All right, let's do some seat questions. I'm going to get us started, and then Jack will finish with the last two, just like we did yesterday. Okay, those are my disclosures, some research funding from the American Lung Association and royalties for a textbook. So let's start with the first question. So you have a 25-year-old woman. She presents for evaluation of shortness of breath and chest tightness that occurs 15 minutes after completing a winter half marathon running a race. Symptoms lasted about 60 minutes, and then they resolved without treatment. She had prepared for the run on her treadmill following a marathon training protocol. She has no history of asthma. She does not smoke. She does not vape. Other than a mild upper respiratory infection the week before the race, she had been in good health, and results from spirometry with bronchodilator testing was performed a week before the event and were normal. So which of the following tests will most likely yield the diagnosis? Technician says to maybe exercise test, laryngoscopy with video stroboscopy, UCAPNIC voluntary hypothermia test, or expiratory high-resolution CT imaging. Okay, great, you got it. So yeah, so here we're worried about exercise-induced bronchoconstriction. So this patient, this woman, is experiencing exercise-induced dyspnea in the setting of outdoor winter marathon running. So exercise-induced bronchoconstriction can be diagnosed, or the best test to assess that. So if you have a patient who there's concern for exercise-induced bronchoconstriction on the boards, you want to think about an indirect challenge test. Often that can be an exercise challenge test, but the UCAPNIC voluntary hypothermia is also an indirect bronchoprovocation test, so that's something that would be appropriate here. What happens with EIB, there's transient narrowing of the airways, usually starts a few minutes after exercise, so about five minutes after exercise. So if somebody gets dyspnea, or wheezing, or tightness, like soon after starting, or peak of exercise, that's usually not exercise-induced bronchoconstriction. That occurs a little bit later. Peaks within 10 to 15 minutes, results by an hour, usually pre-treat with short-acting beta agonist, 5 to 20 minutes. Usually we say 15 minutes before exercise can, and somebody who has frequent symptoms, or they're daily runners, or they're experiencing more frequently can consider maintenance with an inhaled steroid, or a daily leukotriene modifier. The other choices are not correct, because we're not thinking she has cardiac issues going on, so a stress test is not appropriate. Exercise-induced laryngeal obstruction, or EILO, is actually very frequently seen in adolescents and young adults. When they're exercising, they usually will present with this loud wheezing sound. And if you're concerned about EILO, then yes, a laryngoscopy is appropriate, or exercise-induced laryngomalacia. Again, you can get a laryngoscopy. And then this expiratory high-resolution CT imaging can be obtained in some situations when you're worried about ear trapping, but that's such a nonspecific finding that it's not something that would be helpful here. All right, let's move on to the second case. A 55-year-old man presents with intermittent cough and dyspnea for two years. He's otherwise active with no chronic medical problems. He reports intermittent shortness of breath when walking fast. And then these symptoms can persist for several weeks, and then they seem to improve only to return a few months later. He also reports an intermittent dry cough. He smokes a few cigarettes, and he denies any history of asthma and allergies. And on exam, he appears well. He moves about the exam room without any limitations. Chest is clear, and his I to E ratio is 1 to 1. JVP is flat. And then extremities are without edema or clubbing. And this is his spirometry. He has an FVC that is 85% predicted, FEV1 that is 75% predicted, and a ratio of 75%. And that's his chest x-ray, and they're minute, so I'll just tell you they're normal. So the question is, at this point, after counseling him on smoking cessation, what is the best recommendation? Would you obtain lung volume and diffusing capacity, begin an inhaler containing an anticholinergic and a beta agonist, explain that the cough is not related to a cigarette smoking, or warn the patient that he's at risk for developing COPD? »» Okay. So we had a split. So the correct answer here is that what the question's driving at is just recognition of PRISM, preserved ratio, impaired spirometry. So this is a patient who has preserved ratio but reduced FEV1. And this is a recently described entity, but you'll see the publications on PRISM have shot up. This is something that may show up on the boards because it has been in the 2021 interpretation guidelines for spirometry. So patients who have PRISM, they're at increased risk of advancing to COPD independent of smoking status. They are at greater risk of respiratory symptoms, reduced exercise tolerance, and hospitalizations. Mortality risk also appears increased. Some have suggested that obesity may play a role in more of the restrictive PRISM. And then, you know, we're still learning. But the choices that we had, let me just go back here. So the lung volumes and diffusing capacity here, the chest X-ray looked normal. If you're concerned about if it is more a restrictive PRISM, then I think that would be something to consider. It can also be considered, but here the question is really driving at this COPD risk. Studies of using bronchodilators in PRISM have shown, you know, negative results. So there's one big study, a rethink study that was negative. And then the cough could certainly be from, you know, the smoking and smoking cessation may result in improved cough. And then, of course, if this patient meets criteria for lung cancer screening, he should be enrolled. Okay. Here's the next case. A 59-year-old woman with history of chronic rhinosinusitis and latent TB infection presents to the ED with chest discomfort, and she gets a CT chest like most people do. The study is negative for PE, but it does show this right upper lobe and left upper lobe nodule, if you can appreciate that. But there's no metastatic lymphadenopathy. An interventional IR-guided biopsy is obtained, and it reveals this pathology, which is basically palisading epithelioid granulomas, necrotizing vasculitis, elastic stains showing fragmentation of the internal lamina and the vessel wall. If the silver stain and gram stains are unrevealing, cultures are negative, there's no evidence of malignancy, and her labs are normal, including C and Pianca and the MPOPR3 antibodies. She's a non-smoker and has no history of occupational exposure, so it's a very long stem. And the question is, what is the most likely diagnosis? Is it tuberculosis? Is it granulomatosis with polyangiitis or GPA, sarcoidosis, or bronchocentric granulomatosis? »» Okay, great. Actually, it's a bit of a mix here. It's GPA versus bronchocentric granulomatosis, a bit of a stretch. So the correct answer is GPA. If you can see, she's got rhinosinusitis. These nodules were incidentally found. There's necrotizing vasculitis on the path. So even though her ANCA and MPOPR3 antibodies were negative, in this case, she would still meet some of the criteria for GPA. The classic triad is pulmonary, upper airway, and renal manifestations. And then you can have other organ involvement as Dr. Khatunseba reviewed with us yesterday. And in the absence of renal disease, GPA is termed limited disease, but this can be misleading because it can still be a serious illness. And about 10% of patients with GPA can have negative serologies. Tracheal involvement can occur, including subglottic stenosis and bronchial stenosis. And in this case, you know, we're seeing those nodules. The nodules can cavitate, pleural effusions can be present, adenopathy is not usually present. And then in the absence of, so if there's kidney involvement, kidney biopsy is indicated. In the absence of renal involvement, lung biopsy. If it's completed for diagnosis, then a surgical biopsy is usually needed because transbronchial biopsies are often non-diagnostic. And nasal biopsies are not recommended. They have a high false negative rate, and then we reviewed the treatment yesterday. Of course, alternate diagnosis need to be excluded, but since all her cultures were negative, that makes an infectious disease less likely. Bronchocentric glomatosis is characterized by necrotizing glomatous inflammation centered around the bronchi and bronchioles, but usually vasculitis is not present, or vascular involvement is not present. And then sarcoid would be a non-necrotizing granuloma. The necrotizing sarcoid can occur, and vessels can be involved, but that's very uncommon. It's rare. All right, next case. So you have a 20-year-old who presents with one-year history of progressive worsening dyspepsia, occasional abdominal cramping, intermittent chest pressure, borborygmous, followed more recently by dyspnea with moderate exertion. And this is the chest X-ray and some CT scan images. And the question is, which of the following would be considered the next best step? Reassure the patient and prescribe a proton pump inhibitor. Obtain neoadjuvant stereotactic body radiation therapy. Refer for EGD to rule out Barrett's and obtain helicobacter cultures, or refer for surgical treatment of the abnormality. Wonderful. So I think you all got this. Most of you got this right. Refer for surgical treatment. So what we're dealing with here is the boctelic hernia. And usually, it's the most common type of congenital diaphragmatic defect. It's commonly on the left side and in the posterior. So it's on the back. I mean, the general thing with boctelic is back and back. So if it's posterior, it's usually on the left side. And often, the herniated contents can contain fat, but also spleen, stomach, small intestine, and colon. And management is usually surgical. Even if patients don't have symptoms, surgical intervention is recommended. It's slightly different from the myocardial hernia that Dr. Wu reviewed with us yesterday. And here you can see, there it is. So the CT scan shows herniated contents. And the other choices were incorrect. So I think one was the stereotactic radiation therapy. This doesn't look like malignancy. This can be confused with a neurogenic tumor. But even then, if that was the case, you would see extension into the spine and also a connection with the spinal nerve. And usually, if that is treated, that would be surgical and not with radiation. And then, I mean, this is clearly like we're not dealing with Barrett's. This patient is symptomatic, and it's because of this content. So EGD is not indicated here. Okay. We just had a couple of great sleep sessions. So let's do two sleep-related questions. So here's a 45-year-old man complaining of excessive daytime sleepiness, loud snoring, witnessed apneas. These symptoms have been present for the past two years, and they've worsened with a 20-pound weight gain recently. He has hypertension that's controlled on meds. He has a BMI of 27, crowded or pharynx. He was referred for a PSG by his PCP, and the study revealed moderate OSA. As you can see here, he was successfully titrated with CPAP at 8 centimeters of water, but he couldn't tolerate it. It started on home auto CPAP therapy, 6 to 10 centimeters of water. Just couldn't fall asleep with wearing a mask on his nose or face. He cannot tolerate wearing a night guard for bruxism, and he's interested in exploring other treatment options. And here's his results of the sleep study. And the choices are, what would you recommend? Positional therapy, bi-level PAP therapy, hypoglossal nerve stimulator implant, or maxillomandibular advancement? Yeah, I think, I mean, 63% of you got this right. So here, what we're dealing with is really sleep apnea that is really in supine sleep. So as you can see, although the patient's AHI is 25 an hour, the supine AHI is 50 an hour, and non-supine AHI is only 3 per hour. So this is somebody where a positional therapy would be appropriate. He has classic symptoms of sleep disordered breathing. And I know you can't read that, but just to review the other options, so positional therapy makes sense. Hypoglossal nerve stimulator is more invasive. Certainly that's something to be considered if they would fail positional therapy after drug-induced sleep endoscopy. That can be considered. Bi-level PAP therapy is likely not going to be helpful here, because he's not able to tolerate a mask. Maxillomandibular advancement is actually a surgery where you basically advance, break bones and advance the maxilla and the mandible. And that's very invasive, and very few surgical centers offer it. And then the oral appliance, which is the maximandibular advancement devices, could be an option. He's having trouble even just tolerating a night guard with the bruxism. Because of bruxism, it's unlikely to be tolerated. All right. Let's look at the next tracing. This is a 5-minute PSG recording. This is from a CPAP titration study in a patient with history of atrial fibrillation. But his EF is 55% and moderate sleep apnea. During this portion of the study, patient is on CPAP of 4 centimeters of water. Which of the following interventions by the sleep technologist is more likely to resolve the respiratory abnormality observed in this figure during the PAP titration polysomnogram? This is the—so you have the oronasal flow, thoracic effort, abdominal effort, and SpO2 reading. Would you increase the CPAP setting, decrease the CPAP setting, switch to adaptive servo ventilation, or switch to bi-level PAP spontaneous mode without a backup rate? Okay, yeah, 76% of you got this right. I think if there was a choice where they would say expectant therapy, where you just watch them, that would be an option as well. But here what this person has is what would be called treatment emergent central sleep apnea. And they have underlying AFib, but their EF is preserved. So this is somebody, they're only on four centimeters of water, so there's really no option of lowering the pressure on the CPAP. ASV, if this treatment emergent central sleep apnea doesn't resolve on its own, then ASV would be an option here. Okay, last one. A 65-year-old woman presents for evaluation of chronic cough and daily sputum. She has been previously well without upper or lower respiratory symptoms, rhinosinusitis or pulmonary disease until she noted the gradual onset of cough about 18 months ago. So on exam, she has normal vital signs. She's thin, but otherwise well-appearing. She has crackles and inspiratory squeaks and pops in the middle lung field bilaterally. And her PFTs show a total lung capacity that's normal, residual volume that's increased, and 40% predicted, FVC of 85% predicted, FEV1 of 75% predicted, ratio of 65, and DLC of 85%. And her CT chest is shown here. And which of the following tests is most likely to elucidate the diagnosis? Would you get sputum culture for NTM, non-tubercular mycobacteria, serum IgG, immunoglobulin testing, sweat chloride testing, or gene testing for primary ciliary dyskinesia? Okay, my work is done here. Yeah, so, you know, she's somebody who's been well until about a year and a half ago. And if you look at her imaging, she has bronchiectasis in her right middle lobe and lingula and has chronic sputum production. So this is somebody that it would make sense to look for non-tubercular mycobacterial infection. I think the other choices here were quantitative immunoglobulin. So there's no really longstanding history of immune deficiency, recurrent infection, cyanopulmonary or skin infection. So it would be less likely, and it's not as common a cause for bronchiectasis. Yes, if she was younger, you would consider sweat chloride testing, got to rule out CF. But at her age of 65, again, that makes it less likely. Similarly, for PCD, it's more likely to manifest at a younger age. And then just keep in mind some radiographic patterns for bronchiectasis that can give clues to the underlying etiology. So if it's more upper lobe predominant, then think about CF. Central bronchiectasis with a lot of mucus plugging, then you ABPM or ABPA is something to consider. Right middle lobe lingular disease, typically with NTM infection, and then lower lobe with chronic aspiration. So here, I would pass on the clicker to Jack to finish up. All right, great. Thanks, Sandy. I have just two questions that are kind of long, but I think we'll be done. Well, our goal is to be done spot on time. All right, first case, a 62-year-old man with a 40-pack year of smoking presents for further evaluation of his COPD and progressive dyspnea. He has had no hospitalizations, been on inhaled therapy, triple therapy, but his symptoms continue to worsen. His physical exam is normal, BMI of 18, pulse oximetry 92% on two liters of oxygen. And his lung exam diminished breath sounds with a prolonged expiratory phase. And his current PFTs reveal an FEV1 of 35% predicted, TLC 115% predicted, and a diffusing capacity of just 40% predicted. His chest CT shows severe heterogeneous emphysema with predominant upper lobe involvement with hyperinflation. When discussing the risks and benefits of lung volume reduction treatment options with this patient, which of the following statements is correct? A, lung volume reduction surgery has been shown to improve mortality in patients with severe COPD, predominant upper lobe emphysema, and good exercise capacity. B, pursuing bronchoscopic lung volume reduction on the right lung has a better chance of success than on the left. C, the incidence of post-BLVR pneumothorax is 10% to 20%. And D, randomized clinical trials in patients like him have shown improvements in both FEV1 and symptoms. Which one of those four statements is correct? All right, here we go. Yeah, so 40% got the correct answer, but there's a nice split, so there's some good teaching points in here, I think. All right, let's go through those. So hyperinflation from severe emphysema is associated with significant dyspnea and debility, and reduction procedures have been investigated for over 20 years with attempts to reduce the hyperinflation and symptoms. So the lung volume reduction surgery has been shown a survival benefit in select patients, not all. But case volumes are so low these days, less than 200 per year, it's even probably lower than that, mostly due to post-operative complications and prolonged recovery. So more recent explorations of BLVR with endobronchial plugs or thermal ablation or nitinol coils have not shown consistent benefit, but endobronchial valve replacement has been shown to improve both FEV1, six-minute walk, and symptom scores. So like this patient, subjects in these trials had pre-procedure FEV1s less than 45% predicted, an elevated total lung capacity, and heterogeneous emphysema. So choice D is correct. So B is incorrect because for successful endobronchial valve treatment, there should be little to no inter-lobar collateral ventilation. If the fissures aren't well-defined, you've got air moving from one lobe to the other, it's not going to collapse down. So this is typically determined, and I don't personally do this procedure. Some of you in the room may, but my understanding is this is typically done prior to the insertion of a valve with either a quantitative CT assessment or an intraoperatively physiologic assessment. An intact fissure is more common on the left than on the right, accounting for a predominant preference for treatment on the left because it's more likely to achieve the desired results. So choice B was incorrect. Choice A was incorrect because the National Emphysema Treatment Trial is the largest randomized trial for lung volume reduction surgery. And the survival group, excuse me, the group that did the best were those with a predominant upper lobe emphysema like this patient, but poor baseline exercise capacity, not good baseline exercise capacity. And then the third teaching point, due to the intended nature of lung volume reduction, the incidence of post-BLVR pneumothorax in two large clinical trials was 25% to 30%, more than the 10% to 20% that was offered. So that's a lot of patients. And most of these pneumothoraces occur within the first few hours of the procedure. But what's somewhat good, I guess, is even those patients who experience a post-procedure pneumothorax were more likely to have long-term improvement in their lung function and other outcomes, even if they're the unlucky ones who get the pneumothorax. All right, and all these images don't project well. It's the same slice under the windows and the lung windows. On the left, the little red arrows pointing to a little, to me, it looks like a little claw. And that's a cut of the endobronchial valve. And the image on the right, the green arrows are pointing to the pneumothorax in that exact same patient where there's some low-bar collapse there. Sorry, those aren't projecting well. They may better on your screens. Okay, next question, final question for the day. A 57-year-old patient was found minimally arousable by family members after several days of alcohol binge drinking. She was brought to the emergency department found to be afebrile but hypotensive and tachycardic with a pulse ox of 82%. She was promptly intubated, resuscitated with IV fluids, and required norepi to support her blood pressure. After a chest X-ray was completed, a CT scan followed to better assess her chest anatomy. And the images are on the right, again, a little hard to see on this projector. A chest tube was placed and drained several liters of purulent material with immediate improvement in hemodynamics. After two days, she remained on mechanical ventilation and her chest tube was draining approximately 50 mils every six hours while on a negative 20 centimeters of water suction and no evidence of an air leak. Chest X-ray was obtained on day three. That's the lowest image on your screen. And it was similar to what had been seen in the previous two days. A spot pleural pressure was measured with manometry after the patient's ventilator was set to a mode of continuous positive airway pressure of five with no set rate and no pressure support. And those pleural pressures range from negative eight to negative five, fluctuating with the patient's respirations. So the question is, what is the next best step in management of this patient? Would you, A, pursue a surgical decortication, B, place an additional 16 French chest tube, C, place an additional 32 French chest tube, or D, simply remove the current chest tube? What is the next best step of management? All right. So we have 31% saying pursue surgical management and others who want to get rid of the current one. Okay. So the correct answer, best treatment, is this patient's going to need a surgical decortication. So let's go through this for a little bit. So she's 57. You can see on the images, the mediastinal shift on her presenting seat, and the CT basically, like it often does, confirms the chest x-ray. Big hydronuma thorax. And then you can see on the lower part, after three days of what appears to be a functioning chest tube with tidal variations and no air leak, the lung has still not fully inflated. So this is a non-expandable lung. So this patient had a tension empyema clinically manifest with the hypotension tachycardia that responded to pleural space decompression. There's a dramatic shift in the mediastinum, as you can see, and the air leak showing persistent pneumothorax after several days. So the pleural manometry readings were below atmospheric pressure, which would be consistent with an unexpandable lung. This phenomenon is the inability of the lung to expand to the chest wall and all normal apposition between the visceral and the parietal surfaces. And the most common causes are endobronchial obstructions with lobar collapse, chronic atelectasis, and diseases affecting the visceral pleura scarring around it that prevent the lung from expanding. Those are the most common causes of an unexpandable lung. So this is a graph that I want to show because it helps clarify this point of what an unexpandable lung is. It's a terminology that I kind of prefer because the other terminologies that get used include trapped lung or lung entrapment. And those things are often used interchangeably, but the way I look at it is they're not quite the same, even though clinically they might be managed the same way. So if you think about it, this top curve here, these are three different graphs of patients, and the top more horizontal dot line represents somebody with a relatively normal lung, but is subjected to pleural fluid. So an example might be a hepatic hydrothorax. So the lung's healthy, there's just all this fluid there that shouldn't be there. And as you drain the fluid, the pressure in the lung in the pleural space goes down minimally. So the elastance curve is fairly flat, and the pleural pressures stay at or actually above atmospheric pressure. That's how a normal lung would respond to the removal of fluid. On the lung entrapment, the elastance curve is typically, actually let's skip that one. I want to do trapped lung first. So a trapped lung, which is on the far left with the steep vertical elastance curve, typically begins with a pressures that negative and rapidly falls even further with attempts to remove fluid, and this usually causes significant pain. This is a lung that does not want to move one bit. And attempts to try to re-expand it, it's just not going to work, and it's going to cause pain. Lung entrapment, the elastance curve is kind of in between. And there's often a little bit of an inflection point. So the lung, you're able to, as you draw fluid out, it's able to expand a little bit, but then it hits a point where it can't expand anymore, and you'll see a steep decline in pressure when you try to take out additional volume. So trapped lung, lung entrapment. And like I said, there's a big gray area in between these two phenomenon, and often it's hard to tell unless you're going to be doing some very rigorous type of serial manometries, which doesn't get done too often. But so there's a clinical kind of way to look at these two. So I like the term unexpandable lung because it encompasses both. And you can classify, like I said, trapped or lung entrapment based on the underlying etiology or the physiologic parameters we just kind of talked about. So from an etiologic standpoint, the people who first described this, and you can agree with them or not, talked about a trapped lung is more of a primary diagnosis and the result of fibrous tissue overlying the lung from some previous condition that's no longer active. So some old tuberculous pleural effusion that's scarred down, and it's just, boom, it's the TB isn't there, but the scar tissue and the fibrous tissue still is. Whereas lung entrapment is an unexpandable lung due to an active problem, pleural malignancy, an infection, and pyema, or an inflammatory disease. That's lung entrapment in general. So while these terms are often used interchangeably with differences that may seem semantic, there might be some physiologic parameters that support the different terminology. So this patient's pleural pressure was negative, consistent with an unexpandable lung. And while we didn't do a full elastance curve, this was probably lung entrapment from an M-pyema and the formation of a pleural peel. So the definitive treatment for that is going to be a surgical decortication, which is what she went on to. That's why choice A was correct. The existing chest tube appears to be functioning. I mentioned there was a normal tidal swing when you put her on CPAP, and no air leak. So that chest tube is doing what it can. And so adding another chest tube, whether it's a small one or a big one, isn't going to make any improvement in her outcomes. The lung's not going to expand any further. So historically, we would use large chest tubes, these 30 French things, because we thought they were necessary to remove the thick fluid of an M-pyema. But an increasing body of literature now supports smaller bore chest tubes, like a 16 French is an initial approach. But removing this functioning chest tube could risk eliminating the primary means of source control and could result in complications while this patient remains on positive pressure ventilation. So that's why leaving the current one in and not putting in others, that's why that is incorrect. So we're going to stop there.

respiratory medicine

exercise-induced bronchoconstriction

Granulomatosis with Polyangiitis

sleep apnea

emphysema treatment

lung volume reduction surgery

clinical decision-making