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ingested should be identified, as this information may be useful in guiding further
management. Clinicians should contact their regional Poison Control Center; this
is often very helpful in determining active ingredients and the degree of concern
for a given substance (see Chapter 102 Toxicologic Emergencies ). The airway
should be assessed and secured if necessary. Stridor should raise concern for
laryngeal edema and orotracheal intubation is indicated in its presence. The
airway should be visualized during this maneuver and tubes should not be passed
blindly. One exception to this is in the case of ingested hydrofluoric acid, which
requires immediate evacuation, best achieved by nasogastric decompression of
the stomach.
Patients presenting to the ED following a caustic ingestion may become
critically ill and should be closely monitored with this in mind. They should
remain nil per os and large-bore intravenous lines should be placed for fluid
administration. Measures to dilute or neutralize the ingested agent may cause
further complications, and activated charcoal and emetic agents should be
avoided. Two view radiographs of the chest and abdomen should be performed
and reviewed carefully for evidence of pneumomediastinum, pneumoperitoneum,
and pleural effusion. These findings raise concern for full-thickness esophageal or
gastric injury.
Patients with suspected esophageal or gastric injury should receive prompt
gastroenterology and/or surgical evaluation, as early endoscopy is the gold
standard for the assessment of caustic injuries and should be performed within the
first 12 to 24 hours after ingestion. Patients with any concerning history or
findings should be admitted to the appropriate inpatient ward for close monitoring
thereafter, and patients with obvious perforation should receive broad-spectrum
antibiotics and will likely require urgent operative management.

PLEURAL DISEASES
The lung is covered by the densely adherent visceral pleura, which moves
smoothly over the parietal pleura of the chest wall. A thin fluid film and the
friction created by apposition of the pleural layers (like two plates of glass held

together by a film of water) contribute to the full expansion of the lung
mechanically. When air, excess fluid, or purulent material comes between the two
layers of the pleura, the lung may collapse or become significantly compressed
and consideration needs to be given to drainage of the pleural space.

Pneumothorax
PEARLS AND PITFALLS


Tension pneumothorax is a clinical diagnosis and does not require a
radiograph for confirmation if there is hemodynamic compromise.
Exercise caution in sedating patients with pneumothoraces or
converting them to positive pressure ventilation since their
hemodynamic status can be tenuous.
Children with even small pneumothoraces may require admission for
observation.
Current Evidence
A pneumothorax is a collection of air in the pleural space. It can occur for shortor long-term duration and can be static or accumulate progressively. Because
atmospheric pressure is greater than intrapleural pressure, any mechanism that
allows even momentary communication between the atmosphere outside the chest
wall or within the tracheobronchial tree can result in a rapid shift of air into the
pleural space. A pneumothorax may occur spontaneously, or it may be the result
of trauma or a therapeutic intervention. Children with no known predisposing
pulmonary conditions are diagnosed as having a primary spontaneous
pneumothorax. Secondary spontaneous pneumothoraces occur in patients with
underlying diseases such as asthma, cystic fibrosis, or structural abnormalities
such as congenital blebs, pneumatoceles, or congenital pulmonary airway
malformations (CPAMs).
Primary spontaneous pneumothoraces are thought to be the result of sudden
increases in transpulmonary pressure resulting in alveolar rupture. Ruptured

alveoli coalesce into blebs, which usually occur apically and can rupture into the
pleural space. Varying amounts of entering air can lead to a small pneumothorax
or complete collapse of the involved lung (Fig. 124.5 ). Increased intrathoracic
pressure associated with the Valsalva maneuver or forceful inhalation has been
associated with spontaneous pneumothorax but there may be no history of any
abnormal respirations. Genetic predisposition seems to play a role in spontaneous.
Secondary spontaneous pneumothoraces often result from different
pathophysiology; these may involve a defect in the visceral pleura caused by
infection, inflammation, connective tissue disorders, or space-occupying lesions.


FIGURE 124.5 Large pneumothorax involving the entire thorax. Atelectatic lung border is
marked by arrows.

Goals of Treatment
Tension pneumothorax is a life-threatening emergency and needs to be evacuated
immediately. Smaller pneumothoraces may be managed conservatively depending


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