Congenital pulmonary airway malformation mimicking lung cancer in adults: a pitfall in oncologic diagnosis

Introduction

Congenital pulmonary airway malformation (CPAM), previously referred to as “congenital cystic adenomatoid malformation”, is a common pulmonary developmental anomaly that warrants attention due to its atypical presentations (1,2). CPAM arises from abnormal bronchial bud development, and most patients are asymptomatic at birth, but some have cough or respiratory distress (3). In some rare cases, CPAM remains undetected until adulthood. A typical computed tomography (CT) feature is well‑defined, thin‑walled multilocular cysts. However, complications such as recurrent infection or fibrosis can produce solid or solidcystic masses that mimic primary lung cancer, complicating preoperative diagnosis. Although a few reports have described adult CPAM misdiagnosed as malignancy (4,5), systematic analysis of the specific imaging pitfalls is lacking. This dual‑center retrospective study aimed to (I) summarize CT pitfalls leading to misdiagnosis, (II) identify benign clues for correct diagnosis, and (III) construct a practical imaging‑based differential framework to enhance radiologists’ alertness to this disease.

Methods

Ethical statement

This retrospective dual-center study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study protocol was approved by the Ethics Committee of Sir Run Run Shaw Hospital, Zhejiang University School of Medicine (approval No. 2026-2076-01), which including approval for both of the participating centers in this study. The requirement for informed consent was waived due to the retrospective nature of the analysis.

Data collection

To identify patients, we conducted a retrospective search of the databases of Sir Run Run Shaw Hospital and Xi’an International Medical Center Hospital from January 2010 to December 2025 using the keywords “congenital pulmonary airway malformation”, “congenital cystic adenomatoid malformation”, “congenital cystic disease”, and “congenital lung malformation”. Adult patients who had initial radiologic suspicion of lung cancer but who were pathologically confirmed to have CPAM were included. Patients with degraded image quality due to respiratory motion artifacts or ipsilateral pneumothorax that interfered with lesion assessment were excluded. The clinical and imaging data of the patients were analyzed and summarized.

CT image acquisition

With patient’s supine, chest CT was performed with a SOMATOM Force, Definition AS 40 (Siemens Healthineers, Erlangen, Germany), or uCT 510 (United Imaging Healthcare, Shanghai, China) scanner from the thoracic inlet to the lung base. Noncontrast scans were performed under the following parameters: 120 kVp, 100–250 mA, a 512×512 matrix, and a 5-mm slice thickness. Contrast‑enhanced scans were performed with iohexol at a concentration of 300 mg iodine/mL, administered at a dose of 1.5 mL/kg, with a total injection volume of 80–100 mL and an injection rate of 3.0 mL/s; this was followed by a 50-mL saline flush. The arterial and venous phases were obtained at 30 and 70 seconds postinjection, respectively. The window settings for the lung included a width of 1,000–1,500 HU and a level of −500 to −700 HU, while the mediastinal window settings included a width of 300–500 HU and a level of 30–50 HU. Noncontrast lung window and contrast‑enhanced mediastinal window images were reconstructed at a 1.25- or 2-mm thickness.

Image analysis

All CT images were assessed via the picture archiving and communication system (PACS). Two senior radiologists, with 10 to 15 years of experience in cardiothoracic imaging, respectively, jointly reviewed the images without prior knowledge of the pathological diagnosis. Discrepancies were resolved through discussion. The evaluated CT features included (I) lesion location, which was segmented by lung lobe; (II) size, which was measured as the long diameter and short diameter on the maximum cross-section [with the mean diameter calculated as follows: mean diameter = (long diameter + short diameter)/2]; (III) lesion type (classified as air-containing cysts, solid, or mixed); (IV) morphology (classified as round or irregular) and margins (assessed for the presence of spiculation and lobulation); (V) enhancement characteristics, which was measured as the contrast-enhanced value (ΔHU) of the parenchymal region and the same-level chest wall soft tissue on the venous phase and classified as mild (0–20 HU), moderate (21–40 HU), or severe (>40 HU); and (VI) associated findings, including emphysema, atelectasis, and pleural retraction. Circular regions of interest (ROIs) of 10 to 30 mm² in size were placed on the same axial pre- and postcontrast CT images. Each measurement was repeated three times and averaged. ROIs were carefully selected to cover significantly enhanced areas, with necrotic, calcified, and air-containing regions and adjacent anatomical structures being avoided.

Statistical analysis

Given the small sample size and exploratory nature of this study, inferential statistics were not conducted to prevent overinterpretation. Data were summarized with descriptive statistics. Continuous variables (e.g., lesion size and enhancement value) are reported as the mean ± standard deviation or as the median and range, as appropriate. Categorical variables (e.g., presence of lobulation and bronchial communication) are presented as frequencies. All analyses were performed with SPSS software version 26.0 (IBM Corp., Armonk, NY, USA).

Results

This study included six patients, two males and four females, with a median age of 59.5 years (range, 36–62 years). The baseline clinical characteristics of the patients are presented in Table 1. One patient had a history of recurrent cough during childhood. Imaging analysis indicated that the lesions were mainly situated in the right lower lobe (four cases), with an average diameter of 22.3±8.5 mm. Among these, three lesions were solid-cystic and communicated with the bronchi, whereas the other three were solid (including one with marginal calcification). The detailed imaging characteristics are presented in Table 2. Contrast-enhanced CT revealed mild homogeneous enhancement in three lesions (mean enhancement value in the venous phase of 18.7±3.2 HU phase), with the vessel penetration sign observed in all three contrast-enhanced lesions. Associated findings included atelectasis (three cases), emphysema (two cases), and pleural retraction (three cases). Postoperative pathology confirmed CPAM in all cases, without any coexisting malignancy. The mean length of hospital stay was 7.8±3.5 days, the mean duration of postoperative follow-up was 4.5±1.6 months, and no symptomatic recurrence or complications were observed.

Discussion

CPAM, first reported by Ch’in and Tang in 1949 (6), is a rare congenital pulmonary developmental anomaly constituting approximately 25% of congenital lung lesions (7). Its pathogenesis has not been extensively clarified but is generally characterized by abnormal proliferation and dilatation of the terminal bronchioles with impaired alveolar development, which ultimately leads to cystic and/or adenomatoid changes. Lesions typically affect a single lobe, more commonly one of the lower lobes, and this was observed in our case series. In adults, the incidence of CPAM is similar between males and females (approximately 56.4% and 43.6%, respectively), with a mean age of 38.3 years (8); the higher proportion of female patients in our series may be a result of the small sample size. Moreover, the older age at presentation in our cohort compared to averages in the literature (8) may be attributed to the delayed presentation in asymptomatic patients and a prolonged diagnostic process. Clinical manifestations vary based on lesion characteristics and may include productive cough, hemoptysis, pneumothorax, and chest pain (9,10). Approximately 12% of cases are linked to other systemic malformations, most commonly congenital heart disease or gastrointestinal tract anomalies (1). Malignant tumors such as mucinous bronchioloalveolar carcinoma and pleuropulmonary blastoma may also occur Mucinous adenocarcinoma is most commonly associated with type 1 CPAM, arising from malignant transformation of the cystlining epithelium and frequently harboring KRAS mutations (e.g., exon 2 G12V and G12D) (11). In contrast, stromal cells within type 4 CPAM may acquire a somatic Dicer 1 mutation and progress to pleuropulmonary blastoma type I (PPBI) (12). No cases in the present series were associated with other systemic malformations or concurrent tumors.

Analysis of diagnostic pitfalls

CPAM is classified according to the Stocker system (Table 3) (13), which indicates its developmental origins and pathology (2,13,14). Imaging manifestations fall into three patterns (2,15): (I) typical thin-walled cysts (Stocker type I—easy to diagnose; Case 3 had multiple cysts corresponding to dilated bronchi), (II) solid-cystic mass (Stocker type II—challenging when malignant signs such as lobulation/spiculation appear), and (III) solid soft tissue masses (Stocker type III—composed of microcysts <1 cm and resembling pancreatic serous microcystic adenomas) (16,17). The latter two types have higher misdiagnosis rates of up to 27.8% (18).

The misdiagnoses in this series illustrate the above-mentioned challenges and pitfalls. In Case 2 (Figure 1), an infected cystic lesion presented as a ground-glass nodule and was mistaken for adenocarcinoma, mainly because the cystic lucencies (dilated bronchi) were not distinguished from the “sieve-like” pattern of lepidic growth. In Case 3 (Figure 2), a new solid nodule arising from long-standing multicystic lesions was misinterpreted as a malignant transformation, but smooth inner walls and long cord‑like opacities suggested a benign condition. In Case 5 (Figure 3), a homogeneously enhancing solid mass mimicked peripheral lung cancer. Although type I lesions are typically cysts >2 cm, 39% may have small cysts (here ~9 mm) (19); however, significant interstitial fibrous proliferation may obscure cystic spaces on CT and appear as a solid mass. Associated bronchial obstruction, lobulation, and pleural involvement exacerbated the mimicry, but naturally coursing intralesional vessels and coarse marginal calcifications pointed to a benign process.

Figure 1 CPAM presenting as a mixed ground-glass nodule with sieve-like structures (white arrow) and interval changes. (A) Lung window CT (October 22, 2024) demonstrated a ground-glass nodule in the lateral basal segment of the right lower lobe, showing sieve-like structures (white arrow) and traversing vessels. (B) The corresponding mediastinal window depicts an indistinct lesion. (C) Follow-up CT (March 16, 2025) showed a slight increase in the density of the ground-glass component. (D) CT obtained on April 10, 2025, revealed decreased density of the ground-glass area and sieve-like structures communicating with the bronchi. (E,F) Histopathological images (hematoxylin and eosin staining at ×4 and ×20) revealed multilocular cystic lesions within the lung parenchyma, with cysts of varying sizes lined by single-layer ciliated columnar epithelium, accompanied by smooth muscle bundles and inflammatory cell infiltration. CPAM, congenital pulmonary airway malformation; CT, computed tomography.

Figure 2 CPAM with postinfectious organization mimicking tumor progression. (A) Lung window CT (December 22, 2015) showed a well-defined solid-cystic nodule in the lateral basal segment of the right lower lobe, containing internal gas and an air-fluid level, with associated distal obstructive emphysema. (B) The corresponding mediastinal window revealed homogeneous cystic density. (C) Follow-up CT (June 7, 2017) showed resolution of the air-fluid level and mild thickening of the dorsal cyst wall (white arrow). (D) CT (April 22, 2019) demonstrated partial resolution of the cystic component, leaving a residual long, thin-walled cavity communicating with the bronchus and exhibiting smooth margins. (E) CT (August 22, 2023) revealed a newly developed solid component along the dorsal aspect of the cavity, with lobulation, spiculation, and pleural retraction. (F) The corresponding mediastinal window showed focal soft tissue density and a small right pleural effusion. (G,H) Histopathological images (hematoxylin and eosin staining at ×4 and ×20) showed multiple cystic structures lined by pseudostratified ciliated columnar epithelium. The cyst walls contained smooth muscle bundles and vascular structures, with retained secretions in some cavities and extensive chronic inflammatory fibrous proliferation in the surrounding parenchyma. CPAM, congenital pulmonary airway malformation; CT, computed tomography.

Figure 3 Completely solid CPAM mimicking peripheral lung cancer. (A) Lung window CT showed a solid nodule in the anterior segment of the left upper lobe, with bronchial cutoff, clear margins, shallow lobulation, and spiculation. (B) Noncontrast mediastinal window demonstrated a homogeneous soft tissue lesion (approximately 18.6 HU) with coarse marginal calcification. (C,D) Contrast-enhanced mediastinal window CT showed mild homogeneous enhancement (approximately 35.8 HU), internal traversing vessels, and prominently enhanced distal atelectatic lung tissue. (E,F) Histopathological images (hematoxylin and eosin staining at ×4 and ×20) revealed multiple cystic structures lined by pseudostratified ciliated columnar epithelium, surrounded by extensive interstitial fibrous tissue proliferation. CPAM, congenital pulmonary airway malformation; CT, computed tomography; HU, Hounsfield unit.

Identifying key benign clues on imaging

Improving the diagnostic accuracy of adult CPAM requires the recognition of three commonly overlooked benign clues, and appropriate measures should be taken in this regard. First, the cystic nature of the lesions should be carefully evaluated. For lesions that appear solid or solid-cystic on imaging, thin-section CT should be reviewed to identify thin-walled septa, microcysts, or the air-bubble sign, and multiplanar reconstruction may help demonstrate communication between cystic spaces and bronchi, a feature observed in 50% (3/6) of the cases in our series. In the other three cases, no communication with the bronchus was observed. The pathological subtypes were types I and II. CT findings showed solid masses with bronchial occlusion and distal atelectasis (in one case, the mass appeared tubular and distributed along the bronchial course). According to the literature, bronchial occlusion occurs in 18% of type I and 70% of type II cases (20). Second, attention should be directed toward benign biological behavior, including the assessment of long-term stability on prior imaging (1/6) and the evaluation of density changes that parallel episodes of infection with subsequent resolution after anti-inflammatory treatment (1/6), which suggests an inflammatory process rather than tumor progression. Third, the clinical and imaging findings should be interpreted in an integrated manner. In relatively young patients (median age 59.5 years in our study, with the youngest being 36 years), particularly those who are asymptomatic (5/6) and nonsmokers (5/6), CPAM should be considered, especially when accompanied by coarse marginal calcification (1/6), mild homogeneous enhancement (3/6), or the absence of typical malignant features. In our study, we conducted a systematic retrospective analysis of this diagnostic challenge and generated preliminary evidence to support the development of a more reliable imaging-based diagnostic framework for CPAM.

A pathophysiology-based differential diagnostic framework

In the differentiation between CPAM and diseases such as lung cancer, lung abscesses, and pulmonary sequestration (Table 4), systematically deconstructing imaging manifestations based on their pathophysiology is critical. To distinguish CPAM from lung cancer, one must consider more than just morphological similarities such as bronchial obstruction, marginal lobulation, spiculation, and pleural retraction (21). CPAM cysts are developmental anomalies connected to the bronchial tree (1), while cystic components in lung cancer usually arise from tumor necrosis or lepidic growth. This distinction implies that CPAM cyst walls are typically smoother, lack progressive infiltrative growth, and do not exhibit lymph node metastases, which are hallmarks of lung cancer. Positron emission tomography/computed tomography (PET/CT) may aid in diagnosis when necessary. Although high fluorodeoxyglucose (FDG) uptake may also occur in infected or organized CPAM, PET/CT still has clinical value in differentiating CPAM from lung cancer by facilitating the assessment of lymphadenopathy and distant metastasis. Distinguishing CPAM from lung abscesses involves the evaluation of the disease phase. The thick-walled cavity, air-fluid level, and surrounding exudative changes of the lung abscess are common signs of acute suppurative inflammation (22), which can overlap with infected CPAM. However, lung abscesses present with distinct acute infectious symptoms, significantly elevated levels of inflammatory markers, and a transient clinical course. The differentiation from pulmonary sequestration is centered on the critical issue of blood supply. Pulmonary sequestration receives blood supply from anomalous systemic arteries (1). On contrast-enhanced CT or CT angiography, identification of feeding vessels arising from the aorta is diagnostic, whereas CPAM is typically supplied by the pulmonary arteries. In summary, the value of this study extends beyond providing a list of features and further offers a pathophysiology-based framework for differential diagnosis. When atypical solid pulmonary cystic lesions are encountered, their structural origin (developmental vs. neoplastic), temporal characteristics (acute vs. chronic), and blood supply patterns (systemic vs. pulmonary circulation) should be sequentially assessed in order to fit imaging features into a logical chain of diagnostic evidence.

Clinical management, treatment, and prognosis

No standardized guidelines exist for adult CPAM, and thus the comparative benefit between surveillance and early surgery remains controversial (23), with lobectomy remaining the primary form of treatment (8). Meta‑analyses indicate that infection is the most frequent complication of CPAM (74.9%), with pneumonia representing 31.1% of cases While the overall mortality is low (2.4%), most deaths are associated with these complications (8). Surgical indications include symptoms, recurrent infection, diagnostic uncertainty, or suspected malignancy (24). In the meta-analysis, among adult patients with CPAM, the prevalence of concurrent lung tumors was 25.6%; type 1 CPAM accounted for 94.5% of such tumors, with adenocarcinoma being the leading histologic type (72.7%) (8). These findings, demonstrating a non‑negligible prevalence of concurrent lung tumors, lend further support to a more proactive, earlyintervention strategy (25,26). No tumors were found in our series, likely due to the small sample size. Attaining favorable outcomes for patients with CPAM depends on timely treatment. For atypical cases, multidisciplinary discussion and biopsy are advised, and histopathology remains the diagnostic gold standard.

Limitations

This study involved several limitations that should be acknowledged. First, the sample size was small, and not all CPAM subtypes were included, thus limiting the generalizability of the findings. Further validation in larger cohorts is required. Second, the retrospective design with nonuniform imaging protocols across centers might have introduced selection bias and image variability. Third, the absence of a control group with other cystic lesions weakened the discriminative power of the imaging features. Fourth, patients with coexisting malignancies were excluded. Fifth, the visual assessment by radiologists entails subjectivity. Finally, incomplete visualization of the lesion-bronchus connection due to sectioning limitations restricted the pathological correlation. Future multicenter radiomics studies may help establish more objective diagnostic models.

Conclusions

The results of this study indicate that adult CPAM presenting as solid or solid–cystic masses closely mimics lung cancer, posing a high risk of misdiagnosis. To reduce errors, radiologists should apply a pathophysiology‑based framework consisting of the following practices: (I) searching of thin‑section CT images for internal cysts or bronchial communication, (II) comparison with previous imaging to ensure long‑term stability without evidence of progression, and (III) the integration of clinical context (age, symptoms, and smoking history). For cases that remain a diagnostic dilemma after thorough assessment, multidisciplinary discussion or CT‑guided biopsy is advised for histological confirmation and individualized management in order to avoid the unnecessary treatment of benign lesions.

Acknowledgments

None.

Footnote

Funding: This study was supported by the Zhejiang Traditional Chinese Medicine Administration (No. 2025ZL020 to J.W.).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2026-0540/coif). J.W. reports receiving funding from the Zhejiang Traditional Chinese Medicine Administration (grant No. 2025ZL020 to J.W.) through his affiliated institution, Tongde Hospital of Zhejiang Province Affiliated to Zhejiang Chinese Medical University. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of Sir Run Run Shaw Hospital, Zhejiang University School of Medicine (approval No. 2026-2076-01), which covered both participating centers. The requirement for informed consent was waived due to the retrospective nature of the study.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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