Pediatric emergency medicine trisk 4084 4084
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on hemodynamic and respiratory response. Once patients are stabilized, clinicians
should investigate the etiology of the pneumothorax.
Clinical Considerations
Clinical Recognition. The peak incidence of spontaneous pneumathorax occurs in
the adolescent and young adult years with a male predominance. Certain patient
populations are at higher risk. Children who suffer spontaneous pneumothoraces
tend to be tall and thin. Cigarette smoking is a significant risk factor in adults and
illicit drugs such as marijuana and cocaine have also been associated with
pneumothoraces. Patients with collagen vascular disorders such as Marfan
syndrome are also at increased risk. In patients with cystic fibrosis, spontaneous
pneumothorax is the second most common pulmonary complication and usually
occurs in teenage or young adult patients with advanced, diffuse disease. Another
group of children with a high incidence of spontaneous pneumothorax are those
with pulmonary metastases. Children with staphylococcal pneumonia are
especially prone to develop unilateral or bilateral pneumothoraces. Finally, even
though only a very small proportion of asthmatics sustain pneumothoraces, given
that asthma is one of the most common diagnoses encountered in the Pediatric
ED, these patients represent a fair number of cases. Iatrogenic causes of
pneumothorax include thoracentesis or central venous catheter insertion,
bronchoscopy, aggressive positive pressure ventilation (“barotrauma”), or
cardiopulmonary resuscitation. Penetrating and blunt trauma to the chest may
cause injuries to the lung, pleura, esophagus, trachea, and bronchi, all of which
can result in pneumothorax. A more detailed discussion of trauma-related causes
of pneumothorax can be found in Chapter 115 Thoracic Trauma .
A tension pneumothorax requires emphasis because this condition may be fatal
if not recognized early and attended to rapidly. Tension pneumothorax results in
air accumulating in the pleural space with each inspiration. Whether the entry site
of air into the pleural space is through the chest wall, a torn bronchus, or an
injured lung, the physiologic result is that of a one-way valve, whereby air
continues to accumulate in the pleural cavity with inspiration but cannot be
expelled on expiration. This phenomenon continues until the intrathoracic
pressure on the involved side is so high that no further air can enter the pleural
space. This results not only in a complete collapse of the ipsilateral lung but also
in progressive pressure across the mediastinum. This pressure impedes ventilation
of the contralateral lung resulting in further compromise. Hemodynamic
compromise results from rising intrathoracic pressure compromising venous
