Lung hernia: an updated narrative review

Abstract

Background and Objective

Pulmonary (lung) hernia is an uncommon condition in which aerated lung protrudes beyond the normal confines of the thorax through a defect at the thoracic inlet, chest wall, mediastinum, or diaphragm. Although historically linked to trauma, recent reports increasingly involve postoperative patients, including those after lung transplantation, and situations associated with repeated spikes in intrathoracic pressure. We conducted a narrative review to summarize contemporary diagnosis and management.

Methods

We performed a targeted literature search of MEDLINE (via PubMed), ScienceDirect, the Cochrane Library, Taylor and Francis Online, and ClinicalTrials.gov from inception through December 31, 2025. The search was performed in January 2026. We included studies in English or French describing pulmonary or lung hernia of any anatomic subtype or etiology in humans. We extracted data on hernia location, suspected cause, clinical presentation, imaging, management strategy, complications, and outcomes.

Key Content and Findings

The literature is dominated by case reports and small series with heterogeneous definitions and inconsistent reporting of defect anatomy, operative technique, and follow-up. Most published cases involve thoracic or intercostal defects, while cervical hernias are less common and mediastinal or diaphragmatic variants are rare. Computed tomography is the primary diagnostic test, sometimes supported by dynamic maneuvers to reproduce the protrusion. Management is guided by symptoms and anatomy. Observation is often chosen for small, reducible defects, whereas progressive enlargement, pain, impaired reducibility, concern for incarceration, ventilatory dependence, or chest wall instability typically lead to operative repair with reconstruction and selective reinforcement.

Conclusions

More consistent reporting and multicenter data are needed to define progression risk and compare surgical techniques and materials, particularly in high-risk postoperative and post-thoracic transplant populations.

Introduction

Background

Lung hernia, also called pulmonary hernia, is a rare condition in which aerated lung protrudes beyond the normal limits of the thorax through a defect at the thoracic inlet or the chest wall (1,2). It can present as a soft, reducible bulge that enlarges with coughing, Valsalva maneuver, or exertion, and it may be intermittent, which contributes to delayed recognition (1,2).

Although the earliest clinical account is often credited to Roland, who described a supraclavicular pulmonary hernia in the 15th century, lung hernia remains an infrequently reported diagnosis even centuries later (3). However, the true incidence is likely underestimated because small, asymptomatic, or intermittently apparent hernias may go unrecognized, and published literature is subject to reporting bias toward symptomatic, unusual, or surgically treated cases. A comprehensive review in 1994 counted 282 cases, and most contemporary reports still describe the overall literature as only slightly more than 400 cases (4,5).

Rationale and knowledge gap

What has changed is not the definition of lung hernia, but the context in which we encounter it. Many modern studies report tissue vulnerability combined with repeated spikes in intrathoracic pressure, including those from chronic cough, chronic obstructive pulmonary disease (COPD), obesity, and steroid exposure (6-8). These factors can enlarge small defects over time and may convert an incidental finding into a symptomatic problem (6-8). In parallel, contemporary thoracic and cardiac operations create new patterns of chest wall weakness. Less invasive approaches and newer incision sites can still disrupt intercostal support, and transplant incisions may introduce distinct postoperative defect patterns that were uncommon in earlier eras (9,10). In this setting, lung hernia is not always a benign bulge. In selected postoperative cases, especially after transplantation, herniation can affect airway mechanics or regional perfusion and, rarely, progress to parenchymal infarction (11).

Despite these concerns, the evidence remains scattered across case reports and small series. Imaging evaluation varies widely, terminology is inconsistent, and management ranges from observation to repair with diverse techniques and materials, often without clear criteria for escalation (4,5). Data specific to postoperative and transplant populations are particularly fragmented, even though this group may have the greatest clinical risk, the most to gain from early recognition, and a consistent diagnostic and treatment pathway (9-11).

Objective

We conducted a review to synthesize the available evidence on lung herniation, patterns of clinical presentation and diagnostic strategies, and contemporary approaches to observation and surgical repair. We placed special emphasis on postoperative and transplant populations, where standardized evaluation and timely intervention may offer the greatest practical value. We present this article in accordance with the Narrative Review reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2026-0620/rc).

Methods

We performed a targeted literature search in January 2026 covering database inception through December 31, 2025 in MEDLINE (PubMed), ScienceDirect, the Cochrane Library, Taylor & Francis Online, and ClinicalTrials.gov. Search terms combined controlled vocabulary (when available) and free-text keywords related to lung/pulmonary hernia and herniation, supplemented by anatomic and contextual terms (intercostal, chest wall, cervical/supraclavicular, mediastinal/transmediastinal, diaphragmatic, postoperative/iatrogenic, transplant). Reference lists of included articles and key reviews were also screened (Table 1).

Table 1. Search strategy summary.

Items	Specification
Date of search	January 15, 2026
Databases and other sources searched	MEDLINE (via PubMed), ScienceDirect, Cochrane Library, Taylor & Francis Online, ClinicalTrials.gov
Search terms used	“pulmonary hernia; lung hernia; pulmonary herniation; lung herniation; intercostal; chest wall; thoracic inlet; cervical; supraclavicular; mediastinal; transmediastinal; diaphragmatic; transdiaphragmatic”
Timeframe	Database inception to December 31, 2025
Inclusion and exclusion criteria	Included: human reports/studies across all etiologies and anatomic subtypes (case reports/series, observational studies, technical/clinical reports). Language: English or French
	Excluded: non-human studies; non-relevant articles; duplicate records; reports without sufficient clinical/imaging detail to support pulmonary hernia diagnosis
Selection process	Multiple authors screened titles/abstracts and full texts; disagreements were resolved by discussion and consensus. Citation chasing of reference lists was used to capture additional relevant reports

We included English or French reports describing pulmonary/lung hernia of any anatomic subtype and etiology (congenital, traumatic, spontaneous, pathologic, postoperative/iatrogenic, including post-transplant) in humans. Given the rarity of the condition, eligible evidence included case reports, case series, observational studies, and clinically relevant technical/clinical reports. We excluded non-human studies, non-relevant articles, and reports without sufficient clinical and/or imaging detail to support the diagnosis. Duplicated records were removed prior to screening.

Using a standardized extraction form, we captured publication characteristics and key clinical features, including etiology, anatomic location, presentation, imaging approach, defect characteristics, management (observation vs. operative repair and techniques), complications, and outcomes/recurrence where available. Owing to heterogeneity and predominantly case-based evidence, findings were synthesized qualitatively and organized by anatomic subtype and etiology, with attention to postoperative and transplant-associated cases. The study identification and selection process are summarized in Figure 1.

Figure 1.

PRISMA 2020 flow diagram.

Results

Classifications and terminology

Lung herniation occurs when aerated lung protrudes beyond the usual confines of the thorax through a defect at the thoracic inlet, chest wall, or diaphragm (12). Older surgical reports sometimes distinguished a “true hernia” from “lung prolapse” depending on whether the parietal pleura remained intact. In practice, this terminology is used inconsistently and rarely affects management, so we discuss these presentations as part of the same spectrum while noting pleural disruption when it is specifically reported (13,14).

Morel-Lavallée’s 1845 report is generally viewed as the foundational reference for lung hernia classification: he assembled 32 cases and organized them into a practical scheme that integrates both cause and anatomic location, a structure that still underpins most modern descriptions (15). Pulmonary hernias are described by location as thoracic (chest wall, most often intercostal), cervical (apical), mediastinal (including transmediastinal), and diaphragmatic (15).

Thoracic pulmonary hernias are the most common subtype, accounting for 60% to 80% of reported cases, and present as an intercostal lung protrusion through a focal chest wall defect (4,16,17). In traumatic cohorts, thoracic defects remain the most frequent presentation at about 65% (16,17). A practical surgical anatomy concept is that the intercostal spaces contain layered musculature with zones of relative weakness, particularly in anterior parasternal regions and posterior paravertebral regions where muscular coverage is thinner and support differs by compartment. These vulnerable areas become clinically relevant when compounded by trauma, prior incisions, poor tissue quality, or impaired healing, allowing the lung to herniate outward through a discrete defect (18-20).

Cervical pulmonary hernias are characterized by the extension of aerated lung above the superior thoracic aperture into the supraclavicular region and represent approximately 15% to 35% of published cases (16,21-23). In traumatic cohorts, cervical hernias account for a similar proportion, around 35% (21-23). The superior thoracic aperture is formed by the manubrium, first ribs, and T1 vertebra, and the lung apex is covered by apical parietal pleura reinforced by Sibson fascia (suprapleural membrane), which stabilizes the apical pleura against cranial displacement (24,25). Disruption, attenuation, or laxity of this barrier, particularly in the setting of elevated intrathoracic pressure, permits apical lung protrusion into the thoracic inlet corridor (26).

Diaphragmatic lung hernias appear in historical classification schemes but are distinctly uncommon, reported in roughly 1% to 2% of publications, and less than 1% in traumatic series (27,28). This entity is mechanistically unusual because pressure gradients more commonly drive abdominal viscera into the thorax rather than lung into the abdomen. When true diaphragmatic pulmonary hernia is present, it implies a diaphragmatic defect that permits lung tissue to traverse the diaphragm and may overlap with complex combined disruptions rather than an isolated single-plane defect (29,30).

Mediastinal and transmediastinal lung hernias are rare and are inconsistently reported mainly in isolated cases or small series (31-33). In these cases, lung tissue traverses mediastinal boundaries through a structural defect or postoperative space, typically when normal mediastinal restraints are disrupted after major lung resection or trauma.

Etiology and risk factors

Historically, acquired pulmonary hernias have been described most often after trauma and other iatrogenic chest wall defects (1-3). In more recent reports, postoperative and thoracic transplant–associated cases have been increasingly described, reflecting contemporary thoracic and cardiac surgical practice and patient-level vulnerability (9-11).

Trauma is a major, and historically the best-described, etiology of pulmonary hernias (1-3,5). High energy blunt chest trauma can result in lung herniation when the structural integrity of the chest wall is disrupted. The defect most often follows displaced rib fractures or flail segments, rupture of the intercostal musculature, or disruption at the costochondral or costosternal junctions, creating a full thickness weakness through which pleura-covered aerated lung may protrude beyond the thoracic cage (34-36). After the initial injury, ongoing pressure changes during breathing and coughing may enlarge the defect, so traumatic herniation can be identified either immediately or later, particularly when healing is incomplete after severe injury or chest wall stabilization (37,38). Penetrating trauma can create a direct open chest wall defect and, in rare extreme cases, may progress to pulmonary evisceration, in which lung protrudes through the wound without soft tissue coverage, including after gunshot wounds (39,40).

Postoperative and iatrogenic pulmonary hernias result from a focal full thickness weakness of the chest wall created by a surgical or procedural disruption of the intercostal space. They have been described after thoracotomy and mini-thoracotomy, after thoracoscopic access incisions including uniportal video-assisted thoracoscopic surgery (VATS), after minimally invasive cardiac approaches, and through prior tube thoracostomy tracts or sites of rib and chest wall resection (41-46). With the expansion of minimally invasive cardiac surgery performed through a right mini-thoracotomy, postoperative intercostal lung herniation is being recognized more frequently. In a single center experience, Vinck et al. (7) reported nine intercostal lung hernias among 803 adult patients operated through mini-thoracotomy, arising at the prior incision site and most commonly after right second intercostal parasternal access for aortic valve surgery and right fourth intercostal lateral access for mitral valve surgery. The proposed mechanism is a persistent intercostal defect produced by intercostal muscle division or avulsion, retractor-related tissue injury, and intercostal nerve injury with subsequent denervation and muscle atrophy, sometimes compounded by an imperfect layered closure (7). Over time, repetitive pressure changes with breathing and coughing can enlarge the defect, which helps explain delayed presentations months to years after the index procedure.

Iatrogenic pulmonary hernias can also occur when a procedural intercostal tract or access site fails to reconstitute full thickness chest wall support, such as after tube thoracostomy or thoracoscopic port placement, leaving a persistent focal weakness through which pleura-covered lung may gradually protrude (47,48). Pulmonary hernias have also been reported after thoracic spine surgery, including mini-transthoracic approaches for thoracic disc herniation and thoracoscopic thoracic spinal fusion, where intercostal access may leave a focal chest wall weakness that later allows lung herniation (49,50).

Spontaneous pulmonary hernias are rare but are consistently reported, accounting for approximately 30% of all reported cases (51). They most commonly occur through an intercostal space and are typically triggered by abrupt or repetitive increases in intrathoracic pressure, such as particularly forceful coughing, sneezing, or straining (51-55).

Pathologic pulmonary hernias are the least common acquired subtype and arise when the chest wall is weakened or destroyed by local disease rather than by a discrete traumatic or surgical event (3). Reported mechanisms include infectious or inflammatory chest wall processes (classically a chest wall abscess or empyema, including those from granulomatous infections such as tuberculosis) that erode ribs, intercostal soft tissues, and parietal pleura, creating a full-thickness defect through which lung can protrude (3,56-58).

Congenital pulmonary hernias reflect an inborn weakness of the structures that normally restrain the lung at the thoracic inlet or along the anterior chest wall. At the apex, the key “containment” layer is the suprapleural membrane. When this membrane is lax, thin, or partially deficient, the lung apex can protrude into the lower neck, producing the classic cervical (apical) form of congenital lung hernia. In infants and young children, an apical bulge can be a diagnostic gray zone. Some cases represent a benign anatomic variant that becomes less apparent as the chest wall and supporting tissues mature (25).

Congenital pulmonary herniation can also occur through true chest wall defects. When ribs are absent or underdeveloped and the overlying musculature is hypoplastic, the mechanical barrier of the thoracic cage is compromised and lung can bulge through the weak segment (59). A well-recognized syndromic association is Poland syndrome, where variable rib and pectoral muscle defects may permit lung herniation, including neonatal presentations (60,61). Even outside a syndromic diagnosis, isolated congenital rib agenesis has been reported as a classic cause of intercostal lung herniation, with protrusion occurring directly through the segmental defect in the rib cage. Similar presentations have also been described with congenital sternal cleft, where the midline defect in the anterior chest wall can allow lung tissue to bulge outward, sometimes noted in early life (62,63).

Rare connective tissue disorders have also been linked to congenital cervical lung herniation, supporting the concept that abnormal collagen or elastin architecture can weaken the thoracic inlet restraints. Arterial tortuosity syndrome is one reported example, and similar cervical or apical lung herniations have also been described in patients with Marfan syndrome or Ehlers-Danlos syndrome (64-67). In addition, congenital skeletal dysplasias that disrupt normal rib formation, such as spondylocostal dysostosis, can create structural chest wall gaps that permit lung herniation (68).

Several patient and exposure-level factors appear to lower the threshold for pulmonary herniation by amplifying intrathoracic pressure surges, weakening chest wall support, or impairing tissue integrity and healing. Across published series and reviews, commonly reported associations include COPD or emphysema with chronic cough, obesity or high body mass index, systemic corticosteroid exposure, diabetes mellitus, smoking history, and prior thoracic incisions or intercostal access sites (8,69-71). Less frequent but clinically relevant predisposing contexts include connective tissue disorders and neuromuscular chest wall weakness, whereas precipitating events are typically acute pressure spikes from forceful coughing, sneezing, or straining (72-74). Risk factors are shown in Figure 2.

Figure 2.

Pulmonary hernia: key risk factors and common anatomic locations. COPD, chronic obstructive pulmonary disease; CPAP, continuous positive airway pressure; VATS, video-assisted thoracoscopic surgery.

Special attention is warranted in patients undergoing bilateral lung transplantation, where a convergence of risk factors for pulmonary herniation is common. The clamshell thoracotomy, widely used for sequential bilateral lung transplantation, creates a large anterior chest wall incision and intercostal disruption, while recipients routinely receive systemic immunosuppression including corticosteroids and often experience early postoperative coughing and periods of positive pressure ventilation. The resulting pathogenesis mirrors the general mechanism of lung herniation, namely pressure surges acting on a postoperative chest wall weakness with impaired healing, which can allow pleura-covered lung to progressively protrude through the defect and may have a delayed presentation (75-77).

Clinical presentation and complications

Clinical presentation is heterogeneous and depends on the anatomic site and etiology, but many lung hernias are clinically silent. In the natural history cohort reported by Madani et al. (78), most patients were asymptomatic at presentation (33 of 38) and many defects remained stable over follow-up. When symptoms occur, the most typical finding is a soft, reducible chest wall or supraclavicular bulge that becomes more apparent with coughing or straining; patients may also report localized discomfort, pleuritic chest pain, dyspnea, or cough (1-3,78,79). An important clinical clue in acquired postoperative cases is new or persistent pain at a prior incision or drain site, which can precede obvious external protrusion (46,80).

Cervical or apical hernias often present differently, as an intermittent neck or supraclavicular mass that enlarges with cough or Valsalva maneuver and may be soft or crepitant on palpation; these cases are frequently noticed by patients as a “neck lump” during exertion or coughing (81,82). Spontaneous intercostal hernias commonly present after an inciting pressure event, and published case series describe chest pain with focal bulging, sometimes accompanied by ecchymosis (51,83).

Complications are uncommon overall but clinically important when present. Incarceration or strangulation of herniated lung may cause escalating pain and hemoptysis, and can progress to venous congestion, ischemia, or necrosis, prompting urgent intervention in reported cases (83,84). Air-leak related complications have also been described, including subcutaneous emphysema, pneumothorax, pneumomediastinum, and rarely more extensive air tracking patterns in spontaneous cases (51,85). In the setting of positive pressure ventilation, a higher risk of rapid enlargement and incarceration with worsening pain, hemoptysis, or respiratory compromise should raise concern for a complicated hernia (50). At the severe end of the spectrum, open penetrating defects can rarely lead to pulmonary evisceration, a surgical emergency with potential for respiratory and vascular compromise (39).

Diagnostic workup and imaging

Diagnostic confirmation of pulmonary hernia is fundamentally imaging-based because the protrusion may be intermittent and therefore absent on routine “resting” studies. Chest radiography is typically the first-line test, yet it is frequently normal or non-diagnostic; however, the yield improves when the suspected region is imaged in profile and/or under dynamic conditions (expiration or Valsalva maneuver), which can enlarge an otherwise occult hernia. When visible, radiographs may show an aerated extrathoracic parenchymal contour with vascular markings extending beyond the bony thorax (“lung beyond the rib” sign on the lateral/profile view) or a focal hyperlucent area on the frontal projection (“lucent lung” sign); ancillary clues include widening of the involved intercostal space and associated subcutaneous emphysema (Figure 3) (86-88).

Figure 3.

Imaging of an anterior intercostal pulmonary hernia. (A) Lateral chest radiograph suggests focal lung protrusion beyond the expected chest wall contour. (B) Sagittal chest CT (lung window) confirms lung herniation through an anterior intercostal defect. (C) Axial CT (lung window) further delineates the defect and the herniated lung. CT, computed tomography.

Computed tomography (CT) is the modality of choice to establish the diagnosis and define anatomy, directly demonstrating lung (typically covered by pleura) in continuity with the intrathoracic parenchyma traversing a chest-wall or thoracic-inlet defect, while also delineating the hernial orifice/“neck”, the sac, adjacent fractures or postsurgical disruption, and any parenchymal compromise (89,90). Multiplanar reformations are critical; minimum intensity projection (MinIP) and maximum intensity projection (MIP) reconstructions can help assess bronchial or vascular compression, and volume-rendered 3D reconstructions can provide a practical roadmap for operative planning. If the hernia is subtle on standard inspiratory CT (Figure 4), expiratory imaging and/or CT acquired during Valsalva maneuver may unmask or accentuate a protrusion; intravenous contrast (including CT angiography protocols when the neck is narrow and compression is suspected) is recommended to evaluate perfusion and exclude strangulation (89,90). Thoracic ultrasound is a useful adjunct when CT is not immediately available or when a bedside dynamic assessment is desired, typically showing a hyperechoic intercostal lesion corresponding to aerated lung with loss of the normal pleural line between adjacent ribs (91,92). For apical/cervical lung hernias, radiographs often demonstrate a unilateral (commonly right-sided) thoracic-inlet air lucency and may show lateral tracheal deviation; because these lesions are frequently intermittent, studies at mid-inspiration can miss them, and airway fluoroscopy or CT at maximal inspiration may be necessary for confirmation (21-23).

Figure 4.

Imaging of a left anterolateral intercostal pulmonary hernia. (A) Frontal chest radiograph shows subtle left lateral chest wall contour abnormality suspicious for lung protrusion. (B) Coronal chest CT confirms herniation of aerated lung through a left intercostal defect. (C) Axial CT delineates the defect and the herniated lung. CT, computed tomography.

Management principles

Management is individualized because pulmonary hernias are uncommon and the available evidence does not support a single preferred approach for all patients; treatment is guided by symptoms, interval change in the defect, and any complications. Asymptomatic, stable, and easily reducible hernias can be managed with observation, since many remain unchanged during follow-up. In selected patients, nonoperative care focuses on limiting pressure gradients across the defect and reducing dynamic chest wall stress through effective analgesia with chest wall muscle relaxation, activity and strain modification, cough control with optimization of underlying COPD, and close clinical and imaging surveillance with prompt reassessment if symptoms progress or the hernia enlarges (93). François et al. (94) specifically supported nonoperative management of supraclavicular pulmonary hernias, noting that the neck is often wide and not constrained by rib fractures, which may reduce the likelihood of incarceration or strangulation. Supportive measures such as tube thoracostomy and supplemental oxygen may be appropriate when pneumothorax or a clinically significant pleural air leak is present. Operative evaluation is generally warranted for enlarging hernias, persistent or significant pain, impaired reducibility, or any concern for incarceration or strangulation, and it should also be considered when there is ventilatory dependence or chest wall instability. Although supraclavicular hernias are often benign, rare neurovascular complications have been reported, including T1 nerve compression with cervical neuralgia, and successful repair with patch augmentation such as bovine pericardium and adjunctive sealants has been described (23). In case of traumatic chest wall injury, early definitive stabilization should be considered when an intercostal pulmonary hernia accompanies multiple displaced rib fractures and mechanical instability because restoring chest wall mechanics is central to a durable resolution and may help avoid prolonged, unsuccessful, nonoperative management (95).

Surgical techniques and outcomes

Operative repair is principles-based and aims to reduce the herniated lung, address any associated pleural pathology, and reconstruct the chest wall defect in a durable way that restores rib cage mechanics and minimizes recurrence. After exposure of the defect, the lung is reduced and inspected for ischemia or parenchymal injury, with limited nonanatomic resection performed when viability is doubtful. The chest wall is then closed by reapproximating the involved intercostal space and adjacent ribs with pericostal or transmuscular sutures, and reinforcement is added when the defect is large, tissues are attenuated, or tension-free closure cannot be achieved. For selected postoperative or minimally invasive surgery-related defects, a simple rib approximation technique has been described in which sutures are placed directly across the intercostal space between the upper and lower ribs to restore costal margin continuity (96).

When primary repair is insufficient, rigid skeletal stabilization has been described for larger defects or when chest wall instability contributes to recurrence risk. Wiens et al. (97) reported a fixation strategy that applies plate-based stabilization principles to restore structural continuity of the chest wall and support the repair in high-stress regions. Intramedullary titanium rib implants have also been used as an alternative method of rib stabilization, particularly when long-segment support is desired and additional soft tissue dissection is best minimized (98). In traumatic settings, combined approaches have been reported that pair prosthetic defect coverage with stabilization of the injured rib cage, particularly when blunt chest trauma produces both soft tissue disruption and mechanical chest wall instability (99,100). Subotic et al. (101) described mesh interposition for the defect together with plate fixation using a DePuy Synthes system (Johnson & Johnson MedTech) to address concomitant instability and reduce tension on the reconstruction.

Prosthetic reinforcement, when required, most often uses synthetic mesh such as polypropylene, ePTFE, or composite materials, positioned as an underlay or intrapleural patch with adequate overlap and secured to the surrounding chest wall, with soft tissue coverage optimized when local tissues are weak (Figure 5) (102). Biologic reinforcement may be considered when soft tissue quality is poor or infection risk is a concern. Stanizzi et al. (103) reported repair using porcine acellular dermal matrix with durable long-term follow-up, supporting its role as an option in selected patients. Autologous tissue techniques have also been described for traumatic defects, including periosteal flap reconstruction to reinforce closure when prosthetic material is undesirable (104).

Figure 5.

Treatment outcome of an intercostal pulmonary hernia after lung transplantation. (A) Pre-repair CT shows lung herniation through an anterior chest wall defect; (B) Post-repair CT shows hernia reduction with lung contained within the thorax. CT, computed tomography.

Minimally invasive strategies are increasingly reported in selected patients, including VATS for intrathoracic assessment, reduction, pleural washout, and stapled wedge resection when needed, combined with targeted chest wall stabilization when rib fracture instability contributes to the defect (105,106). The supporting evidence remains predominantly observational but is consistent across contemporary series and reports. Operative repair should be principles based: reduction of herniated lung, durable closure of the chest wall defect, and restoration of rib cage stability when fractures or segmental disruption are present. In the largest thoracic surgery series of acquired chest wall hernias (27 patients, predominantly post-thoracotomy), chronic defects were managed with either primary reapproximation of the intercostal space using figure of eight sutures or prosthetic reinforcement when tension-free closure was not feasible, and prosthetic repair was not associated with higher perioperative morbidity compared with primary repair (overall complications 35%: 22% prosthetic vs. 42% primary, P=0.4; median length of stay 4 days) (69).

In an international multicenter experience of operatively managed traumatic rib cage hernias (24 patients), definitive repair most often required mesh reinforcement (75%) and mechanical rib fixation (79%), reflecting that successful treatment commonly demands both soft tissue reconstruction and skeletal stabilization; short-term functional results were generally favorable at a mean follow-up of 6.7 months, with full range of motion in 83% and return to pre-injury activity in 78%, although 21% reported persistent pain at final follow-up (107).

Discussion

In this narrative review, we synthesize contemporary reports of pulmonary herniation across anatomic subtypes and etiologies, with emphasis on postoperative and thoracic transplant–associated presentations. The evidence base is largely limited to case reports and small series with heterogeneous reporting of anatomy, technique, and follow-up; therefore, these conclusions should be viewed as pragmatic clinical guidance rather than comparative effectiveness evidence.

Most published cases involve thoracic or intercostal defects, whereas cervical hernias are less frequent, and mediastinal or diaphragmatic variants are rare. CT is central to diagnosis, but intermittent herniation may yield falsely reassuring studies; provocative imaging with increased intrathoracic pressure (e.g., Valsalva maneuver or expiratory acquisition) can improve detection, and contrast may aid assessment when the neck is narrow or strangulation is suspected. Recent literature also reflects a shift from predominantly traumatic descriptions toward postoperative and iatrogenic cases, often in patients with impaired tissue integrity or recurrent pressure spikes (chronic cough, COPD, obesity, steroid exposure). In transplant recipients, immunosuppression and delayed wound healing may further increase the risk of progression and complications.

Management is individualized based on symptoms and clinical course. Observation can be appropriate for small, stable, reducible defects in asymptomatic patients with counseling and follow-up. Repair is generally preferred for persistent symptoms, enlargement, loss of reducibility, concern for incarceration, ventilatory dependence, or coexisting chest wall instability. Although operative techniques vary, most repairs follow the same principles: reduction and inspection of the lung with limited resection when viability is uncertain, restoration of chest wall continuity (rib or intercostal reapproximation), and selective reinforcement for large defects or poor tissue quality, most commonly using synthetic mesh with adequate overlap, with rigid stabilization when mechanical instability is a contributing factor.

This narrative review covers a broad spectrum of pulmonary herniation, including postoperative/incisional, traumatic, spontaneous, cervical, mediastinal, diaphragmatic, and transplant-associated forms. This broad scope was intentional, given the fragmented nature of the literature and the lack of a recent comprehensive synthesis across major subtypes. However, it is also a limitation. These entities differ in presentation, natural history, complication risk, and technical repair considerations; therefore, our findings should not be interpreted as a uniform treatment algorithm.

The evidence base remains limited, consisting mainly of case reports and small noncomparative series. Reporting is inconsistent with respect to defect anatomy, dynamic imaging, indications for intervention, operative technique, follow-up, and recurrence. Patient-centered outcomes, including chronic pain, pulmonary function, functional recovery, and quality of life, are rarely described. As a result, meaningful comparisons between observation and specific repair strategies remain difficult, particularly in postoperative, transplant-associated, and immunosuppressed patients. This review should therefore be viewed as an updated clinical framework that summarizes shared diagnostic and management principles while emphasizing the need for subtype-specific clinical judgment.

Progress will likely depend on standardization and multicenter collaboration. Future work should prioritize prospective registries with a core dataset that includes defect anatomy (location, size, neck width), imaging approach, symptom burden and relevant physiology, operative details (closure method, reinforcement material, fixation strategy), and patient-centered outcomes with adequate follow-up. High-yield questions include predictors of progression during observation, indications for primary closure versus reinforcement, selection of synthetic versus biologic materials in compromised tissues, the role and timing of rib stabilization when mechanical instability is present, and preventive closure strategies after minimally invasive or high-risk incisions.

Conclusions

Pulmonary herniation is now encountered more often in postoperative and other high-risk patients, not only after major trauma. The current evidence supports a practical approach. The diagnosis should be confirmed and the defect characterized with CT, with dynamic maneuvers when symptoms are intermittent or routine imaging is nondiagnostic. Treatment should be individualized based on symptoms, defect characteristics, and evidence of progression. When operative management is indicated, the primary goal is durable chest wall reconstruction that restores stability and achieves tension-free closure, with selective reinforcement in patients with large defects or poor tissue quality. Future work should prioritize prospective studies with standardized definitions, detailed operative reporting, and longer follow-up to better define natural history and guide technique selection.

Supplementary

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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. Written informed consent was obtained from the patients for publication of the accompanying images.