and Thoracic Trauma

Airway disease

Asthma, cystic fibrosis, interstitial emphysema


Pneumocystis jirovecii, tuberculosis, lung abscess, necrotizing pneumonia, HIV, parasites

Connective tissue diseases

Marfan syndrome, Ehlers–Danlos syndrome, juvenile idiopathic arthritis, systemic lupus erythematosus, dermatomyositis, Birt–Hogg–Dube syndrome

Oncological diseases

Lymphoma, pulmonary metastasis

Congenital malformations

Cystic adenomatoid malformation

Congenital lobar emphysema

Foreign body aspiration


Catamenial pneumothorax

Related to menstrual cycle

When considering pediatric thoracic trauma, pneumothorax may occur in up to a third of patients, most of them associated with extrathoracic and intrathoracic injuries, but one third may present only pneumothorax.

Iatrogenic pneumothorax is a consequence of medical procedures, most of them being performed in the emergency room or intensive care units. The most frequently associated procedures are central venous catheterization, thoracentesis, and positive support by mechanical ventilation (Fig. 56.1). The internal jugular vein and subclavian vein catheterization are procedures with a high-risk for developing pneumothorax. The use of ultrasound techniques has reduced the incidence of pneumothorax by central venous catheterization and thoracentesis in adults. Strategies of protective lung ventilation, with tidal volumes limitation and plateau pressures, have enabled the diminishment of the effects of barotrauma secondary to mechanical ventilation.


Fig. 56.1

Iatrogenic Pneumothorax. Anteroposterior chest X-ray of a 2-year-old patient on mechanical ventilation due to convulsive status. It shows right-sided pneumothorax secondary to insertion of a central venous catheter into the internal jugular vein on the same side

Etiology and Pathophysiology

The increase in transpulmonary pressure is the mechanism described in the appearance of spontaneous pneumothorax. This causes alveolar distension, and if the gradient is high enough, alveolar rupture. It can occur secondary to increased work of breathing, a Valsalva maneuver, positive pressure ventilation, and airway obstruction that causes an obstruction ball valve effect, among others.

Once alveolar rupture occurs, air may reach the perivascular space producing pneumomediastinum; if the air pressure increases, it can go to the neck and face (subcutaneous emphysema), advance toward the peritoneal cavity (pneumoperitoneum), or penetrate the pericardium (pneumopericardium) (Fig. 56.2).


Fig. 56.2

Postinfectious Pneumothorax. Anteroposterior chest x-ray of an 8-month-old patient with severe pneumonia due to adenovirus. It shows pneumothorax, pneumomediastinum, pneumopericardium, and subcutaneous emphysema secondary to mechanical ventilation

Spontaneous pneumothorax seems to occur due to changes in the connective tissue that predispose air leaks from the airways into the pleural space. The mechanisms proposed for both primary and secondary pneumothorax are multiple. Frequently, the existence of subpleural bullae, or bullas, has been associated with the production of primary pneumothorax. In studies performed with computerized axial tomography scans, bullas have been detected in between 28% and 100% of the cases that developed a primary pneumothorax and between 70% and 95% in patients who required video-assisted thoracoscopy surgery (VATS) due to this pathology. In newborns, high transpulmonary pressures during the first breaths contribute to the appearance of primary pneumothorax.

The role of tobacco, both in the development of primary and secondary spontaneous pneumothorax , has also been widely analyzed, especially in adults. Prevalence of smoking in children with primary pneumothorax is between 11% and 14%, while in adults is between 24% and 88%. This supports the theory between time exposure to tobacco and changes in connective tissue and/or chronic bronchiolitis that are observed in adult patients and predisposition to pneumothorax.

A familial form of primary spontaneous pneumothorax has been described, related to a mutation in the folliculin gene, located on chromosome 17, which plays a role in the definition of cell shape, size, and movement. This condition has been associated with the Birt–Hogg–Dube syndrome, in which there is a predisposition to the formation of multiple lung cysts that lead to the development of primary spontaneous pneumothorax.

Secondary spontaneous pneumothorax results in systemic or local inflammation of the lung tissue caused by an underlying disease. In children, asthma and cystic fibrosis are the most commonly recognized chronic respiratory diseases. The mechanism involved in asthma is the chronic inflammation of the small airway, which allows creation of the necessary pressure for the air to escape to the pleural space, although secondary spontaneous pneumothorax has been observed in asthma patients without respiratory exacerbation. The mechanism involved in cystic fibrosis is inflammation and obstruction of the distal airway, due to thick secretions that lead to air entrapment in the alveoli. When the alveolar pressure exceeds the interstitial fluid pressure, the air moves to the interstitium, reaching the hilum, and escaping to the mediastinal pleura. Other mechanisms described are rupture of subpleural bulas at the level of the visceral pleura and Pseudomonas sp. or Burkholderia cepacia infections (Figs. 56.3 and 56.4).


Fig. 56.3

Pneumothorax in Chronic Disease. Anteroposterior and lateral chest X-ray of a 14-year-old patient with cystic fibrosis and advanced lung disease. It shows lateral and anterior pneumothorax on the right side


Fig. 56.4

Pneumothorax in Chronic Disease. Chest CAT scan in a patient with cystic fibrosis. It shows left apical pneumothorax and multiple bilateral subpleural bullas

In newborns, the most common causes of secondary spontaneous pneumothorax are meconium aspiration syndrome (MAS) and hyaline membrane disease (HMD).

Clinical Manifestations

Symptoms and signs of pneumothorax vary according to the patient’s age, level of lung collapse and previous lung volumes. Small pneumothoraxes can be asymptomatic and show normal vital signs. Spontaneous pneumothorax occurs mostly at rest, but it may be caused by situations that increase intrathoracic pressure through the Valsalva maneuver (such as lifting objects or stretching).

Acute chest pain and dyspnea are the most frequent symptoms in pediatric spontaneous pneumothorax. Even without treatment, the symptoms resolve in 1–3 days; however, pneumothorax persists in most patients. Physical examination findings depend on the size of the pneumothorax. Small ones may not be detected clinically. Clinical signs include decreased pulmonary sounds, dyspnea, tachycardia, hyperresonance on percussion, and decreased vocal fremitus. In a minority of patients it can present itself as tension pneumothorax, with respiratory distress, hypoxemia, tachycardia, and arterial hypotension. The latter is a respiratory emergency and requires immediate intervention.

Diagnostic Approach

Once the pneumothorax diagnosis is suggested by the presentation and clinical examination, it is confirmed with an anteroposterior and lateral chest X-ray. Expiratory X-rays have been suggested for detecting small pneumothoraxes, although low yield has been demonstrated. Chest X-rays in lateral decubitus position may be useful in emergencies or intensive care units. In critically ill patients, when pneumothorax is suspected, most chest X-rays are taken in supine position. In these cases, the air moves toward an anterior or sometimes medial location adjacent to the mediastinum, sub pulmonary or lateral, and the lateral costophrenic angle can be distended to the caudal direction, which causes the so-called deep sulcus sign, showing asymmetry of the lateral costophrenic recesses due to a greater depth and radiolucency of one of them; the angle can even extend to the hypochondrium and adopt a triangular morphology (Fig. 56.5).


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Nov 7, 2020 | Posted by in Uncategorized | Comments Off on and Thoracic Trauma
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