From Dust to Casts: Plastic Bronchitis in a Drywall Worker Treated With Thoracic Duct Embolization

Abstract

Plastic bronchitis is a rare pulmonary condition, most frequently observed in children, that can lead to respiratory failure due to airway obstruction. We present the case of a 50-year-old man with occupational exposure to drywall who experienced recurrent episodes of hypoxic respiratory failure, necessitating multiple intubations. He was initially diagnosed with interstitial lung disease and treated with corticosteroids, but showed minimal clinical improvement. Subsequent flexible bronchoscopy revealed a bronchial cast obstructing the left mainstem bronchus. As plastic bronchitis is typically associated with disorders that cause abnormal lymphatic drainage, thoracic duct embolization was performed. The patient also underwent cryoprobe-assisted bronchoscopy for cast removal. Performance of these 2 procedures led to improved oxygenation and resolution of hypoxic respiratory failure, with no further need for mechanical ventilation.

Introduction

Plastic bronchitis is a rare pulmonary condition in adults, characterized by the formation of large, rubbery mucin plugs—or “casts”—that obstruct the airways and can lead to respiratory failure. ¹ Although it is most often associated with congenital heart disease and lymphatic disorders, the risk factors and natural history of plastic bronchitis remain poorly understood. Emerging case reports suggest that environmental exposures may contribute to its development. We present a case of adult-onset plastic bronchitis in a patient with prolonged exposure to drywall dust without the use of personal protective equipment (PPE). While pharmacologic treatments for plastic bronchitis may be more effective in pediatric populations, several innovative surgical interventions have shown promise in managing this condition in adults.^1,2

Case Report

A 50-year-old man with a 30-year history of drywall work, performed without PPE, and no known history of heart disease or malignancy was hospitalized multiple times over a 6-month period due to recurrent episodes (occurring approximately every 2 months) of acute hypoxic respiratory failure.

The initial episode was marked by progressively worsening dyspnea, a productive cough with thick, “noodle-like” mucus, and oxygen saturation levels as low as 81% on room air. Imaging suggested pneumonia, and his symptoms transiently improved with antibiotics, systemic corticosteroids, bronchodilator nebulizer treatments, and inhaled glucocorticoids.

Two months later, he experienced a more severe episode requiring intubation and mechanical ventilation. Bronchos-copy was nondiagnostic, though cultures grew Candida species. He was treated with fluconazole and discharged on systemic corticosteroids, inhaled corticosteroids, a long-acting bronchodilator, and 3 L/minute of supplemental oxygen via nasal cannula.

Approximately 2 months later, he presented again with acute-on-chronic hypoxic respiratory failure. Chest radiograph showed left lower lobe consolidation suggestive of pneumonia, and computed tomography (CT) scan of his chest revealed obstruction of the left mainstem bronchus by a mucus plug. During this hospitalization, a lung biopsy was performed, but it yielded inconclusive results.

Although he was successfully weaned from mechanical ventilation, his respiratory status deteriorated again about 7 days later, necessitating re-intubation. Bronchoscopy at that time revealed a thick bronchial cast obstructing the left mainstem bronchus, raising suspicion for plastic bronchitis. He was subsequently transferred to an academic medical center for further evaluation and management.

During his hospitalization at the academic medical center, chest radiograph again revealed left lower lobe consolidation, and chest CT demonstrated a mucus plug in the left lower lobe. Additional findings included bilateral perihilar ground-glass attenuation with a vague tree-in-bud pattern (which was similar to prior imaging), dense bibasilar consolidation consistent with aspiration sequelae, and numerous moderately prominent mediastinal lymph nodes, many of which were calcified.

Flexible bronchoscopy confirmed the presence of a bronchial cast obstructing the left mainstem bronchus and extending into the left lower lobe (Figure 1A). A substantial portion of the cast was removed using forceps; however, the casts were friable and fragmented easily, resulting in residual obstruction of the left lower lobe bronchus (Figure 1B). Pathologic analysis revealed a cellular bronchial cast composed of mucin, fibrin, and a few macrophages, without evidence of silica crystals (Figure 2).

Figure 1.

Bronchial cast in the left mainstem bronchus. Bronchoscopy performed on hospital day 2 for airway obstruction revealed: (A) a bronchial cast (arrow) in the left mainstem bronchus extending beyond the field of view and (B) the extracted bronchial casts.

Figure 2.

Pathology of the bronchial cast. H&E staining of the bronchial cast: (A) low magnification (2×) showing fibrin (black solid arrow) admixed with serum, mucin (black dashed arrow), and a few macrophages and inflammatory cells (red arrows), (B) high power magnification (40×) showing fibrin (black arrow) and degenerated inflammatory cells (red arrow head), and (C) PAS staining showing mucin with budding yeast forms (black arrow) without silica crystal, high magnification (40×). H&E, hematoxylin and eosin; f, fibrin; mu, mucin; PAS, periodic acid-Schiff.

The following day, lymphangiography demonstrated patent lymphatic flow to the chest with reflux into abnormally dilated bilateral pulmonary lymphatic vessels, which is a common finding in plastic bronchitis. This was followed by coil and glue embolization of the thoracic duct. Due to the persistence of bronchial casts and their previously described characteristics, bronchoscopy with cryoprobe assistance was undertaken to facilitate cast removal, resulting in improved oxygenation. He self-extubated on hospital day 5, and over the following days, his oxygen requirement gradually decreased to his baseline of 3 L/minute. During his admission, he was empirically treated with cefepime for 7 days for presumed hospital-acquired pneumonia. He was discharged to home on 3 L/minute supplemental oxygen and was instructed to continue inhaled glucocorticoids, a long-acting bronchodilator, a long-acting antimuscarinic agent, and low-dose prednisone.

At a follow-up visit ~6 weeks after discharge, the patient reported improvement in his respiratory symptoms, including resolution of his productive cough and reduced dyspnea. Although he continued to require supplemental oxygen at 3 L/minute, he had not experienced any recurrence of respiratory failure since discharge.

Discussion

Plastic bronchitis is a rare and potentially life-threatening pulmonary condition characterized by the formation of large, rubbery bronchial casts that obstruct the airways. The condition was first described as early as the second century AD by the Greco-Roman physician Galen.^3,4 Over the centuries, it has been referred to by various names, including pseudomembranous bronchitis, cast bronchitis, fibrinous bronchitis, Hoffman’s bronchitis, lymphatic plastic bronchitis, and bronchitis fibroplastica.^4,5

Plastic bronchitis is typically associated with disorders that cause abnormal lymphatic drainage, such as congenital heart disease—particularly following the Fontan procedure. ² In adults, however, most cases are idiopathic. ² Documented causes include anatomical abnormalities (eg, thoracic duct stenosis or duplication), surgical history (eg, coronary artery bypass grafting, lung transplantation), and infections (eg, H1N1 influenza, AIDS, Kaposi sarcoma).^1,2,6 Environmental exposures, such as smoke or silica inhalation, have also been implicated.^5,7

Particles in the lungs are cleared by 3 main mechanisms: mucociliary clearance (typically for larger particles >10 microns), bloodstream absorption (for smaller particles <2.5 microns), and lymphatic drainage (for particles ~2-6 microns). ⁸ Drywall dust varies in size depending on its composition, but it is estimated to average between 3 and 10 microns. Inhaled small particles can enter the lymphatic system via stomata in the pleural cavity, travel through pulmonary and mediastinal lymph nodes, and drain into larger lymphatic ducts, including the thoracic duct. ⁹ Accumulation of such particles could impair lymphatic drainage and contribute to bronchial cast formation.

Our patient had a 30-year history of drywall work without PPE. Drywall commonly contains calcium sulfate (gypsum) and silica, and prolonged unprotected exposure may have contributed to the development of plastic bronchitis in this case. A similar report described a stone dealer with silica exposure whose bronchial cast contained silica-laden macrophages. ¹⁰ Although our patient’s cast did not demonstrate such macrophages, the presence of calcified mediastinal lymph nodes and abnormal pulmonary lymphatic vessels on lymphangiography supports a potential link between occupational exposure and the pathogenesis of plastic bronchitis.

Bronchial casts associated with plastic bronchitis are typically acellular, composed primarily of mucin and fibrin with minimal inflammatory content. ¹¹ In contrast, the casts retrieved from our patient demonstrated a cellular composition, including epithelial and inflammatory cells. While casts in plastic bronchitis are often described as thick and rubbery or “plastic-like,” the material in this case was notably translucent and friable, suggesting the possibility of a newly formed lymphatic cast. Microscopic evaluation for silica crystals was negative; however, the absence of identifiable particulates does not definitively exclude environmental exposure as a contributing factor in the pathogenesis of plastic bronchitis in this patient.

Treatment of plastic bronchitis focuses on removing bronchial casts and preventing recurrence. ¹ Both pharmacotherapy and surgical interventions have been utilized in the treatment of plastic bronchitis. Pharmacologic therapies include systemic and inhaled corticosteroids, mucolytics (eg, hypertonic saline, N-acetylcysteine), macrolide antibiotics, sirolimus, and mTOR inhibitors. ¹ However, no single pharmacologic agent has demonstrated consistent efficacy.

Surgical and interventional strategies have become central to the management of plastic bronchitis, with bronchoscopy playing a pivotal role in both diagnosis and therapeutic cast removal. In this case, forceps-assisted extraction was insufficient due to the friable and easily fragmented nature of the casts. Notably, the patient had undergone bronchoscopy with cast removal ~5 days prior, raising the possibility that the observed material represented newly formed lymphatic casts. Given the limitations of forceps in this context, cryoprobe-assisted bronchoscopy was employed to facilitate removal of the residual obstructing casts. The cryoprobe, a bronchoscopic instrument that delivers rapid, localized freezing via compressed gas, enables cryoadhesion to target material. This technique is particularly advantageous for en bloc extraction of soft or friable endobronchial debris, which may otherwise disintegrate with conventional tools, thereby enhancing procedural efficacy and minimizing airway trauma.^{2,12 -14} Additional interventions aiming to reduce cast formation by targeting thoracic duct lymphatic flow, such as thoracic duct embolization and thoracic duct ligation, have been employed.^{15 -17} Among these, thoracic duct embolization is less invasive and has been associated with high rates of symptom resolution.^{15 -17} While these interventions may not completely eliminate plastic bronchitis, they can significantly reduce the formation of large bronchial casts, thereby preventing recurrent episodes of respiratory failure, as observed in our patient.

Although our patient continues to experience chronic hypoxia requiring supplemental oxygen, he has not had recurrent episodes of respiratory failure requiring mechanical ventilation since undergoing thoracic duct embolization. This suggests that the intervention effectively reduced significant cast formation. Given his occupational history, other causes of chronic hypoxia should be explored.

In conclusion, we present a case of adult-onset plastic bronchitis potentially linked to occupational exposure. This case is notable for the identification of an early-stage bronchial cast, which was successfully managed with flexible bronchoscopy and cryoextraction. Thoracic duct embolization should be considered a first-line treatment option in adult-onset plastic bronchitis to prevent further cast accumulation and associated respiratory complications.