Welcome, my name is Jack Buckley, and I am with CHESS, and today we're going to cover some topics from SEEK. These are questions from the Self-Education and Evaluation of Knowledge, our CHESS SEEK products. And if you're interested, you can get the entire collection through your CHESS account. We'll go through here a few of the questions today. The learning objectives are to kind of review some pulmonary topics using a question and answer format. That's a powerful learning tool for many people. And also recognize that the SEEK questions are different than, say, what you might find on a board examination. It's a different type of question that serves a different purpose. And the SEEK questions tend to be very long, very complicated, very detailed, and I think they're much harder than what you might see on a board examination. But they're designed not to test your knowledge as much as they are to teach you multiple points for any given question. Okay, so let's go through one here. A 65-year-old, oh, and by the way, I know some of you are listening while you're driving your car or commuting, and others are looking at this on a screen with no audio. And I'm going to try to adapt my presentation so that it works for both. So I've got both written explanations and details, as well as I'll use my voice for those who are only relying on audio. Question number one, a 65-year-old man has developed ARDS in the setting of bowel sepsis. The CT image of his chest is depicted here in this image here, and you've placed him on volume assist control ventilation with a tidal volume of 6 mLs per kg based on ideal body weight, a set rate of 12 breaths per minute, and a positive end expiratory pressure of 10 with an FiO2 of 55%. His plateau pressure is 29, and his arterial blood gases are acceptable. Which of the following statements accurately reflects your assessment at this time? So I'm going to leave the image up, but here are your possible answers. A, you're not concerned. The clinical parameters are acceptable for the observed clinical scenario. B, you are concerned that the high positive end expiratory pressure is higher in the anterior right lung regions. C, you are concerned that the tidal volume is distributed primarily to the anterior right lung regions. And D, you are concerned that the end expiratory transpulmonary pressure is excessive. Which of these is correct? So I'll ask you to commit. As adults, when we commit to an answer, we don't have to be right, we are more likely to retain it once we learn the correct answer. So the correct answer is C, you are concerned that the tidal volume is distributed primarily to the anterior right lung region. So let's review this. And there's a lot of data here, so if you're reading it, or I'm going to just sit back and listen while I read this out loud. The CT image of the chest shows dense infiltrates in the dependent regions of both lungs as well as the anterior lap bone. This pattern would predict that the delivered tidal volume from a positive pressure breath will distribute almost exclusively to the anterior right lung region. A global tidal volume of 6 mLs ideal body weight delivered to only a quarter of the lungs would translate into the regional equivalent of 18 mLs ideal body weight, a value that raises concerns about regional ventilator injury, excuse me, regional ventilator induced lung injury. That's why choice D is correct and choice A is incorrect. This phenomenon is of regional tidal overstretching has been well documented with chest CT scanning of mechanically ventilated ARDS patients with extensive lung injury. These scans have clearly shown that tidal volume scaled to ideal lung size can be excessive and produce regional tidal over-dispension. Indeed, if it were more practical, CT scans could be an ideal way to scale tidal volume during mechanical ventilation to account for reduced functional lung volume. However, until imaging tools are more readily available to do this, alternative strategies to set tidal volume should be considered. One such approach uses the driving pressure, which is the same as the plateau pressure minus the positive expiratory pressure. As a representative, as a representation of the tidal volume compliance, therefore, so the driving pressure can become a tool to scale tidal volume to actual lung mechanical properties rather than to ideal lung size based on ideal body weight. Some prospective studies to show this approach reduces ventilator induced lung injury and improves outcomes do not exist. This is somewhat theoretical. However, some have suggested based on retrospective analyses that a driving pressure more than 15 centimeters of water reflects regional injury potential. In this patient, the driving pressure is 29 minus 10 or 19 centimeters of water, suggesting that either the tidal volume may be further reduced or perhaps additional PEEP be applied to improve compliance. Pressure applied to the major airways at end expiration, PEEP, is equal in all lung units. So choice B is incorrect. However, the effect of PEEP on lung recruitment will depend on regional lung mechanics and recruitability. End inspiratory transpulmonary pressure is the plateau pressure minus the end inspiratory pleural pressure, which is often measured through an esophageal probe. Values greater than 30 centimeters of water are generally considered excessive. Given that the plateau pressure is 29 in this patient and this patient is passive, the pleural pressure of anything will be positive. So the transpulmonary pressure will thus be less than 29 and choice D is incorrect. All right, that's question one. Moving on to question two, these topics jump around. This one's about lung cancer. A 62-year-old woman is seen for evaluation of a lung nodule detected during baseline low-dose CT screening for lung cancer. She currently feels well, noting dyspnea only with strenuous activities. She has a mild chronic cough without sputum production. She does not have other cardiopulmonary or systemic symptoms. She has not had any recent respiratory infections. She currently smokes half a pack per day, having accumulated 40-pack years. Her medical history includes emphysema. There's no family history of lung cancer. And on her CT scan, there is a nodule described as multilocular atypical pulmonary cyst, approximately 15 by 13 millimeters. And for those who are viewing this, you can see the image on the CT scan. And the question is, which lung imaging reporting and data system, the lung rad system category and management approach is most appropriate for this patient? Option one or option A, this is a category three lung rads and follow up in six months with a low-dose CT scan of the chest. Option B is, this is a category two lung rads nodule with a follow-up of 12 months with a low-dose CT scan. Option C, this is a category 4A and follow-up in three months with a low-dose lung scan is recommended. Or option D, this is a category 4B lesion and evaluation should be pursued immediately. Which of these options is correct? Now, if you're like me who doing C questions, what I like often do is I might be able to eliminate one or two of the responses, but I typically have to look these things up. So if you want to put me on pause, go look at it and come back with your answer. But for those ready to move on, I'm going to reveal the correct answer here. And that is option C, which is category 4A and a follow-up in three months with a low-dose CT. Okay, what's the rationale behind this response? So a multilocular cyst seen on baseline low-dose CT scan of the chest is considered a lung rads category 4A finding. But the recommendation that a follow-up low-dose CT scan should be done in three months. So choice C is the correct answer and A, B, and D are incorrect. So lung cancer that presents as a cystic airspace lesion is not common. But up to 20% of lung cancers missed on baseline low-dose CT scanning have been associated with cystic airspaces. Features that raise suspicion for lung cancer include thickening or nodularity of the wall of the cyst, growth of the cyst size, development of internal loculations, and increase in the solid or nodular portion associated with the cyst. So four morphologic patterns of lung cancer presenting with cystic airspace lesion have been suggested. The first is a nodule that appears to be extending out of the wall of the cystic lesion. The second is a nodule within the cystic lesion. The third is a thickening of the wall of the cystic airspace. And the fourth is a multilocular lesion or the appearance of a cluster of cystic airspaces with soft tissue intermix. And these four types are shown here in this image. A meta-analysis of observational studies that included lung cancers associated with cystic airspaces summarized characteristics of these cancers. Up to one-third of these cancers occurred in individuals who never smoked. The cysts usually had non-uniform walls, over one-third of which were thick, and by thick we mean at least two millimeters, and had irregular margins, while nearly two-thirds had a nodular component. In the majority, the nodular component grew, or the walls thickened over time. And growth of the cystic component was variable. Adenocarcinoma was the histologic diagnosis in 88% of these cancers. The Lung-RADS nodule management system provides guidance on the management of cystic airspace lesions. Thin-walled, unilocular cysts with a uniform wall thickness less than two millimeters are considered benign and are not classified. Pulmonary nodules are distinguished from cystic airspace lesions by wall thickening as the dominant feature. These are managed as solid nodules. A fluid-containing cyst could be infectious and is not classified by Lung-RADS unless other concerning features exist. Otherwise, atypical pulmonary cysts with a growing cystic component of a thick-walled cyst are considered Lung-RADS Category 3 with a follow-up of six months. A thick-walled cyst that is multilocular at baseline, and a thin or thick-walled cyst that becomes multilocular are considered Category 4a with a follow-up in three months. And a thick-walled cyst with a growing wall thickness, a growing multilocular cyst, and a multilocular cyst with increased loculation or a new or increased opacity are all considered Category 4b, and further evaluation is recommended. This patient had follow-up imaging performed, and these are some figures over time. And you can see that the cystic airspace lesion started to develop a solid nodule extending from the wall. So as we move left to right, you can see it's subtle, but there's clearly some solid development of a nodule there. And this led to a right lower lobectomy, which confirmed a T1b N0M0 adenocarcinoma of the lung. Moving on to Question 3, a 65-year-old man with idiopathic pulmonary fibrosis reports a distressing dry cough that interferes with his usual daytime activities and being out in public. He uses profenadone and a histamine H2 receptor antagonist. Pulmonary function test results reveal severe restriction without evidence of obstruction. Esophageal manometry results are normal. Benzonate date is ineffective. In addition to speech and language therapy, which of the following agents should be considered next to address the cough in this patient? A, proton pump inhibitor. Option B, gabapentin. Option C, low-dose opioids. Option D, thalidomide. The correct answer is B, gabapentin. Okay, I'm sorry I rushed that a little bit for those who didn't have time to think that through, but let's go through the explanation about why gabapentin would be the best option. Gabapentin is recommended for the treatment of chronic cough in patients with interstitial lung disease when no clear cofactor has been identified. As is the case in this patient with IPF. So this is why choice B is correct. Gabapentin is a neuromodulating agent that may suppress the central cough reflex. Results from studies in patients with IPF and refractory cough have shown gabapentin, with use of the validated Lester cough questionnaire, to decrease cough frequency and severity and improve quality of life. Using multimodality speech therapy, including cough suppression techniques, vocal hygiene, and psychoeducational counseling to the treatment with this drug class can lead to an even larger improvement in the cough score. Unfortunately, high doses are often required and can limit treatment only to some of the side effects that are most commonly include things like fatigue, dizziness, confusion, dry mouth, and nausea. The cough in patients with IPF is typically described as persistent, dry, and worse during daytime. It's reported in more than 80% of patients with IPF and is more common in individuals with advanced disease and often has a major effect on quality of life. So treatment is aimed at targeting cofactors when found because IPF-related cough is typically refractory to antitussant therapy in the vast majority of patients. Gastroesophageal reflux disease is highly prevalent in IPF patients and is often clinically silent. Study results, however, have failed to demonstrate a change in objective cough counts with proton pump inhibitors, even at high doses, despite showing a decrease in acid reflux events. Although conditionally recommended in previous IPF treatment guidelines, regular antacid treatment for patients with IPF should be prescribed only for patients with a positive workup for acid gastroesophageal reflux. And so choice A is incorrect. Opioids are indicated for unexplained refractory cough that has a substantial effect on quality of life after all alternative treatments have failed. This is why choice C is incorrect. Guidelines recommend that low-dose opiates be considered for symptomatic relief of intractable dry cough in patients with advanced IPF receiving palliative care. Thalidomide, perhaps because of its immunomodulatory properties, has been suggested as a potential agent to treat IPF-related cough on the basis of the results of a small single-centered double-blind crossover study. The study identified improved cough quality of life, although objective cough measurements were not assessed. More than three-quarters of patients experienced adverse effects attributed to the treatment, including constipation, dizziness, and malaise, although no serious adverse effects were reported. So at this time, thalidomide is not considered a routine treatment of cough and IPF, and choice D is incorrect. Although the effect of antifibrotic medications on cough have not been formally studied, findings from uncontrolled observational study in patients with a high cough burden and mild to moderate lung function impairment suggest that profenadone may reduce cough frequency. Reports of topical anesthetics, including nebulized lidocaine, tetracranial lollipops, may suggest a role for these agents in the temporary relief of cough, although controlled clinical trials to assess efficacy and safety remain needed. All right, that was question three. Moving on to question four. This is a 65-year-old woman who presents with an 18-month history of dry cough and progressive dyspnea on exertion for the past 12 months. She is a former cigarette smoker having consumed 20-pack years. Her respiratory symptoms worsened after having an influenza infection eight months ago for which she was treated with a course of antibiotics and prednisone. Her history is significant for hypertension, hyperlipidemia, and early gray hair. Her family history is notable for her father who died from, quote, pulmonary fibrosis, unquote. Review of systems was otherwise unremarkable. No environmental exposures were noted either at work or at home. The physical examination was normal except for bi-basal or crackles noted on lung examination. Laboratory testing revealed an elevated antinuclear antibody at 1 to 320. A comprehensive set of serologic testing was otherwise negative. Pulmonary function testing showed a total lung capacity of 70% predicted, an FVC of 70% predicted, an FEV1 of 75% predicted, and a diffusing capacity of 70% predicted. On a six-minute walk, she was able to walk 1,400 feet, which is 420 meters, with room air, oxygen saturation of 96% at rest, and 94% with exertion. And a representative high-resolution CT scan of the chest is shown here. The question is, which is the best initial management of this patient's condition? A, prednisone, 40 milligrams a day. B, Nintendinib, 150 milligrams twice daily. C, Azathioprine, 150 milligrams daily. Or D, urgent referral for lung transplantation. Take a moment, commit to your answer before I reveal the correct answer. Okay, the correct answer is Nintendinib, 150 milligrams twice a day, option B. Okay, let's go through this. The patient has idiopathic pulmonary fibrosis on the basis of the chest CT imaging, showing the typical usual interstitial pneumonia pattern of peripheral basally predominant reticulation with traction bronchiectasis and honeycomb fibrosis. The usual interstitial pneumonia pattern on high-res CT imaging is diagnostic of IPF if after comprehensive evaluation, there are no relevant home or work exposures to suggest hypersensitivity pneumonitis or occupational lung disease or clinical evidence for connective tissue disease. In this situation, surgical lung biopsy is unnecessary for diagnosis and would subject the patient to an increased risk of morbidity and mortality. And it's been noted, as has been noted in patients with pulmonary fibrosis. Patients with IPF and mild to moderate impairment of lung function should be offered antifibrotic therapy with either Nintendinib or Profenadone, either of which has been demonstrated to slow progression and the decline of FBC by 50% over a 12-month period. The choice B is correct. Prednisone and azathioprine are associated with worse outcomes in IPF patients, including increased risk of mortality and hospitalization is demonstrated in the PANTHER study, especially in the setting of a short telomere disorder as is suggested by the premature gray hair and family history of pulmonary fibrosis. And should not be given as maintenance therapy. So choices A and C are incorrect. A mildly elevated antinuclear antibody is common with age. So the otherwise negative serologies and unrevealing review of systems and physical examination do not support a connective tissue disease as the cause of the interstitial lung disease. The early gray hair and possible family history of interstitial lung disease suggests short telomere syndrome may be present. This is associated with more rapid progression of interstitial lung disease. So referral for discussion of lung transplantation should be more, should more rapid progression occur is appropriate, but not urgent because the lung function shows mild restriction without oxygen desaturation. So choice D is incorrect. Okay, moving along. We've got a couple more. Question five. A 56 year old patient is referred to you by his primary care physician for a thoracentesis. He presented to his physician three weeks ago with mild but progressive dyspnea and exertion and leg swelling. He has no history of chest pain or symptoms suggesting pulmonary infection. He is a lifelong non-smoker with no occupational exposures. He is not taking any medication. His evaluation included a normal electrocardiogram and echocardiogram revealing normal left and right ventricular function. Results of laboratory studies included a normal hemogram, normal thyroid function tests and no elevation of an anti-nuclear antibody level. A chest X-ray is shown here in the top on the right. Take a moment to take a look at that one. On physical examination, the patient is comfortable at rest with normal vital signs. Lung examination reveals dullness in the bases bilaterally. The cardiac examination is normal. There is significant pitting edema to the level of the lower thighs bilaterally. Both upper and lower extremity abnormalities are noted with the hand findings shown in the middle figure. Take a look at those. A thoracentesis was performed on the left side using ultrasound guidance and yields 400 milliliters of slightly milky fluid. There were scant red blood cells microscopically. Cytology findings were negative. Gram stains and cultures were also negative. And the laboratory studies are shown in the bottom figure. And for those listening, a white cell count of 2,700 with a differential of 62% lymphocytes, 32% macrophages, 6% PMNs. Glucose was 80. Total cholesterol was 30. Triglycerides, 85. Albumin, 2.9. Serum albumin is 4.2. LDH is 66. And serum LDH is 90. The patient experienced modest relief of dyspnea following the procedure. However, his dyspnea returned within three weeks and follow-up chest X revealed reaccumulation of the pleural fluid. Based on these findings, which of the following pulmonary abnormalities is this patient most likely to develop in the future? A, anthezema. B, non-small cell lung cancer. C, bronchiectasis. Or D, a malignant mesothelioma. Which of these is most likely for this patient to develop? Okay, I'm ready to reveal the correct answer. And that is bronchiectasis. Okay, why is that the case? Let's go over this. The findings in this patient of a triad of a pleural effusion, lymphedema, and yellow nails, coupled with no alternative diagnosis supported by routine testing makes the presence of yellow nail syndrome most likely. Yellow nail syndrome has strong associations with other respiratory disorders, most prominently chronic sinusitis and bronchiectasis, which is why choice C is correct. So what is yellow nail syndrome? It's a rare syndrome, most often seen in adults over the age of 50, although even rarer cases have been described in the pediatric population. A few case reports have suggested a genetic predisposition to yellow nail syndrome, but there is general consensus that the majority of cases are sporadic. There is no specific laboratory test or tissue finding for the diagnosis, which requires exclusion of other disorders, such as lupus or thyroid-associated pleural disease or other causes of lymphedema. The nail findings are often striking, with slow-growing nails without cuticle or lunula, that's the visible part of the root of the nail, that yellow with time. These may be on either or both of fingers and toes. Yellow nail syndrome is a rare cause of longstanding unexplained pleural effusions. The pathology is obscure. Abnormal development of the lymphatic system is almost always present. Lymphocentigraphy may show lymphatic obstruction, and some have even recommended surgical bypass of obstructed lymph channels when possible. Impaired lymphatic drainage alone would not explain the exudative effusions that are common in yellow nail syndrome, and that we're seeing in this patient. Exudation of the fluid into the pleural space would suggest a degree of capillary leak and or inflammation, but anti-inflammatory treatment is not generally recommended. Since yellow nail syndrome is a rare disorder, there have not been controlled trials evaluating treatment. Most experts recommend a conservative initial approach and the use of compression stockings to reduce leg edema and diuretics to diminish pleural fluid collections. Reports have suggested that vitamin E and azithromycin may have ameliorating effects on the course of yellow nail syndrome. Some patients will have resolution of their infusions and lymphedema with conservative management alone. If pleural effusions recur and are extremely symptomatic, pleurodesis may be required. The emergence of chronic sinusitis or bronchiectasis would warrant treatment directed at these specific disorders. Patients with yellow nail syndrome have not been observed to be at increased risk for malignancy, and this non-smoking patient with no occupational exposure would not be at significant risk for non-small cell lung cancer or malignant mesothelioma, which is why choices B and D are incorrect. Emphysema has not been reported to be associated with yellow nail syndrome, and choice A is incorrect. Okay, moving on to the final question. This is a critical care theme. You are caring for a 45-year-old man requiring mechanical ventilation for COVID-19-associated ARVS. He was intubated three days ago, and there has been an improvement in the gas exchange in the past 24 hours, permitting a decreased FiO2 and positive end expiratory pressure level. On volume-regulated assist control mode, the patient has been synchronous with the ventilator, which is set with a tidal volume of six mils per kid, predicted body weight, and a respiratory rate of 40 per minute. He has been receiving IV sedation successfully, targeted to a Richmond agitation and sedation scale score of minus one to minus two. Sedation has been held twice daily, during which time he promptly responds to simple commands. You went to the room on your daily rounds. He appears well sedated, and no ventilator alarms are noted. And yet a ventilator screenshot on your arrival is shown and is consistent with which of the following. Now, for those of you listening, there's no really way for you to answer this question without taking a break and looking at the image that I've shown here on the right. So if you need to stop and put a pause and come back to this, that's fine. But for those of you who are able to look at the image, it displays a ventilator screen. And the question is, what is going on here? Is this A, an obstructed endotracheal tube? B, is this an endotracheal tube disconnection from the ventilator circuit? C, is this breath snacking? Or D, is this ventilator tube condensation? What's going on based on this display of the ventilator tracings? Okay, the correct answer here is ventilator tube condensation. So let's talk this through. So both the pressure and flow waveforms on the ventilator show, this is the image on this slide that I'm sharing here today is the lower left corner. That's the one I showed you on the previous one. Both the pressure and flow waveforms show a sawtooth pattern most noticeable during the expiratory phase, which signals a pressure fluctuation in the airway sufficient to alter flow, but not necessarily trigger the ventilator above the set respiratory rate of 40. This is termed auto cycling. And should these pressure excursions increase in magnitude, the ventilator could be triggered at an excessive rate. So you can note that the cycling rate of sawtooth pattern might be as much as 200 per minute, which could result in severe respiratory alkalosis, barotrauma, or even hemodynamic compromise. Thus identifying the cause of the auto cycling is important. It's been described to occur from intrathoracic pressure variation related to cardiac contraction, action of mechanical ventricular assist devices. It's been seen with bubbling from a chest tube suction device, or even oscillations in water accumulated in the expiratory limb of ventilator tubing. In this case, the auto cycling was due to condensed water in the expiratory limb, the tubing. And when it was removed, the sawtooth pattern immediately resolved. And that's the image in the middle there. So if you go from left to the middle, you can see the sawtooth patterns in both the pressure and flow waveforms disappear simply by emptying the water out of the expiratory limb of the respiratory circuit. Breath stacking, excuse me, I mean, before I go into, let me talk about the pattern that goes away. Neither if this were an obstruction of the endotracheal tube nor a disconnection from the ventilator would cause this sawtooth pattern seen here. So that's why choices A and B are incorrect. And both of these events would likely trigger ventilator alarms related to high peak airway pressure or low pressure if there was a disconnection, neither of which are seen on these tracings. Now, breath stacking refers to the patient triggering a breath prior to completion of the exhalation of the previous breath. And that's shown in this schematic drawing on the right here. And it's not occurred. Choice C is incorrect. If breath stacking occurred, it could defeat the goal of low tidal volume ventilation typically applied in patients with ARDS. And that concludes six SEEK questions. Thank you all for your time and attention.

SEEK

pulmonary conditions

ARDS

Lung-RADS system

idiopathic pulmonary fibrosis

yellow nail syndrome

ventilator screenshot