Category Archives: Morning Report

Thanks to our fearless leader Dr. Schroedl for presenting an interesting case of pulmonary MALT lymphoma!

Young woman with chest pain and dyspnea – left upper lobe lesion that didn’t respond to empiric treatment for CAP or even an empirical treatment for fungal pneumonia (unknown exact regimen). Bloodwork and noninvasive infectious workup were unrevealing. Initial bronchoscopy and biopsy were unrevealing. Repeat imaging six months later showed persistence of left upper lobe mass.

The patient got a repeat CT-guided biopsy that showed MALT lymphoma! This is a rare disease, and an extranodal low-grade B-cell lymphoma.

Treatment: ritxumab

The patient had good imaging response but persistent dyspnea, which is thought to be asthma that upon further probing, seemed present even prior to these.

Nice review article here: https://erj.ersjournals.com/content/34/6/1408

Thanks, Dr. Schroedl!

Clara Schroedl, MD, MSc, Medicine – Pulmonary/Critical Care

This week in Pulmonary Report, Dr. Ludwig presented the case of a 68 year old man with chronic exertional dyspnea and abnormal PFTs. Her evaluation (which is still ongoing!) tackled a a high-yield and challenging topic – what happens when your patient has restrictive PFTs but doesn’t have parenchymal disease to explain it?

The broad categories of restrictive lung disease can be remembered with the mnemonic PAINT:

In our patient’s case, an HRCT was performed and did not reveal clear parenchymal/pleural causes of restriction, leading us down the “extra-parenchymal” pathway:

Slide: extra-parenchymal causes of restrictive lung dz

Several maneuvers are available to aid in the differential diagnosis of a restrictive PFT

Supine and upright VC may suggest neuromuscular causes of restrictive lung disease.

• Normal lung function – decrease of 3-8% from upright to supine
• Significant diaphragm dysfunction – >15%

Chest wall and diaphragm mechanics

MVV (or maximal voluntary ventilation) wherein patients are asked to take rapid deep breaths for 12 seconds, is demonstrated in the video below:

MVVpred = FEV1 x ~35-40 (lower values suggestive of neuromuscular weakness)

Maximum inspiratory/expiratory pressure (MIP and MEP) are also decreased in neuromuscular disease:

Pre (upright) and post (supine) flow-volume loop

Pre (upright) and post (supine) vital capacity

MIP and MEP

Diaphragm function may also be evaluated using other modalities:

Diaphragm ultrasound for excursion and fractional thickening

Obtaining a diaphragmatic ultrasound

Thickening fraction: [(thickness at end-inspiration—thickness at end-expiration)/thickness at end-expiration]. <20% is indicative of diaphragmatic weakness

Normal diaphragm excursion: 6cm (female) 7cm (male) during deep breathing

Electromyography of diaphragm to assess for innervation

• Using esophageal or surface electrodes below lower frontal/dorsal ribs
• Negative conduction does not distinguish between neuropathic/myopathic causes and may be followed up with nerve stimulation test

Fluoroscopic sniff test can be used to detect unilateral pathology

• Poor sensitivity in bilateral paralysis; accessory muscle use may cause upward displacement of ribs creating appearance of downward displacement of diaphragm
• Sensitivity in unilateral paralysis is ~90%

Finally, some management considerations for respiratory symptoms in the patient with neuromuscular disease:

Consider blood gas testing for hypercapnia when FVC <40% pred

Thanks Amy!

This week, second-year fellow Elen Gusman presented a case of non-expanding lung (NEL) which presented as a post-thoracentesis hydropneumothorax. Ouch!

Representative clip of a right-sided hydropneumothorax

What are 3 causes of NEL?

• Endobronchial lesion –> lobar collapse
• Chronic atelectasis
• Trapped lung

What is trapped lung?

• A commonly encountered cause of non-expandable lung (NEL)
• Fibrinous, restrictive layer on visceral pleura
• Caused by remote inflammatory pleural process
• Often p/w chronic pleural effusion (ex vacuo physiology)

When to suspect trapped lung?

• Chronic/recurrent effusion
• Pain with thoracentesis
• CT with visceral pleural thickening & loculations
• Fluid characteristics: low LDH, protein in exudative range, paucicellular & mononuclear

How do we diagnose?

• Gold standard is pleural manometry & elastance
• Pel = change in pleural pressure [CWP] / volume fluid removed [L]
• 14-25 CWP/L associated with trapped lung

Below is a YouTube video walking through three commonly utilized methods of transducing pleural pressure:

Lung ultrasound (LUS) may also predict trapped lung with an absent “sinusoid sign”

How to obtain:

1. 2D mode U/S with indicator oriented towards head
2. Switch to M mode with indicator through effusion into atelectatic lung
3. Assess for respirophasic variation in position of atelectatic lung (sinusoidal pattern)

How to distinguish trapped lung from lung entrapment?

• Entrapment – active disease, exudative effusion, directly restricts expansion
• Trapped – chronic disease, transudative (except protein) effusion, visceral pleural thickening restricts

StatPearls 2022 “Trapped Lung” (link)

Annals ATS 2019;16(4):506-508. (link)

Semin Respir Crit Care Med 2001;22(6):631-6. (link)

Today’s morning report featured a fascinating case of eosinophilic pleural effusion from second year fellow Ted Cybulski

Second year PCCM fellow Ted Cybulski | http://tedc.cc/  | Twitter: @tdwck

First thing’s first – how do we define pleural fluid eosinophilia (PFE), and what are classic associations to be familiar with?

Some more quick facts:

• Incidence estimated between 5-16% of all pleural effusions
• More common in men (ratios reported between 2:1 and 9:1)
• Malignant in roughly 35% of cases, of which 50% are lung ca.

Here a closer look at the broad categories on the differential diagnosis of PFE:

In our discussion, Dr. Sporn added that pleural fluid protein <4 and effusion size >1/3 hemithorax are suggestive against tuberculous effusion. A couple of other important points about TB effusion:

• Can occur with primary or reactivation of infx
• Pleural fluid ADA >40 u/L argue strongly for TB especially in lymphocytic exudative effusions (90% of cases)
• Eosinophilic effusions are relatively rarer presentation

Below Ted details the association of eosinophil count in PFE with malignancy – while a lower count (<40%) is MC in malignancy, a higher count is not necessarily reassuring. Other characteristics which carry higher risk for malignant effusion include advanced age and higher pleural fluid LDH (cutoff >900 suggested)

Takeaways

• Pleural fluid eosinophilia = >10% eos, found in 6-14% of pleural effusions
• Classic association with trauma, repeated taps, asbestos.
• MC etio malignant
• Lower eos (10-40%), higher LDH (>900) and advanced age associated with higher probability of malignancy
• TB can present with eosinophilic effusion, but classic presentation is lymphocytic exudate with high ADA (>40)

Thanks for leading a great discussion, Ted!

Sources cited

• Krenke et al. ERJ 2009; 34(5):1111-1117 (https://pubmed.ncbi.nlm.nih.gov/19386682/)
• JM Porcel. Lung 2009; 187:263-70 (https://pubmed.ncbi.nlm.nih.gov/19672657/)