Expert consensus on imaging diagnosis of human infection with avian influenza

Introduction

Certain subtypes of the avian influenza virus (AIV) are responsible for the acute respiratory infectious illness known as human infection with avian influenza (HIAI) (1,2). AIV has a segmented single-stranded negative-sense RNA genome and is a member of the genus Influenzavirus A, which is a member of the Orthomyxoviridae family. Type A AIVs are divided into 18 H subtypes (H1–18) and 11 N subtypes (N1–11) according to antigenic variations in the envelope glycoproteins hemagglutinin (HA) and neuraminidase (NA) (3-5). Although humans are not usually infected by AIV, certain subtypes may be able to breach the species barrier under particular situations (6). Prior to the recent emergence of human cases including H7N4, H9N2, H10N8, and H10N3 subtypes (7-13), human infections were primarily caused by H5N1, H5N6, and H7N9 subtypes (14-16).

Standardized diagnostic and treatment procedures are required due to ongoing viral alterations and genomic reassortment, as well as the lack of community immunity against the majority of AIV subtypes. The Chinese Research Hospital Association’s Committee of Infectious and Inflammatory Radiology led a multidisciplinary consensus effort to create evidence-based imaging guidelines for HIAI therapy. This expert consensus was created cooperatively by more than 40 specialists using rigorous methodological frameworks that agreed with the ideals of evidence-based medicine.

Epidemiology

Although the precise cause of HIAI infection is still unknown, sick or dead poultry, poultry that are infected with AIVs, and animals, including pigs and cattle, that are infected with AIV are the main sources of HIAI infection. Potential sources may also include infected humans and animals. The major ways that the disease is spread are through intimate contact with infected birds and inhaling droplets or aerosols carrying AIV particles. There is currently no evidence that humans are particularly vulnerable to AIV; just a few people have contracted the virus and shown symptoms, primarily those who work in chicken farming, transportation, processing, or commerce (1,17). The main viruses responsible for HIAI in the past have been H5N1, H5N6, and H7N9 subtypes, with H5N6 having a higher case fatality rate.

According to World Health Organization (WHO) data (18), there were 969 documented human cases of H5N1 worldwide between January 1, 2003 and March 19, 2025, with 467 fatalities (a case fatality rate of 48.2%). There have been 93 laboratory-confirmed cases of H5N6 in the Western Pacific Region since 2014, resulting in 57 fatalities (61.3% fatality rate). Notably, on June 17, 2024, a case of H5N6 was detected in China’s Anhui Province. WHO has recorded 1,568 human cases of H7N9 since 2013, including 616 fatalities (39.3% fatality rate). In 2019, a case was discovered in the Western Pacific Region.

Other AIV subtype infections have been documented in recent years. The first human case of H5N2 was confirmed in Mexico in April 2024 in a patient who was 58 years old (19). Similarly, during the same period, Vietnam reported the country’s first H9N2 case in a 37-year-old man (20). In 2021, China reported 25 H9N2 cases; Tan et al. (21) detailed the clinical facts. Furthermore, 13 H5 infections were documented in the US in 2024, mostly among farm workers who had come into contact with poultry (22). There have been four cases of H10N3 reported worldwide to date, with the first being in China in 2021 (11-13).

Clinical manifestations

Although rare cases may persist for more than 12 days, the incubation period for HIAI normally lasts between 1 and 7 days. The subtype of AIV infection affects the clinical manifestations. The majority of HIAI cases begin with symptoms like fever and cough that resemble the common cold. Rhinorrhea, sore throat, headache, muscle pains, abdominal pain, diarrhea, nasal congestion, and general malaise may accompany these (5,23). Some instances can spread quickly and have a significant negative effect on the human body, particularly those brought on by subtypes like H5N1, H5N6, H7N9, and H10N8. Severe pneumonia can swiftly progress to acute respiratory distress syndrome (ARDS) in certain patients. The prognosis is affected by age and comorbidities, and patients with underlying medical disorders may eventually die from respiratory failure (24,25). Due to the pulmonary tropism of AIV, HIAI can cause respiratory symptoms as well as conjunctivitis, rhabdomyolysis, empyema, enteritis, myelitis, and encephalopathy (16,26-30).

Laboratory examinations

While total white blood cell counts are usually normal or slightly lower after HIAI, most patients have decreased lymphocyte counts in their blood tests. C-reactive protein levels are typically higher and platelet counts are frequently lower (25). Sputum, tracheal aspirates, bronchoalveolar lavage fluid, nasopharyngeal swabs, throat swabs, and other pertinent samples are examples of respiratory specimens that should be gathered in compliance with the Centers for Disease Control and Prevention’s collection guidelines. Real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR) is used to detect the virus. AIV isolation, positive AIV nucleic acid detection, or a fourfold or higher increase in avian influenza-specific antibody titers in paired serum samples can all be used to confirm a definitive diagnosis of HIAI (31). To guarantee precision and promptness, HIAI diagnosis must be performed by specialist medical facilities and disease control divisions.

Pathogenesis and pathological changes

The respiratory system is the main way that AIV is spread. Through endocytosis, the virus reaches the type II alveolar epithelial cells and the mucosa of the lower respiratory tract, where it replicates and transcribes into the cell nucleus. About 48 hours after infection, viral replication peaks and then progressively decreases, with a few epithelial cells shedding 6–8 days later (32). The virus usually affects the trachea and the epithelial cells of the upper respiratory tract in mild cases. In extreme situations, the virus damages the lower respiratory tract’s epithelial cells. By releasing cytokines and chemokines, infected epithelial cells draw in inflammatory cells like neutrophils and macrophages and stimulate neighboring endothelial cells. Additional inflammatory cytokines, including interleukin-6, interleukin-1β, tumor necrosis factor-α, and chemokine ligand 2, are produced by these activated immune and non-immune cells. These cytokines further stimulate the inflammatory response, disrupt the epithelial-endothelial barrier, and increase the death of epithelial cells. ARDS, shock, encephalopathy, and multiple organ dysfunction are among the conditions that can result from AIV subtypes that can infect a wider range of tissues, such as the H5N1 subtype. These subtypes can cause severe inflammatory responses in multiple organs and high viral titers, which can cause extensive tissue and organ damage (32-34).

Type II alveolar epithelial cells are the target cells for AIV infection. Numerous dispersed hemorrhagic foci, atelectasis, pulmonary hyaline membrane development, necrosis of the bronchial mucosa, lymphocytic infiltration in the alveoli, and significant destruction to the alveolar epithelial tissue are all seen in the lungs during the acute phase of HIAI pneumonia. Proliferation of fibrous tissue takes place in the advanced stages of the illness (1,32,33).

Imaging diagnostic and imaging examination techniques

The Center for Evidence-Based Medicine at the University of Oxford (OCEBM) evidence grading criteria and the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) evidence recommendation strength criteria (35) served as the foundation for the development of the consensus’s standards for evidence quality grading and recommendation strength (Table 1).

Imaging examination techniques

A vital component of HIAI diagnosis and treatment, chest imaging tests are essential for both early HIAI detection and treatment efficacy monitoring. Computed tomography (CT) scans, chest X-rays, and ultrasounds are all forms of chest imaging exams; CT scans are the most commonly used type of examination.

Chest CT scan

High-resolution CT (HRCT) is the recommended option for chest CT scanning, which is the main imaging modality for diagnosing HIAI (see Figure 1 for the process for chest CT imaging). The thoracic inlet to the posterior costophrenic angle is the scanning range. The scanning parameters are as follows: pitch ≤1, automated tube current, tube voltage 120 kV, slice thickness 5.0 mm, slice spacing 1 mm, and reconstruction slice thickness of roughly 0.6 to 1.5 mm using a standard algorithm. Lung and mediastinal windows are used to see the images; the lung window level is set at −500 to −600 Hounsfield units (HU), and the window width is set at 1,500 to 1,700 HU. The mediastinal window level is set at 30 to 50 HU, and the window width is set at 250 to 350 HU. With a window level of 300 to 600 HU and a window width of 2,000 to 3,000 HU, bone window rebuilding is carried out as required. Volume-based CT multiple plane reconstruction (MPR), a technique used in image post-processing, makes it easier to observe lesions, detect them early, and evaluate their type and extent.

Figure 1 Chest CT imaging flow chart for HIAI patients. CT, computed tomography; HIAI, human infection with avian influenza.

Recommendation 1: high-resolution CT scanning is the preferred imaging method for assessing pulmonary lesions in HIAI patients. (Strong recommendation, evidence grades: level IV.)

Chest X-ray examination

Chest X-ray examination can serve as an initial screening tool for HIAI. However, it has a high rate of missed diagnoses for pulmonary lesions, often failing to detect abnormalities in the early stages of the disease. Additionally, it cannot accurately evaluate the status of hilar and mediastinal lymph nodes.

Recommendation 2: chest X-rays can be used as a screening method for HIAI. (Weak recommendation, evidence grades: level IV.)

Chest ultrasound examination

Chest ultrasound examination is a portable, non-invasive examination method that can be used as a supplement to the assessment of intrathoracic lesions when necessary. It can reveal abnormal ultrasound findings in the patient’s chest, including pulmonary consolidation, pleural effusion, or lymph node enlargement (36-38).

HIAI imaging diagnosis

Similar to other forms of influenza, the majority of HIAI patients exhibit symptoms of an upper respiratory tract infection rather than a pulmonary illness, and imaging tests may reveal no abnormalities. Nevertheless, certain strains of AIV cause viral pneumonia by invading the epithelium of the lower respiratory tract, which manifests as aberrant chest imaging results.

Lesions’ distribution in HIAI pneumonia

Patients with HIAI pneumonia typically have lesions in the lower lobes of both lungs, which then quickly extend to the upper lobes of both lungs (39,40). Because of the pulmonary bronchi’s architectural nature and the virus’s free spread through the bronchi and alveoli, lesions can spread between lung segments and lobes, across interlobar fissures to affect neighboring lungs (41). Severe pneumonia can result when lesions affect both lungs’ lobes, making up more than 50% of the lung volume (23). Recent advances in artificial intelligence (AI)-assisted imaging diagnosis (42) have made it possible to screen for pulmonary lesions, determine the volume and proportion of lesions within lung lobes, and, most importantly, use deep learning (DL) to automatically extract implicit disease diagnostic features from large-scale medical image datasets. The main research trends going forward will be identifying the pathogens causing pneumonia, evaluating treatment responses, and assessing prognosis (43). AI diagnosis minimizes the diagnostic burden on radiologists, guarantees good reproducibility, and can increase the clinical diagnostic sensitivity and accuracy of viral pneumonia. It also has a wide range of possible applications.

Recommendation 3: lung lesions in the early stages of HIAI are primarily found in the lower lobes of both lungs and progress rapidly. (Strong recommendation, evidence grades: level IV.)

Imaging characteristics of HIAI pneumonia lesions

HIAI pulmonary lesions exhibit a highly variable nature, with alternating phases of absorption and progression (44), typically manifesting as ground glass opacity (GGO) and consolidation opacity (Figures 2-5), which often coexist. GGO appears in the early stages of the disease, located at the periphery of the lesion, followed by an expansion of the lesion’s extent and increases in density, and progresses to consolidation opacity (1,9,11,39,41,45-48). The pulmonary parenchyma and interstitium are both concurrently involved in GGO, which is characterized by partial collapse of the alveolar gaps, exudation, and edema of the surrounding pulmonary interstitium (49); consolidation opacity is characterized by complete obscuring of pulmonary vascular patterns by lesion density, distributed along bronchial patterns, with pneumonitis bronchial patterns visible between them, and if the lesion involves the entire lung, it presents as a white lung-like change (16,50). The lesion’s appearance is generally tiny, spotty, or mottled, and common findings include thicker bronchial walls within the consolidation opacity and the air bronchogram sign. Additionally, there have been a few isolated instances of H7N9 avian influenza patients in which GGO symptoms were not visible on chest CT scans (51).

Figure 2 Patient, male, 43 years old, presented with fever, cough, sputum production, chest tightness, and shortness of breath for 5 days. Diagnosed with human infection with H5N6 avian influenza, the patient underwent chest CT examination upon admission. (A,B) The same level of lung window and mediastinal window, with multiple areas of consolidation opacity (black arrow) and GGO (white arrow) in all lobes of both lungs. The right lung shows more significant lesions with blurred margins and evidence of air bronchogram signs. (C,D) Reconstructed coronal and sagittal views, providing multi-angle and multi-directional observation of the lesions. The right lung shows extensive consolidation opacity (black arrow), while the left lung demonstrates linear consolidation and GGO (white arrow). CT, computed tomography; GGO, ground glass opacity.

Figure 3 Patient, male, 63 years old, presented with fever, cough, sputum production, and chest tightness for 4 days. Diagnosed with human infection with H7N9 avian influenza, the patient underwent chest CT examination upon admission. (A,B) The same level of lung window and mediastinal window, revealing multiple lesions in both lungs, presenting as consolidation opacity (black arrow) and GGO (white arrow). Within the consolidation opacity, air bronchogram signs are observed, with blurred edges. The mediastinal view shows a large area of consolidation opacity in the right lower lung (black arrow) and small areas of consolidation opacity in the left lower lung, with localized thickening of the pleura. (C,D) Reconstructed coronal and sagittal views showing multiple angles of pulmonary consolidation opacity, with multiple lesions in the right lung, scattered lesions in the left lung, and lesions predominantly distributed on the dorsal side (black arrow). CT, computed tomography; GGO, ground glass opacity.

Figure 4 Patient, male, 51 years old, admitted to the hospital with fever, cough, sputum production, chest tightness, and shortness of breath for 5 days. Diagnosed with human infection with H10N3 avian influenza. Chest CT scan performed after admission. (A,B) Lung window and mediastinal window at the same level, showing consolidation opacity (black arrow) and GGO (white arrow) in all lobes of both lungs, with blurred edges and air bronchogram signs within the lesions. (C) Coronal lung window, showing consolidation opacity (black arrow) and GGOs (white arrow) with a multifocal distribution pattern. CT, computed tomography; GGO, ground glass opacity.

Figure 5 Patient, female, 68 years old, poultry farmer, fever for 8 days, accompanied by chills, slight cough, impaired consciousness, and incontinence. Diagnosed with human infection with H7N4 avian influenza. After admission, a chest CT scan was performed. (A-C) Transverse sections at different levels (lung window): multiple large areas of GGO (white arrows) and consolidation opacity (black arrows) in all lobes of both lungs; scattered patchy GGO (white arrows) in the upper and middle lobes of the right lung and the upper lobe of the left lung. CT, computed tomography; GGO, ground glass opacity.

Recommendation 4: in patients with HIAI, consolidation opacity and GGO are common radiographic signs of pulmonary lesions. (Strong recommendation, evidence grades: level IV).

Treatment outcomes of HIAI pneumonia

The development of pulmonary lesions occurs quickly in patients with HIAI pneumonia, and the absorption of these lesions frequently lags behind the recovery of clinical symptoms and negative viral nucleic acid test results. Four stages—onset, progression, absorption, and stabilization—have been proposed by some researchers to describe the pulmonary lesions of patients with HIAI pneumonia (50,52). Lesions predominantly defined by consolidation may continue to advance following therapy, whereas pulmonary lesions largely characterized by GGOs exhibit considerable absorption after three days (44). Bacterial infections are frequent during HIAI pneumonia and may play a significant role in the mortality and exacerbation of the illness (23,53). Pulmonary lesions may eventually resolve completely or leave residual linear shadows, reticular shadows, subpleural lines, pulmonary emphysema, or pulmonary bullae. Some lesions may progress to interstitial lung diseases such as pulmonary interstitial fibrosis (52) (Figure 6).

Figure 6 Patient, female, 59 years old, presented with fever, cough, and dyspnea for 3 days. Diagnosed with human infection with H7N9 avian influenza. Chest CT scans at different time points after admission (same anatomical location). (A) Chest CT scan on day 5 post-onset, showing extensive patchy consolidation opacity (black arrows) and partial GGO (white arrow) in both lungs. (B) Chest CT scan on day 7 post-onset showing partial GGO (white arrow). (C) Chest CT scan on day 13 after onset. (D) Chest CT scan on day 16 after onset. (E) Chest CT scan on day 23 after onset, showing gradual resolution and improvement of pulmonary lesions. CT, computed tomography; GGO, ground glass opacity.

Recommendation 5: in patients with HIAI, chest CT can be utilized to evaluate therapy results and dynamic changes in lung lesions. (Strong recommendation, evidence grades: level IV).

Mediastinal and pleural changes in HIAI

A comparatively small proportion of patients with HIAI may have pleural lesions at presentation, which might show up on CT imaging as pleural cavity effusion, lobular septal thickening, or subpleural lines. Ultrasound imaging can be used to evaluate pleural effusion, which might present unilaterally or bilaterally, to minimize radiation exposure and help some patients who have mobility issues (38,45,54). These days, certain HIAI patients have also been found to have a greater incidence of pleural effusion, which is thought to be connected to the development of severe pneumonia in these patients (45,55). Some patients with HIAI may develop spontaneous pneumothorax, or pneumothorax, mediastinal emphysema, and subcutaneous emphysema as a result of mechanical ventilation during the course of treatment (40) (Figure 7).

Figure 7 Patient, male, 39 years old, with low-grade fever and cough for 5 days, diagnosed with human infection with H7N9 avian influenza. Chest CT cross-sectional images at different time points after admission (same anatomical location). (A) On the 6th day after onset, small amounts of air accumulation (white arrow) were observed in the mediastinum, left-sided pneumothorax, and small amounts of air accumulation (black arrow) in the subcutaneous soft tissue of the left chest wall. (B) On the 8th day after onset, the lesions improved compared to the previous day. (C) On the 11th day after onset, mediastinal emphysema and left-sided pneumothorax gradually resolved. CT, computed tomography.

Recommendation 6: in patients with HIAI, ultrasound examination can evaluate subcutaneous emphysema, pneumothorax, and pleural effusion. (Weak recommendation, evidence grades: level IV).

Special populations HIAI

A 25-year-old pregnant lady with a H7N9 AIV infection was successfully treated in China in 2013. The imaging features and clinical presentation of the patient were comparable to those of patients in the general community (56). Although pediatric patients with HIAI exhibit similar clinical symptoms and imaging signs to adult patients, children are slightly more likely than adults to develop influenza-associated encephalitis and encephalopathy (IAE) (27,57). In 2003, a case of human immunodeficiency virus (HIV) infection combined with human infection with the H7N2 AIV was reported. The patient had bilateral lung nodules, right hilar consolidation, and enlarged lymph nodes on chest CT, and CD4⁺ T lymphocytes were 300 cells/µL (58). A case of multiple myeloma and human H3N8 avian influenza was documented in 2024. The CT scan revealed consolidation in the left lower lung lobe, which progressed to multiple consolidations in both lungs and minor pleural effusion on both sides before the patient died from a severe infection (59).

Differential diagnosis

In terms of radiological findings and clinical symptoms, HIAI pneumonia is quite comparable to other forms of pneumonia. Multiple pathogen co-infection occurs in certain situations, and pathogen and serological test findings are used to make the diagnosis (60-62).

Mycoplasma pneumoniae pneumonia (MPP)

MPP is more frequently observed in children, with diverse radiological features of the lesions, and the progression of the disease is not as rapid as that of HIAI pneumonia. Typical radiographic signs of MPP in children include thickening of the bronchial walls, tree-in-bud sign, tree-in-haze sign (Figure 8), and widespread pulmonary consolidation (Figure 9). The existence of bronchiectasis should be taken into consideration when pulmonary radiological abnormalities in patients with MPP include pleural effusion, atelectasis, pulmonary consolidation, and alveolar nodules (63,64).

Figure 8 Pediatric patient, male, 6 years old, presented with fever and paroxysmal cough for 3 days and was diagnosed with mycoplasma pneumonia. Chest CT scan was performed on the third day after admission. A and B show thickening of the bronchial wall and narrowing of the lumen (black arrow) in the upper lobe of the left lung, with multiple small patchy shadows scattered around the bronchi, with blurred edges, showing a “tree-in-haze sign” (white arrow). CT, computed tomography.

Figure 9 Pediatric patient, male, 10 years old, with fever and cough for 3 days, diagnosed with mycoplasma pneumoniae pneumonia, chest CT after onset of admission. At the same level (lung and mediastinal windows) in (A,B), 4 days after the disease started, a massive lamellar solid shadow (black arrows) and mostly clogged bronchial tubes were visible in the right middle lobe of the lungs (white arrows). (C) After 40 days of treatment, the patient's second chest CT scan (at the same level as the lung windows) revealed that the lesion in the right middle lobe of the lungs had mostly absorbed. CT, computed tomography.

Coronavirus disease 2019 (COVID-19)

The virus tends to spread freely in the lungs due to the tiny size of coronavirus particles, which are measured in nanometers. This is demonstrated by the numerous dispersed or diffusely distributed GGOs and solid shadows with blurred edges in both lungs, as well as the quick development of lung lesions that primarily affected the lower lobes of both lungs and the peripheral subpleural region. Interlobular septa thickening, vascular wall thickening, and halo indications were observed on chest HRCT; some of these changes were described as “paving stone-like” (65-67) (Figure 10). Individuals with HIAI pneumonia are more likely to have pleural effusions, enlarged hilar mediastinal lymph nodes, and multifocal solid shadows, whereas individuals with COVID-19 have a comparatively high prevalence of “paving stone-like” symptoms (67,68).

Figure 10 Patient, female, 64 years old, with fever and cough for 7 days, diagnosed with COVID-19, chest CT on the 8th day after admission. (A) Transverse and (B) coronal views, scattered multiple GGOs in both lungs (white arrows), with blurred margins, and thickened interlobular septa in the upper lobe of the right lung, with “paving-stone-like” changes (white arrows). COVID-19, coronavirus disease 2019; CT, computed tomography; GGO, ground glass opacity.

Adenovirus pneumonia (AP)

AP is a pneumonia caused by adenovirus (ADV) infection and is one of the more severe types of community-acquired pneumonia in children, with a rapid onset, often with high fever at the beginning of the illness, which may be accompanied by cough and wheezing. AP is characterized by pulmonary emphysema and solid lungs with multilobar involvement as the main imaging features (69,70) (Figure 11).

Figure 11 Pediatric patient, male, 4 years old, coughing for half a month with fever for 8 days, diagnosed with AP, chest CT on the 8th day after the onset of admission. (A-C) Scattered multiple solid shadows (white arrows) are seen in both lungs, with blurred margins, and signs of pneumatic bronchioles are seen within them; the walls of the multiple bronchioles in both lungs are thickened. AP, adenovirus pneumonia; CT, computed tomography.

Respiratory syncytial virus pneumonia (RSVP)

RSVP is caused by respiratory syncytial virus (RSV) infection, which is one of the important viral pathogens causing acute lower respiratory tract infections in children under 5 years of age, the elderly, and immunocompromised populations, and the imaging features of RSVP are multifocal GGOs in pulmonary segments or subpulmonary segments, and solid shadows are relatively rare (71) (Figure 12).

Figure 12 Pediatric patient, female, 6 years old, with cough and fever for 2 days, diagnosed with RSVP, chest CT on the 2nd day after onset of admission. Transverse (A) and reconstructed coronal (B) lung windows with multiple scattered focal GGOs (white arrows) in both lungs with blurred margins. CT, computed tomography; GGO, ground glass opacity; RSVP, respiratory syncytial virus pneumonia.

Recommendation 7: HIAI pneumonia needs to be differentiated from other pathogenic pneumonias, such as Mycoplasma pneumoniae, COVID-19, etc. Confirmation of the diagnosis depends on the results of pathogenetic and serologic tests. (Strong recommendation, evidence grades: level IV).

Update plan

This consensus, developed based on the latest clinical research and advancements in the field, is intended to be supplemented with new research findings approximately 2 to 3 years after its official release. This will ensure continuous improvement and updates to maintain its relevance and accuracy.

Acknowledgments

This expert consensus is initiated by Infectious Disease Imaging Group, Infectious Disease Branch, Chinese Research Hospital Association; Radiology Science editorial department; Radiology of Infectious Diseases editorial department; Elecctronic Journal of Emerging Infectious Diseases editorial department. And we thank Dr. Ruihua Liu from the Fourth Hospital of Inner Mongolia Autonomous Region, for her help and advice on English writing.

Footnote

Funding: The study was supported by the National Key Research and Development Program of China (No. 2019YFE01214001); Shenzhen High-Level Hospital Construction Fund (No. 2022108); Shenzhen Basic Research Program (No. JCYJ20190813153413160); Yantian District Medical and Health Science & Technology Project (No. YTWS20230205); Science and Technology Project for the Construction of High-level Clinical Specialties in Public Hospitals in the Capital Region of Inner Mongolia Autonomous Region (No. 2024SGGZ059); Chongqing Medical Research Project of Science & Health Joint Program (No. 2023DBXM005); and Nanjing Health Technology Development Special Fund (No. YKK21126).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1445/coif). The 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. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patients for publication of this case report and accompanying images.

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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