Medical Image of the Week: Plastic Bronchitis in an Adult Lung Transplant Patient

Figure 1. Representative coronal (A) and axial (B) views of the thoracic CT scan in lung windows revealing bilateral dense consolidations and bronchial filling.

Figure 2. Photograph of bronchial gelatinous casts after bronchoscopic forceps removal.

Plastic Bronchitis is a rare condition characterized by the formation of branching gelatinous casts of the bronchial tree which lead to regional airway obstruction. There are thought to be two classifications of casts; type I being the formation of cellular inflammatory casts while type II are acellular. This entity is a well described complication of the Fontan procedure, a therapeutic intervention in pediatric patients with univentricular congenital heart disease (1). The condition is less well reported and thus recognized in adult populations (2).

Our patient is a 37-year-old man who is status post bilateral lung transplantation undertaken for severe workplace inhalation injury complicated by constrictive bronchiolitis-obliterans. Post-transplant, the patient suffered from refractory severe persistent asthma of the donor lung and therefore was scheduled for elective initial bronchial thermoplasty. Post-procedure the patient developed progressive respiratory distress and ultimately extremis requiring mechanical ventilation. Pulse-dose corticosteroids were initiated given a suspected etiology of acute rejection, although response to therapy was poor. Bronchoscopy was conducted which revealed diffuse fibrin casts of the right lung consistent with the development of plastic bronchitis. Symptoms significantly improved with removal of these casts, although a repeat bronchoscopy with cast removal was necessary shortly afterward. Our patient’s cast formation is unique given that it likely has components of both etiologies given his underlying bronchial hyper-secretory disorder and lymphatic disruption after lung transplant. For this reason, we consider this a unique case in its ability to highlight the overlap of these two pathologic processes in an otherwise unlikely demographic to develop bronchial casts. In our comprehensive literature search, we were unable to find significant description of this disorder in adult lung transplant. However, given the disruption in lymphatics, host vs graft inflammatory factors, and infectious inflammatory factors, it would seem to be a perfect setup pathologically. The underlying pathophysiologic mechanism of plastic bronchitis is believed to be cast formation via pulmonary lymphatic disruption by either surgical intervention or inflammatory processes. Gelatinous casts are formed by way of alveolar capillary leak of proteinaceous material, lymphatic seepage, and exudate accumulation from airway inflammation. The majority of literature regarding this disease processes has been described in pediatric thoracic surgery. Lung transplant, especially in the setting of acute rejection, seems to be a setup for this condition in adult populations.

Sarika Savajiyani DO, Nafis Shamsid-Deen MD, and  Raed Alalawi MD

University of Arizona, College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Singhi AK, Vinoth B, Kuruvilla S, Sivakumar K. Plastic bronchitis. Ann Pediatr Cardiol. 2015 Sep-Dec;8(3):246-8. [CrossRef] [PubMed]
2. Eberlein M, Parekh K, Hansdottir S, Keech J, Klesney-Tait J. Plastic bronchitis complicating primary graft dysfunction after lung transplantation. Ann Thorac Surg. 2014 Nov;98(5):1849. [CrossRef]

Cite as: Savajiyani S, Shamsid-Deen N, Alalawi R. Medical image of the week: Plastic bronchitis in an adult lung transplant patient. Southwest J Pulm Crit Care. 2018;17(1):39-40. doi: https://doi.org/10.13175/swjpcc088-18 PDF 

Medical Image of the Week: Headcheese Sign

Figure 1. Representative image from thoracic CT scan showing ground glass opacities, most prominent in the lower lung fields bilaterally with air trapping.

A 95-year-old woman with a past medical history of breast cancer and mastectomy presented with fevers, cough productive of sputum and progressive dyspnea for 2 weeks. She denies any recent travel or sick contacts but has bird at home since last 10 years. She was afebrile but tachypneic with respiratory rate of 25 and sPO2 of 86% on room air. Her initial chest examination reveals coarse rhonchi in both lungs. Labs were significant for a sodium of 118 mEq/L, leukocytosis to 18,000 cells/mcL without peripheral eosinophilia. Arterial blood gas showed pO2 of 55 mm Hg, pCO2 of 48 mm Hg and pH of 7.44. An initial chest X-ray was positive for extensive bilateral pulmonary infiltrates predominantly in the mid and lower lungs with areas of airspace consolidation. Her urine Streptococcus pneumoniae antigen was negative as well as rapid influenza and a respiratory syncytial virus panel. The high resolution thoracic CT showed scattered ground glass opacities, most prominent in the lower lung fields bilaterally (Figure 1). Small more focal consolidative opacities are seen in the right upper lobe. As there was a juxtaposition of low, normal and high-attenuated area of CT scan, characteristic of the headcheese sign.

The head cheese sign is indicative of a mixed obstructive and infiltrative process (1). The low attenuated regions reflect air trapping suggestive of obstructive small airway disease and vasoconstriction due to hypoxia (2). Expiration CT may be needed to enhance low attenuation areas. This airway pathology leads to mosaic attenuation on HRCT. The most common cause of this radiological sign is hypersensitivity pneumonitis (3). As our patient had a long exposure to bird, it was probably the cause of her lung pathology. Other causes of the headcheese sign such as sarcoidosis, bronchiolitis, mycoplasma pneumonia or desquamative interstitial pneumonitis should be considered.

Learning Points:

1. Headcheese is a radiological sign suggestive of hypersensitivity pneumonitis as most common cause.
2. Occupation or any animal exposure history will be most useful in this scenario.
3. The clinician should rule out other causes such as an infectious etiology or sarcoidosis.

Ajay Adial MD, Danial Arshed MD, Lourdes Sanso MD, and Asma Iftikhar MD

Pulmonary/Critical Care Medicine

New York-Presbyterian/Queens

New York, NY USA

References

1. Webb WR. Thin-section CT of the secondary pulmonary lobule: anatomy and the image--the 2004 Fleischner lecture. Radiology. 2006 May;239(2):322-38. [CrossRef] [PubMed]
2. Hirschmann JV, Pipavath SN, Godwin JD. Hypersensitivity pneumonitis: a historical, clinical, and radiologic review. Radiographics. 2009 Nov;29(7):1921-38. [CrossRef] [PubMed]
3. Patel RA, Sellami D, Gotway MB, Golden JA, Webb WR. Hypersensitivity pneumonitis: patterns on high-resolution CT. J Comput Assist Tomogr. 2000 Nov-Dec;24(6):965-70. [CrossRef] [PubMed]

Cite as: Adial A, Arshed D, Sanso L, Iftikhar A. Medical image of the week: headcheese sign. Southwest J Pulm Crit Care. 2018;16(4):192-3. doi: https://doi.org/10.13175/swjpcc040-18 PDF