Thin-section computed tomography detects long-term pulmonary sequelae 3 years after novel influenza A virus-associated pneumonia

Abstract

Background: The aim of this research was to evaluate long-term pulmonary sequelae on paired inspiration-expiration thin-section computed tomography (CT) scans 3 years after influenza A (H1N1) virus-associated pneumonia, and to analyze the affecting factors on pulmonary fibrosis.

Methods: Twenty-four patients hospitalized with H1N1 virus-associated pneumonia at our hospital between September 2009 and January 2010 were included. The patients underwent thin-section CT 3 years after recovery. Abnormal pulmonary lesion patterns (ground-glass opacity, consolidation, parenchymal bands, air trapping, and reticulation) and evidence of fibrosis (architectural distortion, traction bronchiectasis, or honeycombing) were evaluated on follow-up thin-section CT. Patients were assigned to Group 1 (with CT evidence of fibrosis) and Group 2 (without CT evidence of fibrosis). Demographics, rate of mechanical ventilation therapy, rate of intensive care unit admission, cumulative prednisolone-equivalent dose, laboratory tests results (maximum levels of alanine aminotransferase, aspartate transaminase [AST], lactate dehydrogenase [LDH], and creatine kinase [CK]), and peak radiographic opacification of 24 patients during the course of their illness in the hospital were compared between two groups.

Results: Parenchymal abnormality was present in 17 of 24 (70.8%) patients and fibrosis occurred in 10 of 24 (41.7%) patients. Patients in Group 1 (10/24; 41.7%) had a higher rate of mechanical ventilation therapy (Z = -2.340, P = 0.019), higher number of doses of cumulative prednisolone-equivalent (Z = -2.579, P = 0.010), higher maximum level of laboratory tests results (AST [Z = -2.140, P = 0.032], LDH [Z = -3.227, P = 0.001], and CK [Z = -3.345, P = 0.019]), and higher peak opacification on chest radiographs (Z = -2.743, P = 0.006) than patients in group 2 (14/24; 58.3%).

Conclusions: H1N1 virus-associated pneumonia frequently is followed by long-term pulmonary sequelae, including fibrotic changes, in lung parenchyma. Patients who need more steroid therapy, need more mechanical ventilation therapy, had higher laboratory tests results (maximum levels of AST, LDH, and CK), and had higher peak opacification on chest radiographs during treatment are more likely to develop lung fibrosis.

Figure 1

A 35-year-old woman diagnosed with novel influenza A pneumonia without secondary infection. The patient received cumulative prednisolone-equivalent doses of 850 mg and mechanical ventilation therapy. Laboratory investigations showed the maximum levels of alanine aminotransferase, aspartate transaminase, lactate dehydrogenase, and creatine kinase in the acute stage were 32 U/L, 101 U/L, 1160 U/L, and 201 U/L, respectively. (a) A portable chest radiograph obtained 4 days after the onset of clinical symptoms shows widespread consolidation, with central and lower lung zone predominance; (b) Transverse thin-section computed tomography (CT) scans performed 10 days after the onset of clinical symptoms demonstrate consolidations and ground-glass opacities in the lower lung fields; (c) Follow-up transverse inspiration thin-section CT scans obtained 3 years after the onset of clinical symptoms show residual reticular opacity in the lower lobes and ground-glass opacity in the left lower lobe.

Figure 2

A 24-year-old man diagnosed with novel influenza A pneumonia without secondary infection. The patient without mechanical ventilation therapy received cumulative prednisolone-equivalent doses of 700 mg. Laboratory investigations showed the maximum levels of alanine aminotransferase, aspartate transaminase, lactate dehydrogenase, and creatine kinase in the acute stage were 90 U/L, 69 U/L, 486 U/L, and 1747 U/L, respectively. (a) Transverse computed tomography (CT) scans obtained 18 days after the onset of clinical symptoms through the lower lobes demonstrate ground-glass opacity, parenchymal bands; (b, c) Follow-up transverse thin-section CT scans obtained 3 years after the onset of clinical symptoms; (b) Axial inspiratory image scan demonstrates no clear evidence of lung abnormality; (c) Axial expiratory image shows abnormal low attenuation caused by air trapping, representing failure of the expected increase in lung attenuation.

Figure 3

A 22-year-old man diagnosed with novel influenza A pneumonia without secondary infection, and received mechanical ventilation therapy. The patient received cumulative prednisolone-equivalent doses of 1150 mg. Laboratory investigations showed the maximum levels of alanine aminotransferase, aspartate transaminase, lactate dehydrogenase, and creatine kinase in the acute stage were 39 U/L, 124 U/L, 900 U/L, and 876 U/L, respectively. (a) Transverse computed tomography (CT) image obtained 6 days after the onset of clinical symptoms shows diffuse ground-glass opacity (GGO) and dependent consolidation; (b) Follow-up transverse inspiration thin-section CT image obtained 3 years after the onset of clinical symptoms shows resolution of the GGO and dependent consolidation. However, fibrosis has developed in the anterior portion of the lungs, which showed only mild involvement during the acute phase.