Traumatic Hemoptysis Complicating Pulmonary Amyloidosis

Erwan Oehler, MD¹

Charlotte Courtois, MD² 

Florent Valour, MD¹

¹Department of Internal Medicine

²Department of Pulmonary Medicine

French Polynesia Hospital Center

98716 Pirae, Tahiti

French Polynesia

Case Presentation

We present a 74-year-old man admitted to hospital for a fall occurring at home. His past medical history included histologically-proven pulmonary amyloidosis followed for fifteen years (Figure 1A), without involvement of other organs.

Figure 1A. Frontal chest radiography shows bilateral confluent, somewhat nodular and dense-appearing opacities with a background of faint linear and reticular opacities.

At admission, he complained of left chest pain related to a rib fracture (Figure 1B, arrow).

Figure 1B. Detail radiograph of the left upper thorax shows a fracture (arrow) of a posterolateral rib, superimposed on the background of dense-appearing linear and nodular parenchymal disease.

The next day, he presented with moderate hemoptysis, prompting performance of thoracic CT (Figure 1C and D) which showed a cavity filled with material of soft tissue attenuation.

Figure 1C and D. Axial thoracic CT displayed in soft tissue windows shows extensive bilateral nodular hyperattenuating tissue consistent with alveolar septal / diffuse pulmonary parenchymal amyloidosis. A cystic lesion with internal, dependent soft tissue attenuation (arrow, D) is present, consistent with a hematoma.

This soft tissue-filled cavity was located at the same level as the rib fracture, surrounded by calcified tissue, and presumably reflected a pulmonary parenchymal hematoma resulting from traumatically induced laceration of the inelastic calcified lung tissue.

Discussion

Pulmonary amyloidosis is a rare disease resulting from the extracellular deposition of insoluble fibrillar proteins aggregating in a β–pleated sheet configuration (1). Amyloidosis is classified according to the chemistry of the amyloid protein as AA secondary amyloidosis (SAA protein) -often related to chronic inflammatory disease- AL amyloidosis (monoclonal immunoglobulin light chains of the lambda or kappa type)-secondary to B lymphoproliferative disorders-and hereditary or familial amyloidosis (transthyretin and gelsolin). Dialysis-associated amyloidosis (βR₂R microglobulinemia) and “senile” amyloidosis SAA (wild-type transthyretin) are also recognized. Pulmonary amyloidosis may occur in three forms: tracheobronchial, nodular parenchymal and alveolar septal / diffuse parenchymal patterns (2). The two first forms (which include primitive pulmonary amyloidosis) are often remain localized to the respiratory system, whereas the alveolar septal / diffuse parenchymal form of amyloidosis, whose prognosis is more severe, often presents in a systemically. Parenchymal amyloid nodules grow slowly and generally remain asymptomatic but patients may also present with dyspnea, cough, hemoptysis or recurrent pneumonia (3).

References

1. Chu H, Zhao L, Zhang Z, Gui T, Yi X, Sun X. Clinical characteristics of amyloidosis with isolated respiratory system involvement: A review of 13 cases. Ann Thorac Med. 2012 (4):243-9. [CrossRef] [Pubmed]
2. Gilmore JD, Hawkins PN. Amyloidosis and the respiratory tract. Thorax. 1999;54:444-51. [CrossRef] [PubMed]
3. Vieira IG, Marchiori E, Zanetti G, Cabral RF, Takayassu TC, Spilberg G, Batista RR. Pulmonary amyloidosis with calcified nodules and masses - a six-year computed tomography follow-up: a case report. Cases J. 2009;2:6540. [CrossRef] [PubMed]

Cite as: Oehler E, Courtois C, Valour F. Traumatic hemoptysis complicating pulmonary amyloidosis. Southwest J Pulm Crit Care. 2015;11(4):173-5. doi: http://dx.doi.org/10.13175/swjpcc133-15 PDF