Today we’re joined by Dr. Molly Hayes and talking about an upcoming CME course: Principles of Critical Care Medicine for Non-Intensive Care Specialists. This is a wonderful education course covering a wide array of topics in critical care in a case-based, systematic, and peer-reviewed fashion. The course is interactive and all resources will be available for attendees afterwards for their review. You can sign up at https://learn.hms.harvard.edu/criticalmed and save using the discount code “PulmPEEPS50”!
Meet Our Guest
Dr. Molly Hayes is an Associate 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 additionally is a co-founder of the BIDMC Center for Humanizing the ICU.
Today we have another Pulm PEEPs Pearls episode about a core critical care topic. Furf and Monty will be giving a high level overview of the use of steroids in sepsis including a review of the relevant literature and recent guidelines, and pragmatic bedside points.
Contributors
This episode was prepared with research by Pulm PEEPs Associate Editor George Doumat.
Dustin Latimer, another Pulm PEEPs Associate Editor, assisted with audio and video editing.
Key Learning Points
Why Steroids in Sepsis?
Steroids do not treat the infection — antimicrobials are always first and remain the cornerstone. The goal is addressing critical illness–related corticosteroid insufficiency (CIRCI), where cortisol production cannot keep up with the overwhelming inflammatory demand of septic shock.
Hydrocortisone helps in two main ways:
Blunts the dysregulated inflammatory response — tempers the excessive vasodilation and febrile response that drive harm beyond the infection itself.
Restores vascular sensitivity to catecholamines — sepsis downregulates adrenergic receptors; steroids turn that responsiveness back on.
Clinical takeaway: The first thing you notice is vasopressor weaning (or a bend in the escalation curve) — not a rapid improvement in fever or white count.
Caveat: These trials predate modern sepsis phenotyping. None distinguish hyperinflammatory vs. hypoinflammatory responders — they treat all comers.
The Evidence: Four Landmark Trials
Every IM resident and critical care fellow will eventually journal-club these four. The most consistent signal across all of them is faster shock reversal and reduced vasopressor use; the mortality question remains unsettled.
Trial (Year)
N
Regimen
Key Finding
Annane (2002)
~300
Hydrocortisone + fludrocortisone
Mortality benefit in ACTH non-responders; criticized methodology and messy cortisol-response testing; not cleanly replicated.
CORTICUS (2008)
~500
Hydrocortisone alone
Faster shock reversal but no mortality benefit, regardless of cortisol responsiveness. Raised (later allayed) superinfection concern. Cornerstone for abandoning routine cort-stim testing.
ADRENAL (2018)
~3,800
Hydrocortisone alone
Faster vasopressor weaning; no 90-day mortality benefit.
APROCCHSS (2018)
~1,200
Hydrocortisone + fludrocortisone
Mortality benefit at 90 days.
Bottom line: Faster shock reversal is consistent. Mortality benefit appears in 2 of 4 trials (both used fludrocortisone) but not the others. A 2026 meta-analysis showed benefit for hydrocortisone + fludrocortisone vs. placebo, but
not for hydrocortisone + fludrocortisone vs. hydrocortisone alone — suggesting hydrocortisone drives the main effect.
Who Gets Steroids, and When?
2021 Surviving Sepsis: Consider steroids for norepinephrine or epinephrine ≥ 0.25 mcg/kg/min for ≥ 4 hours despite adequate resuscitation — a reasonable bedside trigger.
Early 2026 update: Moved away from a specific numeric trigger — consider steroids when a septic patient is not responding well to vasopressors or has escalating requirements. Make a clinical decision. (Quality of evidence: low to moderate.)
Go faster than the threshold when: Known/suspected adrenal insufficiency or home steroids, or florid pressor-requiring shock on arrival.
A practical escalation sequence: escalating norepinephrine → add vasopressin (per VASST) → then add steroids if requirements keep climbing.
Do NOT wait for an ACTH stimulation test. It does not reliably predict who responds and only delays treatment. Sepsis is an elevated-cortisol state but can dissociate ACTH and cortisol, and cortisol-binding globulin is depleted — the test is too messy to guide care.
What to Give: The Regimen
Standard dose: Hydrocortisone 200 mg/day, typically 50 mg IV Q6H. (Original trials often used continuous infusions, rarely used in the U.S.) Some start with a 100 mg bolus to gain control.
Higher dose: If chronically on steroids / adrenally insufficient, consider ~300 mg/day (e.g., 100 mg Q8H).
Fludrocortisone: Unsettled. The two mortality-benefit trials added it (50 mcg PO/NG/OG daily), but hydrocortisone already has mineralocorticoid activity and meta-analyses don’t show added benefit over hydrocortisone alone. Most clinicians omit it — adding it is reasonable and safe, just be honest about the uncertainty.
Duration & Tapering
Typical course: ~7 days is most common. Trial practices varied (ADRENAL ~7 days; VANISH used a taper after 6 days; some continue until pressors are off).
No taper needed. You do not need to taper for adrenal insufficiency after a short course — just stop. If pressors dramatically rebound, you can restart, but most patients have gained the benefit they’ll get by day 7.
Pitfalls & Safety
Hyperglycemia: Expected and must be managed (monitor closely; insulin drip if needed). No signal for major DKA / severe complications in the trials.
Superinfection / fungal infection: The most-quoted concern, but the overall literature does not show a convincing, statistically significant increase. Be disciplined about stopping on schedule.
Muscle weakness: Steroids can worsen critical illness myopathy; a short 7-day course likely has limited effect, but be aware.
Other: GI bleeding (follow general PPI prophylaxis guidance) and sodium disturbances (watch for hyper-/hyponatremia).
Two things we know: (1) steroids shorten duration of vasopressor support, and (2) they are relatively safe in sepsis. Whether they improve mortality — and in whom — remains open.
The Five Pulm PEEPs Pearls
Mechanism: Steroids restore catecholamine vascular sensitivity and blunt dysregulated inflammation. The clinical target is vasopressor weaning, not infection treatment.
Evidence: Faster shock reversal is the most consistent finding. Mortality benefit is seen in 2 of 4 trials but not the others — still controversial. Some patients likely benefit; we don’t yet know who.
Trigger: A practical 2021 threshold is levo/epi ≥ 0.25 mcg/kg/min for ≥ 4 hours. Newer guidance drops the strict number — make a clinical decision based on poor pressor response or escalation.
Dose: Hydrocortisone 200 mg/day (e.g., 50 mg Q6H). Adding fludrocortisone mirrors two trials, but meta-analyses find no benefit over hydrocortisone alone.
Safety: Steroids appear safe in sepsis. Monitor and treat hyperglycemia; no marked increase in superinfection.
References and Further Reading
Annane, Djillali et al. “Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock.” JAMA vol. 288,7 (2002): 862-71. doi:10.1001/jama.288.7.862
Sprung, Charles L et al. “Hydrocortisone therapy for patients with septic shock.” The New England journal of medicine vol. 358,2 (2008): 111-24. doi:10.1056/NEJMoa071366
Venkatesh, Balasubramanian et al. “Adjunctive Glucocorticoid Therapy in Patients with Septic Shock.” The New England journal of medicine vol. 378,9 (2018): 797-808. doi:10.1056/NEJMoa1705835
Annane, Djillali et al. “Hydrocortisone plus Fludrocortisone for Adults with Septic Shock.” The New England journal of medicine vol. 378,9 (2018): 809-818. doi:10.1056/NEJMoa1705716
Sun, Alin et al. “Correction: Hydrocortisone combined with fludrocortisone for treatment of adults with septic shock: an updated meta-analysis and systematic review.” Frontiers in medicine vol. 13 1811616. 2 Mar. 2026, doi:10.3389/fmed.2026.1811616
Prescott, Hallie C et al. “Executive Summary: Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2026.” Critical care medicine vol. 54,4 (2026): 715-724. doi:10.1097/CCM.0000000000007089
This week’s Pulm PEEPs Pearls episode is all about spontaneous breathing trials (SBTs). SBTs are a standard part of the daily practice in the intensive care unit, but the exact methods vary across ICUs and institutions. Listen in to hear about the most common methods of SBTs, the physiology of each method, and what the evidence says.
Contributors
This episode was prepared with research by Pulm PEEPs Associate Editor George Doumat.
Dustin Latimer, another Pulm PEEPs Associate Editor, assisted with audio and video editing.
Key Learning Points
What an SBT is really testing
An SBT is a stress test for post-extubation work of breathing, not just a ventilator check.
The goal is to balance sensitivity and specificity:
Too hard → unnecessary failures and delayed extubation
Too easy → false positives and higher risk of reintubation
Common SBT modalities and how they compare
T-piece
No inspiratory support and no PEEP
Highest work of breathing
Most “physiologic” but often too strict
Pressure support (PS) + PEEP (e.g., 5/5 or 8/5)
Offsets ETT resistance and provides modest assistance
Easier to pass than T-piece
CPAP (0/5)
No inspiratory help, but provides PEEP to counter ETT resistance
Sits between PS and T-piece in difficulty
Evidence favors pressure-supported SBTs for most patients
Leads to earlier extubation and fewer ventilator-associated risks
Bottom line: A 30-minute PS 5/5 SBT is evidence-based and appropriate for most stable ICU patients
When a T-piece still makes sense
T-piece SBTs are useful when:
Cost of reintubation is high
Difficult airway
Prior failed extubation
Pretest probability of success is low
Prolonged or difficult weaning
Tracheostomy vs extubation decisions
Need to mimic physiology without positive pressure
In LV dysfunction or pulmonary edema even small amounts PEEP may significantly improve physiology
Some centers use a hybrid approach: PS SBT → short confirmatory T-piece before extubation
CPAP as a middle ground
Rationale:
Allows full patient effort while compensating for ETT resistance
Evidence:
Fewer and smaller trials
Possible modest improvement in extubation success
No clear mortality or LOS benefit
Reasonable option based on patient physiology, institutional protocols, and clinician comfort
No single “perfect” SBT mode
Across PS, T-piece, CPAP, and newer methods (e.g., high-flow via ETT) there are no consistent differences in mortality or length of stay
What matters most:
Daily protocolized screening
Thoughtful bedside clinical judgment
Matching SBT difficulty to patient-specific risk
Institutional variation is normal—and acceptable
Examples:
PS 10/5 in postoperative surgical ICU patients
PS 5/0 as an intermediate difficulty option
Key question clinicians should ask: What does passing or failing this specific SBT tell me about this patient’s likelihood of post-extubation success?
Take-home pearls
SBTs are stress tests of post-extubation physiology.
PS 5/5 for 30 minutes is a strong default for most ICU patients.
T-piece trials are valuable when false positives are costly or physiology demands it.
CPAP is reasonable but supported by less robust data.
Consistency, daily screening, and judgment matter more than the exact mode.
References and Further Reading
Burns KEA, Khan J, Phoophiboon V, Trivedi V, Gomez-Builes JC, Giammarioli B, Lewis K, Chaudhuri D, Desai K, Friedrich JO. Spontaneous Breathing Trial Techniques for Extubating Adults and Children Who Are Critically Ill: A Systematic Review and Meta-Analysis. JAMA Netw Open. 2024 Feb 5;7(2):e2356794. doi: 10.1001/jamanetworkopen.2023.56794. PMID: 38393729; PMCID: PMC10891471.
Burns KEA, Sadeghirad B, Ghadimi M, Khan J, Phoophiboon V, Trivedi V, Gomez Builes C, Giammarioli B, Lewis K, Chaudhuri D, Desai K, Friedrich JO. Comparative effectiveness of alternative spontaneous breathing trial techniques: a systematic review and network meta-analysis of randomized trials. Crit Care. 2024 Jun 8;28(1):194. doi: 10.1186/s13054-024-04958-4. PMID: 38849936; PMCID: PMC11162018.
Subirà C, Hernández G, Vázquez A, Rodríguez-García R, González-Castro A, García C, Rubio O, Ventura L, López A, de la Torre MC, Keough E, Arauzo V, Hermosa C, Sánchez C, Tizón A, Tenza E, Laborda C, Cabañes S, Lacueva V, Del Mar Fernández M, Arnau A, Fernández R. Effect of Pressure Support vs T-Piece Ventilation Strategies During Spontaneous Breathing Trials on Successful Extubation Among Patients Receiving Mechanical Ventilation: A Randomized Clinical Trial. JAMA. 2019 Jun 11;321(22):2175-2182. doi: 10.1001/jama.2019.7234. Erratum in: JAMA. 2019 Aug 20;322(7):696. doi: 10.1001/jama.2019.11119. PMID: 31184740; PMCID: PMC6563557.
Burns KEA, Wong J, Rizvi L, Lafreniere-Roula M, Thorpe K, Devlin JW, Cook DJ, Seely A, Dodek PM, Tanios M, Piraino T, Gouskos A, Kiedrowski KC, Kay P, Mitchell S, Merner GW, Mayette M, D’Aragon F, Lamontagne F, Rochwerg B, Turgeon A, Sia YT, Charbonney E, Aslanian P, Criner GJ, Hyzy RC, Beitler JR, Kassis EB, Kutsogiannis DJ, Meade MO, Liebler J, Iyer-Kumar S, Tsang J, Cirone R, Shanholtz C, Hill NS; Canadian Critical Care Trials Group. Frequency of Screening and Spontaneous Breathing Trial Techniques: A Randomized Clinical Trial. JAMA. 2024 Dec 3;332(21):1808-1821. doi: 10.1001/jama.2024.20631. PMID: 39382222; PMCID: PMC11581551.
Mahul M, Jung B, Galia F, Molinari N, de Jong A, Coisel Y, Vaschetto R, Matecki S, Chanques G, Brochard L, Jaber S. Spontaneous breathing trial and post-extubation work of breathing in morbidly obese critically ill patients. Crit Care. 2016 Oct 27;20(1):346. doi: 10.1186/s13054-016-1457-4. PMID: 27784322; PMCID: PMC5081985.
Yi LJ, Tian X, Chen M, Lei JM, Xiao N, Jiménez-Herrera MF. Comparative Efficacy and Safety of Four Different Spontaneous Breathing Trials for Weaning From Mechanical Ventilation: A Systematic Review and Network Meta-Analysis. Front Med (Lausanne). 2021 Nov 22;8:731196. doi: 10.3389/fmed.2021.731196. PMID: 34881255; PMCID: PMC8647911.
Furf and Monty are back today with another Pulm PEEPs Pearls episode, and discussing the use of methylene blue for patients with septic shock. They review the clinical scenarios when this comes up, the mechanism, some key data, and some take aways, all in 15 minutes! Let us know any other topics you’d like covered on the show and make sure to like, give us 5 stars, and subscribe wherever you’re listening to this podcast.
This episode was prepared in conjunction with George Doumat MD. Goerge is an internal medicine resident at UT Southwestern and joined us for a Pulm PEEPs – BMJ Thorax journal club episode. He is now acting as a Pulm PEEPs Editor for the Pulm PEEPs Pearls series.
Key Learning Points
Clinical context: when does methylene blue even come up?
This is not a first-line sepsis drug.
It’s considered in catecholamine-refractory vasoplegic septic shock, typically when:
Norepinephrine is at high dose
Vasopressin is on board
Often a 3rd or 4th vasopressor is being used (e.g., phenylephrine, angiotensin II)
The phenotype is strongly vasodilatory/vasoplegic (warm, distributive shock) rather than primarily cardiogenic.
Mechanism of action (why it might help)
Methylene blue:
Inhibits inducible nitric oxide synthase and guanylate cyclase.
Blunts excess nitric oxide and cyclic GMP–mediated vasodilation, which are key in vasoplegic sepsis.
Practical translation:
It restores vascular tone and can make the vasculature more responsive to catecholamines.
It’s also used in post-CPB vasoplegia (e.g., after cardiac surgery, especially in patients on ACE inhibitors) and has migrated from that world into ICU sepsis practice.
Typical dosing strategy (as described in the episode)
If there’s a response, consider a continuous infusion or repeat bolus.
Key nuance: unlike other pressors that start as drips, methylene blue is often trialed as a bolus first to see if it’s doing anything.
What does the evidence suggest?
Most data are from small, single-center, heterogeneous studies, so evidence quality is low. Meta-analyses and systematic reviews (through ~2024–25) suggest:
Hemodynamics
Can increase MAP (roughly 1–10 mmHg across studies).
May shorten total vasopressor duration (one meta-analysis ~30 hours less, though this is not definitive).
Secondary physiologic effects
Some small improvements in PaO₂/FiO₂ (P/F) ratio in certain studies.
Clinical outcomes
Possible reduction in hospital length of stay (≈ up to 2 days in some pooled analyses).
Some signal toward lower short-term mortality, but:
Studies are small
Heterogeneous
Evidence is very low certainty
Bottom line:
There’s a repeatable signal that methylene blue:
Raises MAP
Helps reduce catecholamine requirements
But hard clinical outcomes (mortality, LOS, ventilator days) remain uncertain.
Safety profile & important adverse effects
Things to watch for:
Methemoglobinemia
Serotonin syndrome
Especially in patients on SSRIs, though in life-threatening refractory shock the hosts still lean toward using it with caution.
Pulse oximeter artifact
Can distort SpO₂ readings.
Urine discoloration
Blue/green urine—benign but striking.
Notably:
Methylene blue is both a treatment for and a potential cause of methemoglobinemia, depending on context and dosing.
Guidelines & where it fits in practice
Surviving Sepsis Campaign 2021:
Does not recommend methylene blue for routine use in septic shock.
No major critical care society includes it in standard septic shock bundles or protocols.
The hosts frame methylene blue as:
A rescue therapy, not guideline therapy.
Something to consider only in refractory vasoplegic shock, ideally with:
We are so excited to be launching a new series here at Pulm PEEPs! We’ll be talking about high yield topics in 15 minutes or less. In this series, Furf and Monty will tackle core points and provide an overview, key points, and further reading. We’re starting with a key point review of Immune Checkpoint Inhibitor Pneumonitis. Let us know if there are other topics you want to hear about!
Key Learning Points
Epidemiology & Pathophysiology
Increasingly common as immunotherapy use grows in oncology.
Caused by immune activation from PD-1, PD-L1, or CTLA-4 inhibitors.
Any new respiratory symptoms in a patient currently or previously on ICI → consider ICI pneumonitis.
CT findings are variable: can mimic organizing pneumonia, NSIP, ARDS, or diffuse ground glass opacities. Imaging pattern does not determine severity grade.
Diagnosis is of exclusion — infection and malignancy progression must be ruled out first.
Today we’re talking about a topic that is relevant for all critical care physicians but under-examined: ICU Acquired Weakness. We are joined by two excellent guests to walk through a case and discuss the diagnosis, pathophysiology, prevention, and treatment of ICU Acquired Weakness. Check out our associated infographics and key learning points below.
Meet Our Guests
Jim Devanney is a Physiatrist who just completed a neurocritical care fellowship at BIDMC. He is transitioning to a clinical associate position at University Health Network – University of Toronto where he will be working as a PM&R consultant within the ICU.
Kalaila Pais is a third year internal medicine resident at BIDMC, interested in pulmonary and critical care and medical education and is returning for her third Pulm PEEPs episode.
Key Learning Points
Definition & Clinical Presentation
ICU-AW refers to new-onset, generalized muscle weakness that arises during critical illness, not explained by other causes.It typically presents as:
Symmetric, proximal > distal weaknessRespiratory muscle involvementPreserved cranial nerve functionNo sensory deficits in myopathy (sensory loss points toward neuropathy)
Differential Diagnosis Using Neuroanatomical ApproachAn anatomical approach (central → peripheral) helps localize the etiology weakness
Today, we’re virtually visiting the University of Virginia for another Fellows’ Case Files. This is a fantastic case that covers ARDS, the infectious work up of an immunosuppressed patient, and the evaluation of undifferentiated shock. Please let us know what you think of the episode and always feel free to reach out with interesting cases!
Meet Our Guests
John Popovich completed his residency training and chief year at UVA and has stayed on there for his pulmonary and critical care fellowship.
Tim Scialla is an associate professor of medicine at UVA. He completed his residency and fellowship at Johns Hopkins Hospital where he was also an ACS. His clinical and research focuses are advanced airways disease. He is also the program director of the PCCM fellowship.
Matt Freedman completed his residency training at Virginia Commonwealth University and is currently a second year fellow at University of Virginia.
Case Presentation
Patient: 52-year-old male with psoriasis, HIV/AIDS (CD4 count: 71), presenting with progressive shortness of breath, fever, non-productive cough, and weight loss.
Today is our third episode in our collaborative series with BMJ Thorax. Our mission at Pulm PEEPs is to disseminate and promote pulmonary and critical care education, and we highly value the importance of peer reviewed journals in this endeavor. Each month in BMJ Thorax, a journal club is published looking at high yield and impactful publications in pulmonary medicine. We will be putting out quarterly episodes in association with Thorax to discuss a journal club publication and synthesize four valuable papers. This week’s episode covers four articles related to obstructive sleep apnea therapies, and the use of non-invasive ventilation and high flow nasal cannula for intubation and COPD exacerbations.
Meet Our Guests
Chris Turnbull is an Associate Editor for Education at Thorax. He is an Honorary Researcher and Respiratory Medicine Consultant at Oxford University Hospitals. In addition to his role as Associate Editor for Education at BMJ Thorax, he is also a prominent researcher in sleep-related breathing disorders.
Natalie McLeod is a resident in respiratory medicine and is currently doing a clinical fellowship in sleep and ventilation at Oxford University Hospitals.
To submit a journal club article of your own to Thorax, you can contact Chris directly – christopher.turnbull@ouh.nhs.uk
To engage with Thorax, please use the social media channels (Twitter – @ThoraxBMJ; Facebook – Thorax.BMJ) and subscribe on your preferred platform, to get the latest episodes directly on your device each month.
We are podcasting today directly from ATS 2025 in San Francisco! Every year, in collaboration with the ATS Critical Care Assembly, we highlight some of the scientific symposium programming from the conference. Today, Furf and Monty sit down with the three chairs of the scientific symposium entitled: Mechanical Ventilation of the Future: New Foundations For Ventilator Strategies.
Meet Our Guests
Juliana Ferreira is an Associate Professor at the University of Sao Paulo, Brazil where she is also co-director of the pulmonary and critical care fellowship program. She is an MD, PhD, and a physician scientist with specific interests in mechanical ventilation and medical education. Finally, she serves ATS as the ATS MECOR Latin America Director.
Bhakti Patel is an Assistant Professor Medicine at the University of Chicago. She is a dedicated researcher and educator. Her research focuses on non-invasive ventilator support.
Akram Khan is an Associate Professor of Medicine at Oregon Health and Science University. Akram is a pulmonary, critical care, and sleep provider with specific clinical interests in critical illness, pulmonary vascular disease and sleep apnea. Additionally, he is an accomplished translational science researcher.
We’re back with another edition of Fellows’ Case Files! Today, we’re virtually visiting Rutgers University, Robert Wood Johnson Medical School to work through a fascinating pulmonary case. Enjoy, and let us know your thoughts.
Meet Our Guests
Khalil El Gharib completed his residency training at Northwell at Staten Island University Hospital Program and is currently a first year fellow at Rutgers Robert Wood Johnson Medical School.
Sabiha Hussain completed her residency training at Robert Wood Johnson Medical School and her fellowship training at Columbia Presbyterian Medical Center in New York. She is currently a Professor of Medicine and the fellowship Program Director.
Case Presentation
Patient: 28-year-old male with Asperger’s syndrome and IgA nephropathy.
Symptoms: 3-month history of progressive dry cough and dyspnea on exertion; later developed mild hemoptysis.
Notable exposure: Questionable black mold in the patient’s apartment.
Initial Workup and Diagnostic Reasoning
Vital signs: Hypoxemia (SpO₂ 91% on room air).
Exam: Inspiratory crackles.
ABG findings: Elevated A–a gradient (~50), indicating a gas exchange problem.
Chest X-ray: Bilateral, patchy infiltrates without specific lobar preference.
Initial management: Discharged with empiric antibiotics for presumed multifocal pneumonia.
Re-Presentation and Further Testing
Symptoms worsened; now with blood-tinged sputum.
Chest CT: Showed diffuse ground-glass opacities (GGOs) without fibrosis, consolidation, or lymphadenopathy.
Imaging and Pathology
Pathology images a courtesy to Dr Isago Jerrett, pathology resident at RWJMS
Key Learning Points
Diagnostic Framework for Hypersensitivity Pneumonitis (HP)
New classification: Based on fibrotic vs. non-fibrotic phenotype (not acute/chronic).
CT features of HP:
GGOs with lobular air trapping.
“Three-density sign” (normal lung, low-density air-trapping, and ground-glass opacities).
BAL: Typically shows lymphocytic predominance in chronic HP, neutrophilic in early stages.
