Introduction The Organ Injury Scale for chest wall trauma, last updated in 1992, governs the diagnosis and management of nearly half of all trauma patients. When this scale is used in association with the abbreviated injury score (AIS) and the trauma injury severity score (TRISS), overall survival following trauma can be estimated. There is presently no standardized scoring system for blunt chest wall trauma in the setting of lung herniation.

Methods A systematic review of the literature on blunt chest wall trauma was completed and all reports of lung hernias since 1500 compiled. Four hundred cases of blunt trauma to the chest leading to lung herniation were identified and used to develop a classification scheme for extrathoracic lung herniation, adapt the organ injury scale for chest wall trauma to include extrathoracic lung hernias, and elucidate a treatment algorithm based on the type of lung hernia.

Results Lung hernias can be divided into anterior and posterior; anterior hernias can be further divided into intercostal and parasternal. Intercostal hernias should be managed acutely by way of anterior chest wall exposure and potential thoracotomy due to the significantly higher risk of incarceration and/or strangulation.

Discussion Anterior lung hernias should be grade III (AIS 3), parasternal lung hernias as grade IV (AIS 4), posterior lung hernias or the presence of any incarcerated lung as grade V (AIS 4), and strangulated lung hernias as grade VI (AIS 5). Incarcerated or strangulated lung has a high reported morbidity and mortality.

Extrathoracic Lung Herniation from Blunt Trauma: A Review

David Lo, MD and Mark L. Shapiro, MD

Department of Surgery, Duke University Medical Center, Durham, North Carolina.

Contact: Mark L. Shapiro, MD. E-mail This e-mail address is being protected from spambots. You need JavaScript enabled to view it .

Citation: Lo D, Shapiro M. Extrathoracic lung herniation from blunt trauma. J Surg Radiol. 2010 Jul 1;1(1). Download PDF Extrathoracic Lung Herniation from Blunt Trauma: A Review 7219 Kb Received May 28, 2010. Accepted June 2, 2010. Epub June 2, 2010. Copyright: © 2010 Surgisphere Corporation. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Contents - Introduction - Case Report - Discussion - Conclusion - Acknowledgements - References

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Introduction

Blunt thoracic trauma, of which the majority may be attributed to motor vehicle collisions (MVC), is responsible for over 25% of all trauma-related death.^1-4 Potentially severe injury to major vital structures can occur in the chest, particularly in the presence of multiple rib fractures.⁵ Direct blunt force trauma, or secondary trauma from fractured ribs or crush injury, can lead to life-threatening disruption of the bony skeleton, lungs, pleural membrane, trachea and bronchi, heart, great vessels, esophagus, thoracic duct, and diaphragm. Concomitant injury to other organ systems elsewhere in the body may also be present and further contribute to the overall morbidity and mortality, particularly in patients with fractures of the sternum or scapula.^6-8

Blunt thoracic trauma has been well described as far back as ancient Egypt, where trauma from animals and falls were the major contributors to morbidity and mortality from non-penetrating injuries to the chest.⁹ The Edwin Smith Surgical Papyrus describes blunt thoracic trauma, along with the management of a variety of other forms of injuries experienced by those living in ancient Egypt around 3000 BC.^9,10 The Chirurgia Magna, written in 1365 by De Chauliac, further elucidates the connection between rib fractures, pneumothorax, and hemoptysis; the original relationship between hemoptysis and rib fractures was first documented by Hippocrates in the 5^th century.^11,12

Heimlich valves, chest drainage systems, and tube thoracotomy became more prevalent during the American Civil War, as knowledge of the potentially devastating morbidity and mortality caused by pneumothorax and blunt thoracic trauma were more appreciated.^13,14 With the development of the automobile, the incidence and prevalence of blunt thoracic trauma has risen considerably and MVCs now account for over 75% of all blunt thoracic injuries.^15-17

Case Report

VJ is a 40 year-old unrestrained male driver involved in a high energy motor vehicle collision in which his vehicle was struck head-on by a larger vehicle at an excess of 90 mph. There was significant driver compartment intrusion with severe damage noted to the windshield, dashboard, and steering wheel, requiring prolonged extrication. The patient was minimally responsive at the scene with a reported GCS of 5 (E1V3M1). A King airway was placed for depressed GCS and agonal respiration. Upon arrival to our trauma bay, a level I trauma alert was initiated.

Standard Advanced Trauma Life Support (ATLS) was performed with focus directed at the potential life-threatening issues related to the visible chest contusion and the airway. Given the difficult airway due to significant facial trauma, the anesthesia emergency airway team was activated to assist with an endotracheal intubation, which was achieved successfully. The chest was inspected and auscultated with evidence of bilateral breath sounds, though significantly reduced on the right. However, during simultaneous assessment of the patient’s circulation, he had a manual systolic blood pressure of approximately 60 mmHg and a pulse exceeding 130 bpm with no large bore IV access; a right groin cut down was performed and the great saphenous vein cannulated by a MAC Cordis. Four liters of lactated Ringers were rapidly infused leading to a significant improvement in his hemodynamics.

Bleeding from several facial lacerations and fractures was controlled with pressure. Palpable pulses were appreciated in three out of his four extremities. Nonpalpable pulses were noted in his left lower extremity, secondary to a femur fracture and associated soft tissue edema and hematoma.

The secondary survey was then completed, including a complete physical examination. The patient was found to have an extensive right chest wall deformity and a compressible soft mass palpable under his right breast. Minor abrasions on his extremities, small lacerations on his face, and a marked left thigh deformity were also identified. An orthopedic evaluation at this time confirmed the presence of a comminuted left femur fracture along with a partially shattered right patellar. A portable chest X-ray was completed and revealed asymmetric opacification of the left chest with a suspicion for hemothorax on the right, numerous right-sided rib fractures with adjacent pleural opacity, and a widening of the mediastinum (Figure 1).

Figure 1. Portable chest X-ray in a patient involved in an MVC with right sided rib fractures, hemothorax, and a widened mediastinum. An endotracheal tube is seen with the tip 2 cm from the carina. Pleural opacification on the right side near the rib fractures represents hemothorax. No definite pneumothorax can be appreciated on this limited evaluation.

Once the patient was hemodynamically stable, he was transported to the CT scanner for imaging of his head, face, cervical spine, thoracic spine, lumbar spine, chest, abdomen, and pelvis, and CT angiogram (CTA) of his neck and bilateral lower extremities; the mechanism of his trauma and the nature of his injuries was sufficient indication for such comprehensive imaging in order to rule out injuries to other organs. CT of the face was completed due to the presence of several palpable facial fractures. CTA of the neck was obtained to rule out dissection of the carotid artery in a patient with significant facial and sinus fractures at high risk for an extension injury from a high energy MVC. CTA of the lower extremities was completed to assess potential vascular disruption in the absence of palpable pulses in his left lower extremity and the presence of a complex femur fracture. Catheter-based angiography for altered mental status revealed intimal disruption of the internal carotid artery, leading to the initiation of therapeutic heparin.

Figure 2. A. CT of the brain showing diffuse pneumocephalus (arrows) within the anterior and middle cranial fossa secondary to a displaced fracture of the sphenoid bodies and posterior sphenoid sinuses. B. CT of the face showing a partially displaced right temporal bone fracture (arrows) traveling through the middle ear canal and mastoid process. C. CT of the face showing longitudinal fracture (arrow) of the left external auditory canal into the greater wing of the sphenoid. The ossicles are intact bilaterally. D. Arteriogram of the right common carotid artery showing an eccentric wall irregularity near the petrous portion of the artery (arrows). This may reflect a focal area of intimal injury or even a possible dissection flap.

No intracranial hemorrhage was identified on the CT of the brain; however, pneumocephalus was present secondary to a displaced sphenoid body fracture passing through the sphenoid sinus. Bilateral temporal bone fractures through the petrous portion of the bone proximal to the geniculate ganglion of the facial nerve were present. The external auditory canal was disrupted on the left without injury to the otic capsule (Figure 2).

Most notably, the chest CT revealed a disruption of the anterosuperior chest wall with concomitant complete dislocation of the sternoclavicular joint. The first rib was also avulsed from the sternum on the right side. The anterior and posterior aspect of the first rib, and the lateral aspect of ribs 2 through 9 were fractured on the right, with multiple anterior and lateral fractures seen on ribs 2 through 5 and the subsequent creation of four distinct flail segments. The anterosuperior chest wall/pleural rupture defect was seen with an intercostal herniation of the right lung apex through the defect. A moderate right-sided pneumothorax and extrathoracic air collection with marked right chest wall subcutaneous emphysema in a contained chest cavity were noted (Figure 3). Three-dimensional reconstruction later revealed total disruption of the pectoralis major and minor muscles with subtotal disruption of ribs 3, 4, and 5. No injury to the heart or great vessels was present on imaging (Figure 4).

Figure 3. A. Coronal image from CT of the chest, abdomen, and pelvis. Demonstrated is an extrathoracic hernia of the right lung apex through a large defect in the chest wall. Note the contrast with the relatively normal lung on the left side. B. More anterior image from the same series showing the large extrapleural air collection below the pectoralis major and a pneumothorax on the right.

Figure 4. Three-dimensional reconstruction windowed for bones and muscles. A. Anterior-posterior view demonstrating the large chest wall defect, predominantly over ribs 3 to 5 (circle). The intercostal contents have been displaced and an open defect can be appreciated. B. Right lateral view demonstrating lateral fractures of ribs 1 to 12 (arrows). Additional review of these images permitted visualization of four separate flail segments from ribs 2-5. The dislocation of the clavicle at the sternoclavicular joint and the first rib from the sternum were also evident (uppermost arrow).

CT of the abdomen and pelvis revealed no injuries. Reconstructions of his cervical, thoracic, and lumbar spine confirmed the injuries described above in addition to some gas tracking between L3 and L4. Imaging of the neck was negative for disruption of the carotid artery, while the lower extremity runoff confirmed a displaced fracture through the greater trochanter, a completely displaced comminuted fracture of the mid-femur, and a nondisplaced left femoral condyle fracture (Figure 5). The superficial femoral artery, popliteal artery, and distal lower extremity vessels were patent.

The patient was transported to the surgical ICU, where a right-sided tube thoracostomy was performed and a 36-Fr. chest tube was successfully inserted. Approximately 250 mL of blood immediately returned with further improvement in the patient’s oxygenation and heart rate. Additional plain films of his extremities were completed, revealing a vertical fracture through the left calcaneus, multiple fractures of the metatarsals, a patellar fracture with effusion, an intertrochanteric left hip fracture, and a femoral diaphysis fracture leading to angulation (Figure 5).

Figure 5. There were 11 separate fractures to the patient’s left leg, including three separate fractures to the femur, patellar fracture with dislocation, tibia/fibula fracture, vertical calcaneus fracture, and four metatarsal fractures. A subsequent CT scan of the left lower extremity was obtained to assist with operative planning.

A repeat hematocrit at this point revealed a drop from 42% on arrival to 22%. Concern for bleeding into the left thigh and right chest in the setting of volume dilution and need for ongoing fluid resuscitation led to the transfusion of two units of packed red blood cells. An improvement to 26% was noted on a repeat hematocrit later in the day.

The decision was made to perform a rib plating to treat the flail chest and lung hernia. The rib plating materials became available on hospital day 4 and the patient subsequently underwent an anterior chest wall exposure, titanium rib plating over the flail segments on ribs 2-5, Alloderm bio-prosthetic graft repair of the pleural defect after reduction of the lung hernia, repair of the pectoralis major, tracheostomy, and percutaneous endoscopic gastrostomy (PEG) tube placement.

The chest wall incision was made inferior to the sternal notch and extended to the fourth rib, followed by a circumlinear incision along the inferior mammary fold toward the mid-axillary line. After incision through the subcutaneous tissues, we confirmed that the pectoralis major had been entirely disrupted and had retracted laterally. A significant portion of the pectoralis minor was also disrupted and retracted. A significant defect in the anterior chest wall was appreciated, with total disruption of the first and second interspaces and anterior disruption along the third interspace. Pleural disruption was evident and an intercostal lung hernia was present (Figure 6).

Figure 6. A photograph taken during surgery indicating the sizeable chest wall defect, seen between the two universal plates (white arrowheads), and the destruction of the chest wall above the right-most rib plate (right black arrowhead). The plates are located above the ribs and have not yet been screwed into place. The tissue seen above the right-most plate is lung; there was total disruption of the intercostal muscles and pleura secondary to the tremendous blunt force trauma experienced by this patient. The Allys clamp is located on the remaining stump of the pectoralis major muscle. The remainder had retracted laterally toward the axilla (top of image).

The second and fifth ribs had an anterior and anterolateral fracture, and the fifth rib in particular also had a weakness in the costochondral cartilage proximal to the sternum. 15 cm titanium alloy rib plates were used to reapproximate the ribs and reduce the fractures. Titanium screws were placed medially and laterally into the rib to secure the plate, thereby repairing these two flail segments. The third and fourth ribs had a predominant anterior fracture but a difficult-to-reach lateral fracture. Reduction of only one of these fractures was necessary to correct the flail segment, and 10 cm titanium alloy rib plates were used to complete this repair (Figure 7).

Figure 7. All four rib plates are now screwed in with titanium alloy screws (black arrowheads). The nylon stitches seen inferiorly, laterally, and superiorly (white arrowheads) are anchoring an Alloderm bioprosthetic graft into place to help close the pleural defect. This later sealed the pleural cavity and allowed us to remove the chest tube on postoperative day 7 with successful reinflation of the lung.

Alloderm bioprosthetic graft was used to recreate the pleura and thereby close the significant chest wall defects. A 10 x 8 cm piece of Alloderm was secured inferiorly, laterally, and superiorly and anchored to the ribs with care taken to avoid damage to the neurovascular bundle along the inferior rib margins. A new chest tube was placed into the pleural cavity, one Blake drain placed between the Alloderm and rib margin to prevent the formation of a seroma, and two Blake drains placed into the subcutaneous space. The pectoralis minor and major muscles were reapproximated, along with the remnant of the fascia and subcutaneous tissues. The skin was closed with staples. A tracheostomy and PEG tube placement were completed in the standard manner. The entire operation took about nine hours to complete, and was well-tolerated by the patient.

Two days later, the patient was taken to the operating room by orthopedics for an intramedullary nail placement into the left femur. The patient was eventually extubated, tolerated oral feeds, had progressive improvement in his mental status, and was discharged to home with home health after approximately a month of hospitalization. The patient’s overall prognosis was initially poor given the extent of his injuries in the setting of multisystem trauma (Table 1).

Discussion

Rib Fractures

Rib fractures are the primary marker of additional intrathoracic and intraabdominal injuries. An increase in the number of such fractures leads to a nonlinear increase in overall morbidity and mortality (see Table 2).^18,19 Mortality may range from 3-20% or higher in patients with over six rib fractures, and is primarily related to the nature of the other associated injuries.¹⁹ For example, patients with an Abbreviated Injury Score (AIS) over 45, such as those with avulsion of chest wall tissues or flail chest with more than three affected ribs may have an overall mortality that approaches 20%.^5,19-21 Patients with concomitant intraparenchymal lung hematoma or hilar vessel disruption secondary to blunt thoracic trauma also have a dramatic increase in mortality.²¹

Pneumothorax and Hemothorax

Over 20% of patients with blunt thoracic trauma will present with pneumothorax and/or hemothorax.^22-24 Rib fractures may lead to violation of the pleura to cause pneumothorax. Transection of the intercostal or internal mammary arteries, or laceration of the lung can lead to hemothorax. Tube thoracostomy and/or thoracotomy may be necessary for symptomatic patients to avoid the cardiopulmonary compromise that can occur in tension pneumothorax or severe hemothorax.

Flail Chest

More serious rib fractures can lead to destabilization and paradoxical movement of the chest wall (flail chest), thereby compromising respiratory function and increasing the work of breathing.²⁵ In critically-ill patients with injuries to other body systems, flail chest and subsequent hypoventilation can prolong recovery and contribute to higher morbidity and mortality.^26,27 Hypercarbia and respiratory acidosis may occur secondary to the increase in work of breathing and disruption of normal pulmonary physiology. Compliance of the chest wall is markedly diminished secondary to pain and the disruptive mechanics of multiple rib fractures, leading to a decrease in tidal volume.²⁸ This leads to a marked reduction in alveolar minute ventilation and contributes to hypoxia.^28,29

Lung Herniation

Etiology

An uncommon, but potentially devastating injury is the disruption of the enclosed chest wall (i.e. multiple rib fractures or separation of the costochondral and/or sternoclavicular joints) that leads to herniation of the lung parenchyma and pleural membranes through the thoracic cage. First described in the 16^th century, about 400 cases of lung herniation secondary to thoracic trauma have been reported.^30-57 The incidence of acquired pulmonary hernia has increased with more acute injuries encountered with MVCs, blast trauma, and modern warfare.^33,34,39 Anterior dislocations comprise about 99% of all lung herniations, likely due to the anterior-posterior direction of most injuries encountered during an MVC; the significant reinforcement of the larger latissimus dorsi, trapezius, subscapularis, rhomboids, and periscapular muscles, and the scapula itself makes posterior herniation a rarity.^{30,33-35,37,38,40-57}

Pathophysiology

Anterior lung hernias can be divided into intercostal herniations and parasternal herniations (Figure 8). Both can occur secondary to blunt thoracic trauma, but out of nearly 400 reported lung hernias, only three have been described in the scientific literature since 1960 as being of the parasternal type.^45,49,58 Parasternal hernias occur when there is a disruption between the sternocostal ligament and the costochondral joint, leading to a disruption of the costal cartilages flanking the sternum (Figure 9 [Publisher note: permission not granted to reproduce this image online]). Direct injury to this region typically presents as an avulsion of these cartilages and interruption of the underlying pleura. Due to lateral retraction of the rib cage, the potential for incarceration and strangulation of the lung may be lower than in intercostal hernia.

Figure 8. Proposed algorithm for dealing with anterior and posterior hernias of the lung. Anterior lung hernias can be divided into intercostal and parasternal hernias. Based off a review of more than 400 cases in the literature, we propose that all intercostal hernias be taken to the operating room for a reduction of the hernia and repair of the defect due to the high risk of incarceration and/or strangulation. There are few cases of posterior or parasternal hernias described in the literature (dotted lines), so their overall management remains unclear. Parasternal hernias, due to the larger defect in the chest wall, may be managed conservatively if they remain asymptomatic.

Figure 9. Illustration reviewing the anatomy of the chest wall, including the interchondral and costochondral joints, costal cartilages, and their relationship to the ribs. The costoclavicular ligament connecting the ribs to the clavicle is also shown. Parasternal lung hernias occur between the costochondral joint and sternocostal ligament. Intercostal hernias occur between rib levels and typically involve a substantial defect of the chest wall. Illustration used with permission of Elsevier. July 2010.

Anterior intercostal lung hernias comprise about 98% of all lung hernias. In this instance, blunt force trauma to the anterior chest leads to the fracture of one or more ribs with concomitant disruption of the underlying pleura. Fracture of ribs in more than one location, thereby creating a flail segment, appears to be a component in most cases.^{34-40,43,46,47,51,53-56} A flail segment may provide sufficient disruption of the chest wall to permit a section of lung to herniate through the defect. The nearby proximity of other ribs, some of which may not necessarily have any fractures, has the potential of creating a small opening that can entrap a herniated lung and lead to ischemia of the affected segment.

Posterior herniation of the lung appears to be as rare as parasternal herniations.⁵⁹ Few cases exist in the literature, particularly in a trauma setting.^59-61 The posterior rib cage is significantly better reinforced than the anterior, with bony support for the former provided by the scapula and multiple layers of muscles providing significant reinforcement. The paraspinous muscles near the midline provide significant structural support, while the trapezius and latissimus dorsi provide significant support throughout the back. Near the scapula, the rhomboids, subscapularis, and superior and inferior supraspinatus muscles further reinforce the mechanics. In addition, the direction of most blunt trauma is from anterior to posterior, further limiting the incidence of posterior lung herniation.

Presentation

Lung herniation may be entirely asymptomatic, or present with acute infarction of a devascularized section.^{29, 30,37,45,46,62} Some trends are apparent in the literature: parasternal hernias and anterior hernias through large disruptions of the anterior chest wall are less likely to present with compromise of the lung and/or incarceration.^45,49,58 Small disruptions of the chest wall with only one or two flail segments are more likely to present with incarceration and/or strangulation.^44-46,62

Asymptomatic patients may have no overt subjective or clinical symptoms, other than a potentially palpable defect in the chest wall on physical examination.⁶² Symptomatic patients may present with a pneumothorax, or crepitus along the chest wall.⁴⁶ Pulse oximetry may reveal values below 100% due to a significant pathologic shunt from a partially devascularized or poorly aerated hernia segment. In more severe cases, tension physiology or vascular compromise of the affected segment may occur.^44-46,62

Diagnosis

Many patients with pulmonary hernias are asymptomatic. However, the diagnosis of lung herniation should be suspected in all patients with significant blunt trauma to the chest, particularly when there is known disruption of the parasternal ligaments, fracture of multiple rib segments with or without flail chest, or a significant chest wall defect. Additionally, difficulty with oxygenation, relative hypoxia, and a pneumothorax with extrapleural soft tissue crepitus are indicators of potential hernia.

After completing the standard ATLS survey and appropriately stabilizing the patient, a chest X-ray should be completed as the initial imaging. While a lung hernia may not always be evident on a simple portable film, plain films of the chest do provide key information on the presence and extent of a pneumothorax or any other acute conditions that must be treated prior to more advanced imaging.^35,63

The next step in diagnosis is CT scan of the chest with IV contrast. Rib fractures are associated with visceral injury, particularly when multiple segments are fractured.^5,18-21 A CT scan of the chest will help rule out concomitant damage to the great vessels, the heart, and extravasation from pulmonary lacerations. Further, three-dimensional information regarding the nature of the fractures, the precise location of the lung hernia, and the extent of the chest wall defect can be obtained and used for operative planning. Additional imaging as dictated by the nature and severity of the trauma should also be completed in the stable patient.

Staging / Grading

The chest wall injury scale staging and grading system classifies injuries that can occur to the chest wall and assigns an abbreviated injury score to each injury. These scores can be used in conjunction with the Trauma Injury Severity Score (TRISS; see Table 1) to determine the overall chance of survival following blunt or penetrating injury to the chest.

Based off our review of the literature, we propose a modification to the chest wall injury scale to also include pulmonary hernias (Table 3). Grade I and II injuries have no pulmonary hernia reflecting a small defect and implying insufficient force to cause a significant chest wall disruption. Grade III injuries may have anterior lung hernias in conjunction with several flail segments, typically necessary in order to permit herniation of lung tissue. A significant amount of force is typically present, as indicated by the displaced sternal fracture that may also be present. Grade IV injuries may have a significant chest wall defect, three or more flail segments, or a parasternal lung hernia. As discussed above, we believe a parasternal lung hernia may require substantially more force to disrupt the more malleable costochondral joints at multiple locations on the sternum. A grade V injury implies severe traumatic forces leading to bilateral flail chest and/or a posterior lung hernia. Further, due to the severity of symptoms, an incarcerated lung hernia also qualifies as a grade V injury due to the concomitant morbidity and mortality from pulmonary entrapment. Finally, we classify a strangulated lung hernia as a grade VI injury due to the serious mortality associated with devascularized and necrotic lung.

Management

Morel Lavallée first classified lung hernia according to anatomic location and to etiology in the 1845.⁶⁴ However, to date, no more than 400 cases of pulmonary herniation have been documented. Of the reported cases, approximately 20% are described as congenital and 80% as acquired, of which the majority are traumatic in origin secondary to partial anterior traumatic chest wall defects due to small segmental rib fractures or costochondral dislocation. Herniation of lung parenchyma usually occurs through the intercostal spaces (65% of cases) or in the supraclavicular region (35% of cases). As noted above, most lung hernias secondary to blunt chest trauma arise more often in the anterior chest wall near the sternum. Controversy continues to exist regarding the role of surgical repair versus conservative treatment.

Although surgical intervention for chest wall trauma and instability is not a recent phenomenon, the current literature regarding chest wall stabilization without pulmonary herniation hinges on conservative management by selective intubation, pain control (i.e., epidural or patient-controlled analgesia), and mechanical ventilation. Surgeons of the early 20th century used external traction devices to stabilize the incompetent chest wall after recognizing the high mortality associated with flail or “crushed” chest. With the utilization of positive pressure ventilation in the management of chest wall instability and flail chest gaining popularity in the early 1940’s, external traction became obsolete. In the 1960s and 1970s, however, a minority of surgeons recognized that selected patients with flail chest might still benefit from surgical fixation if a trial of mechanical ventilation failed. The majority of rib and sternal fractures heal without surgical intervention. The debate over the indications, if any, that would support operative repair continues even though many patients with fractures in other body regions benefit from timely open reduction and internal fixation. Nevertheless, two prospective randomized series compared surgery versus conservative management of flail chest found that the surgically repaired group demonstrated significantly fewer days on the ventilator and in the ICU, lower incidence of pneumonia, and better pulmonary function in the absence of severe pulmonary contusions.^65,66 In this review of the literature, the authors seek to address the question as to whether operative repair of chest wall fracture should be more widely applied.

With regard to pulmonary hernia secondary to traumatic chest wall injury, both operative and conservative management have been recommended. A general accepted therapeutic regimen does not exist. Although surgical repair is the usual treatment of choice in most published literature, spontaneous reduction of pulmonary hernias in asymptomatic patients have also been reported. The decision to operate is usually based on the size of the hernia and the possibility of incarceration of the lung given the type of chest wall injury that has occurred. Few case reports, including those in the pediatric literature, have shown that lung hernia, when asymptomatic or small, can be managed conservatively and does not require surgical intervention. However, large lung hernias should be repaired, if it produces constant pain, recurrent infection, respiratory distress, non-viable herniated pulmonary tissue, and potential of heavy exertional activity or increase in intrathoracic pressure.⁶⁷

Of the two types of herniation, the intercostal lung hernias usually protrude through thoracic wall defects secondary to segmental costal or sternal fractures or associated costochondral dislocation. In such cases, the disruption the chest wall and the pleura allow the herniated part of the lung to become entrapped subcutaneously with fractured bones forming the outlet with associated pneumothorax, especially when mechanical ventilation with positive end-expiratory pressure is used which makes conservative management difficult. This could be life-threatening in patients with already diminished respiratory reserve because it abruptly worsens the respiratory condition, or in the case of tension pneumothorax. In the event that a small outlet is formed, intercostal pulmonary hernias may lead to incarceration or strangulation of the lung parenchyma, with resultant hemoptysis and pain at the herniation site. Intercostal hernias are usually symptomatic with considerable threat of complications. Accordingly, surgical repair is routinely recommended. However, in the presence of asymptomatic and uncomplicated intercostal lung hernias, conservative management has been proposed. In these cases, serial clinical and radiographic (chest X-ray and CT scan) follow-up is recommended.

Conclusion

Our patient presented with an intercostal pulmonary hernia. The decision for operative therapy was driven by on the size of the hernia, patient’s symptoms, and the possibility of incarceration of the lung given the extent of chest wall injury that had occurred. Through our literature review, we propose a classification scheme based on extent of injury and on the type of pulmonary hernia to help guide the therapeutic management decision: surgery versus conservative treatment more definitively.

Acknowledgements

We gratefully acknowledge the efforts of Dr. Sapan Desai and Dr. Cynthia Shortell, who made significant contributions to this manuscript. We also appreciate the assistance of Dr. Steven Vaslef and Dr. Danny Jacobs in reviewing an advanced copy of this manuscript.

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