Extrathoracic acquired lung hernias can be classified by etiology into traumatic, spontaneous, and pathologic (
5). PTLH is further divided into three subtypes based on the exact location of the chest wall defect: intercostal (space between the ribs), parasternal (space between the ribs and the sternum), and supraclavicular (superior thoracic aperture). Diaphragmatic lung hernias, either posttraumatic or congenital, are generaly categorised separately due to their separate and different etiological, underlying defect mechanism, and management plan.
Chest wall weakness due to muscle disruption and or bone fractures (ribs, sternum, clavicle) and increased intrathoracic pressure (coughing, heavy lifting, chronic obstructive pulmonary disease) are the cornerstones for posttraumatic lung hernia formation (
6). Increased intra-abdominal pressure can also be transmitted to the chest, causing increased intrathoracic pressure. Due to the strong support of the paraspinal and back muscles (trapezius, rhomboids and latissimus dorsi), the anetrior and lateral sides of the chest wall are considered to be the weakest points of this cavity and herniation of the lung more frequently occurs in these locations.
The three point immobilization of the chest through the seat belt with the shoulder harness and the lap belt and relative immobiliztaion of the left chest compared with the right chest combined with the subsequent shear force across the intercostal, claviculosternal and sternocostal junctios (seat belt injury) have been proposed as a possible mechanism for PTLH (
Although spontaneous regression of the PTLH has been reported in the pediatric population (
5), in the majority of the cases, especially in sizable hernias, the regression of the hernia sac and adequate coverage by the scarred tissue is extremely unlikely. The observation that most of the PTLH do not resolve spontaneously and the fact that thoracic strapping would impair chest wall motion increase the risk of atelectasis and subsequent infection and reduce the pulmonary compliance. These facts have forced the medical community to abandon this old-fashioned management of PTLH ( 6).
Early detection and management of the PTLH is important in preventing incarceration and strangulation of the herniated lung segment and decreasing the longterm sequela of the hernia including pain, cough spells, and chest wall buldging or deformity. The possibility of the intercostal PTLH becoming further complicted by fomation of a pneumothorax or even tension pneumothorax, especially if the patients require positive pressure ventilation, is a real concern in cases where the diagnosis or management is dealyed (
While CT scan with multiplannar image reconstruction and maximum and minimum intensity projection reformats is the most accepted radiologic tool for evaluation of these patients, plain chest radiograph with tangential views and valsalva maneuver can be very helpful and should be the first approach in radiologic evaluation (
4). In cases where CT scan is unavailable, transthoracic ultrasound can assist with the diagnosis ( 4). In situations where the lung tissue is severly compressed against a small hernia orifice (chest wall defect), contrast enhanced CT scan is mandatory to evaluate for possible strangulation or lung infarction (CT pulmonary angiograophy protocol) ( 4). In cases where inspiratory chest CT is nondiagnostic, an expiratory exam with valsalva manuever may help to establish the final diagnosis.
While conservative management in supraclavicular PTLH is generaly deemed a sufficient approach by most authors (larger thoracic wall defect in such cases reduces the risk of strangulation) (
1, 7), surgery is the most acceptable management in intercostal or parasternal PTLH ( 1). Indications for surgery include relief of pain, incarceration or strangulation prevention, nonviability of the lung tissue, optimization of pulmonary function, prevention of respiratory failure, and cosmetic reasons ( 3). In some previous reports PTLH patients presented with shortness of breath and even respiratory failure ( 2, 3).
The spectrum of reported surgical approaches varies from primary repair with pericostal stitches (similar to our case), or concurrent placement of wire sutures (
3) to repair using prosthetic grafts (intrathoracic polytetrafluoroethylene Gore-Tex patch) ( 3, 5, 8), mesh (synthetic/biologic) ( 9), or periosteal/muscle flaps ( 8). A hernia sac is generally not present in these cases since the pleura is usually disrupted. If a sac is present then it should be removed. Video assisted open repair can be used and is helpful in further assessment of lung segment viability following the hernia reduction, evacuation of hematoma, and evaluation of the inner surface of the cavity and the diaphragm for any small missed injuries and to ensure adequate lung expansion ( 1). The efficacy of the surgical approaches remains to be confirmed by further studies.
The current case is an example that PTLH can have delayed presentation even up to a few decades following trauma. The fact that the patient had a remote history of severe chest wall trauma at the exact same place of the lung herniation and lack of any recent injuries to explain the hernia has made us believe that this case is an example of delayed presentation of PTLH although spontaneous origin especially in an adult is always a very unusual possibility. Patient and medical team education is warranted to help with early detection of such cases. Surgical repair, especially in the cases with intercostal or parasternal hernia, is mandatory to prevent further complications. We suggest that in patients with even a remote history of blunt chest trauma, physical examination and preoperative evaluation including assessment for possible PTLH be considered before patients undergo positive pressure ventilation. We also suggest that PTLD be considered as a differential diagnosis for the patients with blunt traumatic chest injuries and rib fractures as this would affect the surgical management.