The "Galaxy Sign" on Screening LDCT: A 60mm Cluster That Wasn't Cancer

A 69-year-old man was referred to the respiratory multidisciplinary team following identification of a branching pulmonary nodule on a low-dose CT scan undertaken as part of a lung cancer screening program. He was an ex-smoker with a history of exertional breathlessness and an occasional productive cough, without hemoptysis, fever, or weight loss. He worked as a taxi driver with no known occupational exposures or recent travel abroad. His demographics — an older male ex-smoker with a pulmonary mass — placed him squarely in the high-risk zone for primary lung cancer.

Figure 1

LDCT: 60mm LUL cluster with central 20mm dense focus — the "galaxy sign"

Low-dose CT demonstrating a 60 mm cluster of prominent, dense nodules with a central 20 mm confluent solid focus in the left upper lobe. The pattern — a dense central opacity surrounded by smaller satellite nodules whose density decreases toward the periphery, resembling a galaxy of stars — is the "galaxy sign," first described by Nakatsu et al. in 2002 in sarcoidosis. In a lung cancer screening context, this size (60mm) and solid component trigger LungRADS 4 classification and immediate concern for malignancy.

The screening CT pattern was immediately referred for FDG PET-CT, which demonstrated heterogeneous uptake with a relatively low SUVmax of 3.1 within the pulmonary lesion. More tellingly, there were multiple prominent, slightly enlarged bilateral hilar and mediastinal lymph nodes demonstrating symmetrical, markedly increased FDG uptake with SUVmax of 12.5 — far exceeding the metabolic activity of the primary lesion itself. No destructive or FDG-avid osseous lesions were identified.

Figure 2

PET-CT: mild uptake (SUVmax 3.1) in the LUL lesion — disproportionately low

FDG PET-CT demonstrating heterogeneous, mild uptake within the 60 mm left upper lobe lesion (SUVmax 3.1). This is the key metabolic clue: a 60 mm solid-appearing lung mass in a smoker with SUVmax 3.1 is metabolically atypical for primary lung cancer (which typically shows SUVmax >5–7 at this size). The disproportionate mismatch between lesion size and metabolic activity, combined with the galaxy sign morphology, should prompt granulomatous disease at the top of the differential.

Figure 3

PET-CT: bilateral hilar lymphadenopathy with SUVmax 12.5 — sarcoidosis pattern

FDG PET-CT demonstrating symmetrically enlarged bilateral hilar lymph nodes with markedly increased uptake (SUVmax 12.5) — dramatically exceeding the SUVmax of the primary pulmonary lesion (3.1). This pattern — symmetrical bilateral hilar FDG avidity greater than the pulmonary lesion — is characteristic of sarcoidosis. In primary lung cancer with nodal spread, the nodal uptake is typically asymmetric and correlates with or exceeds the primary lesion's SUV. Symmetric bilateral hilar hypermetabolism with a metabolically quiet lung lesion should trigger the sarcoidosis differential.

Figure 4

PET-CT: mediastinal lymphadenopathy with high FDG uptake

FDG PET-CT demonstrating enlarged mediastinal lymph nodes with markedly increased FDG uptake. The mediastinal nodal involvement in combination with bilateral hilar disease creates the classic "lambda sign" of sarcoidosis — a lambda-shaped distribution of hilar and mediastinal lymphadenopathy visible on PET imaging. This constellation — galaxy sign on CT, low primary lesion SUV, high symmetric nodal SUV — built a compelling case for sarcoidosis before any tissue was taken.

Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) of a mediastinal lymph node was performed. Histopathology demonstrated reactive sinus histiocytosis and anthracosis with prominent fibrosis, along with scattered epithelioid histiocytes at the periphery of fibrotic-appearing areas. No acid-fast bacilli, fungal organisms, or amyloid were identified on special stains. Bronchoalveolar lavage cultures were negative for bacterial, fungal, and acid-fast organisms. The findings were interpreted as possibly representing burnt-out granulomatous inflammation — consistent with advanced, fibrotic-phase sarcoidosis — without evidence of malignancy.

Figure 5

EBUS-TBNA histopathology: fibrosis and anthracosis — burnt-out granulomatous inflammation

Photomicrograph of the mediastinal lymph node demonstrating reactive sinus histiocytosis, anthracosis (carbon pigment deposition from air pollution or tobacco exposure), and prominent fibrosis with scattered epithelioid histiocytes at the fibrotic periphery. The absence of necrotizing granulomas, viable granulomata, acid-fast bacilli, or malignant cells, combined with the imaging constellation, supported a diagnosis of pulmonary sarcoidosis in its fibrotic (burnt-out) phase. The patient was reenrolled into the screening program with planned CT surveillance rather than surgical intervention.

Correlation of the imaging studies and histology led the multidisciplinary team to diagnose pulmonary sarcoidosis. A repeat low-dose CT was planned and the patient was reenrolled into the screening program — avoiding thoracic surgery, mediastinoscopy, or systemic treatment for a cancer that did not exist.

Discussion

The galaxy sign is a clinically important pattern to recognize in lung cancer screening populations precisely because it is uncommon enough to be unfamiliar yet distinct enough — when seen — to redirect away from a malignancy workup. First described by Nakatsu et al. in 2002, the galaxy sign represents coalescent interstitial granulomas in the lung parenchyma: a central dense confluent opacity with multiple smaller satellite nodules at its periphery whose density decreases toward the edge, resembling a galaxy of stars. The radiological pitfall in lung cancer screening is that the satellite nodules can appear fused and be misinterpreted as spiculated margins — the hallmark radiological feature of primary lung adenocarcinoma. Recognition that the "spiculation" is actually satellite nodules, not tumor infiltration, is the critical distinction.

The PET pattern in this case is the second teachable point. Primary lung cancers of 60mm typically generate SUVmax values well above 5; values below 3.5 at this size should trigger a benign or granulomatous differential. Moreover, the pattern of symmetric bilateral hilar hypermetabolism with SUVmax far exceeding the primary lesion (12.5 vs. 3.1) is virtually pathognomonic for sarcoidosis. In metastatic lung cancer with nodal spread, nodal SUVmax typically correlates with or is exceeded by the primary tumor. The inverse relationship here — quiet primary, hot nodes — argues strongly against malignancy even before tissue sampling. EBUS-TBNA confirmed burnt-out granulomatous inflammation, and the patient avoided an operation that would have been unnecessary and potentially morbid given his age and comorbidities.