Beyond the Usual Course: A Rare Case of Persistent Traumatic Pulmonary Pneumatoceles With 8-Year Favorable Evolution

Introduction

Traumatic pulmonary pneumatoceles (TPPs) are rare sequelae of chest trauma, with reported incidence varying widely depending on patient population and diagnostic modalities [1]. They are more frequently encountered in young patients, especially children [2]. Most TPPs follow a benign and self-limiting course, typically resolving spontaneously within weeks to months under conservative management [3]. Nevertheless, large, persistent, or complicated lesions may pose diagnostic and therapeutic challenges in pediatric populations.

We present the case of a young child who developed 2 ipsilateral and large TPPs following severe blunt chest trauma, with sequelae persistence for nearly 8 years. To the best of our knowledge, this is one of the longest documented radiological follow-ups of a pediatric TPPs in the literature, providing unique insights into its natural history and long-term management.

Case Report

We report the case of a 1-year, 7-month, 11-day-old boy (587 days old) who was admitted to the emergency department following a high-impact motor vehicle collision. He was an unrestrained passenger sustaining injuries in a high-mechanism, multiple-rollover motor vehicle accident involving both parents. Upon admission to the trauma unit, he presented with severe traumatic brain injury, craniofacial hemorrhaging (epistaxis and otorrhagia), and a right temporo-occipital hematoma with associated tissue loss. Due to respiratory failure (tachypnea and refractory hypoxia), he required emergency endotracheal intubation and mechanical ventilation. Initial chest radiography (Figure 1) demonstrated a right mid-clavicular fracture without associated rib fractures. No pneumothorax or pleural effusion were noted bilaterally, although scattered alveolar opacities (predominantly on the right side) were consistent with pulmonary contusions. While radiographs of the spine and extremities were unremarkable, a whole-body computed tomography (CT) scan identified a displaced right temporo-occipital skull fracture with overlying epidural and subcutaneous hematomas (Figure 2). A chest CT scan revealed extensive pulmonary contusions in the right lung, along with 2 large, irregularly marginated, thick-walled cavities in the upper and lower lobes, measuring 52×38 mm and 39×35 mm, respectively, both containing air-fluid levels (Figure 3). A small right-sided pneumothorax was also identified. No sternal or rib fractures were observed. Following an emergency craniotomy for hematoma evacuation, the patient was managed conservatively for a stable pneumothorax and remained in the intensive care unit for 18 days. He was successfully weaned from mechanical ventilation after 10 days with no infectious complications or need for chest tube placement. After a favorable clinical course, he was discharged 27 days after admission. Follow-up chest CT prior to discharge demonstrated partial clearance of the TPPs, with decreased intra-lesional fluid levels but no reduction in overall size. A decision was made to continue conservative management with close clinical and radiological surveillance, contingent upon informed consent obtained from the parents after multidisciplinary discussion with the involved specialties. Subsequent follow-up revealed complete resolution of the upper lobe pneumatocele within 3 years, while the lower lobe lesion persisted but evolved into a thin-walled, air-filled cavity without communication with the tracheobronchial tree. The most recent thoracic CT, performed 7 years, 10 months, 10 days after the accident, demonstrated stability with a slight increase in the size of the lower lobe pneumatocele, measuring 78×75×47 mm (Figure 4). Despite this radiological progression, the child remained entirely asymptomatic, with no episodes of dyspnea, hemoptysis, or recurrent pneumonia during the entire follow-up period. Management consisted of annual clinical and radiological follow-up (low-dose CT or radiography) and ongoing family counseling, with surgical intervention reserved for eventual clinical complications or disease progression. Considering the absence of complications, the favorable long-term outcome, and the family’s preference, surgical resection was not pursued. The patient remained under surveillance until the age of 10 years (8 years 5 months after trauma), with no symptoms and a normal lifestyle, including regular school attendance. In accordance with the family’s wishes, the multidisciplinary team elected to maintain the existing follow-up protocol.

Discussion

TPPs, first described by Fallon in 1940 [4] and subsequently recognized as a traumatic complication by Greening et al in 1957 [5], are defined as thin-walled, air-filled cystic lesions of the lung lacking epithelial lining, often containing air, fluid, or blood. In the literature, these entities have also been referred to as traumatic pneumatoceles, pulmonary pseudocysts, cavitary pulmonary lesions, or cavitating hematomas [6–8].

Reported incidence varies considerably according to the studied population and diagnostic modality, ranging from 0.24% to nearly 10% of trauma cases [9,10]. The condition is significantly more prevalent in children (as presented in our case), a finding attributed to the increased compliance of the pediatric chest wall, which facilitates energy transmission to the pulmonary parenchyma [2, 7]. Ulutaş et al reported no significant difference in TPPs development between blunt and penetrating injuries [1], although blunt trauma remains the predominant mechanism [8,11].

They are more commonly observed in males and often coexist with other traumatic injuries, including pulmonary contusions, parenchymal lacerations, pneumothorax, or abdominal trauma [3,9]. TPPs tend to involve the right lung more frequently and are often multiple, subpleural, and located within the lower lobes [2,9,12]. Their occurrence is not directly correlated with the number of rib fractures; rather, chest wall biomechanics and the site of impact are more relevant [13,14].

The pathogenesis involves parenchymal laceration due to shearing forces, most often following blunt trauma. The widely accepted “chest rebound” mechanism describes initial compression-induced injury followed by rapid recoil, generating pressure differentials that facilitate cystic cavity formation [8,13]. In most cases, the visceral pleura remains intact and vascular injury is minimal. The resulting air-filled cavities expand until intrapulmonary pressure equilibrates [12]. Mechanical ventilation (particularly when using positive end-expiratory pressure) can exacerbate this process by further increasing intrathoracic pressures and promoting air leakage [7].

Clinically, TPPs are frequently asymptomatic or present with nonspecific symptoms such as chest pain, mild dyspnea, hemoptysis, mild fever, leukocytosis, dyspnea, hypoxemia, and even respiratory distress, usually within 12–36 h after the trauma [9,12,15]. In our case, a combination of TPPs, extensive pulmonary contusions, and severe traumatic brain injury resulted in profound hypoxemia, necessitating the initiation of mechanical ventilation.

Because these manifestations overlap with other thoracic injuries, imaging is essential for accurate diagnosis. Chest CT is the standard method for diagnosis, with sensitivity approaching 96% compared to only 24% for chest radiography, especially for lesions smaller than 2 cm [6,15]. Typical CT findings include thin-walled, air-filled cavities, occasionally containing air-fluid levels. Radiological classification reported by Wagner et al in 1988 describe 4 distinct types of TPPs, based on mechanism of injury and anatomical distributions [16]. Lesion size varies widely in the literature, from 3 mm to 15 cm, with a typical range of 1–6 cm (including children and adults) [1,17]. Larger cavities are generally associated with more severe trauma. In our case, the observed lesions (measuring 52 mm and 39 mm along their major axes), were considered exceptionally large relative to the patient’s age (under 2 years) and lung volume (occupying nearly the entire right lung), and thereby markedly exacerbating the associated hypoxemia.

Differential diagnoses encompass congenital, inflammatory, infectious, systemic disease (Bechterew’s disease, Wegener granulomatosis, Sjogren syndrome), and neoplastic cystic lung lesions, highlighting the importance of follow-up imaging to monitor morphological evolution and to exclude malignancy in atypical or persistent cases [1].

Most cases have spontaneous resolution, with radiological healing occurring between 7 days (for TTPs less than 2 cm) and 10 months (for complex and blood-filled cavities) [1,17,18]. Rapid size reduction, sometimes up to 50% within the first week, has been reported [19]. In some cases, lesions evolve into pulmonary hematomas before complete resolution, occasionally leaving residual fibrotic scarring [2].

Although the prognosis is generally favorable, complications can occur within the first 10 days, including enlargement, infection, abscess formation, rupture with secondary hemorrhage or pneumothorax, hemoptysis, respiratory deterioration, and mediastinal or surrounding organs compression [6,9,20]. Early signs of such complications include persistent fever, leukocytosis, and worsening radiographic findings, underscoring the importance of vigilant clinical and radiological monitoring during this period [15,17]. Routine prophylactic antibiotics are not recommended, although secondary infections have been documented.

Management of TTP’s is predominantly conservative. Approximately 40% of patients require intensive care, 30% need intubation, and infectious complications occur in 4% to 38% of cases [7,9]. Chest tube drainage is generally reserved for associated pneumothorax, hemothorax, or hemopneumothorax [17]. Surgery is rarely indicated and is reserved for specific situations [1,2,21], including large (>4 cm) and complicated lesions (eg, respiratory distress, hemorrhage, disseminated intra-vascular coagulation, intra-operative increase in size), persistent or enlarging cavities, uncontrolled hemorrhage or massive hemoptysis, rupture into the pleural space with persistent air leak, and clinical deterioration despite optimal supportive care.

Thoracotomy with parenchymal repair is the preferred approach. Lung-sparing procedures (eg, wedge resection, segmentectomy) are favored over lobectomy, which is reserved for anatomically complex or non-resectable lesions. Pneumonectomy is contraindicated given the localized nature of TPPs and the associated high morbidity [12]. In selected cases of simple, infected cavities unresponsive to medical therapy, percutaneous drainage can be considered [1].

In our case, despite the significant size of the pneumatocele, conservative management proved to be a viable strategy. This approach was justified by the child’s excellent general condition, the absence of complications or secondary infections, and the favorable clinical progression. Furthermore, both the initial management strategy and the long-term follow-up plan were supported by the parents after thorough consultation. Long-term surveillance via periodic chest CT was instrumental in this process, allowing close monitoring of the progressive resolution of the upper lobe pneumatocele and the gradual emptying of the lower lobe cavity. Ultimately, this clinical and radiological success confirmed that a conservative strategy could be safely maintained for over 8 years after the trauma.

Conclusions

TPPs are rare pediatric post-trauma complications that typically resolve quickly; however, our case proves that large cavities can persist for years without functional impairment. The key clinical takeaway is that lesion size and persistence alone should not mandate invasive intervention. In asymptomatic patients without complications, clinicians should prioritize conservative management and long-term radiological surveillance. This approach is a safe, effective alternative to surgery, preventing unnecessary invasive procedures in the pediatric population.