PulmPEEPs

The Pulm PEEPs are extremely excited today to be launching our series on Chronic Obstructive Pulmonary Disease in partnership with the ATS Clinical Problems Assembly. We are joined by Dr. Bob Wise and Dr. Wassim Labaki to discuss the classification and initial workup of COPD, and management strategies from inhalers to pulmonary rehabilitation. Make sure to listen today and in the coming weeks for the rest of our COPD discussion.

Meet Our Guests

Dr. Bob Wise is a Professor of Medicine at Johns Hopkins School of Medicine and has served as the Medical Director of the Pulmonary Function Lab at the Johns Hopkins Asthma and Allergy Center. Bob is a leader in the care of patients with obstructive lung disease and his research focus has been conducting multi-center clinical trials in airway disease and is also a master physiologist. Bob has been involved in various capacities with ATS throughout his tenure as well and received the ATS CP Assembly Sreedhar Nair Lifetime Achievement Award in COPD.

Dr. Wassim Labaki is an Assistant Professor of Medicine in the Division of Pulmonary and Critical Care Medicine as well as the Medical Director of the Lung Volume Reduction Surgery Program at the University of Michigan. Wassim was the recipient of the Early Career Investigator Award in COPD from ATS in 2019 and currently is on the Program Committee of the ATS Clinical Problems Assembly.

Key Learning Points

Modified Medical Research Council (mMRC) Dyspnea Scale

mMRC Grade 0 = Only breathless with strenuous exercise

mMRC Grade 1 = Short of breath when hurrying on level ground, or walking up a slight hill

mMRC Grade 2 = Walking slower than people of the same age due to dyspnea, or stopping due to dyspnea when walking at my own pace on level ground

mMRC Grade 3 = Stopping for breath after walking 100 meters / a few minutes on level ground

mMRC Grade 4 = Too breathless to leave the house or breathless with getting dressed / undressed

References and links for further reading

1. Clinicians. Global Initiative for Chronic Obstructive Lung Disease – GOLD. Accessed April 11, 2022. https://goldcopd.org/clinicians/
2. Miami CF 3300 P de LB. COPD Foundation | Take Action Today. Breathe Better Tomorrow. Accessed April 11, 2022. https://www.copdfoundation.org
3. Barnes PJ. Chronic Obstructive Pulmonary Disease. New England Journal of Medicine. 2000;343(4):269-280. doi:10.1056/NEJM200007273430407
4. Celli BR, Wedzicha JA. Update on Clinical Aspects of Chronic Obstructive Pulmonary Disease. New England Journal of Medicine. 2019;381(13):1257-1266. doi:10.1056/NEJMra1900500
5. Criner GJ, Martinez FJ, Aaron S, et al. Current Controversies in Chronic Obstructive Pulmonary Disease. A Report from the Global Initiative for Chronic Obstructive Lung Disease Scientific Committee. Ann Am Thorac Soc. 2019;16(1):29-39. doi:10.1513/AnnalsATS.201808-557PS
6. Martinez FJ, Agusti A, Celli BR, et al. Treatment Trials in Young Patients with Chronic Obstructive Pulmonary Disease and Pre-Chronic Obstructive Pulmonary Disease Patients: Time to Move Forward. Am J Respir Crit Care Med. 2022;205(3):275-287. doi:10.1164/rccm.202107-1663SO
7. Rodriguez-Roisin R, Rabe KF, Vestbo J, Vogelmeier C, Agustí A, all previous and current members of the Science Committee and the Board of Directors of GOLD (goldcopd.org/committees/). Global Initiative for Chronic Obstructive Lung Disease (GOLD) 20th Anniversary: a brief history of time. Eur Respir J. 2017;50(1):1700671. doi:10.1183/13993003.00671-2017
8. Singh D, Agusti A, Anzueto A, et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease: the GOLD science committee report 2019. Eur Respir J. 2019;53(5):1900164. doi:10.1183/13993003.00164-2019

This week the Pulm PEEPs, David Furfaro and Kristina Montemayor, are joined by three outstanding critical care doctors and medical educators to discuss the evaluation of patients with undifferentiated shock. We cover everything from the basics about defining shock, to advanced POCUS techniques to clarify the etiology of shock. Listen today and let us know your favorite technique for evaluating shock in the ICU.

Meet Our Guests

Molly Hayes is an Assistant Professor of Medicine at Beth Israel Deaconess Medical Center and Harvard Medical School, the Director of the MICU at BIDMC, and the Director of External Education at the Carl J Shapiro Institute for Education and Research. She is also a course director for a yearly CME course on principles of critical care medicine run by BIDMC and HMS.

Nick Mark is a Pulmonologist and Intensivist at Swedish Medical Center in Seattle, Washington. He is also the founder of ICU One Pager, which produces high yield critical care education one-page guides that have been downloaded by thousands of learners.

Matt Siuba is an Assistant Professor of Medicine and intensivist at the Cleveland Clinic, where he is the associate program director for the Critical Care Medicine fellowship. He founded and runs the website Zentensivist.com, has his own associated podcast, and is a senior editor at CriticalCareNow.com.

Key Learning Points

Key graphics

Definition of shock

— Shock is defined as inadequate oxygen delivery to meet the body’s needs. Decreased perfusion and oxygen delivery leads to cell injury and death

— If you define just as hypotension, you will miss people who have cryptic shock, and categorize some people with shock who don’t have it

— Cryptic shock = a patient with normal blood pressure (MAP > 65), but who still has shock based on inadequate O2 delivery

— O2 delivery is broken down in to cardiac output and arterial oxygen content

Causes of shock

— Shock can be divided into three large categories:

1) A pump problem – low cardiac output. This includes cardiogenic and obstructive shock. Make sure to remember to look for tamponade and valvulopathies.

2) A pipe problem – low systemic vascular resistance. This includes distributive shock. Distributive shock is most often due to sepsis but can be due to anaphylaxis, endocrinopathies, cirrhosis, or spinal shock.

3) A tank problem – low preload. This includes hypovolemic and hemorrhagic shock. Make sure to remember about high intrathoracic pressure, which can decrease effective preload.

Examining a patient with undifferentiated shock

— See if the patient is on the “Shock BUS” by examining their brain (mental status), urine output, and skin

— Feel if their skin is warm vs cold and if it is mottled

— Feel the patient’s pulses to see if they are bounding, normal, or thready

Point of Care Ultrasound

— “Ultrasound is the new stethoscope”

— The first step is to always look at the heart and look for chamber size and function. You can then look for pericardial effusion

— Point of care ultrasound then includes looking at the lungs for signs of fluid overload, consolidation, or pneumothorax

— A complete ultrasound also involves looking at the abdomen and at the extremities for DVT

— More specific ultrasound techniques include looking at:

1) IVC exam to estimate right atrial pressure. This test is often misused. It is most helpful in states when the patient has low stroke volume and trying to figure out if they have cardiac limitation to stroke volume vs if they are hypovolemic.

2) Velocity time index as a measure of cardiac output to trend with interventions

References and links for further reading

1. Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726-1734. doi:10.1056/NEJMra1208943
2. Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):762-774. doi:10.1001/jama.2016.0288
3. Chukwulebe SB, Gaieski DF, Bhardwaj A, Mulugeta-Gordon L, Shofer FS, Dean AJ. Early hemodynamic assessment using NICOM in patients at risk of developing Sepsis immediately after emergency department triage. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2021;29(1):23. doi:10.1186/s13049-021-00833-1
4. Hernández G, Ospina-Tascón GA, Damiani LP, et al. Effect of a Resuscitation Strategy Targeting Peripheral Perfusion Status vs Serum Lactate Levels on 28-Day Mortality Among Patients With Septic Shock: The ANDROMEDA-SHOCK Randomized Clinical Trial. JAMA. 2019;321(7):654-664. doi:10.1001/jama.2019.0071
5. Wang J, Zhou D, Gao Y, Wu Z, Wang X, Lv C. Effect of VTILVOT variation rate on the assessment of fluid responsiveness in septic shock patients. Medicine (Baltimore). 2020;99(47):e22702. doi:10.1097/MD.0000000000022702
6. Sweeney DA, Wiley BM. Integrated Multiorgan Bedside Ultrasound for the Diagnosis and Management of Sepsis and Septic Shock. Semin Respir Crit Care Med. 2021;42(5):641-649. doi:10.1055/s-0041-1733896
7. Yuan S, He H, Long Y. Interpretation of venous-to-arterial carbon dioxide difference in the resuscitation of septic shock patients. J Thorac Dis. 2019;11(Suppl 11):S1538-S1543. doi:10.21037/jtd.2019.02.79
8. Volpicelli G, Lamorte A, Tullio M, et al. Point-of-care multiorgan ultrasonography for the evaluation of undifferentiated hypotension in the emergency department. Intensive Care Med. 2013;39(7):1290-1298. doi:10.1007/s00134-013-2919-7
9. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically lll. Emerg Med Clin North Am. 2010;28(1):29-56, vii. doi:10.1016/j.emc.2009.09.010

We are extremely excited to introduce our new Pulm PEEPs Meet the Patients series. Teaching and learning medicine is an incredible journey, and the goal is always to be improving patient care. Patients are our best teachers about the diseases we encounter, so the goal of this series is to spend more time with patients with pulmonary disease and with those who have been critically ill. For our first episode, we are thrilled to be joined by Katie Fielding.

Katie s an educator and spent 13 years teaching high school science. She now specializes in integrating technology into the classroom to enhance education. Katie was diagnosed with CF as an infant and has spent years as a patient advocate. She works closely with the Cystic Fibrosis Foundation and serves on the Adult Advocacy Council.

Katie gives us an incredible perspective about what it is like to live with Cystic Fibrosis, how her life has changed with modern therapies, and how to be the best provider possible.

This week, we have another great case episode on Pulm PEEPs! We are joined by Emily Fridenmaker who helps us think through a fascinating case presenation.

Meet Our Guests

Emily Fridenmaker is a Pulmonary, Critical Care, and Sleep Medicine fellow at the University of Kentucky College of Medicine. She went to medical school at West Virginia school of medicine and did her internal medicine residency at Charleston Area Medical Center

Patient Presentation

A middle-aged woman presents with 2-3 weeks of mild but progressive shortness of breath with exertion associated with low-grade fevers, worsening night sweats, and fatigue. Further history reveals a progressive non-productive cough and weight loss. She has a past medical history of neurologic dysfunction over two years and a working diagnosis of chronic inflammatory demyelinating polyneuropathy and is pursuing treatment in Mexico due to cost limitations. She has been receiving prednisone 10 mg daily and azathioprine. Aside from travel history to Mexico, her social history is notable for prior employment in a candle factory, and for hiking with some cave exploration. She is a former 20 pack-year smoker and has rare alcohol use.

Key Learning Points

References and links for further reading

1. McKinsey DS, McKinsey JP. Pulmonary histoplasmosis. Semin Respir Crit Care Med. 2011;32(6):735-744. doi:10.1055/s-0031-1295721
2. Cuellar-Rodriguez J, Avery RK, Lard M, et al. Histoplasmosis in solid organ transplant recipients: 10 years of experience at a large transplant center in an endemic area. Clin Infect Dis. 2009;49(5):710-716. doi:10.1086/604712
3. Wheat LJ, Slama TG, Norton JA, et al. Risk Factors for Disseminated or Fatal Histoplasmosis. Ann Intern Med. 1982;96(2):159-163. doi:10.7326/0003-4819-96-2-159
4. Smith JA, Kauffman CA. Endemic fungal infections in patients receiving tumour necrosis factor-alpha inhibitor therapy. Drugs. 2009;69(11):1403-1415. doi:10.2165/00003495-200969110-00002
5. Poplin V, Smith C, Milsap D, Zabel L, Bahr NC. Diagnosis of Pulmonary Infections Due to Endemic Fungi. Diagnostics. 2021;11(5):856. doi:10.3390/diagnostics11050856
6. Wheat LJ, Freifeld AG, Kleiman MB, et al. Clinical Practice Guidelines for the Management of Patients with Histoplasmosis: 2007 Update by the Infectious Diseases Society of America. Clinical Infectious Diseases. 2007;45(7):807-825.
7. Azar MM, Hage CA. Clinical Perspectives in the Diagnosis and Management of Histoplasmosis. Clinics in Chest Medicine. 2017;38(3):403-415. doi:10.1016/j.ccm.2017.04.004
8. Threadcraft MA, Case R. Vape-Associated Pulmonary Injury (VAPI) Presenting With a “Miliary” Pattern on Imaging. Cureus. 13(2):e13385. doi:10.7759/cureus.13385
9. Raoof S, Amchentsev A, Vlahos I, Goud A, Naidich DP. Pictorial essay: multinodular disease: a high-resolution CT scan diagnostic algorithm. Chest. 2006;129(3):805-815. doi:10.1378/chest.129.3.805
10. Sharma BB. Miliary nodules on chest radiographs: A diagnostic dilemma. Lung India. 2015;32(5):518-520.
11. Purek L, Laroumagne S, Dutau H, Maldonado F, Astoul P. Miliary mesothelioma: a new clinical and radiological presentation in mesothelioma patients with prolonged survival after trimodality therapy. J Thorac Oncol. 2011;6(10):1753-1756. doi:10.1097/JTO.0b013e31822e295a

This week we are absolutely thrilled to be joined by three Interstitial Lung Disease experts to discuss the workup and differential for a patient with a new presentation of suspected ILD. This is also our first episode in a collaboration between the Pulm PEEPs and the American Thoracic Society Clinical Problems Assembly. In a series of episodes, we will be joined by pulmonary experts from around the country who are leaders in the ATS CP Assembly to provide content on common and cutting-edge topics in PCCM.

Meet Our Guests

Sonye Danoff is an Associate Professor of Medicine at Johns Hopkins and is Co-Director of the John Hopkins Interstitial Lung Disease and Pulmonary Fibrosis program. She also serves as the Assembly Chair of the Clinical Problems Assembly for the American Thoracic Society.

John Kim is an Assistant Professor of Medicine at UVA and has both clinical and research expertise in interstitial lung disease with a focus on pulmonary fibrosis.

Shweta Sood is an Assistant Professor of Medicine at Penn Medicine whose expertise is in Interstitial Lung Disease. She is an integral part of fellowship training where she leads the monthly ILD conference for fellows as well as provides didactics for ILD cases.

Consult Patient

A 66-year-old man who is a never smoker with a past medical history of hypertension and osteoarthritis was admitted to the hospital after presenting with progressive dyspnea on exertion to dyspnea at rest and was found to be hypoxemic. He reports 4 months of progressive dyspnea on exertion but on further questioning, thinks he was last normal about 1.5 years ago when he could walk 2 miles at a time. Currently, he can only walk 0.25 to 0.5 miles before needing to stop. He reports an intermittent, dry cough throughout the day that is not associated with eating, position, or sleeping. A full ROS is negative including for rashes or joint pains. His family history is notable only for hypertension and hyperlipidemia. He is a never smoker, drinks in moderation 1-2 x a week, and lives in the suburbs with his wife. His house has central heating and air conditioning, they have no pets, and they have carpeted floors. He is a retired police detective.

His physical exam is notable for fine crackles at the bilateral bases on pulmonary auscultation, and he is breathing comfortably on nasal cannula although mildly tachypneic to 18 breaths per minute. He has no signs of volume overload, no peripheral clubbing, no rashes, and joint exam does not reveal swelling or synovitis.

Key Learning Points

Take away points from our guests:

— ILD is a symptom, not a diagnosis

— The first time a patient is evaluated for interstitial lung disease is the best chance for making the diagnosis so take the time to evaluate them thoughtfully

— Start the physical exam with the hands first. The hands can reveal a lot about the patient (clubbing, cyanosis, joint, skin, and nailbed findings) and it establishes a personal connection

— When doing the pulmonary exam, percuss first from top to bottom to learn the size of the lungs, and then listen from bottom to top

— When reading a CT scan the simplest approach is “Is it a UIP pattern or not?”. This can be your first diagnostic divide. UIP is consistent with IPF, and in select circumstances connective tissue disease, occupational lung disease, or advanced hypersensitivity pneumonitis. Non-UIP patterns have a broader differential

— A multi-disciplinary interstitial lung disease conference is the gold standard for establishing an ILD diagnosis

Gathering the history:

— Ask about onset: acute or chronic. “When was the last time your breathing was entirely normal?”

— Symptoms can be shortness of breath, a lingering cough, or often fatigue and decreased energy. Occurrence is important! Do symptoms occur only with exertion or at rest too?

— “Have you ever had chest imaging before?”

— Take a thorough exposure history, and the weird questions are all necessary! Ask about birds and feathers (pet birds, bird feeders, down pillows or blankets, hunting, taxidermy), mold or water damage, organic or inorganic compounds from work (landscaping, ship yards, coal mines)

American College of Chest Physicians – Interstitial Lung Disease Patient Questionnaire

Physical Exam:

— Assess stability first and foremost

— Lung findings: crackles, inspiratory squeaks (often in hypersensitivity pneumonitis)

— Look for evidence of alternative diagnoses: volume overload, liver disease, signs of infection

— Evaluate for signs of connective tissue disease: examine the skin around the forehead and mouth for signs of scleroderma, look for rashes, perform a thorough joint examination and look at their hands, and assess muscle strength

Imaging:

— Order a high-resolution CT scan without contrast. High resolution means thin slices that are 1-2 mm thick. Contrast should be avoided if possible because it makes looking for subtle reticulations or ground-glass opacities harder

— Inspiratory and expiratory films help evaluate for gas trapping. If present, this may indicate hypersensitivity pneumonitis

— Prone films allow you to distinguish reticular changes in the dependent portions of the lungs from atelectasis

Reading the CT scan:

— Look at the distribution first. Is it uniform from top to bottom or not? Is it subpleural, peripheral predominant, or central?

— Identify key features: reticulation, traction bronchiectasis, honeycombing, ground-glass opacities, cysts, and nodules

Laboratory evaluation:

— ANA, Scl-70, DS DNA, anti-RNP, anti-centromere, RF, CCP, SSA, SSB, RNA pol 3, HIV, myositis panel, Hypersensitivity pneumonitis panel

Pulmonary function tests:

— A restrictive ventialtory defect is the classic pattern and can tell you about severity. In ILD, TLC, VC, FRC, and RV are generally all reduced in proportion

— Identify if there is obstruction or not, because if present this may indicate co-existing emphysema, or hypersensitiy pneumonitis

–The DLCO can be helpful for disease severity, and for raising concern about other co-existing diagnoses such as pulmonary vascular disease, or emphysema

— A DLCO < 50% predicted may predict that the patient will need oxygen with exertion and the patient should be walked

6 Minute Walk Test:

— This should be performed for all new patients, because it is important for prognosis

— In the first year after diagnosis, a 6MWD should be performed every 3 – 4 months to assess disease trajectory. It can be done every 6 – 12 months after that.

Differential Diagnosis:

Silo ILDs in to two large buckets

1) An exposure, trigger, or underlying cause is present: hypersensitivity pneumonitis, medication induced, occupational lung disease, connective tissue disease, granulomatous disorder

2) Idiopathic interstitial pneumonia

References and links for further reading

1. Raghu G, Collard HR, Egan JJ, et al. An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis: evidence-based guidelines for diagnosis and management. Am J Respir Crit Care Med. 2011;183(6):788-824. doi:10.1164/rccm.2009-040GL
2. Raghu G, Brown KK. Interstitial lung disease: clinical evaluation and keys to an accurate diagnosis. Clinics in Chest Medicine. 2004;25(3):409-419. doi:10.1016/j.ccm.2004.05.007
3. Bradley B, Branley HM, Egan JJ, et al. Interstitial lung disease guideline: the British Thoracic Society in collaboration with the Thoracic Society of Australia and New Zealand and the Irish Thoracic Society. Thorax. 2008;63 Suppl 5:v1-58. doi:10.1136/thx.2008.101691
4. American Thoracic Society, European Respiratory Society. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias. This joint statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was adopted by the ATS board of directors, June 2001 and by the ERS Executive Committee, June 2001. Am J Respir Crit Care Med. 2002;165(2):277-304. doi:10.1164/ajrccm.165.2.ats01
5. Lederer DJ, Martinez FJ. Idiopathic Pulmonary Fibrosis. New England Journal of Medicine. 2018;378(19):1811-1823. doi:10.1056/NEJMra1705751
6. Travis WD, Hunninghake G, King TE, et al. Idiopathic nonspecific interstitial pneumonia: report of an American Thoracic Society project. Am J Respir Crit Care Med. 2008;177(12):1338-1347. doi:10.1164/rccm.200611-1685OC
7. Wijsenbeek M, Cottin V. Spectrum of Fibrotic Lung D...

Dave Furfaro, Kristina Montemayor, and Ansa Razzaq are back to tackle another pulmonary case! Listen in and solve the case yourself, and we’ll share some diagnostic pearls along the way. Let us know any additional thoughts on Twitter.

Patient Presentation

The is patient is 57-year-old man with hypertension and asthma who presents with dyspnea and left-sided pleuritic chest pain for 3 weeks. He was in his usual state of health until 3 weeks prior to admission, when he developed dyspnea and sharp left-sided chest pain that worsens with deep breathing. His symptoms are accompanied by unintentional 30-pound weight loss over the past several months as well as an intermittent cough that is nonproductive.

On physical exam, he is mildly tachypneic and saturating well on room air with otherwise normal vital signs. He has decreased breath sounds at the right lung base.

Key Learning Points

**Spoilers Ahead** If you want to think through the case on your own we advise listening to the episode first before looking at the infographics below

Physical Exam Pearls

Reasons for decreased breath sounds on physical exam

1. Increased thickness of chest wall

2. Reduced airflow to part of the lung

3. Overinflation to part of the lung

4. Something between the lung and chest wall — air or fluid

Determine bradypnea and tachypnea quickly by matching your breahting rate to the patient’s respiratory rate

Pleural Effusions

Transudative effusion partial differential: heart failure, nephrotic syndrome, hepatohydrothorax, fluid overload, hypoalbuminemia, urinothorax, amyloidosis*, chlothorax*, hypothyrodism*, malignancy*, sarcoidosis*

*these effusions often present as exudates but can be transudates

Exudative effusion partial differential: Infection, hemothorax, malignancy, connective tissue disease, chylothorax, pancreatitis, esophageal perforation.

Sarcoidosis

Key Elements of Diagnosis:

1. Is there a compatible presentation (imaging, physical exam)

2. Detection of non-necrotizing granulomatous inflammation in one or more tissue samples

3. Exclusion of other disease that may present similarily

Pulmonary stages of sarcoidosis:

Key to remember that patients don’t always progress through these stages. The system is useful for prognosticating and determining treatment based on the risk for disease progression.

Treatment for pulmonary sarcoidosis

Patients with stage 1, and even many with stage 2, often don’t require treatment

The first-line agent is oral glucocorticoids and the typical starting dose is prednisone 20 – 40 mg by mouth daily. The patient should be evaluated closely, and ideally, this dose can be tapered starting at about 4 – 6 weeks. Following this, the prednisone dose is tapered slowly over 6 months – 1 year while monitoring for symptom recurrence.

Second-line steroid-sparing agents are methotrexate, azathioprine, or mycophenolate. These are often used if the patient relapses, or is on more then 10mg daily for 3 months after the initial taper with intolerance of steroids

Third-line agents: tumor necrosis factor (TNF)- alpha antagonists (small molecule or monoclonal antibody therapy)

References and links for further reading

1. Light RW. Pleural Effusion. New England Journal of Medicine. 2002;346(25):1971-1977. doi:10.1056/NEJMcp010731
2. Feller-Kopman D, Light R. Pleural Disease. New England Journal of Medicine. 2018;378(8):740-751. doi:10.1056/NEJMra1403503
3. Sarcoidosis: An FP’s primer on an enigmatic disease. MDedge Family Medicine. 2021;70(3). doi:10.12788/jfp.0177
4. Iannuzzi MC, Rybicki BA, Teirstein AS. Sarcoidosis. New England Journal of Medicine. 2007;357(21):2153-2165. doi:10.1056/NEJMra071714
5. Drent M, Crouser ED, Grunewald J. Challenges of Sarcoidosis and Its Management. New England Journal of Medicine. 2021;385(11):1018-1032. doi:10.1056/NEJMra2101555

We are excited to bring you another episode in our Pulm PEEPs Top Consults series! Kristina Montemayor and David Furfaro, are joined by Sandy Zaeh to discuss the assessment and management of a patient with a severe asthma exacerbation. We’ll follow a consult patient from the emergency department to the ICU, and cover everything from the physiology of pulsus paradoxus in asthma to how to manage the ventilator in status asthmaticus. Listen today and please send any questions our way on Twitter @pulmPEEPS.

Meet Our Guests

Sandy Zaeh is an Instructor of Medicine and Pulmonary & Critical Care Medicine physician at Yale School of Medicine.

Key Learning Points

References and links for further reading

1. Chung KF, Wenzel SE, Brozek JL, et al. International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma. European Respiratory Journal. 2014;43(2):343-373. doi:10.1183/09031936.00202013
2. Rodrigo GJ, Rodrigo C, Hall JB. Acute asthma in adults: a review. Chest. 2004;125(3):1081-1102. doi:10.1378/chest.125.3.1081
3. Godwin HT, Fix ML, Baker O, Madsen T, Walls RM, Brown CA. Emergency Department Airway Management for Status Asthmaticus With Respiratory Failure. Respir Care. 2020;65(12):1904-1907. doi:10.4187/respcare.07723
4. Althoff MD, Holguin F, Yang F, et al. Noninvasive Ventilation Use in Critically Ill Patients with Acute Asthma Exacerbations. Am J Respir Crit Care Med. 2020;202(11):1520-1530. doi:10.1164/rccm.201910-2021OC
5. Brenner B, Corbridge T, Kazzi A. Intubation and Mechanical Ventilation of the Asthmatic Patient in Respiratory Failure. Proc Am Thorac Soc. 2009;6(4):371-379. doi:10.1513/pats.P09ST4
6. Laher AE, Buchanan SK. Mechanically Ventilating the Severe Asthmatic. J Intensive Care Med. 2018;33(9):491-501. doi:10.1177/0885066617740079
7. Leatherman J. Mechanical ventilation for severe asthma. Chest. 2015;147(6):1671-1680. doi:10.1378/chest.14-1733

This week on Pulm PEEPs, Dave Furfaro and Kristina Montemayor are joined by experts in the field of critical care medicine and ARDS to discuss all things PEEP! Drs. Roy Brower, Sarina Sahetya, Todd Rice, and Elias Baedorf-Kassis discuss everything ranging from PEEP basics to their approach to optimizing PEEP in patients with ARDS.

Meet Our Guests

Roy Brower is a Professor of Medicine at Johns Hopkins where he served as the MICU director for over 33 years, and he has been one of the pioneers for lung-protective ventilation for patients with ARDS.

Elias Baedorf-Kassis is an Assistant Professor of Medicine at Beth Israel Deaconess Medical Center and Harvard Medical School. He is the Medical Director of Respiratory Care at BIDMC, and helps lead the VV-ECMO program.

Todd Rice is an Associate Profess of Medicine in the Division of Allergy, Pulmonary, and Critical Care Medicine at Vanderbilt University and Vice President for Clinical Trial Innovation and Operations in the Vanderbilt Institute for Clinical and Translational Research.

Sarina Sahetya is an Assistant Professor of Medicine at Johns Hopkins Hospital and does research in the diagnosis of treatment in ARDS.

Key Learning Points

• The plateau pressure can be measured on the ventilator with an inspiratory hold maneuver
• Extrinsic PEEP is applied by the ventiilator, while intrinsic PEEP, or auto-PEEP, occurs when there is incomplete emptying of the lungs due to inadequate time for exhalation. This often happens with obstructive lung disease. Intrinsic PEEP can be measured on the ventilator with an end-expiratory hold maneuver
• We utilize PEEP in all intubated patients to minimize atelectasis. When patients are supine, the heart moves back 2 cm and the diaphragm raises by 2 cm, so often the left lower lobe of the lung is compressed and there is atelectasis there. This is often seen on CXR:

References, Image Sources, and Further Reading

1. Higher versus Lower Positive End-Expiratory Pressures in Patients with the Acute Respiratory Distress Syndrome. New England Journal of Medicine. 2004;351(4):327-336. doi:10.1056/NEJMoa032193
2. Amato MBP, Meade MO, Slutsky AS, et al. Driving Pressure and Survival in the Acute Respiratory Distress Syndrome. New England Journal of Medicine. 2015;372(8):747-755. doi:10.1056/NEJMsa1410639
3. Writing Group for the Alveolar Recruitment for Acute Respiratory Distress Syndrome Trial (ART) Investigators. Effect of Lung Recruitment and Titrated Positive End-Expiratory Pressure (PEEP) vs Low PEEP on Mortality in Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial. JAMA. 2017;318(14):1335-1345. doi:10.1001/jama.2017.14171
4. Beitler JR, Sarge T, Banner-Goodspeed VM, et al. Effect of Titrating Positive End-Expiratory Pressure (PEEP) With an Esophageal Pressure-Guided Strategy vs an Empirical High PEEP-Fio2 Strategy on Death and Days Free From Mechanical Ventilation Among Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial. JAMA. 2019;321(9):846-857. doi:10.1001/jama.2019.0555
5. LaFollette R, Hojnowski K, Norton J, DiRocco J, Carney D, Nieman G. Using pressure–volume curves to set proper PEEP in acute lung injury. Nursing in Critical Care. 2007;12(5):231-241. doi:10.1111/j.1478-5153.2007.00224.x
6. Hess DR. Respiratory mechanics in mechanically ventilated patients. Respir Care. 2014;59(11):1773-1794. doi:10.4187/respcare.03410
7. Sahetya SK, Hager DN, Stephens RS, Needham DM, Brower RG. PEEP Titration to Minimize Driving Pressure in Subjects With ARDS: A Prospective Physiological Study. Respir Care. 2020;65(5):583-589. doi:10.4187/respcare.07102
8. Umbrello M, Chiumello D. Interpretation of the transpulmonary pressure in the critically ill patient. Ann Transl Med. 2018;6(19):383. doi:10.21037/atm.2018.05.31
9. Kenny JES. ICU Physiology in 1000 Words: Driving Pressure & Stress Index. PulmCCM. Published February 13, 2016. Accessed January 1, 2022. https://pulmccm.org/review-articles/icu-physiology-in-1000-words-driving-pressure-stress-index/

The Pulm PEEPs are joined again by Natalie West to discuss a patient who presented with a chronic, productive cough. Listen in today as we work through our differential diagnosis, interpret basic pulmonary testing, and share our clinical reasoning along the way. We have some fantastic diagnostic and treatment teaching points, so once you’ve solved the case check out the takeaways and infographics below. Please let us know any additional insights you have on Twitter!

Patient Presentation

A 50-year-old woman, who is a never smoker, with a past medical history of recurrent pancreatitis presents to the pulmonary clinic with a chronic, productive cough. Her cough has been present for 3 years and has increased in frequency to now being present daily. In the last three months, the cough has also worsened and is productive of small amounts of yellow to green sputum. She has a history of chronic post-nasal drip and sinus infections, and uses intranasal steroids, but has not noted changes in these symptoms. There is no significant family history of pulmonary disease, and an exposure history review of symptoms is negative.

On physical exam, she was a thin woman who appeared her stated age and was breathing comfortably on room air. Her exam was notable for mild expiratory wheezing, primarily on auscultation of the right posterior lung field. She had no cyanosis, clubbing, evidence of volume overload, or abdominal tenderness.

Key Learning Points

**Spoilers Ahead** If you want to think through the case on your own we advise listening to the episode first before looking at the infographics below.

Differential Diagnosis of Chronic Cough

Three most common causes: upper airway cough syndrome, GERD, cough variant asthma

Additional etiologies to consider: chronic bronchitis, post-infectious after a respiratory tract infection, bronchiectasis, ACE inhibitors, lung cancer, eosinophilic bronchitis, interstitial lung disease

Imaging Pearl

Evaluating Bronchiectasis

Making a New Diagnosis of Cystic Fibrosis in an Adult

Sweat testing

Sweat testing should be done in CF accredited center. Inform patients that there are no needles involved. Pilocarpine and electrical stimulation are applied to the arm or leg to stimulate the sweat gland, and then sweat is collected on filter paper, a gauze, or a plastic coil. From there, the amount of chloride in the sweat is calculated

Results

< 30 normal

31 – 60 indeterminate

> 60 is positive and Cystic Fibrosis is likely

What do you do with an Indeterminate test?

Patients with milder phenotypes of Cystic Fibrosis can have a normal or indeterminate sweat chloride level, and 10% of adults diagnosed with CF have a normal sweat chloride. If the sweat chloride test is indeterminate or normal, but suspicion is high for CF, then genetic testing for the whole array of mutations should be performed

References and links for further reading

1. Morice AH, Millqvist E, Bieksiene K, et al. ERS guidelines on the diagnosis and treatment of chronic cough in adults and children. European Respiratory Journal. 2020;55(1). doi:10.1183/13993003.01136-2019
2. Barker AF. Bronchiectasis. New England Journal of Medicine. 2002;346(18):1383-1393. doi:10.1056/NEJMra012519
3. Bronchiectasis: a case-based approach to investigation and management | European Respiratory Society. Accessed November 23, 2021. https://err.ersjournals.com/content/27/149/180016
4. Rowe SM, Miller S, Sorscher EJ. Cystic Fibrosis. New England Journal of Medicine. 2005;352(19):1992-2001. doi:10.1056/NEJMra043184
5. Shteinberg M, Haq IJ, Polineni D, Davies JC. Cystic fibrosis. The Lancet. 2021;397(10290):2195-2211. doi:10.1016/S0140-6736(20)32542-3
6. Jain R. Diagnosing Cystic Fibrosis in Adults: Better Late Than Never. Annals ATS. 2018;15(10):1140-1141. doi:10.1513/AnnalsATS.201806-432ED

Pulm PEEPs hosts, Kristina Montemayor and David Furfaro, bring our first episode in our Top Consults series. In this series, we will bring in experts to work through the most common pulmonary and critical care consults. Whether you are the consulting physician, or a pulmonologist responding to the page, these episodes are geared to give you all the information you need to care for your patients!

Today, we are joined by Chris Kapp and Matthew Schimmel, two interventional pulmonologists, to discuss hemoptysis. Chris and Matt will help us work through two hemoptysis consults, and together we’ll provide a framework for thinking about hemoptysis, outline some key components of the evaluation, and delve into treatment options.

Key Learning Points

Hemoptysis Evaluation

Hemoptysis Management

Life-Threatening or Large Volume Hemoptysis

1. Stabilize the patient! Make sure the airway is protected either by the patient coughing themselves, or intubation if needed. Provide hemodynamic support with IVF, blood products, and pressors if needed. If it is known which lung has the bleeding the patient can be positioned so the lung with the bleeding is down. This protects the non-bleeding lung.
2. Correct any bleeding diathesis If the patient is on anti-coagulation, or has any reversible bleeding diathesis, these should be corrected immediately to reduce further bleeding.
3. Localize the bleed If the patient is stable, they should undergo a CTA to localize the bleeding. If they are not stable to make it to a CT scan, a bronchoscopy should be performed.
4. Bronchoscopic treatment In addition to clearing blood from the airway, bronchoscopy can localize the bleeding. With available expertise, bronchoscopic treatments can be performed such as ice saline, topical epinephrine, or balloon tamponade to isolate the bleed.
5. Definitive therapy with arteriography and embolization Patients with life-threatening hemoptysis should ultimately undergo arteriography and embolization of any bleeding vessel. If this is not possible, then surgery can be needed in some cases.
6. A note on diffuse hemoptysis If there is not one distinct bleeding lesion, then localizing and treating the bleed becomes more difficult. For diffuse alveolar hemorrhage, evaluation should be performed for if it is primary, and due to an immunologic cause and capillaritis, or secondary to a systemic disease and / or bleeding diathesis. These investigations will guide available treatment options. Capillaritis from an immunologic cause, such as lupus or vasculitis, can be treated with systemic glucocorticoids and an additional immunosuppressive agent such as cyclophosphamide or rituximab.

Non-life-threatening or Small Volume Hemoptysis

1. Monitor for clinical worsening Patient’s should be monitored, either in the in-patient or out-patient setting, for increased volume or frequency of hemoptysis and for any clinical worsening, such as desaturations or decreased ability to clear the airway.
2. Correct any bleeding diathesis If the patient is on anti-coagulation, or has any reversible bleeding diathesis, these should be corrected immediately to reduce further bleeding. In pattients with non-life-threateneing hemoptysis this requires careful consideration of balancing the risk of bleeding vs the benefits for continuing anti-coagulation.
3. Evaluate for underlying cause Patient’s should undergo imaging and evaluation for the underlying cause of the hemoptysis. This may be evidence of an underlying infection, a pulmonary embolism, or new lung lesions making the patient at risk. If the source can’t be found on non-invasive imaging, and there is no clear systemic source such as an infection, a bronchoscopy is warranted. Any underlying cause should be treated and investigated further.
4. Inhaled Tranexamic Acid Nebulized tranexamic acid is well tolerated and can help resolve hemopytysis without invasive procedures.

References and links for further reading

1. Gagnon S, Quigley N, Dutau H, Delage A, Fortin M. Approach to Hemoptysis in the Modern Era. Can Respir J. 2017;2017:1565030. doi:10.1155/2017/1565030
2. Radchenko C, Alraiyes AH, Shojaee S. A systematic approach to the management of massive hemoptysis. J Thorac Dis. 2017;9(Suppl 10):S1069-S1086. doi:10.21037/jtd.2017.06.41
3. Davidson K, Shojaee S. Managing Massive Hemoptysis. Chest. 2020;157(1):77-88. doi:10.1016/j.chest.2019.07.012
4. Lara AR, Schwarz MI. Diffuse Alveolar Hemorrhage. CHEST. 2010;137(5):1164-1171. doi:10.1378/chest.08-2084
5. Wand O, Guber E, Guber A, Epstein Shochet G, Israeli-Shani L, Shitrit D. Inhaled Tranexamic Acid for Hemoptysis Treatment: A Randomized Controlled Trial. Chest. 2018;154(6):1379-1384. doi:10.1016/j.chest.2018.09.026