplant recipients is poor, with mortality rates approaching 80%. So back to our question, A, being the correct answer. B, as we talked about, DAH is equal in allo and auto, and in fact, maybe a little bit higher in auto. Hemoptysis occurs in much less than 50% of patients, and you do not need transbronchial biopsy for this diagnosis. It's a diagnosis made on BAL, serial BAL. Question five, this is a 63-year-old woman who presents with fatigue, vague right anterior chest pain, dry cough, and occasional dyspnea. Past medical history is unremarkable. Exam reveals a pale woman, but is otherwise normal. Hemoglobin is eight with normal indices, otherwise a normal exam, I'm sorry, otherwise normal labs. A chest CT is obtained, and the remainder of the CT is unremarkable without parenchymal disease or mediastinal adenopathy, and an I-131 scan is negative for uptake in the thorax. And here is her CT, and as I mentioned, on lung windows, there was no parenchymal disease, and there was no additional mediastinal adenopathy on the soft tissue series. So what is the most likely diagnosis in this patient? Is it A, teratoma, B, lymphoma, C, intrathoracic thyroid, or D, thymoma? And we'll pause for a few seconds. And the correct answer here is thymoma. So thymoma is the most common cause of an anterior mediastinal mass in adults, usually located adjacent to the junction of the heart and great vessels, round or oval in shape with smooth margins, as was the case with our patient. Clinically, they develop in patients between the ages of 40 to 60 with an equal sex distribution. About 60% are asymptomatic, 40% may have vague symptoms, including cough, dyspnea, and chest pain. And whether they're benign or malignant depends on several factors. Distribution, benign is more common. If they're contained within the capsule, that's characteristic of benign thymomas, whereas malignant invade through the capsule. Benign do not spread. Malignant can invade locally. Treatment is surgery for the benign, for the malignant surgery, and sometimes radiation. Prognosis is good for benign thymomas and poor for malignant thymomas. Of interest, thymomas have associated findings. So myasthenia gravis can be seen in 10 to 50% of patients with thymomas. It's due to thymic production of autoantibodies directed against the acetylcholine receptors. Patients may have pure red cell aplasia in about 5% with normochromic normocytic anemia. Our patient happened to have that associated finding. You can see myocarditis, hypogammaglobulinemia, Cushing syndrome, or megaesophagus have also been described. And here again, we have our CT, and note that it's a very smooth margins, well-contained, and of soft tissue density. The other options given in the differential diagnosis in this question, so teratomas, they're germ cell tumors in children and young adults, usually symptomatic at presentation. Lymphomas, most commonly in young adults, they may have systemic and constitutional symptoms. Depending on the location and size, airway obstruction can result. An intrathoracic thyroid may be seen in middle-aged women. They often extend above the thoracic inlet, and the I131 scan may be positive. And then lipomas would tend to have fat density on CT, not seen in our case. So again, thymoma was the correct answer here. Question six, this is a 55-year-old man with pemphigus vulgaris on chronic corticosteroid treatment who presents with dyspnea fevers that have been worsening over 72 hours, progressing to hypoxemic respiratory failure. Notable history, he's a recent immigrant to the US, came from Cambodia. He goes back frequently, including trips in the last few months. He's a never smoker. On exam, he's intubated, lung exam reveals crackles and wheezing. His white cell count is 12,000, with 28% eosinophils, and he undergoes BAL. Here is his imaging. And here is the BAL. What is the likely diagnosis? Is this A, disseminated coccidioidomycosis? Is it B, strongyloidiasis? Is it C, hyper eosinophilic syndrome? Or D, acute eosinophilic pneumonia? And I'll give you a little time to think about it. And the correct answer is B, strongyloidiasis. So this patient has strongyloidiasis estercoralis. It's most often due to auto infection in an immunocompromised host. Remember, this patient was on chronic corticosteroid treatment. Patients present with cough, wheezing, dyspnea, fever, maybe some hemoptysis. The chest X-ray shows opacities that can progress to ARDS as occurred in this patient. Peripheral eosinophilia is present. And the diagnosis can be made on BAL or on biopsy, showing eggs or larvae. And there is an ELISA available as well. And treatment is with antiparasitic drugs such as thiobendazole or ivermectin. Another example of the parasite is shown here. So this is not COX-C. We didn't see COX-C on BAL. We clearly saw the parasite. Hyper eosinophilic syndrome is a diagnosis of exclusion with six months of unexplained peripheral eosinophilia or shorter than that in the presence of end organ damage and acute eosinophilic pneumonia. We've already talked about this patient is already on steroids. So it'd be unlikely to develop. And it is unusual to have this degree of peripheral eosinophilia early on. So this patient has B strongyloidiasis. Question seven. A 57-year-old man underwent a bilateral lung transplantation for COPD. The donor was CMV positive. The recipient was CMV antibody negative. The post-op course was complicated by some initial weaning difficulties. He improved and went to rehab two months post-op. Subsequent to that, he remained well with no new pulmonary complaints. He underwent routine surveillance transbronchial biopsies to monitor for rejection at one and two months after transplant, and no abnormalities were noted. He underwent monthly monitoring of his blood for CMV PCR or antigen, and these have been negative. And now you're seeing him at four months follow-up. He feels relatively well, but he has noted low-grade fever and mild cough with some yellowish sputum production. Current meds include tacrolimus twice daily, prednisone, mycophenolate mofetil twice daily. He's on trimethoprim sulfa three times a week, prophylaxis, and he's on valgan cyclover daily, although the dose had recently been decreased due to renal insufficiency. Physical exam is normal. PFT, specifically FEV1, is decreased by about 12% from his baseline. Tacrolimus level is therapeutic, and our CMV studies are pending. Here is the CT. Transbronchial biopsies perform for these symptoms, the URI symptoms, worsening PFTs, and interstitial changes on imaging. And here is the pathology. I'll let you look at that for a moment. And the question is, the abnormalities demonstrated are most likely due to A, post-transplant lymphoproliferative disease, or PTLD, B, acute cellular rejection, C, cytomegalovirus infection, or D, pneumocystis jeroveci infection. And I'll let you think about that. And the correct answer here is CMV infection. So pathologically, what one sees in CMV are intranuclear inclusion bodies with the classic owl eyes appearance. And the image on the right with the black arrows is pointing to this classic appearance. You see markedly enlarged or cytomegalic cells. They have amphiphilic purple intranuclear inclusions and multiple small basophilic blue intracytoplasmic inclusions. But really, when you see this owl eyes appearance, you think of CMV infection. Here's the example of the imaging, small opacities, nodules. There may be thickening of the interlopular septa. You may see ground glass opacities. You may see tree and bud or patchy consolidation. So a whole range of radiographic appearances in CMV. A fall in transplant immunosuppression usually peaks at one to six months after transplant. And so during that time when immunosuppression is the highest is when we see most of our opportunistic infections, including those due to viral organisms, specifically CMV. You can see a pneumocystis jeroveci. We certainly prophylax for that. And in the fungal family, you can see aspergillus or candida. CMV infection, specifically CMV pneumonitis, is associated with a long-term development of bronchiolitis obliterans and chronic lung allograft dysfunction or CLAD. And the most severe CMV infections occurred due to primary infection in those who are donor positive and recipient negative. So that was the situation in our case, CMV donor positive, but our recipient was CMV negative. You can also get secondary CMV infection that's due to reactivation of latent disease that's unmasked with immunosuppression. And the presentation, it can range from asymptomatic, meaning just detected in the blood with elevated CMV PCR. It can be a flu-like illness. You can see full-blown pneumonitis as in our case. Retinitis is described, hepatitis, colitis, or gastroenteritis. And we monitor at our monthly visits or as clinically indicated with serial measures of CMV, PCR, or antigenemia in the blood. Treatment is with IV ganciclovir or high-dose oral valganciclovir. And we certainly institute CMV prophylaxis in all our lung transplant patients, although the duration and regimen vary. So if you're recipient negative, donor positive, our situation, you may certainly at least a year and may be lifelong with oral valganciclovir. If you're recipient positive, variable, but usually at least a year. And those who are CMV negative and donor negative, so negative, negative, are usually a shorter interval of prophylaxis, and some may use acyclovir in this situation. And of course, there's concern about CMV resistance in this patient population. So let's talk about some of the other options on the slide. PTOD or post-transplant lymphoproliferative disorder, the highest incidence is in the first year of post-transplant. It's clearly related to B-cell proliferation by Epstein-Barr virus. Radiographically, patients get nodules. They may see adenopathy. You can have extra pulmonic involvement. And treatment includes rituximab as well as a decrease in immunosuppression. And here's what a PTOD biopsy might look like. You can see a proliferation here of lymphocytes homogenous. Acute cellular rejection usually occurs in the first three months, but can occur up to two years or more post-transplant. And patients present with nonspecific dyspnea, a fever, leukocytosis. In some cases, there may be a cough, maybe hypoxemia or malaise, but they can be asymptomatic. Early on, the chest x-ray may show a perihylar infiltrate, a small effusion, or can be unchanged from baseline. And the diagnosis for ACR requires transbronchial biopsy, which shows perivascular lymphocytic infiltrates. And treatment is with corticosteroids, usually with good response. And here's an example of the path you might see in ACR. And on your right, you can see a small pulmonary vessel with a lymphocytic infiltrate surrounding the vessel. So that's ACR. So A is incorrect. It was early. We didn't see it on biopsy. ACR, the timing was okay, but we didn't see the characteristic lymphocytic vasculitis on the transbronchial biopsy. And that CT would be unusual. And for PJP, the patient was on adequate prophylaxis, not seen on this biopsy. And again, the CT would be a little bit unusual. Okay, question eight. So short answer. Which of the following underlying diseases is well described to recur in the allograft following lung transplantation? Is it A, sarcoidosis, B, cystic fibrosis, C, idiopathic pulmonary arterial hypertension, or D, usual interstitial pneumonia? Which is well described to recur in the allograft following transplantation? Okay, and the correct answer here is sarcoidosis. There is a long list of disease recurrence following transplantation, and this probably isn't a complete list, but sarcoidosis is by far the most common. We talked about LAM recurring, giant cell interstitial pneumonitis can recur, DIP and LIP can both recur, IPH has been shown to recur. We know that broncho, what we used to call bronchovelar cell carcinoma, recurs. LCH can recur, PAP, and diffuse panbronchiolitis. But sarcoidosis is the one that is most commonly described to recur. Now, this may be an incidental asymptomatic finding of isolated granulomas on a transbronchial biopsy or on autopsy specimens. Less commonly, it's symptomatic recurrence requiring corticosteroid treatment, although that has been described. When one performs molecular studies in lung transplant recipients with sex mismatched lungs, it suggests that the recurring granulomas are of recipient origin. And the reason we may not see disease recurrence in some other diseases is that it takes, many of these diseases take a long time to develop in relation to the current lung transplant survival rates. So again, the answer is A, sarcoidosis. The other three diseases here have not been reported to recur and certainly not frequently. And now our last question, this is a 22-year-old woman who she was found unconscious in a pool of vomit with an empty one-quart bottle of bourbon nearby. She was taken by ambulance to the ED and she was endotracheally intubated. Vomit was found in the posterior pharynx during the intubation. In the ICU, SAT is only 88% despite receiving 100% oxygen by mechanical ventilation. She's set in DCAC mode with a set volume of 400, set rate of 14, a PEEP of 8, and FIO2 of 100%. Exam findings were remarkable for a healthy-appearing female. She's deeply sedated. There are her height and weight. Blood pressure is 80 over 50. Heart rate is 130. Her respiratory rate is 14. She's not overbreathing. She has diminished breath sounds and dullness to percussion over the left hemithorax. The endotracheal tube is positioned at 25 centimeters at the incisors. And here is her chest radiograph. And I'll let you study that for a moment. So this is after intubation. And the question is, which of the following is the most appropriate next step in her management? A, place the patient in the left lateral decubitus position. B, perform flexible bronchoscopy. C, insert a chest tube into the left hemithorax. Or D, reposition the endotracheal tube. And I'll let you think about that for a moment. And the correct answer here is to reposition the endotracheal tube. So here we have an arrow at the tip of the endotracheal tube, and one can see that we have a right main stem intubation resulting in left lung atelectasis. So right main stem intubation is a very important step in the treatment of endotracheal atelectasis. So right main stem intubation resulting in total atelectasis of the left lung. You would also note that there's an ipsilateral shift on the imaging. You can see that the mediastinal contents is shifted to the left. The proper position of the endotracheal we know is two to six centimeters above the crina. And case series indicate that malposition of endotracheal tubes with the tip too low occurs at about 10% of emergent intubations as occurred in our case. Post-intubation chest radiography is of value to confirm proper positioning because we often know that clinical evaluation may be unreliable. So the differential of a pacified hemithorax in the intubated patient in the ICU, widespread unilateral parenchymal lung disease, a massive pleural effusion, but here you would expect if that's what was going on in the left hemithorax, you'd have contralateral shift of the mediastinal contents, not ipsilateral. A hemothorax, again, you would expect contralateral shift if it was on the left. Total lung atelectasis as in our case and other clues as we mentioned to this being the cause is that the mediastinal contents have shifted towards the opacified hemithorax. You can also see contralateral tension pneumothorax causing a contralateral shift, but not present in our case. So choice A, the left lateral decubitus position, you might consider this if this was a situation of hemoptysis where spillage can worsen the hypoxemia. We also know that putting the dependent lung down can worsen or will worsen the hypoxemia. Bronchoscopy would not be indicated. That could be indicated for a well-positioned tube in the situation of a mucus plug resulting in atelectasis, but that is not the case here. And then C, inserted chest tube into the left hemithorax. No, one might consider that if it was a massive pleural effusion, but we have excluded that the shift would be contralateral. And in our case, it's ipsilateral. So really the correct answer here is reposition the endotracheal tube, which has been misplaced in the right main stem. And that was done. And shortly after that, the left lung achieved full expansion. So with that, I'd like to conclude. I want to thank you for your attention. And this is my email. If you think of any questions or comments, please feel free to email me and I wish you all the best of luck on your boards. Thank you so much.

LAM

rapamycin

actinomycosis

penicillin

eosinophilic pneumonia

CMV infection

thymoma recurrence

endotracheal tube